Table of Contents

1. Internal Medicine
A. Dennatology .......................................................................................................................... 1
B. Diabetes Mellitus .................................................................................................................... 16
C. Infectious Disease
1. Work-up ........................................................................................................................... 23
2. Osteomyelitis ................................................................................................................... 31
3. Septic Arthritis ................................................................................................................. 34
4. mv .................................................................................................................................. 47
D. Neurology .............................................................................................................................. 49
E. Oncology
1. Bone Tumors .................................................................................................................... 58
2. Soft Tissue Tumors .......................................................................................................... 67
F. Peripheral Vascular Disease
1. Deep Venous Thrombosis and Pulmonary Embolism ..................................................... 69
2. Arterial Disease ................................................................................................................ 71
G. Radiology
1. MRI .................................................................................................................................. 74
2. Bone Scans ....................................................................................................................... 79
3. CT .................................................................................................................................... 83
H. Rheumatic Diseases
1. Gout and CPPD ................................................................................................................ 83
2. Charcot Disease ............................................................................................................... 89
3. Lyme Diesease ................................................................................................................. 92
4. Rheumatoid Arthritis ....................................................................................................... 94
5. Osteoarthritis .................................................................................................................... 100
6. Paget's Disease of Bone ................................................................................................... 101
7. Seronegative Spondyloarthropathies (General) .............................................................. .1 03
2. Pharmacology
A. Antibiotics .............................................................................................................................. 114
B. Antifungals ............................................................................................................................. 120
C. Local Anesthetics ................................................................................................................... 126
D. Steroids .................................................................................................................................. 128
E. General Medications
1. SedativeslHypnotics ......................................................................................................... 133
2. Antipruritics ..................................................................................................................... 134
3. Antiemetics ...................................................................................................................... 13 5
4. Laxatives .......................................................................................................................... 136
5. Antidiarrheals ................................................................................................................... 13 7
F. Analgesics
1. Narcotics .......................................................................................................................... 138
2. NSAIDS .............................. , ............................................................................................ 142
G. Tables and Fonnulas .............................................................................................................. 151
3. Perioperative Management
A. Hospital Charting ................................................ '" ........................ '" ..................................... 159
B. Perioperative Complications .................................................................................................. 163
C. Anemias ................................................................................................................................. 167
D. Blood Transfusions ......................................................................... ; ...................................... 169
E. Pre-and Post -Operati ve Management .................................................................................... 171
4. Principles of Surgery
A. Regional Nerve Blocks .......................................................................................................... 180
B. Bone Healing ......................................................................................................................... 183
C. Wound Healing ...................................................................................................................... 189
D. Principles and Techniques of Fixation ................................................................................... 192
E. Biodegradable Fixation .......................................................................................................... 202
F. Suture Materials ..................................................................................................................... 203
5. Forefoot Surgery
A. Accessory Bones .................................................................................................................... 209
B. Ossification of Bones ............................................................................................................. 211
C. Digital Surgery
1. Anatomy ........................................................................................................................... 211
2. Nail Surgery ..................................................................................................................... 213
3. Hammertoes/ClawtoeslFloating Toes/Overlapping Fifth Toes ....................................... 217
4. Polydactyly ...................................................................................................................... 221
5. Predislocation Syndrome (Lesser MTPJ Instability) ....................................................... 223
D. Lesser Metatarsal Surgery
1. Brachymetatarsia .............................................................................................................. 224
2. Lesser Metatarsal Surgery ................................................................................................ 226
3. Tailor's Bunion ................................................................................................................. 228
4. Joint Implants ................................................................................................................... 230
E. Amputations ........................................................................................................................... 233
F. Intermetatarsal Neuroma ........................................................................................................ 235
G. First Ray Surgery
1. Anatomy of the First Ray .................................................................................................. 239
2. Radiology of the First Ray ................................................................................................ 241
3. Surgery of the First Ray
a. Soft Tissue Procedures ............................................................................................... 245
b. Proximal Phalangeal Osteotomies ............................................................................. 246
c. Distal Metatarsal Osteotomies ................................................................................... 246
d. Proximal Metatarsal Osteotomies .............................................................................. 249
e. Joint Destructive Procedures ...................................................................................... 251
f. Hallux LimituslRigidus .............................................................................................. 258
g. Hallux Varus .............................................................................................................. 262
6. Rearfoot and Ankle Surgery
A. Bone Grafting ......................................................................................................................... 264
B. Inferior Calcaneal Spur and Plantar Fasciitis ........................................................................ .266
C. Endoscopic Plantar Fasciotomy ............................................................................................. 268
D. Metatarsal-Cuneiform Exostosis/Haglund's Deformity ......................................................... 269
E. Equinus .................................................................................................................................. 272
F. Flatfoot ................................................................................................................................... 274
G. Cavus Deformity .................................................................................................................... 279
H. Tarsal Tunnel Syndrome ........................................................................................................ 282
I. Triple Arthrodesis .................................................................................................................. 283
J. Tendon Transfers ................................................................................................................... 284
K. Ankle Surgery
1. Medial Ankle Instability .................................................................................................. 287
2. Lateral Ankle Instability .................................................................................................. 287
3. Dislocating Peroneal Tendons ......................................................................................... 289
4. Arthroscopy ...................................................................................................................... 290
5. Ankle Fusions .................................................................................................................. 292
7. Plastic Surgery
A. Wound Healing ....................................................................................... : .............................. 294
B. Split Thickness Skin Grafts ................................................................................................... 295
C. Skin Flaps .............................................................................................................................. 298
D. Skin Plasties ........................................................................................................................... 299
8. Pediatrics
A. Metatarsus Adductus .............................................................................................................. 302
B. Clubfoot ................................................................................................................................. 31 0
C. Calcaneovalgus ...................................................................................................................... 315
D. Vertical Talus ......................................................................................................................... 317
E. Torsional Abnormalities ........................................................................................................ 320
9. Emergency Medicine
A. Anaphylaxis ........................................................................................................................... 325
B. Chest Pain .............................................................................................................................. 326
C. Electrocardiogram .................................................................................................................. 327
D. Comatose Patient ................................................................................................................... 329
E. Shock ...................................................................................................................................... 330
10. Trauma
A. General Fracture Management. .............................................................................................. 333
B. Digital and Sesamoidal Fractures .......................................................................................... 336
C. Metatarsal Fractures ............................................................................................................... 337
D. Fifth Metatarsal Base Fractures ............................................................................................. 338
E. Midfoot Fractures
1. LisFranc's Fractures ......................................................................................................... 340
10. Rearfoot Fractures (Contined)
F. Rearfoot Fractures
1. CuneifonnlCuboidlNavicular Fractures .......................................................................... .342
2. Talar Fractures ....................................................................... , ......................................... 343
3. Calcaneal Fractures ................................................................... , ...................................... 347
G. Syndesmosis Sprains .............................................................................................................. 351
H. Ankle Fractures ...................................................................................................................... 353
I. Tibial Plafond Fractures (Pilon Fractures) ............................................................................ .356
1. Physeal Fractures ................................................................................................................... 357
K. Open Fractures ....................................................................................................................... 362
L. General Trauma
1. Avascular Necrosis .......................................................................................................... 364
2. Compartment Syndrome .................................................................................................. 364
3. Osteochndritides .............................................................................................................. 366
M. Gunshot Wounds .................................................................................................................... 367
N. Soft Tissue Trauma
1. General Guidelines ........................................................................................................... 368
2. Chronic Regional Pain Syndrome .................................................................................... 370
3. Nerve Injury ..................................................................................................................... 370
O. Tendon and Ligament Trauma
1. Achilles Tendon Ruptures ................................................................................................. 374
2. Ligamentours Ankle Injuries ........................................................................................... 375
P. Vascular Trauma .................................................................................................................... 377
Q. Nail Bed Injuries .................................................................................................................... 377
R. Puncture Wounds ................................................................................................................... 378
S. Bite Wounds ........................................................................................................................... 379
T. Burns ...................................................................................................................................... 379
U. Cold Injuries ........................................................................................................................... 380
INTERNAL MEDICINE
INTERNAL MEDICINE
INTERNAL MEDICINE
INTERNAL MEDICINE
INTERNAL MEDICINE
INTERNAL MEDICINE
INTERNAL MEDICINE
INTERNAL MEDICINE
INTERNAL MEDICINE
INTERNAL MEDICINE
INTERNAL MEDICINE
INTERNAL MEDICINE
INTERNAL MEDICINE
INTERNAL MEDICINE
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INTER.NALTvlEDI ( ' ~ I N 1 ~
DERMATOLOGY
I. SKIN LAYERS
A Epidermis
1. Stratum Corneum: horny, keratin layer
2. Stratum Granulosum: granular layer
3. Stratum Lucidum: seen with thick horny layer (palms & soles)
4. spiny layer
tUIllCti<m as macrophage of the epidermis and process contact
antigens
5. Stratum Genninativum: basal cell layer
I ,.... only cell of the epidermis capable of division. They divide
an ... ~ ~ D l I .... Total turnover time is 28 days (14 days of migration and 14
. = melanin which is t:mnsferred to keratinocytes. Melanin protects
. skin from UV radiation. In whites, found mostly in basal cell layer. In blacks,
found throughout the epidermis.
Langerhans cell
Keratinocyte
Melanocyte
. 6
... . -.
.:. I
Layers of the Epidermis
B. Dermal-Epidermal Junction (Basement Membrnne Zone)
1. Lamina Lucida
2. Lamina Densa
3. Sublamina Densa
C. Dermis
..
Stratum
malpighii
1. Papillary Dermis: immediately beneath epidermis. Thin haphazardly arranged collagen fibers,
abundant ground substance. and delicate elastic fibers.
2. Reticular Dermis: extends to the subcutaneous fat. Coarse elastic fibers and thick collagen
bundles arranged mostly parallel to skin surface.
1
.. .. .
. .
..
II. SKIN STRUCTURES
A Hair Follicle: hair growth proceeds through distinct phases
prolonged gro\\-1h
CatageD.: short lived interphase
T eIogen: final resting phase
Diagramatic
Anatomy ofa
Hair Follicle
Phases ofthe growth cycle of a hair

growing hair ;". ....... ..',

)!-,l ... ..
CATAGEN
ANAGEN
Cells of hair bulb produce hair shaft which is completely keratinized and has no living cells. Hair
color is due to the amount and type of melanin.
B. Eccrme:6laoos: found in highest concentration on palms, soles, and axillae. Secretory coil located
in dermis transmits sweat directly to skin surface for cooling of body.
2
C. found primarily in axillae and anogenital and serves as a scent gland.
De1lVed from hair germ and opens directly into pilosebaceous follicle lather than skin surface.
Become active at puberty.
D. SebaceOOsGIaDds: found on all body parts except palms and soles. Produces oil (sebum) that is
hm,r follicle. This lubricates and protects the hair and skin.
E. AIreCtOresPilorUm: smooth muscle attached to the base of the hair follicle. Contract in response to
cold or fright "Goose Bumps".
nerve
[
P8PiD8fY
DERMIS
reticular
J
r . ( l
; / I. ... , ..
I, ... '_ ....... _ ....
-. ... 1 ... -- 1 -'-.) "'
_.'.1 I ) \i .... 1.' "-
'. J .' '.' :
" -
Diagramatic cross section of the skin and panniculus
m. SKIN LESIONS
A change in color of normal skin without elevation or depression < lern in
diameter. (Freckle)
2. Patch: similar to macule but > I em.
3. Papule: circumscribed solid elevation, I ern in diameter.
4. Wheal: an edematous papule.
5. Nodule: similar to papule but > 1 cm
6. Tumor: similar to nodule but > 2 cm
7. Plagye: an elevation above the skin with a plateau-like surface.
8. Vesicle: elevated lesion < I em, containing clear fluid
9. Bulla: similar to vesicle but> 1 em.
10. Pustule: similar to vesicle but filled with neutrophils and dead bacteria Fluid is white or yellow
(pus).
3
Macula
Papule
Nodule
Pustule
Vesicle
Bulla
Tumor
Wheal
B. Secondary Lesions
1. Scale: an excess of horny material on the skin.
2. Crust: scab consisting of dried blood, serum. or pus.
3. Erosion: scooped out and shallow break. No damage to the dermis.
4. Fissure: linear form of an erosion.
5. IDeer: deep lesion involving the dermis.
1. Eschar: darlc colored, hard to remove crust on ulcer.
Secondary Lesions
Scale
Crust
Excoriation
Fissure
Erosion
Ulcer
Scar
4
C. , The rim is different from the center.
2. Linear: long, thin lesion or smaller lesions in a long, thin line.
3. Target or Iris: concentric rings like an archers taIget.
4. Imbricated: target lesions with normal skin between the abnormal zones. Very rare.
5. Serpiginous: snake-like. Partially circular and undulating
6. Geographic: outline of a continent on a map. .
7. Vegetating: lesion bas a surface that grows outward in uneven, fleshy tufts that feel soft.
8. Venucous: wart-like. Tufts ofprottuding lesion are hyperlreratotic, not soft.
9. Zosteriform: conforming to the distribution of a nerve root
10. PolYCYclic or Circinate: annular lesions grow together; parts of their circles form larger lesion.
11. Grouped: several similar lesions located in close proximity surrounded by a large area of normal
skin.
D.:'

The folloWing aspects should be included in every description:
1. Size
2. Color
3. Consistency: soft, medium, :firm.
4. Configuration: shape or outline of lesion.
5. Margination: sharp or diffuse.
6. Surface ChaIacteristics: smooth or rough.
IV. BACTERIAL INFECTIONS OF THE SKIN
A: Iriiiietimi' .
1 t A SUperficial skin infection due to s. pyogenes & s. aureus, alone or together. Especially
common in children in hot, humid climates.
2. Small. thin-walled vesicles or pustules on an erythematous base rupture to form characteristic
yellow-brown (honey-colored) crusts. Removal of the crusts reveal a superficial. moist base.
Lesions do not ulcerate.
3. Commonly found on the face and extremities.
4. Involved areas may be pruritic. Regional lymph node involvement is common but other
systemic manifestations areI3fe.
5. (Mupirocin, Bacitracin. Neomycin)
. Clindamycin)
B. Ecthyma
1. A superficial skin infection caused by Group A Strep. And or S. aureus.
2. Begins as vesicles or bullae that rupture to form crusts. Removal of crust reveals an ulceration.
Heals with scarring.
3. Lesions are typically erythematous. circular. and multiple. Most commonly involve the lower
e",'tremities.
4. \freatDtent: pml3i1tibiotics (Dj.cloxacillin)
- ! .. '., .,' : ... .
c. !En$meJa!rand,elliiJitist ...., .......
1. When a Strep. infection spreads into and when it
,. involves the deeperdermisand
2. S. Pyogenes releases enzymes to facilitate rapid spre3<iofthe infection through tissue planes and
prevent abscess .erytheIna; develop. The enzymes also produce
systemic manifestations confusion; and hypotension).
3. PredisposiIlg factors: edema, SkID- burns, surgery, or radiation.
4. Most common sites are the face and lower extremities.
5. Erysipelas unlike cellulitis has a shaIply demarcated and elevated border.
6. Both needle aspiration and skin biopsy of the lesion usually fail to yield organisms.
5
7. Causative agents: Usually Strep.
S. aureus- around abscess or open wound
H. influenzae- facial cellulitis in young children (6-36 months).
P. multocida - cat and dog bites.
P. aeruginosa & other gram (-) organisms- common in immunocompromised
hosts.
8. Treatment: Mild- Ora} antibiotics
Severe- Intravenous antibiotics
Signs and sytnptoms JJJaY worsen after therapy is initiated because the antimicrobial rapidly kills
the bacteria causing the release of potent enzymes.
D. Furuncles and Carbuncles
1. A'ftiiU:riCltS is an infection of the hair follicle that produces an inflammatory nodule with a pustule
centeilliiough which the hair emerges.
2. A several adjacent hair follicles and begins as a nodule which enlarges to create
an inflamnlatory mass that discharges pus from multiple follicular orifices. They occur
..E!'edominantly on the back of the neck and is more common in diabetics.
3. (5. the most common cause of both.
Treatment: Small furuncles- moist heat to promote drainage.
Carbuncles & Large furuncles- I&D
E. Folliculitis
1. Inflammation at the opening of the hair follicle. Pathogenesis involves occlusion of the follicular
ostium.
2. Skin lesions are erythematous papules or pustules surrounding the individual hairs most
commonly on the scalp and extremities.
3. Predisposing factors: chemicals, trauma, tight clothing, excessive sweating, occlusive dressings,
immersion in water.
4. :allrilllibis the most common cause. P. aeruginosa is common with inadequate disinfection of
swi11lI1liD.g pools. hot tubs, and whirlpools.
5. A-eatment: Systemic antibiotics.
F. Erythrasma
1. ASiiPerficial infection., usually asymptomatic involving intertriginous areas (groin, axillae, toe
webs). Scaling, fissuring, and maceration of toe weDs (particularly the fourth).
2. Causative organism is Corynebacterium minutissimum (gram positive bacilli). This organism
produces porphyrins so all lesions fluoresce with a or pink "coral" with a Wood's lamp.
3. In other areas the lesions are scaly, brown or red, sharply demarcatedpatcnes.
4. Treatment: Wash with
Whitfield's or topical miconazole

EfYtbromyciil
G. Necrotizing Fasciitis (Hemolytic Streptococcus Gangrene)
1. A fulminating infection of thcf Thrombosis of subcutaneous vessels
occur with gangrene of underlying tissues,
2. Disorder a cut3neous injuiy (puncture wound or laceration) and most commonly
: involves
3. Early in course, affected area becomes red, ho(aDdedematoUs. Between.days 2 and 4, skin"
assumes a Blisters may be present. Process advances to areas of frank
cutaneous gangrene with eventual sloughing.
4. Radiographs usually reveal
5. S. pyogenes but more commonly a mixture of aerobic and anaerobic
._" .. ,
6. Treatment Immediate I&D
Intravenous antibiotics
6
V. CUTANEOUS SIGNS OF BACfERIAL INFECTION
A. Bacterial Endocarditis
1. An infection of native or prosthetic cardiac valves most commonly due to various Strep. & Staph.
2. Infection causes vegetations of fibrin, platelets, blood cells, and organisms to form on the valve.
These vegetations can break off and obstruct small and medium sized vessels.
3. Most patients have a fever and a heart murmur.
4. Four skin signs can occur:
a. Petechiae: small reddish-brown, nonbalancing macules or slightly raised papules most
commonly found on the extremities and mucous membranes. Develops in 10-20010 of the
cases.
b. Splinter Hemorrhages: 1-3mm brown.. red, or black linear discolorations beneath the nail
plate. Occurience is 20%.
c. Osler's Nodes: red or pwple painful nodules on pads of fingers and toes. Present in IO%.
d Janeway's Lesions: nontender, erythematous macules on palms and soles. Occurrence is
15%.
B. Disseminated Gonococcal Infection
I. N. gonofihea is transmitted by seA"Ual activity. Disseminated disease occurs when gonococci
enter the bloodstream usually from an asymptomatic location (urethra, pharynx, rectum).
2. Clinical features:
a. Arthralgias: usually involving several joints (wrists, hands, knees). Septic arthritis can occur.
b. Tenosynovitis: pain, swelling, and erythema along tendon sheaths. Pain on movements.
c. Skin Lesions: begin as tiny red papules or petechiae and become vesicular and pustular with a
gray necrotic center on an erythematous base. Usually located on extremities. Occurrence is
50-70%. Will usually clear in 4 days but new lesions may appear.
3. Treatment: Ceftriaxone
C. Staphvlococcal Scalded Skin Syndrome
1. Infection or mucous membrane colonization with toxin producing S. aureus which causes the
skin to cleave at the granular cell layer.
2. Fever and irritability precede a generalized macular eruption which progresses to diffuse
erythema Vesicles and bullae then develop followed by skin separation. Skin sloughs leaving a
moist, red base that quickly dries.
3 . Vesicular fluid is usually sterile. Nikolsky's sign, shearing of normal epidermis in response to
lateral pressure is present.
4. Occurs mostly in children < 5 years old
5. Treatment: Systemic antibiotics
POSSIble drainage of abscesses
Possible intravenous fluids
VI. VIRAL VESICULAR DISEASES
A Herpes Simplex
1. Charncterized by small, grouped vesicles on a red base.
2. Lesions are painful, self-limited, and usually recurrent Recurrences average 2 a year.
3. Although the lesions can occur anywhere, HSV -1 is most often associated with oral-labial lesions
and HSV-2 with genital lesions.
4. Fever blisters and cold sores are the most common presentation of reactivated HSV infection.
Lesions occur at the oral mucocutaneous border and outer portion of the lips. The vesicles
progress to ulcerated areas that heal without scars.
5. Lesions usually crust ",ithin 4-5 days and completely disappear within 10 days. Vtral shedding
ends when lesions have crusted.
6. PrimaIy infection results most often from direct contact with another infected person.
7. Factors that initiate reactivation: UV radiation, fever, emotional stress, fatigue, trauma,
menstruation. and pregnancy.
8. HSV's contain a linear double stranded DNA molecule.
7
9. Treatment: Acyclovir
Palliative Care: analgesics, antipruritics
B. Varicella (Chickenpox)
1. Highly contagious disease caused by primary infection with varicella-zoster virus, a member of
the herpes family.
2. Experienced by most children, usually in the spring.
3. Characterized by 2 or 3 successive crops of widespread pruritic, small, clear vesicles with pink
halos on the scalp, face, mouth, and trunk.
4. Lesions begin as macules and progress through papules, vesicles, and pustules that crust and heal
usually without scarring. Distinctive feature is that in one area of the body all of the stages of a
lesion can be seen.
5. Incubation is about 14 days. Constitutional signs (fever, chills, myalgias, and arthralgias) may
precede the rash by 1-3 days. Crusting of the lesion usually occurs by day 6 with complete
healing in 1-3 weeks.
6. Disease is acquired by direct contact \\'ith lesions or inhalation of infected airborne droplets.
7. Treatment: Isolation
Antipruritics and antipyretics (Nonsalicylate- aspirin can cause Reye' s Syndrome)
Topical antibiotic ointment
C. Herpes Zoster (Shingles)
1. Characterized by painful, small, grouped vesicles occurring on an inflamed base and usually
localized to 1 or 2 dermatomes without crossing the midline.
2. Vesicles tend to enlarge and become pustular in 3-4 days then erode and crust in 7-10 days.
Patient is contagious until vesicles form crust. Scarring is common.
3. Rash is usually preceded by a prodrome of fever, malaise, headache, and localized pain and
parasthesias lasting 1-4 days. Lymphadenopathy is also common.
4 . Varicella results from primary infection and herpes-zoster represents reactivation of the latent
virus.
5. Treatment: Usually self-limiting and treatment is unnecessary
Acyclovir
Topical Zostrix (Capsaicin) to reduce pain
D. Hand-Foot-And-Mouth Disease
1. A relatively benign, highly contagious, self-limiting disorder usually seen in infants and young
children.
2. Acquired by direct contact and caused most commonly by coxsackie virus A16 or enterovirus 71.
3. After an incubation of 1-3 days, 2-8mm bright, red macules appear on the tongue, hard palate,
and buccal mucosa. These lesions develop into thin-walled gray vesicles surrounded by a red
halo. Healing takes 7-10 days.
4. Cutaneous lesions on the sides and dorsum of the hands, feet, fingers, and toes occur after the oral
lesions. Initially, these lesions appear as red papules with small, thin, gray vesicles appearing in
the center. They are usually oval or linear and run parallel to skin lines and usually resolve in 10-
14 days.
5. Sore throat and mouth, anorexia, malaise, and fever are also common.
6. Treatment: Symptomatic therapy- disease is usually self-limiting.
VII. VIRAL WARTS (VERRUCAE)
Warts are benign growths caused by papilloma viruses of the papovavirus group. They are slow-
growing, DNA-containing viruses that replicate in the nucleus of cells. They can occur on all areas of the
body and are very common on the foot. Warts are housed in the epidermis. Upon debridement, pinpoint
bleeding occurs because the vessels in the dermal papillae are cut. Remember, the dermal papillae have
finger-like projections that interlock with the epidermis.
8
A Verruca Vulgaris
1. Most common form of wart.
2. Seen on fingers, bands, and knees most commonly in children.
3. Firm nodule extnbiting vegetations with thrombosed capillaIy loops. These are the warts blood
supply and are pathognomonic for warts (looks like black dots on the skin).
B. VenucaFlantaris
1. Trauma at pressure sites on plantar surface of the foot allows penetIation by wart virus.
2. Hyperkeratotic plaque with thrombosed capillaries form (may not be noticeable until
debridement).
3. Tender on lateral compression.
c. Mosaic Warts
1. Very large, diffuse group ofwarts with ill-defined boundaries. May look similar to a callous.
2. No pinpoint bleeding upon debridement because the dermal papillae are not pushed superficially.
Lesion has a more horizontal than vertical arrangement.
D. Histology of Warts
1. Large vacuolated "swiss cheese effect" of warty plug.
2. Pyknotic nuclei: small, shrunken cells.
3. Basophilic inclusion bodies surrounded by a peri-nuclear halo.
E. TreaunentofWarts
l. Acid Therapy
a. Best conservative approach.
b. SOOAl Monochloracetic acid (Monocete) is best for sharply cimnnscribed warts.
c. 60% Salicylic acid can also be used alone or in combination with the monochloracetic acid.
d For the mosaic warts, it is better to use the monochlomcetic acid because it doesn't spread out
upon weigbtbearing and destroy surrounding good skin, like the salicylic acid paste does.
e. Treatment takes about 6 weeks, has a success rate of 75-800/0, and is often painful.
2. Surgical Excision: must be down to the level of the superficial fascia.
3. Ctyotherapy (Freezing): very painful and not vety effective.
4. Laser Surgery
F. Molluscum Contagiosum
1. An epidermal DNA poxvirus which resides in the kemtinocyte. The virus multiplies and forms
globules of viml proteins (molluscum or Henderson-Patterson bodies).
2. Historically, the disease was recognized as a highly contagious childhood condition. More
recently, it has become a sexually transmitted disease.
3. Incubation period avemges 4-8 weeks.
4. Individual warts occur as asymptomatic smooth-surfaced, flesh-colored, hemi-spherical papules
seveml millimeters in diameter. In 250/0, these lesions are surrounded by a flat, erythematous
halo. This centml umbilication is pathognomonic.
5. In children, face, extremities, and sometimes trunk are involved. Lesions spontaneously involute
over seveml months. Total course is about 2 years.
6. In adults, inner thighs, pubis, and genetalia are usually involved Resolution is quicker than in
children.
VIII. DERMATOPHYTES AND SUPERFICIAL FUNGI
Dermatophytes are capable of colonizing or infecting kemtinized tissue such as hair, nails, and
stIatum corneum. Infections are caused by members of the genem Microsporum, Trichophyton, and
Epidermophytes. A KOH prepamtion can be performed in order to identify the species by culture.
A Tinea Pedis (Athlete's Foot)
1. T. mentagrophytes, T. rubrum, and E. floccosum are the main causative agents.
9
2. Itching and foul odor are the most common symptoms.
3. Four classifications:
a. Chronic Interdigital: characterized by maceration and dermatitis in the toe webs. Skin is
white with a foul odor.
b. Chronic Papulosquamous Hyperkeratotic: characterized by fine, dry, white scales that may be
patchy or cover the foot in a moccasin-like distribution. Usually occurs bilaterally and is
associated with T. rubrum
c. Vesicular or Subacute: characterized by tense vesicles and bullae containing a serous fluid.
Usually associated with T. mentagrophytes and is the form most responsible for an id reaction
on other parts of the body.
d. Acute Ulcerative: a rapid spread of an eczematoid vesiculopustular process. Secondary
bacterial infection can occur and the vesicular fluid turns purulent. Can involve large areas of
the foot and can appear with cellulitis,. lymphangitis, and lymphadenitis.
4. Treatment: Appropriate hygiene- avoid going barefoot, wash and dry feet daily.
B. Tinea Capitis
Topical imidazole agents (usually for 2-4 weeks)
-Clotrimazole (Lotrimin)
-Miconazole (Micatin)
-Econazole (Spectazole)
-Ketoconazole (Nizoral)
-Sulconazole (Exelderm)
-Oxiconazole (Oxistat)
1. Scalp ringworm caused by T. tonsurallS.
2. Non-inflammatory type is characterized by multiple scaly lesions and areas of broken hair.
e. Tinea Barbae
1. Commonly referred to as barber's itch and is most often seen in farm workers in contact nith
animals.
2. The superficial form appears with scaling, erythema, and broken hair associated with T. rubrum
and T. violaceum.
3. In deeper form&. perifollicular pustules, crusting, and exudates are seen associated with T.
verrucosum and T. mentagrophytes.
D. Tinea Faciale
I. Presents as erythematous, scaling, pruritic lesions on the face and neck
2. Causative organisms are T. rubrum, T. mentagroph}1eS, and M. canis.
E. Tinea Corporis
1. Characterized by 1 or more circular, sharply circumscribed, slightly erythematous, dry, scaly
patches 'with progressive central clearing on the trunk and limbs.
2. T. rubrum, and T. mentagrophytes are most commonly involved
3. Majocchi's granuloma consists of perifollicular and granulomatous, slightly elevated nodules
occurring on the lower leg.
F. Tinea Cruris
1. Commonly known as "jock itch".
2. Appears as well demarcated, scaling, circinate lesions with erythematous raised borders involving
the groin and intertriginous areas.
3. T. rubrum, T. mentagrophytes, and E. floccosum are most common
G. Tinea Versicolor
1. Characterized by finely scaling, guttate or nummular patches occurring on the upper trunk and
extending onto the neck and arms.
2. Caused by dimorphic yeast, Pityrosporum orbiculare.
H. Tinea Manum
1. Clinical presentation ranges from mild, asymptomatic scaling to discrete vesiculopustular plaques
and patches .
2. Involvement of one hand and both feet is common and unexplainable.
3. T. rubrumis most common.
L Tinea Nigra
10
1. A superficial infection of the stratum corneum caused by Exophiala wernecki. Usually found in
tropical and subtropical areas.
2. An asymptomatic, nonscaling, dark brown to black lesion on the palms, soles, and fingers.
IX. SUBCUTANEOUS AND DEEP FUNGAL INFECTIONS
A Mycetoma <Madura Foot)
1. An infection caused by a wide variety of agents (bacteria and fungi found in soil and plants)
resulting in an indolent condition consisting of a triad of tumefaction, draining sinuses, and grains
(microcolonies of organisms).
2. Infection begins as an initial implantation that forms a locally invasive indolent tumor-like mass.
The mass slowly enlarges and sinus tracts form, and edema and induration lead to scarring into a
wooden fimmess in parts of the tissue. New nodules fonn and more sinus tracts develop and
destruction of the tissue and bone occur.
3. Treatment: 1&D of abscess and surgical debridement
Antimicrobial therapy depending on the causative organism
X. PAPULOSQUAMOUS DISEASES
A Psoriasis
1. A chronic, inflammatory rash with increased and rapid epidennal proliferation resulting in
accumulation of stratum corneum.
2. Classic lesion is well-circumscribed , erythematous plaque with a dry, silvery scale appearing on
extensor surfaces of the limbs. Lesions are bilateral and symmetrical in distribution.
3. Lesion exhibits the Koebner phenomenon which means replication of skin in an area of pressure
due to scratching.
4. Removal of the scales results in pinpoint bleeding known as the Auspitz' sign.
5. Nails are involved in 50010 of the cases and present with pitted depressions and onycholysis.
6. Different types include: plaque, guttate, erythrodermic, pustular, and arthritic.
7. Histopathology: Epidermis- hyperkeratosis and acanthosis with elongated rete ridges. Also see
Munroe's
abscesses (a collection ofneutrophils in the stratum corneum).
Dermis- capillary proliferation with perivascular inflammation.
8. Treatment: Lubricants
Tars
Anthralin (hydrocarbon ointment)
Topical corticosteroids
Phototherapy- Ultraviolet B (UVB) radiation
Oral psoralen plus ultraviolet A (pUV A)
Psoralen is a drug derived from plants which when activated by long wave UV
light is phototoxic and melanogenic. The UV light causes binding of the
psoralen to DNA thus inhibiting DNA production; therefore, inhibiting cellular
production.
Systemic therapy- methotrexate, retinoids, cyclosporin, hydroxyurea vitamin D3
B. Reiter's
I. A seronegative asymmetric arthropathy. Syndrome consists of conjunctivitis, urethritis, and
arthritis.
2. Disease has a strong male preponderance (9:1) and most patients have an HLA-B27 haplotype.
3. Classic lesion is termed keratoderma blenorrhagicum. Very similar to pustular psoriasis on the
palmer and plantar skin but lesions of Reiter's have a tbicklayer of keratin overlying the pustules.
4. Penis may also be involved with moist, red plaques.
5. Treatment: NSAlD's
Immunosuppressive agents
11
C. Lichen Planus
1. An inflammatory dermatitis of unknown etiology that is primarily papular in origin.
2. Violaceous, polygonal, flaHopped, pruritic papules displaying a lace-like pattern of white lines
on their surfaces (Wickham's striae).
3. Lesions appear on flexor surfaces of the wrists and foreanns, lumbar area, penis, ankles, anterior
aspects of the legs, and dorsum of the hands. Lesions display the Koebner phenomenon.
4. Mucous membranes are affected in over 50%.
5. Nails are involved in about 1O%. Most common changes are thinning and longitudinal ridging of
the nail plate and onycholysis.
6. Variants include: annular, linear, hypertrophic, atrophic, bullous, ulcerative or erosive, lupus
erythematous overlap, pemphigoides, and planopilaris or follicular.
7. Histopathology: Epidermis- hyperkeratosis "With degeneration of the basal ceUlayer. Damaged
cells release melanin. Acanthosis resulting in a "sawtooth" appearance. Clusters of eosinophilic
bodies result from keratinocyte degeneration and are seen along the epidermal-dermal junction.
Dermis- band-like lymphOCytic infiltrate in upper dermis.
8 Treatment: Oral, intralesional, and topical corticosteroids
Antihistamines
Phototherapy
Systemic retinoid therapy
Dapsone
D. Pitvriasis Rosea
1. Acute, self-limiting, inflammatory disease of unknown but suspected viral etiology affecting
children and young adults with the highest incidence in the winter.
2. Lesions are found to oval, eI}1hematous papules and plaques with an inncr collarette of scale.
The center usually shows some clearing.
3. First cutaneous manifestation is a "herald patch" usually on the trunk that begins as a small
erythematous papule and rapidly a round to oval patch 2-10 cm in diameter. Lesions are
distributed along lines of cleavage on the trunk and proximal extremities to produce a "Christmas
tree" pattern.
4. Treatment: Topical corticosteroids
Ultraviolet light
E. Pityriasis Rubra Pilaris
1. Characterized by hyperkeratotic follicular papules, salmon colored scaly plaques, and palmer-
plantar keratoderma.
2. Striking feature is "island sparing" - normal appearing skin within sheets of erythema.
3. Lesions usually appear first on the upper half of the body, often in the scalp, and spread caudally.
4. Plantar lesions can extend up the sides of the feet to produce a sharply demarcated "keratodermic
sanda!". Fissuring is common.
5. Treatment: Topical steroids, emollients, andkeratolytics
Systemic retinoids
Methotrexate
Oral Vitamin A
XI. ECZEMATOUS DISEASES
Eczema is a Greek word meaning "boiling over". We use it as a general term. The hallmark of all of
the eczemas is the presence of itching. All conditions can appear in the acute, subacute, or chronic
phases. Treatment of eczema of unknown etiology is usually topical corticosteroids.
A. Atopic Dermatitis
1. A genetic disorder sometimes associated with ast:hJ:na, allergic rhinitis, or hay fever.
2. Frequently immunoglobulin E is increased in the serum.
3. Skin disease usually starts in infancy and many children experience resolution after 2-6 years.
12
4. 3 phases are: infantile, childhood, and adolescent or adult
5. Sites commonly affected are: face, scalp, diaper areas and buttocks, hands, antecubital and
popliteal fossae.
6. Aggravating factors: extreme temperature changes, sweating, bacteria, soaps, and detergents.
B. Contact Dermatitis
1. Allergic Contact Dermatitis
a. A cell-mediated, type IV, delayed immunologic reaction.
b. 2 phases: First is sensitization in which the patient becomes allergic to the chemical. The
second occurs with continued or repeat exposure to the allergen.
c. Eruptions usually appear as itchy feet, generally of a chronic nature secondary to shoegear
breaking down and putting the feet into contact with various components of the shoes.
Dorsum of the foot is the most common area.
d 2 common allergens in shoes are mercaptobenzothiazole and tetramethylthiuratll, which are
used in rubber adhesives. Phenolic resins, leather tanning agents, and formaldehyde have also
been identified as allergens.
e. A diagnosis can be confirmed with a patch test by cutting out a small sample of the shoe and
placing it on the patients back. A shoe contact dermatitis kit is also available.
2. Irritant Contact Dermatitis
a. Represents 80% of contact dermatoses and results from non-immunologic physical or
chemical damage to the skin.
b. Skin reactions may be acute, as with exposure to acids. or chronic, due to repeated damage
from a weaker agent.
C. Seborrheic Dermatitis
1. Usually occurs at 20-40 years of age and persists for life.
2. Occurs in hairy areas and clinically consists of mild erythema covered with a greasy scale.
3. Most common forms:
a. Scalp seborrhea can mimic psoriasis but is less scaly, more diffuse, and more easily managed
b. Facial seborrhea appears with a mild erythema and greasy scale in the paranasal area.
c. Truncal seborrhea occurs as small circinate or petaloid patches in the central chest.
d Flexmal seborrhea occurs in the axillae, groin, and inframammary areas and is similar to the
scalp lesions.
4. Patients can have 1 or several forms simultaneously.
5. Etiology is unknown but evidence favors Pityrosporum ovale.
6. Treatment: Keratolytic shampoos- Zinc pyrithione (Sebulon, Danex, Head and Shoulders)
Selenium sulfide suspension (Selsun Blue)
Salcylic acid and sulfur (Sebulex)
Topical steroids
Tar preparations
Antifungals (Ketaconazole)
D. Stasis Dermatitis
1. Characterized by erythema, dependent edema, and hemosiderin pigmentation of the distal lower
legs, particularly medially.
2. Most commonly occurs as a consequence of phlebitis or varicose veins, which lead to venous
insufficiency, venous hypertension, and eventually stasis dermatitis.
3. Stasis ulcers are a complication of uncontrolled disease.
4. Treatment: Control the venous insufficiency- support stockings, elevation, diuretics
E. Dvshydrosis (pompholyx)
1. A non-inflammatory, idiopathic, recurrent vesicular eruption on the palms and soles.
13
2. ChaIacterized by symmetrical, tense, deep-seated, pruritic, burning vesicles, 1-5 mm in diameter,
on the sides of the digits and the volar aspects of the palms and soles. Vesicles may coalesce to
form bullae or evolve into sterile pustules that dry and shrink or rupture.
3. The cause is unknown but the patient is usually a type A personality; thus a psychogenic basis is a
possibility. Disorder is exacerbated with stress.
4. Treatment: Usually responds very poorly to all therapy other than systemic steroids
Topical corticosteroids and antihistamines
Cool water soaks
XII. CUTANEOUS DRUG REACTIONS
A. En1hema Multiforme
1. Syndrome characterized clinically by acute, self-limited, but often recurrent episodes and by
symmetrically distributed round, fixed skin lesions.
2. Primary lesion is a round, erythematous papule. Over hours to days the papules evolve in several
different patterns.
3. Lesions may enlarge and coalesce to produce, small plaques or may evolve with concentric zones
to reveal target lesions. Outer zone of target lesion is erythematous and central portion is white,
yellow, or gray.
4. In 25%, the lesions are limited to the oral cavity.
5. Treatment: Topical corticosteroids
Antihistamines
B. En1hema Multiforme Major (Stevens-Johnson Syndrome)
1. Usually follows a 1-14 day prodrome offever, malaise, cough, sore throat, arthralgia, and
myalgia.
2. Inflammatory bullous lesions suddenly appear on the mucous membranes which are
characteristically covered by hemorrhagic crusts.
3. Bilateral purulent conjunctivitis appears. Nares, pharynx, larynx, and lower respiratory tract can
be involved.
4. Skin involvement varies from urticarial to target or bullous lesions.
5. Complications include: blindness, renal failure, pneumonia, scarring of the skin, and nail loss.
6. Treatment: Large doses of systemic steroids
Mortality of patients not treated is 5-15%
C. Erythema Nodosum
1. Most often presents with the sudden onset of ill-defined, tender, erythematous nodnles or plaques
distributed symmetrically over the anterior lower legs.
2. Initially lesions are red, slightly elevated, and 1-5 em in diameter with diffuse borders. Nodnles
evolve through color changes of a bruise from red to blue to yellow with a green tint
3. Nodules may last between 1-2 weeks and usually resolve without scarring. Entire episode
subsides over a 3-6 week period.
4. Fever, malaise, and arthralgias may precede lesions.
5. Females are affected more than males (9:1).
6. Etiologic factors include: infectious agents, sarcoidosis, inflammatory bowel disease, and drugs
such as sulfonamides and oral contraceptives.
7. Treatment: NSAID's
Oral potassium iodide
Steroids are not that effective
XIII. GRANULOMATOUS DISEASES
A. Necrobiosis Liooidica Diabeticorum
1. ChaIacterized by several, sharply but irregularly demarcated patches, usually on the shins.
14
2. Indmated patches appear yellowish in center and violaceous at the periphery.
3. About 75% are females and about 213 have diabetes mellitus.
4. Histopathology: Degeneration or necrobiosis of collagen with polymorphic cellular infiltrates
composed
of lymphoid cells, fibroblasts, and histiocytes.
5. Treatment: Topical corticosteroids
Intralesional steroid injection
B. Gnmuloma Annulare
1. A benign, usually self-limiting disorder of unknown etiology.
2. Occurs predominantly in children and young adults. Affects women more commonly than men
3. 4 clinical types: localized, generalized, perforating, and subcutaneous (deep).
4. Localized is the most common and presents with a limited number of asymptomatic, flesh-
colored to red-purple, 1-5 mm. dermal papules, often arranged in an arciform or annular pattern.
5. Lesions found most commonly on the hands and feet. Involvement of the arms, legs, trunk, and
face may also occur.
6. Histopathology: Focal degeneration of collagen with an intlammatoty infiltrate and fibrosis
within the
dermis.
7. Treatment: Spontaneous resolution occurs in 50% within 2 years.
XlV. NAIL DISORDERS
A Psoriasis: subungual keratosis, nail pitting, onycholysis, discoloration (oil spots).
B. Lichen Planus: longitudinal grooving and ridging, shedding of nail plate and atrophy of nail bed,
ptetygium
formation, subungual hyperpigmentation
C. Darier's Disease: longitudinal subungual red and white streaks, distal wedge-shaped subungual
keratoses.
D. Alopecia Areata: pitted (stripped) nails.
E. Onycholysis: separation of nail plate from nail bed- psoriasis, hypothyroidism, hyperthyroidism,
pregnancy,
moniliasis, tetracyclines, artificial nails.
F. Clubbing: biliary cinhosis, chronic respiratory illnesses, congenital heart defects, familial (Increase
in
Lovibond's angle > 180 degreesJ.
G. Sooon Nails (Koilonychia): faulty iron metabolism, familial, inflammatoty skin diseases, idiopathic.
H. Onychogryphosis: hypertrophy and curvature- trawna or circulatoty disorder.
I. AnOnychia: Stevens-Johnson syndrome, epidermolysis bullosa, absence of nails.
J. Beau's Lines: transverse furrows- systemic illness, trawna.
K. Onychoschizia: splitting of distal nail plate into layers, dehydration of nail plate.
L. Half and Half Nails: proximal white, distal red- renal disease.
M. Muehrcke's Lines: narrow, white, transverse bands occurring in pairs- hypoalbuminemia.
N. Mee's Lines: white transverse lines, single or multiple- arsenic poisoning.
o. Onychorrhexis: brightness with breakage of nail.
P. Terry's Syndrome: distal 1-2 mm normal pink color, proximal end has white appearance- cirrhosis.
Q. Racquet Nails: inherited disorder.
R Median Nail Dystrophy: inverted fir tree- trauma.
S. Leukonychia: white discoloration of nail plate, bed, or matrix.
T. Yellow Nail Syndrome: pulmonaty disease and lymphedema.
15
DIABETES MELLITUS
Pathogenesis
Group of disorders characterized by glucose intolerance. Insulin produced by beta cells in the pancreas
decreases blood glucose by inhtbiting glycogen breakdown and facilitates entry of glucose into the tissues.
When tissues fail to use glucose, hyperglycemia results. Diabetes affects 2-5% of the population in the U.S.
Types
a. Type 1 (IDDM) Insulin dependent diabetes was formerly called juvenile-onset diabetes but
now is referred to as type I because it is not restricted to the juvenile age group. It is
characterized by abrupt onset, polyuria, polydipsia, polyphagia, and often rapid weight loss.
b. Type 11 (NIDDM) Non-insulin dependent diabetes was referred to as adult onset. Symptoms
are often less pronounced than type 1. Patients with NIDDM present with thirst, pruritus and
fatigue. Obesity is present in 60-90% of these patients.
c. Secondary
1. Pancreatic disease: hemochromatosis, pancreatic deficiency, pancreatectomy
2. Hormonal: Cushing's syndrome, acromegaly, pheochromocytoma
3. Drug-induced: thiazides, diuretics, steroids, phenytoin
4. Genetic syndromes: lipodystrophy, myotonic dystrophy, ataxia, telangiectasia
d. Impaired glucose tolerance (lGT) , also known as chemical, latent, borderline,or subclinical
e. Gestational: glucose intolerance with onset during pregnancy
Distinguishing Features of DM
Features
age onset
prevalence
Ketosis
weight
complication
genetics:HLA
monozygotic twins
100%
islet cell antibody
insulin secretion
hyperinsulinism
insulin treatment
required
insulin resistance
defect
Diagnosis
IDDM
<30
.2-.3%
common
nonnaI
frequent
yes
40-50010
yes
severe deficiency
always
occasional:poor control excess antibody
a. Classic symptoms: polydipsia, polyphagia, polyuria
NIDDM
>30
2-4%
rare
obese (80%)
frequent
no
Concord near
no
moderate to
usually not
usual: receptor
b. Hypergylcemia: fasting plasma glucose level greater than l40mgldl on more than one
occasion
c. Oral glucose tolerance test: 75g glucose dose dissolved in 300ml water after overnight fast;
plasma glucose above 200mgldl at both 2 hrs and at least one other time between zero and 2
hrs.
d Hemoglobin Alc: (gylcosylated hemoglobin) Concentration in normal individuals 3-6%;
patients with DM have two-to threefold elevation. Is a rough reflection of the mean level of
circulating glucose for the previous 2 to 3 months (life of RBC-120 days).
16
Treatment
a. Diet : is the cornerstone of treatment Objectives include providing nutrition with a balance of
protein, fat and carbohydrates and to normalize weight
b. Oral Hypogylcemics: Sulfonylureas are recommended for patients with symptomatic NIDDM
who cannot be controlled by diet alone and in whom an addition of insulin is impractical or
unacceptable. (For a detailed discussion see pbarmacology section.)
c. Insulin : Used primarily for the type I (lDDM) diabetic who is hypoinsulinemic and prone to
ketosis. Also can be provided for type II diabetic who is not compliant with diet.(see
pharmacology section for details)
Complications
A Acute:
I.Ketoacidosis: precipitating factors- infection. omission of insulin. new onset diabetes
a. chamc. by pH <7.2 .hyperglycemia, hyperventilation. inc. anion gap. hyponatremia,
hyperkalemia, inc. BUNtCr ketones in blood and urine
b. absolute insulin deficiency leads to inc. lypolysis, inc. fatty acids in the blood and ketosis
c. Dx.:polyuria, polydypsia, nausea, vomiting. abdpain, dehydration,. altered mental status,
acetone halitosis
d. Tx:
-fluids to restore intravascular volume with monitoring of cardiac and renal function
-bicarbonate ifDKA associated with shock/coma, arterial pH of <7.1, severe hyperkalemia
-K replacement (monitor ECG to ensure no hyperkalemia)
-insulin, monitor electrolytes
-phosphate (insulin inc. cellular uptake of phosphate and dec. plasma levels)
2.Hyperosmolar Nonketotic Hyperglycemic Coma
a. glucose>600mgldl without ketosis-see in type II more common
b. Signs: lethargy ,confusion. seizures, coma, dehydration. hypertension, polyuria, polydypsia
c. Tx: fluid replacement, insulin, electrolytes( esp. K + and phosphate)
3.Infection: at increased risk due to triopathy
A) neuropathy, B) vascular insufficiency,and C) immunopathy
a. immune status decreased due to granulocyte depletion and defective phagocyte ingestion
b. nephropathy can compromise antibiosis
c. Infections can include epidermophytosis, ascending un pyelonephritis, septicemia and
gas infections
d (see section on diabetic foot infections for details)
4.Hypoglycemia-plasma glucose <50mgldl
B. Chronic:
a. due to I )IDDM -imbalance btw.insulin and glucose,2)reactive-insulin secretion vs.
absorption of food 3)insulin overproduction-pancreatic tumor or alcohol ingestion
b. Dx.: Whipple's triad-I)risk of hypoglycemia,2)BS 40mgldl or less3)immediate
recurrence following admin. of glucose
c. Tx.: related to cause(ie insulinoma-surgery) adjustment of dosage and patient education
d somogyi phenomenon: hypoglycemia results in rebound hyperglycemia-may be due to
excess secretion of counterreguJatory hormones(glucagon and epinephrine)
I.Atherosclerosis
a. Possibly due to oxidation of LDL
b. macroangiopathy- plaque occluding larger vessels(Ml, HfN, CV A)
c. microangioapathy-increase basement membrane thickening(neuropathy, nephropathy,
retinopathy)
d. high incidence of lower extremity disease-ant tib. Post.tib and peronael arteries usually
affected(see PVD section)
2.Retinopathy
a. increased capillary permeability
b. microaneurysms
c. hemorrhages
d retinal detachment
17
3.Nephropathy
a.Diffuse:
1. widening of glomerular basement membrane
2. mesangial cell thickening
b.Nodular:
1. accumulation of PAS-positive material at the glomerular tufts(Kimmelsteil-Wilson
lesion)
2. hylanization of afferent glomerular arterioles
c.Tx:
1. strict control of blood sugar
2. control HTN
3. decrease protein in diet
4.Neuropathy
Anatomic Classification
structure
signs/symptoms
nerve root
pain,dermatome sensory loss
mixed nerve
vascular
pain, weakness, sen. loss,
reflex change
nerve terminal
sen loss(stocking-glove)
absent reflex mild weakness,
nerve tenninal(muscle)
anterior thigh pain with
weakness
sympathetic ganglion
postural hypotension,
impotence,gastrophy,
anhydrosis,arhtropathy
a. Pathogenic mechanisms
disorder
radiculopathy
mononeuropathy
polyneuropathy
amyotrophy
autonomic neuropathy
etiology
probably vascular
probably
metabolic
unknown
unknown
1. sorbitol pathway-schwann cell hyperosmolality due to sorbitol excess, swelling, and
destruction
2. occlusion ofvasa nervorum
3. decreased nerve myoinositol
4. decreased nerve conduction
5. altered myelin synthesis and deficient repair
6. motor and sensory neuropathy
7. autonomic disorders
8. neurotrophic factors:nerve growth factors
2. Treatment:
1. antidepressants-amitriptyline 10-25mg qd, nortriptyline 300mg tid
2.
3. topical-<:apsaicin
4. analgesics/sedatives
18
Diabetic Charcot Foot:
a. pathophysiology:
1 newopathy: loss of pain perception. proprioception and sympathetic activity
2.trauma: increased weight bearing promotes joint degenerntion and subluxation
b. stages:
l.development: destructive phase. joint laxity, subluxation.osteochondral fragmentation
2.colescence: absorption of debris and fusion of larger fragments to adjacent bone
3.reconstruction: revascularization and remodeling of bone and fragments
c. clinical features:
vascular neuropathic
bounding pulse
erythema
swelling
warmth
absent/diminished
pain
proprioception
vibrntion
deep tendon reflexes
d. treatment:
I. casting/immobilization
2. accommodative foot gear
3. reconstructive surgery
Diabetic Foot Ulcers:
skeletal
rocker bottom deformity
medial tarsal subluxation
digital subluxation
crepitus
hypermobility
I. abnormal pressure distribution secondary to newopathy
-accentuated by faulty biomechanicslbone distortion
-poorly fitted shoes
2. secondary to cuts or puncture wounds from foreign bodies
3. high infection rnte often with multiple organisms
4. prevention is cornerstone of tx.
-adequate shoe gear
-proper hygiene
-control of blood sugar
-firequentinspection
Diabetes and Surgery:
1. good metabolic balance prior to surgery
-normal vital signs/electrolytes
-blood glucose btw. 100 and 200 mgtdl
-renal and hepatic status
-preopEKG
cutaneous
ulcer
hyperkeratosis
infection
hyperhydrosis
2. prefernble to admit patient to hospital the day before surgery to adjust insulin dose
3. glucose measurements several hrs before and after surgery
Management during Minor Procedures
I. those patients undergoing local anesthesia
2. will be given oral nutrition immediately postop.
3. no change in diet, oral hypogycemic or insulin regimen
4. monitor glucose 1 hour before and 1 hour after surgery
Management during Major Procedures
l.Preop. eval
-type I vs type II
-type of therapy (diet, oral , insulin)
19
Pharmacology:
-diabetic control
-evaluate for any systemic complications
-admit to hospital a day prior to surgery or 2-3 days if poor control
-preop labs (ECG, UA, Chemistry, CBC, glycolsylated hemoglobin)
-schedule early in day-better equilibrium btw insulin dose and caloric intake
-if diet controlled and stable, fasting blood glucose on the morning of surgery
-if oral hypogycemics, discontinue the morning before the day of surgery
-if on insulin and controlled 250mgfdl), give liz the usual dose on morning of
surgery
2. Intraoperative and Postoperative Management
a. Important considerations
-blood glucose should be between lOO-200mgfdl
-frequent intraop glucose testing to avoid iatrogenic hypoglycemia
b. Methods of management
preop start IV with l000ml5% dextrose (D5W) \\'ith 40mEqIL ofKCL run
at lOOmllhr (need to dec. rate in pts. with CHF or renal failure)
administer liz of usual morning insulin,glucose test immediately after
surgery
continue IV fluids at 80m11hr, monitor blood every 4 to 6 hr with
appropriate
regular insulin coverage
-or-
low dose continuous regular insulin
IV solution consist of 100 U of regular insulin added to 500 ml of .5%
normal saline solution
Glucose level:
following surgery, hydration status and glucose most important info.
diet controlled, glucose <300mgfdl can manage on diet alone 12 to 24
hrs after surgery
oral hypogycemics, if glucose under control, can start oral agent the day
following surgery
taking insulin, requires frequent (every 4 hrs for the first 12 postop hrs)
glucose
testing- insulin given only if patients glucose values> 300mgfdl -only
regular
insulin is to be used at intervals of 4 to 6 hrs.
Insulin: a source- beef, pork, human
admin. - is a protein structure usually given subcutaneously
adverse IX. - mainly sx. of hypoglycemia
-tachycardia
<anfusion
-vertigo
-diaphoresis
b. preparations: 1. Rapid acting
-crystalline zinc or regular-can give subq or IV
-semilente-only given subq
2.Intennediate
-isophane or NPH(neutral protamine hagedom)-only subq
20
3. Prolonged
Protamine zinc-max effect in 24hr
ultralente-given with semilente to form lente an intermediate
acting form
4.Humalog 70/30
Oral Hypoglycemics: used in patients with NIDDM
mechanism: -stimulate insulin release from beta cells
-reduce serum glucagon levels
-increase binding of insulin to target tissues
adverse rx.: -GI disturbances
-hypoglycemia
-pruritus
-nausea
-anemia
drug interactions: 1. Displace from plasma proteins
-clofibrate
-phenylbutazone
-salicylates
-sulfonamides
2. reduce hepatic metabolism
-dicumarol
-chloramphenicol
-monoamine oxidase inhibitors
-phenylbutazone
3. decrease urinary excretion
-allopurinol
-probenecid
-salicylates
-sulfonamides
Biguanide: (metformin)
classification: antihypergylcemic NOT hypoglycemic
mechanism: -decrease intestinal glucose absorption
-increased periphernl glucose uptake
-iner. Insulin-mediated glucose uptake
-decreased hepatic glucose production
advantage: -gylcemic control without weight gain (which occurs "With
insulin and hypogylcemic agents)
-reduces total serum cholesterol
-inereases HDL
-decreases trigylcerides
adverse rx: most serious is lactic acidosis
risk factors (contraindications)
-renal insufficiency
-hepatic disease
-severe cardiovascular disease
-severe pulmoDary disease
temporary discontinue;
-IV contrast medium
-infection
-surgery, trauma
-acute MI, angina
21
-stroke
-dehydration
-severe GI illness
Drug rx: oral sulfonylureaslinsulin
alcohol-iner lactic acidosis
cimetidine-iner metformin levels
nifedipine
cationic drugs (ranitidine,triamterine, trimethoprim)
nephrotoxic drugs
aggressive use of diuretics
Dose: 500mg tablets BID
Rezulin (Troglitazone)
-Troglitazone is a thiazolidinedione antidiabetic agent that lowers blood glucose
by improving target cell response to insulin
-Troglitazone decreases hepatic glucose output and inereases insulin-dependent
glucose disposal in skeletal muscle. Its mechanism of action is thought to
involve binding to nuclear receptors Peroxisome Proliferator Activated Receptor
(PP AR) that regulate the trans...'Tiption of a number of insulin responsive genes
critical for the control of glucose and lipid metabolism.
-Rezulin is indicated to improve glycemic control in patients with type 2
diabetes mellitus as an acljunct to diet and exercise in combination with (not
substituted for):
A sulfonylurea drug for patients who are not adequately controlled with a
sulfonylurea alone or,
A sulfonylurea drug together with metformin for patients who are not
adequately controlled with the combination of a sulfonylurea and metformin
or,
Insulin in patients who are not adequately controlled with insulin alone.
-Contraindications
-Severe idiosyncratic hepatocellular injury has been reported
during marketed use , Rezulin therapy should not be initiated if the
patient exhibits clinical evidence of active liver disease or increased
serum transaminase levels (AL T> 1.5 times the upper limit of normal)
-Thus, dose adjustment in patients with renal dysfunction is not necessary
-Rezulin is not indicated as initial therapy in patients with type 2 diabetes.
-Rezulin is available in 200, 300 and 400 mg tablets as follows
-Rezulin should be taken with a meal.
Combination Therapy
Sulfonylureas
Metformin
Insulin
22
Infection Work-Up
Def'mition: Invasion of the body by hannful organisms (pathogens) such as bacteria, fungi, and viruses
with an initiation of an inflammatory response by the host.
Infectious Dose: Minimal number of viral particles necessary to establish a disease state: I X 10
6
This
allows for differentiation between colonization and infection.
Key: Diagnose an infectious process quickly and accurately. Diagnosis is made by clinical exam, NOT by
ancillary tests. Make diagnosis then implement a proactive treatment plan.
Goals: To establish a treatment plan, work to answer 2 questions:
A Is hospitalization required?
Outpatient versus in-patient therapy. Oral antIbiotics versus IV antIbiotics
B. Is surgical intervention warranted?
Bedside debridement versus OR I&D
I. History (Subjective):
A Chief Complaint
B. History of Present Illness
C. NLDOCAT
1. Any previous ulceration or infection?
2. Any recent antibiotic usage?
3. Trauma?
4. Last meal?
5. Check shoegear for foreign body or signs of irritation.
6. Constitutional signs & symptoms: fever (highest temp & when?), chills, night sweats,
rigors (violent shaking), nausea, vomiting, loss of appetite, dianhea, weight loss, general
malaise/fatigue, myalgias.
History of.. .. (begin to think empirically):
negative
Post-op
IV line sepsis
Implant
Scratching
Puncture Wound
Pseudomonas
Diabetic Infection
IV Drug Abuse
Water Related
volnificans,
Fever
Dog/Cat Bites
Human Bites
Staph. aureus
Staph. epidermidis
Staph. epidermidis
Tinea info with secondary bacterial info = gram
Cellulitis = Staph & Strep Osteomyelitis =
Polymicrobial
MRSA, MRSE, Pseudomonas
Pseudomonas, Aeromonas hydrophilia Vibrio
Mycobacterium marinum
Pasteurella multicida
Eikenella corrodens
Body temperature is regulated by the hypothalamic thermoregulator), center in response to various
stimuli. The stimuli affecting the hypothalamus are endogenous pyrogens secreted by leukocytes
and Kupfer cells. Other stimuli are bacterial endotoxins, phagocytosis, and certain immune
reactions. The endogenous pyrogen then increases the set point and temperature is raised Two
signs of increased set point are chills and shivering.
Gram negative bacteria tend to cause more of an intense fever. Gram positive bacteria tend to
evoke a profound inflammatory response, which releases endogenous pyrogens. It is believed that a
certain threshold of endogenous pyrogens is necessary for fever to occur. It is for this reason we
may not see fevers with early localized infections.
23
General Guide to Post-Op Temperature Elevations
107 Anesthetic Hyperthermia
106
lOS Blood Transfusion Reactions
104 Closed Abscesses
103 AtelectasislPneumonitislDrug ReactionslLiver Disease
102 Wound Infection
101 Draining Abscess
100 Benign Post-op FeverlPost-anesthesia Overshoot
99
98 Usual Range ofNonnal
97
96 Post-op Hypothermia
II. Past Medical Histon':
A. Diabetes: What type and for how long? Last BG? Classic triad (neuropathy, nephropathy,
retinopathy).
B. Cardiovascular: CABG (how many bypasses and when?), H1N, Murmurs, MVP, MI (last one),
phlebitis.
C. LungILiverlRenal disease.
III. Medications: Note dosages and frequencies. If on antibiotics: how long and why?
IV. Allergies: Penicillin, Local anesthetics, Iodine/Shellfish. Note type of reaction.
V. Past Surgical History: List all surgeries, dates, & physicians and/or hospital. Get medical records
on recent lower extremity surgeries.
VI. Social History:
A. Cigarettes, Alcohol, IV Drugs (how long & how much?).
B. Occupation: Is patient on feet at work.
C. HIV risk factors.
vn. Family History:
A. Are parents still alive? If not, what was cause of death.
B. Person to contact in case of emergency.
VIII. R e ~ i e w of Systems:
A. HEENT: headaches, glaucoma. retinopathy, eye or ear infections, sinusitis, sore throat, stiff neck
B. CVS: HTN, MI, CHF, MVP, murmur, angina, dyspnea, phlebitis, claudication
C. Resp: COPD, asthma, bronchitis, recent cough or cold, TB, pneumonia
D. GI: ulcers, GERD's, diarrhea, constipation (last bowel movement), hepatitis
E. GU: urgency, frequency, nocturia, hematuria, retention, incontinence, UTI, renal stones, SID's
F. MS: Muscle or joint pain, arthritis (type & how long?). Is patient ambulatory? Any assistive
devices?
G. Neuro: CV AfTIA, seizures, vertigo, syncope, paralysis, NM disorder, peripheral neuropathy
IX. Physical Examination (Objective):
A. Geneml appearance of patient:
Does patient look sick? Are they diaphoretic, flushed, disheveled, poor attitude?
B. Vital Signs: Preliminary way to detennine the amount of stress the infection has placed upon
patient.
1. Temperature: Note Tmax in past 24 hours & Tpres
2. Blood Pressure: May decrease during infection.
3. Pulse: May increase during infection.
4. Respiratory Rate: may increase during infection.
S. Finger Stick Blood Glucose in Diabetics: Usually elevated during infection.
24
Septic Patient: Elevated temperature, bypotensive, tacbycardic. tacbypnic.
C. Bacteremia:
L Definition: simple presence of bacteria in the blood stream that have clinical manifestations.
2. Significance: method by which infections can be spread to distant foci.
D. Septicemia:
1. Definition: clinical state in which in addition to bacteremia there are fever, cbills, & other
clinical symptoms.
2. Significance: represents failnre of the body to localize infection.
E. Don't limit exam to the lower extremity:
1. Look for other sources of infection:
a. Eyes, ears, nose, throat
b. Respiratory Tract
c. SBE
d Phlebitis, IV line sepsis
e. Gastrointestinal Tract
f. Genitourinary Tract
g. Skin: decubs or ulcerations on other parts of body.
X. Lower Extremity Examination:
A. Vascular Status:
1. Pulses:
a. If non-palpable then check with Doppler. If non-audible or weak with Doppler, get non-
invasive
arterial studies (pYR.'s).
b. ABI < 0.45 is inadequate for healing in diabetics. At least 30mmHg needed to heal
digital wounds.
c. May need arteriogram and vascular surgery consult for possible bypass.
d Question for ischemic rest pain/relief of pain with dependency of limb
2. Capillary Refill: Also check color and temperature of digits.
B. Neurological Status:
1. Check all sensory, motor, & reflex functions.
2. Determine level & duration of neuropathy ifpresent
a. Use Semmes-Weinstein monofilameDts. Comes in 3 sizes. If patient cannot feel the 5.07
size, protective threshold is lost.
e. Ortbopedic Status:
1. Note all boney prominences.
2. Note foot type and deformities.
3. Previous amputations?
4. Pain \\<ith range of motion of affected joint versus tenderness upon palpation.
D. Dennatologic Status:
1. Assess for the 5 CARDINAL SIGNS OF INFLAMMATION:
a. Dolor - Pain This is the most indicative sign. Even neuropathic patients will have pain.
b. Rubor - Redness
c. Calor - Heat
d. Tumor - Swelling
e. Functio Lasea - Loss of Function
At the site of inflammation, blood vessels dilate and there is an increase in blood flow to the area
causing RUBOR & CALOR Then there is extravasation of phagocytes and fluid into the
perivascular space resulting in TUMOR This edema causes stretching of the cutaneous nerve
fibers and the patient experiences DOLOR which causes FUNCTIO LASEA
Always uote Intensity of tbe signs of inflammation & compare to the contralateral limb.
25
2. Wound Evaluation:
a. Location - digits, interspaces, boney prominences, plantar space.
b. Size - always measure after debridement
c. Base - granular, fibrotic, fatty, necrotic, macerated
d. Depth - Does wound probe to bone or track up tendon sheaths or fascial planes? Is bone or
tendon exposed?
Wagner Classification of Diabetic, Neuropathic, & Vascular Foot Lesions
o - No open lesions, may have keratosis.
I - Full thickness ulceration that does not go beyond skin.
2 - Beyond full thickness of skin. Tendon or joint capsule may be exposed.
3 - Ulceration open to bone. Osteomyelitis is present.
4 - Wet or dry gangrene with or without cellulitis localized to the forefoot.
5 - Gangrene to extensive portion offoot or whole foot. Foot salvage is not possible.
c. Drainage - serous, serosanguinous, hemorrhagic, liquefactive, purulence.
f Odor - foul odor indicative of anaerobes, fruity odor indicative of pseudomonas.
g. Margins of Wound - viable, nonviable, necrotic, undermined, irregular border, punched-out,
keratotic, hyperpigmented indurated, macerated
h. Surrounding Tissue
1. Erythema versus Cellulitis (outline borders with marker to monitor regression or
progression).
Erythema - abnormal redness of the skin due to capillary congestion such as inflammation.
CeUuIitis - an acute spreading infection of the skin and connective tissue. More wide-spread
than erythema and boundaries are not clearly demarcated (Most common organisms
associated with cellulitis are Group A Strep & Staph aureus.)
2. Edema - as edema decreases, you will see an increase in skin lines.
3. Lymphadenopathy - check for lumps in groin & behind knee.
4. Lymphangiitis - "blood poisoning". Red streaks up legs along lymphatic channels.
Infection is drained from the body via lymphatics. Lymph nodes can become swollen during
this process due to excess bacteria & increase in pressure from the edema. If lymph nodes
become overwhelmed, lymph drainage can be blocked and red streaks can occur (#1 org. is
grp. A Strep)
Bacteria can also seed the blood via l}rophatics and cause a bacteremia which can lead to a
septicemia.
XL Medical Imaging:
A Conventional Radiographs:
1. Always order even with soft tissue infectious. Need baseline radiographs.
2. Examine for:
a. Soft tissue swelling.
b. Gas in soft tissues. (May also be able to feel crepitation in skin clinically.)
c. Foreign Body.
d Trauma
e. Osteomyelitis:
Periosteal reaction.
Lytic changes with sclerotic border.
Cortical breaking.
Osseous destruction.
Sequestrum, involucrum, cloaca, Brodie's abscess (chronic changes).
3. Lag time can be 10-14 days.
26
The following medical imaging modalities should only be used as an adjunct to therapy. They should only
be used if the results would alter a treatment pJan or benefit the patient. They should never be relied upon
to make a diagnosis. Diagnosis is made by CLINICAL EXAM. Please see the section on Radiology of
Infection for complete discussion of each.
B. Nuclear Scinitigraphy (See radiology section).
C. CT Scan. (See radiology section).
D. MRI. (See radiology section).
XII. Laboratory Evaluation:
FIRST LINE TESTS SECOND LINE TESTS
1. CBC with diff I. ESRlCRP
2. Chemistry Panel 2. Blood Cultures
a. BUN 3. Urinalysis
b. Creatinine 4. Urine Culture
c. Glucose
TESTS FOR SURGERY
1. Pf,PTT
2. LFT's,. TFT's
3.CXR
4.EKG
First line tests should be performed upon initial presentation of patient to aid in diagnosis & establish
appropriate treatment protocol. Second line tests can be performed after initial presentation. They may
help monitor patients progress or help rule-out other sources of infection. Tests for surgery should be
performed initially only if patient needs to go to the OR immediately. (Do not order if they are not
medically indicated)
Please see section on "Pre & Postop Management: Hospital Charting" for normal lab values.
A. Complete Blood Count (CEC):
1. Hemoglobin (Hgb).
2. Hematocrit (Hct).
3. Platelets (pIts).
4. White Blood Cells (WBC): Usually> 10,000 for infection (Leukocytosis).
a. Differential:
Granulocytes (Contain granules in cytosol)
Neutrophils:
Polymorphonuclear (PMN) cells
Band cells
Basophils
Eosinophils
Agranulocvtes
Monocytes
Lymphocytes
PMN's: Mature neutrophil. Initial killer cell, actively phagocytic. Contains lysozymes &
lactoferrin. Half-life is 6 hours but functions last for 1-2 days. Maturation tinie is 14 days.
Band cells: Immature neutrophil Nucleus is elongated & twisted It is less deformable &
less motile; therefore, less effective in phagocytosis & killing. Increases during acute
infection (Left Shift).
Basophils: Contain heparin, histamine, & other substances to contract smooth muscle &
increase permeability of blood vessels.
Eosinophils: Function unknown.
Increased in (NAACP): Neoplasms,. Allergens, Addisons, Collagen vascular diseases, Parasites
Monocytes: Second line of phagocytic response (replaces neutrophil within 24 hours).
Activated into macrophage at inflammatory site.
A Macrophage is an aggressive phagocytic, bactericidal, & long-lived cell. It
processes antigen & delivers them to lymphocytes for specific antibody
production.
Lymphocytes: Possess cellular mediators for immunity.
B cells are produced from bone marrow & produce specific antibody.
T cells are produced from thymus & produce specific sensitized lymphocytes.
27
Laboratory diagnosis of infection:
Leukocytosis (increase WBC's) with a shift to the left (increase band cells).
During acute infection, the body tries to fight the infection by increasing the number of WEC' s,
specifically neutrophils. Unfortunately, the neutrophils do not have time to mature before they are
needed to try to "kill" the infection and band cells are produced.
B. Chemistry Panel:
1. BUN: Measures hydration state. Less specific for renal function. BUNICr may be elevated in
dehydrated state. Follow levels closely
2. Creatinine: Best hematologic index of renal function. Use to measure creatinine clearance for
proper antibiotic dosages.
3. Glucose: Stress of infection may cause an increase & may complicate wound healing.
4. Electrolytes: Na, K Cl, CCh.
C. Second Line Tests:
1. Erythrocyte Sedimentation Rate (ESR):
a. Detennined by measuring the distance in mm a column of erythrocytes falls in 1 hour.
b. NON-SPECIFIC: inflammation, infection, malignancy, renal disease, connective tissue
disease, age.
c. Use as a baseline to monitor effectiveness. Draw every 5-7 days.
2. C-Reactive Protein: Similar to ESR but more difficult to perform & more expensive.
3. Urinalysis: (+) leukocytes & nitrates (probable UTI). If there are an increase in the squamous
epithelial cells, the sample was probably contaminated (need to repeat test). Check urine culture
to detennine specific organism(s).
4. Blood Cultures:
a. Used to diagnose bacteremia; however, most bacteremias are intermittent & a (+) culture
can be difficult to obtain.
b. Take as soon as possible after the onset ofa fever (usually 101).
c. Need 2-3 cultures at least 20 minutes apart & from different sites. This increases the
chances of catching the organism.
d Must utilize aspetic technique to avoid skin contaminants.
DECISION MAKING
#1 Does tbe patient need to be admitted?
Outpatient versus Inpatient therapy.
Oral antIbiotics versus IV antIbiotics.
1. Outpatient Therapy:
a. Localized signs of infection with no systemic manifestations.
b. Benign medical history (patient is not immunocompromised).
c. Can be sent home on oral antibiotics.
2. Inpatient Therapy:
a. Extension of infection.
b. Systemic manifestations.
c. Need IV antibiotics.
d Require surgical intervention.
e. Immunocompromised host.
Diabetes
Peripheral Vascular Disease (vascular surgery consult)
HIV
Cancer
Rheumatoid Arthritis
Steroid Therapy
Elderly
28
Jmmunocompromised patients may not be able to elicit an inflammatory response & the infection
may look benign. The typical redness, rn-elling. & heat may not be present but this does not mean that the
infection is localized. Their immune system cannot fight the infection as effectively as a healthy patient:
therefore, what may look benign can tum into a rapidly progressing & fatal infection. Caution should be
used with these patients and hospitalization even for localized infections should be considered
#2 Is surgical intervention necessary?
Bedside debridement versus OR I&D
1. Bedside Debridement:
a. Localized infection.
b. Neuropathic patients.
c. Better evaluation of the wound
2. Operating Room Incision & Drainage:
a. Unknown extent of infection.
b. Wound probes to bone or bone is exposed
c. Wound tracks up fascial planes or tendon sheaths.
d Abscess.
e. Gas in soft tissues: Needs immediate I&D.
XIII. Treatment:
A Systemic Therapy (Antibiotics):
1. Oral versus IV.
2. Choose according to clinical scenario:
a. Diabetes: polymicrobial
b. Cellulitis: Group A Strep, Staph aureus
c. Gas: clostridium
d Foul odor: anaerobes
e. Fruity odor: pseudomonas
f. Jnterspaces: gram ( -)
g. Golden purulence: Staph aureus
3. Start broad & narrow spectrum pending culture results & sensitivities. Good options for
intial therapy are Ancef7Flagyl or BactrimlFlagyl or Unasyn (will vary depeding of hospital
micro. resistance profile)
4. Obtain cultures before starting antibiotics. May get negative cultures if patient is already on
antlbiotics.
5. Calculate Creatinine clearance prior to dosing Abx
B. Local Therapy (Wound Care):
1. Incision & Drainage:
a. Use general anesthesia or spinal if extent of infection is unknown. Infection may track
up leg beyond the boundaries of a local block.
b. Don't use a tourniquet Need to differentiate healthy, bleeding tissue from necrotic
tissue. If a tourniquet is used, drop it before final debridement to ensure adequate
debridement.
c. Plan all incisions. Final goal is wound closure.
d Debridement (Remember the 3 D's: debridement, drainage, decompression):
Do not separate tissue planes. Initial incision should be down to bone.
Resect all infected, necrotic soft tissue and bone.
Careful handling of skin edges, especially in patients with PVD.
e. Cultures:
Soft tissue swabs: gram stain, aerobic, anaerobic, fungal, acid-fast.
Bone: obtain pieces for culture & biopsy.
Request sensitivities on all cultures
29
f. Irrigation:
Need high power for lavage. Pulse lavage apparatus or 60cc syringe with an 18
gauge blunt tip needle. The high power and pressure facilitates debridement.
lrrigant solution is irrelevant, usually use normal saline.
Adding antibiotics to irrigant solution offers no benefit.
g. Wound should be packed open:
Use plain Nu Gauze packing on smaller wounds & 4X4 gauzes or Kerlix on larger
wounds.
Perform daily dressing changes on wound & monitor for signs of healing.
When all signs of infection have been irradicated wound can be closed, usually 3-4
days after initial 1&D.
2. Daily Wound Care (Bedside):
a. Irrigation.
b. Local debridement.
c. Packing.
d. Wet to Dry Dressings:
1. Absorbs fluid exudates.
2. Facilitates debridement upon removal.
3. Solutions:
Saline: isotonic, drying.
Betadine: drying, antimicrobial, can be caustic to tissues.
Dilute Betadine: less drying & less caustic to tissues.
Dakins (hypocblorate, usually 114%): antimicrobial, promotes granulation
tissue.
Acetic Acid (usually WYO): antimicrobial, good for pseudomonas.
e. Monitor for healthy tissue. Final goal is wound closure.
f. Biologic & Synthetic Membrane Dressing:
I. Not used often, but if desire to use, granulation tissue must be present.
2. Materials:
Porcine skin graft.
Amniotic membrane.
Epiguard: A synthetic membrane with 2 layers. The inner layer is made of
polyurethane. Granulation tissue grows into & attaches to this layer. The
outer layer is composed of teflon. This layer is breathable and bacteria
impermeable.
g. Elevate limb. This encourages venous & lymphatic drainage to reduce edema & improve
local blood flow. Patients with compromised circulation should have legs level in bed,
not elevated
3. Wound Closure:
a. Primary Closure: never use unless all necrotic tissue is excised & no signs of infection
exist.
b. Delayed Primary Closure:
Usually 3-4 days after initial 1&D.
Excise all necrotic, non-viable tissue.
Obtain bleeding skin edges.
Irrigation.
Culture.
Suture: Avoid closure of deep tissues. Utilize non-reactive materials (Nylon,
Prolene).
c. Secondary Intention: for large wounds that cannot be reapproximated
d. Skin Grafts (Apligraft}
30
Patients with severe PVD require lower extremity bypass surgery or angioplasty prior to closure
Osteomyelitis
I. Definitions:
A. Hematogenous Osteomyelitis: Usually occurs in children & is primarily a medically treated disease.
When it occurs in adults, it is usually a smgically treated disease. Now increasing incidnce in the
elderly >50 yrs
-Primarily long bones LE and the hwnerus
-Vertebrea in 1he elderly
-So Aureus, S1rep in neoneates
Lew and Waldvogel, NElM' 336: 1997
-GNRs in elderly, immlDlocompromised patients
-Pseudomonas in IVDAs and long tenn indwelling urinary ca1hetcrs
B. Contiguous Osteomyelitis(direct extension): Direct infection of bone from and exogenous source or
spread of infection from a near by infected focus.
-Prothesis, implants, open fractw'es primary concerns con
C. Osteomyelitis in a patient with vascular impairment: These patients have difficulty mounting an
inflammatory response. They also have poor delivery of antIbiotic to the infection site.
-vascularity needs to be addressed to insme adequet healing
D. Acute Osteomyelitis: Suppurative infection accompanied by edema, vascular congestim, & small
vessel thrombosis.
E. Chronic Osteomyelitis: Nidus of infected dead bone or scar tissue, an ischemic soft tissue envelope,
& a refractory clinical course.
F. Sequestrum: Piece of necrotic tissue, usually bone, that has become separated from smrolDlding
heal1hy tissue.
G. Involucrum: The sheath of new bone that forms around a sequestrwn.
H. Brodie's Abscess: A chrmic abscess of bone surrolDlded by dense fibrous tissue and sclerotic bone.
II. Classification:
Waldvogel
Hematogenous Osteomyelitis
Contiguous Focus Osteomyelitis
Osteomyelitis associated with Vascular Disease
Chrmic Osteomyelitis
III. Clinical Evaluation: (Please see infection work-up.)
IV. Imaging Modalities:
A. Radiographs:
Oemy-Mader
Anatomic Stage
1. Medullary Osteomyelitis
2. Superficial Osteomyelitis
3. Localized Osteomyelitis
4. Diffuse Osteomyelitis
Physiologic Stage
A. NormalHost
B. Systemically Compromised
Host (BS)
Locally Compromised Host (BL)
C. Treatment is worse than the
Disease
l. Need 30-50% resorption to detect osseous changes on x-ray. This can take 10-14 days.
2. Always take x-rays for an infection. Can act as a baseline & monitor the regression or
progression of the infectious process.
3. Signs (In order by which appears first):
Soft tissue swelling.
Periosteal reaction (thickening or elevatim).
Focal osteopenia.
B. Please refer to Radiology of Infection for bone scans, MRI. & CT.
31
v. Diagnosis:
A. Bone biopsy:
1. Definitive diagnosis.
2. Bone culture & microscopic examination of bone.
3. Utilize imaging modalities to determine best area to take biopsy.
B. Hematogenous Osteomyelitis may be diagnosed with positive blood cultures with a positive bone
scan.
VI. Treatment:
A. Primary Goals:
1. Adequate drainage.
2. Thorough debridement.
3. Obliteration of deadspace.
4. Antimicrobial coverage.
B. Primary Surgical:
1. Debridement of all nonviable & marginally viable tissue.
2. Antibiotic Polymethylmethacrylate Impregnated Beads (PMMA):
a. Indications for use:
Deadspace maintenance followed by bone grafting, bone fusion, or primary closure.
Debridement & closure.
Combined debridement & internal fixation procedure.
Systemic disease which contraindicates adequate systemic levels of organ toxic
antibiotics, such as aminoglycosides.
b. Gentamycin is the traditional antibiotic used with PMMA beads because it is not heat labile
and the curing process of the PMMA is an exothermic process. Other antibiotics may be
used; however, the antibiotic must be added in the dough phase of the PMMA. This
prevents the heat degradation of the antibiotic. Antibiotics that have been used include:
Gentamycin
Cephalosporins- Cefazolin, Moxalactam, Cefotaxime
Tobramycin
Vancomycin
Ticarcillin
c. Procedure:
Mix & construct the beads on a wire and place in the wound.
Close the wound over the beads.
Leave the beads in for about 2-4 weeks.
d. Mechanism
Immediate ans sustained release of antibiotic in the local area
Release of antibiotic declines exponentially with time
3. Ingress-Egress Systems:
a. Closed suction irrigation. A closed system in which continual flushing of the wound is
accomplished through inflow tubing (ingress) & outflow tubing (egress). There are many
problems with this system, such as contamination of the outflow tubing (usually
pseudomonas).
4. Bypass Surgery: (Consult vascular surgery for options.)
C. Secondary Surgical- Reconstructive:
1. Papineau bone graft: This technique is for filling bone defects. SmaIl cancellous chips are
packed into bone deficits when the wound is granular. This graft is given time to take then
various closures can be used.
2. Bone Fusion: Used after resection when infections are near articular surfaces.
3. Delayed primary closure.
4. Tissue transfer/Skin grafting.
5. Bead therapy, bone grafting, & closure.
32
VII. Follow-Up:
A. Goal is to prevent rectnTence.
B. Antibiotics:
1. Customarily 6-8 weeks following last surgery or since initial clinical resolution of infection
when no surgery has been performed.
2. The word "cure" is inappropriate. It is possible for an area to activate for up to 20 years.
3. Follow-up intervals:
First 6 months: every month.
6 months-I year: every 3 months.
1 year-2 years: every 5 months.
Local Antibiotics/Antibiotic Beads
The implantable admixture of antibiotic to any of several carriers for the purpose of localizing increased
antibiotic concentrations at specific target tissue sites.
Selected antibiotic should meet the following criteria:
A. H2O soluble
B. nontoxic to tissue
C. bactericidal (preferably)
D. available in powder form
E. heat stable if used with PMMA
Carriers may be:
A. biological
1. cancellous bone graft
2. demineralized bone matrix
3. Ca ++ hydroxyapatite
B. biologically inert
1. polymethyl methacrylate (PMMA)
2. plaster of paris
* commercially prepared antibiotic carriers are available in Europe, and are expected to be
available in the United States after further investigation of possible toxicities
Miclau et al compared the elution oftobramycin from various carriers, and found:
A. cancellous bone graft eluted 70% of its antibiotic within the first 24 hours of implantation, and
had non-measureable levels at 14 days
B. demineralized bone matrix released 45% of its antibiotic within the first 24 hours of
implantation, and had non-measurable levels at 14 days
C. plaster of paris eluted 17% of its antibiotic in the first 24 hours after implantation, with
measurable levels of antibiotic up to 21 days post-implantation
D. PMMA eluted 7% of its antibiotic within the first 24 hours of implantation, with trace amounts
measurable up to 14 days post-implantation
PMMA, the most commonly used carrier for implantable antibiosis, usually comes in half-packs (20 g) or
full-packs (40-60 g); consists of
A. monomer (liquid)
B. polymer (powder)
* the monomer and polymer are mixed together (an exothennic reaction) with the antibiotic
powder ootil a doughy consistency is achieved, at which time small beads are fashioned and placed on 26
or 28 gauge wire like pearls on a necklace. The hardened beads are then implanted into a dead space in
which high local levels of antibiotic are desired, typically within an area of debrided osteomyelitic bone or
the space previously occupied by osteomyelitic bone after resection. (N.B. no one wearing contacts should
be in the surgical suite during preparation of the beads, as offensive vapors have been linked to morbidity
with those individuals)
33
Suggested Ratio of Antibiotic:PMMA
Antibiotic
Amount of Antibiotic AmountofPMMA
Cefazolin
4-8 g 40-60 g
Cefotaxime
4-8 g 40-60 g
Nafcillin
4-8 g 40-60 g
Tobramycin 5-10 g 40-60 g
Vancomycin 4-8 g 40-60 g
Ticarcillin 6-13 g 40-60 g
Clindamycin 4-8 g 40-60g
Diffusion (Elution) of Antibiotic from PMMA depends on:
A. type of cement used (Palacos vs. Simplex vs. CMW)
B. coefficient of diffusion for each antibiotic
C. concentration of antibiotic within the bead
D. size/surface area/roughness of the bead
E. amount of fluid that moves past the bead
Bead Properties
A. smaller beads = more surface area to total volume, leading to increased elution rates
B. higher concentrations of antibiotic within a bead leads to increased pore size and roughness,
each leading to increased rates of elution
C. Ciemy proposed a ratio of 1:5 when adding antibiotic powder to the PMMA powder; e.g. for
every 109 of powdered PMMA polymer, add 2 g powdered antibiotic, stating that any higher ratio would
prevent proper hardening of the PMMA
D. most studies conducted with 1-2 g antibiotic to 40-60 g PMMA in literature
Complications with Antibiotic-Impregnated PMMA Beads: very few
A. if the cement is used for fixation, mechanical strength is compromised with greater than 1 ()O/O
antibiotic content (not an issue with beads)
B. care should be used in patients with renal disease, though local antibiotic concentrations 10-50
times greater than the toxic serum levels can be achieved without the serum ever absorbing enough to
achieve those toxic levels
C. no allergic reactions have been reported to date in the literature
Disadvantages
A. second procedure required for bead removal, typically after 10-14 days
SEPTIC ARTHRITIS
Infectious arthritis stands apart from other rhemnatic disocders because cure rather than mere control is
possible. Whether oc not this goal can be achieved depends upoo the type of ocganisrn, promptness in initiating
therapy, medical status of the individual, and prioc status of the involved joint Almost any pathogen may affect
articular cartilage and periarticular tissues. A multitude ofbacteria, viruses, mycobacteria, and fimgi have been
associated with arthritis.
MECHANISMS OF SEPI'IC ARTHRITIS
I. DIRECT JOINT INVASION BY THE MICROBE : pathogens may invade the joint directly and produce
on-going inflammation and destruction. Examples include direct joint innoculation (puncture wound) oc
hematogenous spread.
2. JOINTS MAY BE AFFECTED INDIRECIL Y AS A RESULT OF:
34
A the resulting immune response of the affected host For example, in Hepatitis-B arthritis circulating
imnnme complexes appear to mediate the polyarthritis that accompanies the prodromal stage of this
infection.
B. miaobial debris that may persist in the joint and perpetuate an inflammatory respoose. even after the
organism is no longer in the joint. This appears true in some cases of gonnococca1 arthritis in which an on-
going synovitis is associated with sterile joint fluid that is non-inflammatory, so called " post-infectious
sterile arthritis."
c. unknown mechanisms. This applies to almost all of the reactive arlhritides, such as those associated with
gastrointestinal infections with some of the enteric gram negative organisms (Shigella sp., Yersinia sp.).
ACUTE BACI'ERIAL ARTHRITIS
PREDISPOSING FACTORS AND ASSOCIATED CONDITIONS
1. Rhewnatoid arthritis
possible mechanism for association
damaged joint is a good nidus for infection
compromised defenses from medications
defective phagocytosis (?)
important clinical features
usually due to Staph. aureus
treatment results often poor
2. Crystal-induced arthritis
possible mechanism for association
synovial fluid acidosis may promote crystal deposition
enzymatic" strip-mining" of cartilage
important clinical features
identification of crystals in the joint does not rule out septic arthritis
3. Severe osteoarthritis, Charcot joints, Hemarthroses
possible mechanism for association
joint disorganization, chronic synovitis, and bloody effusions all provide nidus for bacteria
important clinical features
always send bloody joint fluid for culture
4. Chronic systemic disease (SLE, sickle cell anemia, cancer, etc.)
possible mechanism for association
impaired generalized defenses due to chronic illness, phagocytic deficiencies, and medications
important clinical features
often due to Staph aureus or gram negative bacilli
consider Salmonella sp. in patients with sickle cell
35
ACUTE BACTERIAL ARTHRITIS
PREDISPOSING FACTORS AND ASSOCIATED CONDmONS
I. Rheumatoid arthritis
possible mechanism for association
damaged joint is a good nidus for infection
compromised defenses from medications
defective phagocy10sis (?)
important clinical features
usually due to Staph. aureus
treatment results often poor
2. Crystal-induced arthritis
possible mechanism for association
synovial fluid acidosis may promote crystal deposition
enzymatic" strip-ruining" of cartilage
important clinical features
identification of crystals in the joint does not rule out septic arthritis
3. Severe osteoarthritis, ChaIrot joints, Hemarthroses
possible mechanism for association
joint disorgmization, chronic synovitis, and bloody effusions all provide nidus for bacteria
important clinical features
always send bloody joint fluid for culture
4. Chronic systemic disease (SLE, sickle cell anemia, cancer, etc.)
possible mechanism for association
impaired generalized defenses due to chronic illness, phagocytic deficiencies. and medications
important clinical features
often due to Staph aureus or gram negative bacilli
consider Salmonella sp. in JB1ients with sickle cell
PATHOGENESIS
Acute bacterial arthritis occurs most often by hematogenous dissemination from a primary source of infection.
However, joint sepsis may also result from the extension of an adjacent soft tissue infection or adjoining
osteomyelitis.
Three stages of cartilage destruction have been described:
36
1. Initial events include liberation of lysosomal enzymes from PMN's and synovial lining cells
resulting in the loss of proteoglycan from cartilage. If the infectious process is resolved early, a
restomtion of proteoglycan matrix may be achieved and chondrocyte damage avoided.
2. Dming the second stage, increased mechanical stress and inadequate nutrition result in
chondrocyte damage.
3. In the last stage, enzymes released from PMN's and synovial lining cells with the altered joint
mtrlJanics gradually destroy the collagen network.
CLINICAL FEATURES
Septic arthritis usually affects one joint, but may involve two or more joints. The involved joint is geneI3lly red,
hot, swollen and acutely painful. There is also extreme pain and limitation with range of motion. The knee
followed by the hip and ankle are the most commonly involved joints in non-gonococcal septic arthritis.
Systemic features include fever ( may be low gtade ), chills and rigors. A careful physical exam may reveal an
infectious focus involving any site, but the usual sowces include the skin, nasopharynx, sinuses, lungs, cervix,
and the rectum.
JOINT DISTRIBUTION
%OFCASES
JOINT ADULTS ClllLDREN
knee 55 40
hip 11 28
ankle 8 14
shoulder 8 4
wrist 7 3
elbow 6 11
others 5 3
LABORATORY TESTS
Peripheral leukocytosis occurs in the majority of patients with acute bacterial arthritis. An elevated ESR is also
genetally found.
Patients suspected of having septic arthritis should have blood cultures and cultures of regions that may be the
primary SOUICe of infection ( physical examination will help to determine areas that may need to be cultured ).
Blood cultures may be positive in up to 75% of patients.
A diagnosis of septic arthritis is established by gram stain and a positive synovial fluid culture. A typical joint
infection demonstI3tes a purulent effusion with a synmial fluid white count greater than 50,000 cellsIcmm and
more than 9()01o PMN's. Gram stain and culture are obligatory if septic arthritis is suspected.
INCIDENCE OF ORGANISMS IN ACUTE BACTERIAL ARTHRITIS IN ADULTS
Gram-positive cocci
Gram-negative cocci
( N. gonorrhoeae )
Gram-negative bacilli
TREATMENT
45%
50%
5%
1. Treatment should begin immediately after the suspicion and/or confirmation of the diagnosis.
37
2. Antibiotics are chosen primarily on the basis of the synovial fluid gram stain and are acljusted based on the
culture results.
3. Oosed needle aspiration should be performed at least once daily to drain the affected joint.
4. Open surgical drainage is indicated if there is a lack of response to therapy ( joint fluid cultures remain
persistently positive or patients remain febrile after 3-4 days of antIbiotic therapy ); Some studies espouse
immediate open surgical drainage.
S. The infectedjoint should be kept at rest to prevent mechanical stress; generally using a splint will provide
adequate immobilization and reduce pain and trauma
6. As joint symptoms resolve, passive range of motion exercises should be started to avoid joint contractures.
7. Weightbearing should be deferred until inflammation has completely resolved
SYNOVIAL FLUID EXAMINATION (IMPORTANT POINTS)
Cultures are nearly 100010 positive in non-gonococcal bacterial arthritis, but only 2S-S0% positive in gonococcal
arthritis.
Gram stain smears are approximately 7S% positive with gram positive cocci, SO% with gram negative bacilli,
and less than 25% in gonococcal arthritis.
1be leukocyte and differential leukocyte counts are generally greater than SO,OOO cellslcmm and greater than
80% PMN's, but these results can also occur with noninfectious inflammatory arthritis.
Synovial fluid glucose is less than 50% fasting, simultaneous serum glucose but may not be present and may be
seen with Rheumatoid arthritis.
RADIOGRAPIDC TESTING
Radiographic examination of affected joints may reveal only soft tissue swelling early in the course of the
disease. Juxta-articular osteopenia appears about 7-10 days after the onset of joint infection. If the joint
infection is not eradicated, progressive joint space narrowing may develop. Late radiographic findings include
joint subluxation and eventual joint destruction.
Radioisotope scanning may be helpful in localizing sites of infection, however the findings are non-specific and
radionuclide imaging generally has little role in the initial evaluation of acute septic arthritis.
RADIOGRAPIDC-PATHOLOGIC CORRELATION
PATHOLOGIC ABNORMALITY
edema and hypertrophy of soft tissue
synovial membrane with
fluid production
hyperemia
inflammatory pannus
with chondral destruction
pannus destruction of bone
fibrous or bony ankylosis

BACIERIA (# OF CASES) < 2 YRS 2-6YRS >6YRS
RADIOGRAPmC ABNORMALI1Y
joint effusion,
swelling
osteoporosis
joint space loss
marginal and central erosions
bony ankylosis
TOTAL
38
S. aureus 49 36 81 166(34%)
H influenza 154 19 1 174(36%)
Streptococci 27 23 24 74(15%)
Gram neg. 24 9 6 39 (SOlo)
bacilli
S. pneumoniae 23 4 3 30(6%)
482
From series by Fink and Nelson. Speiser et al, PeltoJa and Vahvaven, Borella et el., and Samilson et a1.
39
INODENCE OF ORGANISMS IN CHILDHOOD SEPTIC ARTHRITIS
Gram-positive cocci
70%
Gram-negative cocci 5%
Gram-negative bacilli <15%
H. influenza 10%

(DISSEMINATED GONOCOCCAL INFECTION)
Gonococcal arthritis is the most common form of acute bacterial arthritis. Joint involvement occurs during
dissemination of the gonococcal infection from a primary source of infection.
CLINICAL MANIFESTATIONS
The organism initially infects mucosal cell surfaces. Typically the primary infection involves the reproductive
but may involve the pharynx or rectum.
Disseminated gonococcal infections occur in approximately 1-3% of all primary infections. Dissemination
seems to occur more commonly in females, generally around the time of menstruation. *** An important note
is that patients with complement deficiencies are at an increased risk of gonococcal bacteremia.
Most patients with disseminated gonococcal infections are less than 40 years of age and relate a history of
promiscuity and unprotected sexual intercourse. Again the primary sites of infection are the urethra in males,
cervix: in females, auf the rectum and phaIyn.x in both sexes.
Patients disseminated disease may have systemic findings that include fever, chills, and malaise. A migratort
polyarthritis is the most common initial joint manifestation, and subsequent findings may localize to one or
more joints. Any joint may be involved
Peri-articular pain and swelling are common, and tenosynovitis is found in a significant number of patients.
Typical skin lesions are a frequent manifestation, generally beginning as smaI1 erythematous macules, which
may develop into pustular lesions characterized by a grey, necrotic center with a hemhorragic base.
LABORATORY TESTS
Peripheral leukocyte counts may be normal or moderately elevated Synovial fluid analysis reveals an
inflammatory fluid with a variable number of white cells ranging from a few thousand to several hundred
thousand per cubic millimeter. Joint fluid cultures are positive in less than half of all patients even under ideal
conditions.
DIAGNOSIS
Disseminated infection should be suspected in young, sexually active [patients who develop an acute migratory
polyarthritis, tenosynovitis, and/or a characteristic rash. Primary source and joint cultures along with synovial
fluid analysis should be performed
40
TREATMENT
1. Antlbiotics : Ceftriaxone ( Rocephin ) IM/IV or

Cefotaxime ( C1afman ) IV then,
Cefuroxime axetil ( Ceftin ) po or
Amoxici1IinlclavuJanate ( Augmentin ) po or
Ciprofioxacin ( Cipro ) po
Parenteral antiobiotics are generally contimJed for 24-48 hours until symptoms begin to resolve, and then
patients are switched to enteral antibiotics to complete a 7-10 day course of therapy.
2. Joint aspiration
3. Joint immobilization
VIRAL ARTHRlTIS
Viral arthritis often begins with non-spec.ific symptoms such as ma1aise and fatigue, headache, neck. stiffness,
sore throat, and nausea and vomiting. Joint involvement is generally polyarticular, and the arthritis is usually
short-lived and rnrely results in joint damage. Laboratory tests are non-specifi.c. The following are some of the
most conunon causes of viIal arthritis :
1. Hepati.tis-B - joint manifestations may be seen in 10-30010 of patients . The arthritis is generally self-limiting.
2. Rubel1a - may occur in natural rubella infection or after immunization ",ith the live attenuated "irus.
3. Parvovirus B 19
4. HlY related arthropathy
FUNGAL ARTHRITIS
A wide variety of fungi may cause joint infection, which may arise either from direct extension from a focus of
osteomyelitis or by hematogenous dissemination. The arthritis is usually monolpau.ciarti.cular, most often in
large weighfuearing joints, and generally follows a chronic or indolent course. Synovial fluid analysis and
allture are variable, often providing little to no diagnostic value. Fungi that may be associated with infectious
arthritis may be grouped as superficial or deep organsims. Although normal hosts may develop fungal arthritis,
there is usually some predisposing factor that increases susceptIbility to infection. The diagnosis can be made
by synovial fiuid culture or synovial tissue biopsy.
SUPERFICIAL
Sporothrix schenckii
Candida albicans
Actinomyces israelii
" Maduromycoses"
DEEP
Aspergillus fumigatus
Histoplasma capsuIatum
Cryptococcus neoformans
Coccidioides immuns, Blastomyces dermatitidis
MYCOBACTERIAL BONE AND JOINT INFECTIONS
Extrapulmonary tuberculosis occurs in approximately 1-2.6% of patients with tuberculosis.
It is generally believed that skeletal TB is caused by dissemination of bacilli by hematogenous spread or
lymphatic drainage:from another area of lB. TB arthritis most frequently involves weightbearingjoints and is
usually monoarticular. A positive tuberculin skin test is obtained in most patients, and in about 50010 a previous
personal or family history is present.
S)'U.ovial pathology reveals a chronic granulomatous reaction with giant, Langhan-type cellular infiltration.
Acid-f3st staining of the synovium or surrounding tissue may reveal the organisms.
41
Radiographically the affected joint may reveal only soft tissue swelling or more advanced changes with
destruction of peri-articular bone, narrowing of the space, and osteoporosis. Chest X-ray abnonnalities of past
or present 1B may be present in 50010 of patients.
ARTHROCENTESIS AND SYNOVIAL FLUID ANALYSIS
Synovial fluid is an invaluable source of diagnostic information. One of the most important reasons to perfonn
synovial fluid analysis is to rule out bacterial infection in severely inflamed joints. There is no other sufficiently
reliable way to differentiate septic arthritis from acute crystal-induced arthritis. Arthrocentesis may be
therapeutic as well as diagnostic. For tense effusions in which the intra-articular pressure is higa removal of the
fluid will relieve symptoms and at least theoretically decrease joint damage.
TECHNIQUE
1. The joint should be moved through its I31lge of motion to resuspend its contents.
2. Anatomic landmarks defining the joint surface should be identified and may be outlined with a pen or
marker.
3. The specific area of the joint to be aspirated is identified and may be marked with the retracted portion of a
ball point pen.
4. The skin should be cleansed of obvious dirt with soap and water.
5. The skin can be infiltrated with a local anesthetic.
6. A brief scrub with a betadine solution followed by an alcohol swab should provide adequate protection.
7. Do not touch the skin at the aspiration site after cleansing!
8. It is a mistake to select a small needle with the intention of sparing the patient pain. VIscous material flows
with great difficulty, if at all, through needles smaller than 20 gauge.
9. Stretch the skin slightly, penetrate the skin, aspirate gently, and advance the needle slowly until fluid
appears in the syringe.
10. After removal of the needle, apply gentle compression at the puncture site for several minutes. Then apply
a band-id or light dressing.
C. COMPLICATIONS OF ARTHROCENfESIS
1. Iatrogenic infection of a previously sterile joint (it has been estimated that infection occurs in less than 1 in
10,000 instances of diagnostic arthrocentesis ).
2. Bleeding at the puncture site and presumably within the joint; in anticoagulated patients who develop acute
arthritis, anticoagulation itself is not a contraindication to arthrocentesis.
3. Possible injury to cartilage by the needle.
4. Occasionally patients may experience a vasovagal ( syncopll ) episode during or after the procedure.
SYNOVIAL FLUID ANALYSIS
I. GROSS EXAMINATION
1. VOLUME : can serve as one measure of the severity of a process, but low volume does not mean the
absence of an important intIa-articular rrocess.
2. VISCOSITY : fluid of normal viscosity holds together and stretches approximately one inch before
separating. Low viscosity fluid drops from a syringe like water. VIscosity is generally decreased in
intlannnatory joint fluids.
42
3. COLOR AND CLARITY: if newspJpef print cannot be read through the fluid, it generally suggests an
inflammatory process. The plastic of some syringes makes fluids appear falsely cloudy, so examine the
fluid in a glass container (ie. test tube ). NoIIDal and noninflammatory joint fluids are a transparent straw or
yellow color depending on the amount of albumin or bilirubin present.
II. MICROSCOPIC EXAMINATION
1. WET MOUNT: Useful for identification of cells, cartilage 1iagments, lipid droplets, cytoplasmic inclusions,
and some crystals. Sickled red cells may be seen in effusions of patients with sickle oeIl disease.
2. CRYSTAL ANALYSIS: A polarizing light microscope provides the gold standaId for crystal identification.
Monosodium urate crystals of gout are needle shaped or long with blunt ends, and display a strong
negative birefringence. CPPD crystals display a weak positive birefringence. The number of crystals
associated with human disease is increasing and includes calcium oxalate associated with renal failure,
crystals of protein in dysproteinemic states, cholesterol crystals in chronic inflammatory diseases, and
apatites.
3. GRAM'S STAIN: Useful iftbere is any suspicion of joint infection. Based on gram stain finding:; bacteria
can classified into broad groups to allow empirical therapy. The following steps are used in preparing a
slide:
A flame the smear
B. add crystal violet
C. Gram's iodine
D. wash with 95% alcohol
E. safranin
4. OIlIER STAINS:
Prussian blue: stain for iron that may show iron in synovial
lining cells in pigmented viUonodular synovitis or
hemochromatosis.
Ziel-Nielson : may be helpful in evaluating poSSible
tuberculosis.
Congo red : amyloid deposits show an apple-green birefringence
on polarized light examination.
Alizarin red S : a calcium stain used for apatite crystals.
ID. SPECIAL LABORATORY JESTS
1. CULTURES: if joint infection is suspected the fluid should be sent for culture and sensitivity. The
following type of cultures can be sent: aerobic, anaerobic, gonococcaL fungal, and tuberculosis.
2. MUCIN CLOf lEST: several drops of syno"ial fluid are added to about 20 mI. of 5% acetic acid in a small
beaker allowing one minute for a clot to form A " good clot " from notmal or osteoarthritis fluid forms a finn
mass that does not fragment on shaking. A n poor clot" like that from many inflammatory fluids fragments
easily and forms flakes, shreds, and cloudiness in the surrounding fluid " Good mucin clot " generally
reflects the normal integrity of hyaluronate.
43
3. LEUKOCYIE COUNT AND DIFFERENTIAL: will provide infonnation about the level of joint
inflammation.
4. GLUCOSE: synovial fluid glucose concentration is normally slightly less than that of blood glucose. A very
low level of glucose in the synovial fluid suggests joint infection Occasional effusions in Rheumatoid
arthritis have a S)'novial fluid level ofless than half that ofblood
RHEUMATIC DISEASES CHARACTERIZED BY SYNOVIAL FLUID ANALYSIS
NONINFLAMMATORY
Osteoarthritis
Trauma
Osteochondritis dessicans
Neuropathic arthropathy
Sickle cell disease
Osteochondromatosis
Hypertrophic osteoarthropathy
Ochronosis
Hemochromatosis
Acromegaly
Amyloidosis
HEMORRHAGIC
Trauma with or without fracture
Postsurgical
Pigmented villonodular S}novitis
Synovioma
Neuropathic arthropathy
Hemangioma
Coagulation disorders
Hemophilia
von Wtllebrand's disease
Therapeutic anticoagulation
Sickle cell disease
Thrombocytopenia
Ehlers-Danlos syndrome
Scurvy
CLASSIF1CATION OF SYNOVIAL EFFUSIONS
EXAM NORMAL NONINFLAMM
color straw strawlyellow
WBC(mm3) <200 200-2,000
PMN(%) <25 <25
culture (-) (-)
mucin finn firm
clot
INFLAMMATORY
Rheumatoid disease
Reiter's syndrome
Psoriatic arthritis
Ankylosing spondylitis
Ulcerative colitis
Acute crystal synovitis
Systemic lupus erythematosus
VIral or fungal infections
SEPTIC
Bacterial infections
INFLAMM.
yellow
2,000-75,000
>50
(-) often(+)
friable
SEPTIC
variable
>100,000
>75
friable
44
Tuberculosis of Bones and Joints
Amer Thoracic AssI.>cAmer J Resp and Clin Care Med, 149:
INlRODUCTION
1. The prevalence of tuberculosis bas been rising since 1986, with moIbidity increasing 14% from
1985 to 1993.
2. Urban areas of developed countries are more likely to encounter patients who have tuberculosis
3. Factors that contribute to increased rate include:
a. suppression of the immune system
b. development of drug-resistant strains of Mycobacterium
c. aging population
d inaeased number of health-care workers who are exposed to the disease
4. mv remains the leading known risk: for the reactivation of latent tuberculosis infection
5. Spinal tuberculosis has existed for at least 5000 years
6. Pott noted the association between tuberculosis involvement of the thoracic spine and paraplegia
7. The sanitarium setting, in the era before antitubercular drugs, was considered to be successful
treatment in that era, still bad a 60% mortality rate within six years after discharge from the
sanitorium
THREE RELATED ORGANISMS
1. Mycobacterium tuberculosis - most common
2. Mycobacterium africanum - found outside Northwestern Africa
3. Mycobacterium bovis - found in areas not utilizing milk pasteurization
MYCOBACTERIUM TUBERCULOSIS
4hin rod, with round ends, nonmotile, without capsule, resists decolorization with strong mineral acids and
alcohol; hence, is considered an acid-alcohol-fast or acid-fast bacillus.
-grows only on enriched medium containing egg and potato base or serum (albumin) base
-visible colonies appear at around 2 to 4 weeks, secondary to o ~ 1 ' g e n tension. Increased oxygen tension, as
in the lung, allows the organism to grow freely.
INCIDENCE
-one-thiId of the global population is infected with Mycobacterium tuberculosis
-M. tuberculosis is the cause of 3 million deaths per year
-ten million persons are presently infected, and 9()0" of new activated cases come from this infected pool of
individuals
-in non-Hispanic white people, the median age at diagnosis is 61 years
-among the American minority, the median age of diagnosis is 39 years
-one-thiId of patents with tuberculosis who are also infected with mv will have extrapulmonary disease,
with or without a pulmonary component
SITE OF INFECTION
-Tuberculosis has been reported in alI bones of the body
-In the U.S., the spine is involved 5OO" of the time
Thoracic spine 50%
Cervical spine 25% Pott's Disease- TB of the vertebra
Lumbar spine 25%
-other reported areas are less common,
pelvis 12%
hip & femur loo"
knee & tibia 10%
nbs 7%
ankle or shoulder 2%
elbow or wrist 2%
multiple sites 3%
-extrapulmonary tuberculosis is more common in children than in adults
-most common extrapulmonary involvement in children is the superficial lymph nodes(scrofula)
45
DIAGNOSIS OF MUSCULOSKELETAL TUBERCULOSIS
CLINICAL
1. Localized pain
2. Associated fever
3. weight loss
4. truncal rigidity
5. muscle spasm
6. neurological signs
7. cold abscess (swelling without inflammation) - strongly suggestive of TB osteomyelitis
o Tubercular skeletal lesions demands further evaluation of other organ involvement, i.e. lungs, intestinal
tract and kidneys. One-third of patients with bone or joint 1B have a history of pulmonaty involvement
PLAIN RADIOORAPHS
1. NO SPECIFIC RADIOORAPIDC FINDINGS
2. osteopenia
3. soft-tissue swelling
4. minimal periosteal reaction
5. narrowing of joint space
6. cysts in bone adjacent to joint
7. enlargement of the epiphysis in children
8. subchondral erosions
9. new-bone formation
BONE SCANS - not terribly helpful
SKIN TESTS
discovered the material tuberculin that was the antigenic component of Mycobacterium
tuberculosis. This was later precipitated out to reveal the purified protein derivative (PPD)
of the PPD test depends on exposure to M tuberculosis, immunosuppresion of the
host and Pfe'rious exposure to bacille Calmette-Guerin (bCG).
least 20% of debilitated or malnourished patients who have extensive disease have a false-
negative skin test
infected patients with concomitant 1B are prone to be anergic and will therefore provide a
negative skin-testing.
01HER TESTS
1. ESR - neither specific nor completely reliable
2. ELISA (enzyme-linked immunosorbent assay) - reported sensitivity of 60 - 800/0., but these
tests may be negative for patients who have advanced disease.
3. Chromatography-not widely available
4. Nucleic Acid Probes-not widely available
5. Polymerase Chain Reactions-not widely available
Crn.,TURE
diagnosis depends on recognition of Mycobacrerium tuberculosis on either histologic
study or culture or both.
BIOPSY
and possible operative treatment are reserved for patients who fail to respond to
adequate
chemotherapy, who have substantial neurological impainnent(as in rn infected vertebrae), or
in whom either resistant strains or other disease entities are suspected.
46
TREATMENT
1. If patient is suspected of having tuberculosis, that patient must be placed in an isolation
room
2. operative intervention should be delayed until the patient is no longer infectious
3. Medical treatment
a. contact Center for Disease Control for most recent guidelines
b. consult an specialist
4. Antibiosis
a. minimum of three to which the organism is susceptible
b. at least one of these must be bactericidal
c. Possible antibiotic selection includes, but is not limited to,
Isoniazid 3-5 mg/kglday
Pyridoxine 10 mg QD
Rifampin 10 mg/kglday
Pyrazinamide 20-25 mg/kglday
Ethambutol 15-25 mglkglday
StreptomycinlS-20 mglkglday
5. Optimum duration of treatment, 6-9 months for patients with pulmonary involvement alone.
Patents with extrapulmonary tuberculosis require 12-18 months of treatment
MANAGEMENT of HIV
L Definition: a human retrovirus that infects lymphocytes and other cells bearing the CD4 surface
marker. Infection leads to lymphopenia, CD4lymphocyte deficiency and dysfunction, impaired cell-
mediated immune response, and polyclonal B-cell activation with impaired B-cell response to new
antigens.
1. AIDS: characterized by opportunistic infections and unusual malignancies
II. Standard of Care
1. Document CD4 count every 3-4 months as long as CD4>50. Do not need to follow CD4 count<50.
Viral load testing every 3-4 months.
2. All HIV -infected patients should have the following regardless of CD4 count:
A PPD/anergy panel
1. IfPPD is (+) give INH for I year.
2. Anergy panel-Checks the ability to host an immune system response. Want it red and
raised.
B. RPRlFfA: IfRPR is reactive, get an LP.
C. Pneumococcal vaccine: Get every 3-5 years.
D. Influenzal shot: Get every year. This is controversial.
E. Hepatitis screen and heptavax series if HBV serology is negative.
F. Cervial pap smear for all women eveyr 6-12 months.
G. Toxoplasma titer.
3. CD4 of 500 begin combination antiretroviral therapy using:
A AZT 200mg TID + a second reverse transcriptase inhibitor +/- a protease inhibitor.
1. AZT: can cause megaloblastic anemia, neutropenia, GI effects, anxiety, dark blue nails.
B. Other nucleoside reverse transcriptase inhibitors include:
1. DOl: can cause pancreatitis, peripheral neuropathy.
2. DOC: can cause month ulcers, peripheral neuropathy.
3. D4T
4. 3TC: has the least amount of side effects.
C. Protease inhibitors: (saquinavir, indenovir, nalfinC\ic, ritonavir, amprenovir)
1. Decrease markedly and prolong life.
2. Be selective with patient: Have to be compliant with medication. If doses are missed
resistance can form
47
D. Nonnucleoside ribonuclease reverse transcriptase inhibitors:
1. viramine
2. delavadine
3. efavirenz
4. CD4,200 begin PCP (Pneumocystis carinii pneumonia) prophylaxis:
A. PCP prophylaxis should be started regradless of CD4 count if patient has oropharyngeal candidiasis
(thrush), fevers, weight loss/wasting syndrome.
B. PCP prophylaxis drug therapy:
l. Bactrim I DS on Mon., Wed, and Fri. This is the drug of choice. Can cause rash, fever,
neutropenia, GI effects, liver dysfunciton.
2. Dapsone: Second drug of choice. Must check for G6PD-can cause hemolytic anemia.
May also use dapsone plus pyrimethamine.
3. Aerosolized pentamidine: Third drug of choice. Can still get PCP in upper lobes. Can
cause cardiomyopathy, damage to retina. Can also give monthly IV pentamidine.
C. To diagnose PCP:
1. WH wil be increased
2. If gallium scan is (=) possible PCP, if (-) definitely NOT PCP.
3. Get ABG, ifp02<75, start tapering doses of steroids (ie, prednisone 40mg BID x 5 days,
40 mg QD x 5 days, 20 mg QD x 5 days).
4. Bronchoscopy.
D. PCP tretment:
1. Bactrim
2. Pentamidine: Second drug of choice. Must correct for renal insufficiency. Can cause
pancreatitis, life-threatening hypoglycemia and hypertension.
5. CD4<75 begin MAC (Mycobacterium avium complex) prophylaxis:
A. Rifabutin: Drug of choice for prophylaxis. Can cause GI effects and hepatotoxicity. Second line
choices include clarithromycin or azithromycin.
B. Can cause bone marrow suppression and pancytopenia Need to check AFB in blood. May also be
found in respiratory or GI tract.
C. Treatment for MAC is for life. Usually clarithromycin + one other drug (ethambutol, clofazimine,
ciprofloxacin, rifabutin).
6. CMV (cytomegalovirus):
A Retinits: Most common place it presents. Usually patient is at end stage disease. Treat for life.
B. May be found in bone marrow, liver, urine, blood.
C. Treatment (There is no prophylaxis available):
1. Ganciclovir. Can cause bone marrow suppression and neutropenia. Oral fonn can be used
for CMV colitis.
2. Foscamet: Assocaited with renal failure and electrolyte abnormalities. May have some
anti-retroviral properties.
D. Recurrences occur frequently and require reinstitntion of high dose induction therapy.
E. +Note-CMV, MAC, lymphoma all can present with fever, bone marrow suppression, pmcytopenia,
and an increase in LFT's.
7. Kaposis
A Can be found in skin, mouth, GI tract, liver (can cause biliary obatruction), lung (these bleed
easily- prognosis very poor).
B. Treatment is chemotherapy. Intralesion interferon can be injected for skin lesion.
8. TB
A. Rise with increase in my. With this see an increase in extra-pulmonary TB.
B. If patient has been incarcerated, homeless, or lived in a shelter, should be tested for TB.
C. Treatment for patients with HIV and 'IB should be for one year.
9. Peripheral neuropathy:
A About 50% ofHIV patients will have this.
B. Treatment:
1. Elavil: as much as their blood pressure can tolerate.
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2. MoIpbine.
3. Mexilitine.
10. Other possible infections:
A Toxoplasmic encepablitis: Prevention-do not eat raw meat, wash all vegetables, stay away from
cats. Prophylaxis is Bactrim or dapsone plus pyrimethamine.
B. Cryptosporidosis: Found in contaminated drinking water. No available prophylaxis.
C. Cryptococcus: Avoid sites contaminated with pigeon droppings. Treatment is fluconazole.
D. Coccidiomycosis: F01D1d in soil, fanns. Preferred treatment is fluconazole. "Alternate drugs
include itraconazole, ketaconazole, amphotericin B.
E. Histoplasmosis: F01D1d in chicken coops. caves, bini roosting sites. Treatment is fluconazole.
F. Candidiasis: F01D1d on mucosal smfaces and skin. Treatment is an oral azole (fluconazole).
Can also use topical nystatin or clotrimazo1e.
Herpes Simplex: Treatment is acyclovir until lesions have resolved. Can use IV
foscamet for strains resistant to acyclovir.
H. Varicella-Zoster: Effectiveness of acyclovir is questionable.
1. Human Papillomavirus: May need biopsy of cervix.
1. Bacillary angiometosis: Looks similar to Kaposis. Treatment is erythromycin.
K. Seborrheic Dermatitis.
NEUROLOGY
Nemologic disonlers may lead to various lower extremity manifestations including cavus deformities, equinus,
pes planus, spasticity, paralysis, gait abnormalities and diminished sensation
1 DIAGNOSTIC WORKUP:
l.History of illness
- Should be obtained from all available sources.
- Utilize a problem oriented fonnat i.e.NLDOCAT.
a. Patient
b. Family/Guardian
if patient is a child, ascertain pregnancy course delivery, APGAR score,
developmental milestones.
c. Other healtbc.are professionals
2.Past medical history
3.Past surgical history
4.Cunent medications
5.Family history
6.Social history - occupation, EtOH, illicit drugs, SID'slHIV
II. PHYSICAL EXAM
-a complete neurologic exam should be performed. Neurology consultation is highly recommended.
1. Mental status check - obtained by obseIvation and. during history taking.
- Assess general appearance, level of consciousness, orientation, affect, cognition.
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2. CI3Dial nerves
I. Olfactory- sense of smell
II. Optic- visual acuity and fields
aanopsia- loss in 1 eye
b. bi-temporal hemianopsia- loss temporal fields
c.homonymous hemianopsia-loss complete field,L or R (see Fig. 1)
ill. Occulomotor >
IV. Trochlear extraocular eye motions
VI. Abducens >
V. Trigeminal- Motor- muscles of mastication
- Sensory- entire face via 3 divisions
VII. Facial- Motor- muscles offacial ex-pression
- Sensory- anterior 213 tongue
VII. VestIbulocochlear - hearing
IX. Glossopharyngeal - sensory posterior 1/3 tongue
X Vagus -uvula midline, normal voice, gag response
Xl Spinal accessory - Motor sternocleidomastoid and trapezius
XII. Hypoglossal - motor tongue
3. Motor exam - evaluate symmetry, function and muscle tone
a Lower extremity
Tl2-L3 - Iliopsoas
L2-4 - Adductors, Quadriceps
lA - Tibialis anterior
L5 - Abductors, EBL, EDL, EDB
S I - Gluteus maximus, PL, PB, TP, Gastrosoleus
S2-3 - Instrinsics
b. Upper extremity
C5 -Deltoid
C5-6 -Biceps
C6 - Wrist extensors
C7 - Triceps, Wrist flexors, Finger extensors
C8 - Finger flexors,
C8-Tl - Hand intrinsics
c. Manual muscle test grading
5 - Normal - Complete ROM ag;rinst gravity with full resistance
4 - Good - Complete ROM ~ gravity with some resistance
3 - Fair - Complete ROM against gravity
2 - Poor - Complete ROM with gmity eliminated
I - Trace - Evidence of slight contractility. No ROM
o -Zero - No evidence of contractility
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4. Sensation - determine if sensory loss is localized to a single dermatome or stocking-glove distribution
a Posterior colwnns
-Vibratory
-2-point discrimination
-Position sense
't h. OO'erjor spinotha1am.ic
-Light touch
\t" c. 8!ternl spinotha1am.ic
'1 -Pain and tempeIature
5. Reflexes
a Deep tendon
U - Patellar tendon
Sl - Achilles tendon
C5 - Biceps tendon
C6 - Brachimadialis tendon
C7 - Triceps tendon
Grading ofDTR's
-!{) - absent
+ I - hypoactive
+2 -normal
+3 -hyperactive
+4 - pathologically brisk: / clonus
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b. Pathological reflexes - assesses UMN dysfunction
Babinski - not present - plantarflexion of toes
- Present - dorsiflexion of halllLX and fanning of lesser toes.
6. Cerebellar tests
a.Rhomberg
b. Rebound
c. Rapidly alternating movements
d Heel to shin
e. Tandem walking (heel to toe)
7. Orthopedic lower extremity exam
a. assess deformities present
- mild, moderate, or severe
- flexible or rigid
- location - rearfoot, midfoot, forefoot or combination of deformities
- compensatory mechanisms present
- evaluate weightbearing and non-weightbearing
- gait analysis
-sensory ataxic - demyelinating peripheral neuropathies, spinocerebellar
degeneration, Vit Bl2 deficiency, M.S.
-steppage - peripheral or spinal motor nerve lesions, polio, CMf, progressive
muscular atrophy
-myopathic - Muscular dystrophy and other myopathies
-<:erebellar ataxic - cerebellar lesions
-extrapyramidal- PaIkinson's
-spastic - CV A, tumor, tramna, corticospinal lesion, M.S., c.P.
-apractic - Alzheimer's, normal pressure hydrocephalus
-hysterical
8. Labs and Special Studies
may include CPK, aldolase, EMGlNCV, muscle and nerve biopsies, lumbar puncture, cr
scan, MRI, X-rays and other procedures.
ill. Differentiation on Upper Motor Neuron (UMN) and Lower Motor Neuron (LMN) dysfunction
Voluntary control
Tone
Reflex arc
Pathologic reflexes
Atrophy
UMN LMN
lost lost
splStic flaccid
present absent
present not present
little or none significant
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N. Neurologic Diseases affecting the lower extremities
1. Caws Foot - 75% of patients with a pes cavus deformity will have an underlying neurologic
problem (Brewerton et al.)
Congenital causes:
CHARCOT-MARJE-TOOm DISEASE (Peroneal muscular atrophy)
-most common neuromuscular disorder resulting in cavus foot. Symmetric
hereditary motor and sensory nemopathy that is progressive.
-3 modes of inheritance
l. Autosomal dominant- affects 30/100,000 and is slowly progressive
2. X-linked recessive- affects 3.61100,000 and is more severe, onset during
adolescence
3. Autosomal recessive- affects 1.41100,000, is rapidly progressive and severely
disabling
females> males 3-5:1. Seen primarily in Ca)!casians
deformities- caws, caVOvarus, equinocavoV311lS due to overpowering of
muscles. Rigid or Flexible
CHARCOT-MARJE-room DISEASE (cont)
PL> TA produces a plantarflexed medial column
TP> PB produces a rearfoot varus
-Contracture of plantar fascia increases cavus
-FDL > EDL and intrinsics leads to clawtoes
generalized LE atrophy leads to the development of "stork leg" or
"inverted champagne bottle" deformity.
-present with high steppage or marionette gait
-progressive atrophy of distal UE leads to "monkey fist" or "skeleton hand"
deformity.
-Diminished sensation in stocking-glove distnbution
-NCVare delayed by awroximately 50010
-Diagnosis based on positive family history and clinical findings. Recently
available is a blood test to diagnose the Type I autosomal dominant form.
DEJERINE-SOTTAS DISEAE (Hypertrophic interstitial polyneuropathy)
-autosomal recessive
-progressive disease with onset in childhood to early adulthood.
~ weakness and sensory loss of primarily the lower extremities.
-peripheral nerves are enlarged and frequently palpable due to "onion bulb"
fonnation of the nerves
-nerve biopsy reveals concentric proliferation of Schwann cells around an area of
demyelination.
FREIDRICH'S ATAXIA
-recessively inherited disease
-idiopathic degeneration of the posterior and lateral colmnns of the spinal cord
-onset in late childhood and early adolescence, rapidly disabling.
-weakness oflower extremities, anterior and lateral compartments. Later upper
extremity
weakness, primarily ulnar nerve distribution.
-stocking-glove sensory loss.
-cerebellar involvement with incoordination, nystagmus, dysarthric speech, ataxia.
-no lab abnonnality is diagnostic however, sensory action potentials are absent or
markedly
decreased NCV remain nonna! or decrease slightly with disease progression.
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ROUSSY-LEVY SYNDROME
-autosomal dominant inherited disease
-slowly progressive
-common findings include resting tremor, clwnsy gait, atrophy of the distal LE's
and UE's, abnormal equilibrium, and absent D1R's.
REFSUM'S DISEASE (Heredopathia atactia polyneuritiformis)
-autosomal recessive, hypertrophic sensory-motor polyneuropathy
-metabolic neuropathy caused by a disturbance in lipid metabolism which leads to
an accumulation of phytanic acid
-males = females
-periods of acute exacerbations
-retinitis pigmentosa, ataxia, ichthyosis, deafness, distal extremity weakness with
gait distwbances, diminished D1R's.
-sennn phytanic acid levels are >50010 above normal.
SPINAL DYSRAPHISM
CEREBRAL PALSY
-failure of mesoderm and neuroectoderm to fuse and form the neural tube
-Types:
1. Spina bifida-Iack of closure of vertebral arches, primarily lumbar
2. Spina bifida occulta- not accompanied by protrusion of meningeal or
spinal
elements
3. Spina bifida cystica- protrusion of meninges
4. Meningoradiculocele- protrusion of meninges and nerve roots
5. Meningomyelocele- protrusion of meninges and spinal cord.
-leg weakness with feet in equinovarus position
-(timinished D1R, sensmy loss feet and saddle area
-may be associated with hydrocephalus
-associated with congenital abnormalities and mental retardation
-caused by static brain lesion acquired in utero, during delivery or months after birth.
-commonly due to trauma, asphyxia or premature birth
-irreversible, non-progressive brain deformity
-classification:
-Spastic (65%)
1. Spastic diplegia- BIL LE spasticity- scissoring gait, variable mental
impairment
2. Spastic quadriplegia- severe BIL UE and LE spasticity, severe
intellectual impairment
3. Spastic hemiplegia- unilateral spastic hemiparesis, less severe mental
impairment
-Athetoid (20%)
-Ataxic
-Rigid
-Tremor
-Atonic
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-treatment ofCP
-Physical therapy
-Surgical intervention-release contractures
-Muscle relaxants
MUSCULAR DYSTROPHY
-familial disoIders that lead to degeneration of muscle fibers, due to enzymatic defect
-Types:
L Docbenne' Pseudohypertrophic - most common sex-linked inherited
myopathy, diagnosed during early childhood due to slow motor
development SOOIo show pseudohypemophy of ca1f musculature due to
fill deposition which can be seen on biopsy. Girdle weakness leads to the
classic
"Gower's sign" utilized when going from the
floor to standing. Ankle equinus and
equinovarus deformities are common.
Progressive and the ngority of pdients are
wheelchair bound by age 20. Elevated CPK
levels are noted
2. Becker MD. - similar pattern of muscle weakness as Duchenne
however, less aggressive. Patients with Becker MD. often walk to
approximately age 35 and have longer life spans.
3. Facioscapulohumeral MD. - mildly progressive, affects faciaI and
shoulder muscles with weakness and atrophy. Lower extremity weakness
usually oca:as 20-30 years later.
4. Myotonic MD. - multisystemic disorder, onset I3Dges from birth to 50
years of age. Presents with tonic JIWSCle spasms. Often a foot drop
develops.
5. Limb giIdle MD. - diagnosis of exclusion, has inconsistent features.
Initial }ESeDtation of shoulder and pelvic giIdle weakness and atrophy.
SYRINGOMYELIA
-progressive disorder, onset usually 2nd-3rd decade
-characterized by muscle atrophy, dissociated
anesthesia, pamparesis with neurotrophic changes including neurogenic
osteoarthropathy (Charcot), loss ofD1R
by a tubular dilatation in the spinal cord most commonly in the cervical
-diagnosis easily made with MRI or cr
2. Peripheral neuropathy ( COMMON CAUSES)
-Hereditary
-CMT
-Dejerine-Souas
disease
-Amyloidosis
-Acquired
-Diabetic
-Myeloma
-Guillain-Barre'
-Malignancy
-Uremia
-CtyOglobulinemia
-HlV
-Tangier's disease
-Fabry's disease
-Abetalipoproteinemia
-Freidrich's ataxia
-Hypothyroidism
-Sarcoidosis
-Alcoholic
-Collagen-vascular
-Acromegaly
-VitaminB
55
-Toxic (ie drugs, chemicals)
<hloramphenicol
-isoniazid
-nitrofurantoin
-DaJEone

-metronidazole
-hydralazine
-phenytoin
-lead
-cyanide
-thallium
-zerit
-Infectious
-leprosy
-diphtheria
-IHV
-Entrapment
-aupal and tarsal tunnel
3. Various neurologic disease
1. PARKINSON'S DISEASE
-lithium
-pyridoxine
-disulfuram
-ethionamide
-vincristine
-gold
-amiodarone
-colchicine
-arsenic
-mercwy
-trichloroethylene
-ddI
-herpes zoster
-Lyme disease
-progressive disorder, characterized by eosinophilic inclusious in the
neurons of the substantia nigra.
<haracterized by rigidity, resting tremor, bradJkinesia, loss of postural reflexes,
festinating gait Dementia occurs in 50010 of patients.
-males=females, onset 40-60 years of age
-multiple drugs utilized in treatment including levodopl, caIbidopl, amantadine,
bromocriptine. pergolide. Physical therapy helpful to improve
function.
2. MULTIPLE SCLEROSIS
-chronic CNS disease of unknown origin
by inflammatory demyelinating plaques in white matter of eNS.
Infiltration oflymphocytes, plasma cells and macrophages.
-ooset at around 30, 2: 1 female:male
-course is relapsing and remitting
-optic neuritis is most common presenting SJDlPI:om
-LE affected> UE often with SJmIicity and futigue
-cerebellar involvement with ataxia, scanning dysarthria and intention tremor
-autonomic symptoms- incontinence, impotence and orthostatic hypotension.
-often see peISOnaIity changes, memory loss, dementia and emotional lability.
-MRI diagnostic in >90% of cases
-mean survivalawrox. 25yrs and is improving
-avoid physical and emotional stress, infections and prolonged exrposure to
extremes of temperature.
3. CEREBRAL VASCULAR ACCIDENT
-rapid onset of a nemologic deficit involving a vascular territory of the brain and
lasting for greater than 24 hams. < 24 hours considered a transient ischemic attack
(TIA).
-most often due to thrombosis or embolic event as well as hemorrhage from
aneurysm or A V malformation.
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-presentation varies with the vessel involved and portion of the brain infarcted.
-cr scan diagnostically helpful
-Genemlly, early flaccid paralysis followed by increasing spasticity and
development of synergistic patterns.
-Physical therapy and orthotic fabrication can improve functional ability
4. EPILEPSY
-characterized by abnonnal, recurrent, excessive discharges from neurons.
-50010 have no 1lIJ.<b-lying neurologic disorder
-other etiologies include EtOH withdrawaL head trauma, hypoglycemia, meningitis,
encepbalitis
-most seizures last 30-90 seconds
-Classification
l.Focal (Partiallocal)- originate from a localized portion of the brain
-Simple focal
-motor- focal motor with march Jacksonian
-sensory- somatosensory, visual,auditory, gustatory
-autonomic- epigastric sensation, pallor,sweating, flushing,
piloerection, pupillary dilatation
-psychic- dysphasia., affective, cognitive, illusions.
hallucinations.
-Complex focal
-simple focal followed by impairment of consciousness
-impaired consciousness at onset sometimes with automations.
-Any focal seizure may evolve to a secondary generalized seizure.
2.Generalized - no focal component,therefore no prodrome, aura or focal
motor or sensory symptoms.
-Absence (petit Mal)
-impairment of consciousness only, may show mild
clonic,atonic,tonic component.
-Myoclonic seizures
-Tonic
-Tonic-Clonic (Grand mal)
-Atonia (astatic) seizures
3.Unclassified
-Status epilepticus
-condition in which patient has a series seizures \\'ithout total recovery of
consciousness. Most common cause in compliance with seizure
medications.
-AnticonvuIsants (ie. phenytoin, carbamazepine) are most commonly utilized.
Need to
obtain therapeutic blood levels.
5. MYASTHENIA GRAVIS
-Acetylcholine (Ach) receptor antibodies destroy the receptor sites on the
postsynaptic membrane. Results in miniature end plate potentials that are reduced
in size and number.
-Due to an autoimmunoplthy
-Ha1.lma1k is exercise induced fatigue that is resolved with rest.
-Often get double vision and ptosis, difficulty with che,viog. Only involves skeletal
muscle.
-Ach receptor antibody found in the serum of>90%
57
-Tensilon (edrophonium) is helpful diagnostically.
-EMG shows classic changes of decrement
-5% of patients have an associated thymoma which is most easily diagnosed with
CT scan.
-Treatments include long term anticholinesterase meds or disease modifying drugs
such as Immuran. Also plasmaphoresis has been found to be effective.
MG (cont)
-*** Eaton-Lambert syndrome is similar to myasthenia gra"is however, it involves
a defect in neuromuscular transmission due to a decreased number of Ach packets
released at the presynaptic terminal.
- use certain meds such as aminoglycosides and tetracycline with caution
6. GUllLAIN-BARRE' SYNDROME (Acute idiopathic polyneuritis)
-immunologically mediated demyelinating polyneuropathy
-affects all ages and se"{es
-bimodal peaks of occurrence- 15-35 yrs and 50-75yrs
-usually preceded by a viral or mycoplasma infection. surgery, immunization or
in patients with systemic lupus erythematosis (SLE) and lymphomas.
<haracterized by rapidly progressing symmetrical motor weakness in a distal to
proximal fashion. Can lead to severe respiratory paralysis and occasionally cranial
nerve involvement
<auses stocking-glove paresthesias
-decreased or absent DTR's
-may cause autonomic dysfunction including-brndycardia/tachycardia,
hypotension/hypertension.
-diagnosis-lumbar puncture reveals elevated CSF protein and the presence of a fe.v
mononuclear leukocytes.
-EMG reveals decreased NCV and prolonged latencies
-functional recovery occurs usually 2-4 weeks
BONE TUMORS
I
ccmr H:M. F1nous IIYSPt.4S fit
---ua
1

i

1
CEL{.1UMCIt
aUlD; oI1Eli'f'Sn'5EIl
.,.,. ICII'"
58
CIassification: Histologically based on the cell or tissue type from which the lesion originates. Osseous,
Cartilaginous and Fibrous are the origin of most primaIy benign and malignant neoplasms in bone.
Diagnosis:
Subjective symptoms(NLDOCAT)
Past medical history
Clinical evaluation of objective signs
Radiogrnphic evaluation:
Helps to determine the rate and aggressiveness of the bone
tumor
1. Pattern ofbone deslruction:
a) Geographic -least aggressive, well defined
b) Moth eaten -more aggressive, less defined
c) Permeative - highly aggressive
2. Sclerotic border:
-slowly growing lesions are associated with reactive sclerosis of the surrounding
bone
-sclerosis can be of variable thickness and partially or completely surround the
lesion
3. Cortical involvement:
-bone cortex serves as a barrier to Iateral expansion of the tumor
-nonaggressive medullary lesions may cause little change in the endosteal surfuce,
however, some benign lesions
such as aneurysmal bone cysts can expand rnpidly
-aggressive lesions cause endosteal erosion and can penetrate the corte.x in more
than one pJace
4. Periosteal reaction:
1. Continuous
a. Cortex destroyed
smooth shell - due to expansile pressure benign lesions (giant cell,
enchondroma, fibrous dysplasia)
lobulated shell - due to ,'31iation of growth rate
ridged shell - AKA "soap bubble" due to slowing rate of
prolifemtion (non-ossifying fibroma, enchondroma)
b. Cortex present
solid - implies slow growth rate, can be seen in osteoid osteoma,
enchondroma and eosinophilic granuloma
undulating - variant of solid, seen with periostitis, hypertrophic
osteoartbropath
lamellar - may be single or onion skin in appearance
parallel or spiculated "hair on end" -often associated with
malignancy (Ewing's sarcoma)
2. Interrupted
a Buttress
solid appearing wedge ofbone, forms at margins
of slowly enlarging lesion( chondromyxoid
fibroma, malignant change oflong-standing benign lesion)
b. Codman Triangle
suggests aggressive malignant lesion seen in
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osteosarcoma and chondrosarcoma
c. Lamellated Reaction
onion skin appearance can be seen in malignant
(osteosarcoma) and benign lesions (eosinophilic granuloma)
3. Complex
Sunburst pattern, highly suggestive of osteosarcoma
5. Size and Shape:
In general, malignant tumors are larger than benign tumors, often >6Cm
Elongated lesions in which the greatest lesional diameter is 1.5 times the least
diameter may be indicative of Ewing's sarcoma, histiocytic lymphoma,
chondrosarcoma and angiosarcoma.
6. Soft tissue involvement:
If lesion leads to cortical breakthrough than it is aggressive
7. Skeletal location oflesion:
Tumors may predominate in areas of red, or hematopoietic,
marrow. These include metastatic disease, plasma cell myeloma, Ewing's sarcoma
and histiocytic lymphoma.
The tendency for these tumors to involve appendicular and axial skeleton in the
young and only the axial skeleton in aged is related to the changing distnbution of
red marrow.
Some tumors are more prevalent in areas of rapid bone growth such as distal femur
and proximal ubia.
Tibia: increased incidence of adamantinoma, nonossifying
fibroma and chondromyxoid fibroma, osteosarcoma, osteoid
osteoma, Giant cell tumor
Fibula: non-ossifying fibroma, aneurysmal bone cyst, Ewing's sarcoma, lipoma
Foot chondromyxoid fibroma, aneurysmal bone cyst,
chondroblastoma, osteoid osteoma, osteoblastoma, enchondroma, lipoma
8. Location oflesion in bone: (Fig.!)
Transverse plane:
Central .......... Solitary bone cyst, enchondroma
Eccentric ........ Aneurysmal bone cyst, giant cell tumor,
osteosarcoma, chondrosarcoma, fibrosarcoma, chondromyxoid
fibroma
Cortical ......... Non ossifying fibroma, osteoid osteoma
lID..1acorticallParosteal .... Osteochondroma, juxtacortical
chondromas, parosteal osteosarcoma
Longitudinal plane:
Epiphysis ........ Chondroblastoma
Metaphysis. ...... Osteosarcoma
Diaphysis ........ Ewing's sarcoma, retinaculum cell sarcoma, multiple myeloma and
metastases
Physeal .......... Giant cell tumor
MetalDiapbyseal..Unicameral bone cyst, enchondroma
9. Trabeculation:
-may reflect residual trabeculation displaced by tumor or
new bone formation due to the tumor
Pattern
delicate, thin
coarse, thick
lobulated
delicate, horizontally
oriented
striated, radiating
Tumor
Giant Cell tumor
Chondromyxoid fibroma
non ossifying fibroma
aneurysmal bone cyst
hemangioma
60
10. Matrix Pattern:
Size
~ tumors produce matrix that calcifies or ossifies
Cartilage tumors:
-calcific circles (rings) -<hIe to endochondral bone
formation .
-flocculent
-fleck-like (stippled)
11. Patient age: (Fig.2)
~
1. 1 year
2. 1 year to 10 yrs.
3. 10 years to 20 yrs.
4. 10 years to 30 yrs.
5. Skeletally immature
~
6. Skeletally mature to
5Oyrs.
7. 30 years to 60 yrs.
8. 50 years to 80 yrs.
Lesion
Melaslatic neuroblastoma
Ewing's sarcoma
Aneurysmal bone cyst
Osteosarcoma
ChondrobJastoma
Lesion
Giant aill tumor
ChondrosaIcoma
PrimaIy lymphoma
Malignant fibrous histiocytoma
FibrosaIooma
Multiple myeloma
Metastasis
Benign versus Malignant Bone Lesions
Benign
Small
Malignant
Large
Soft tissue mass
Periosteal reaction
Margins
None Large
Rare Common
Sclerotic None
Zone of transition
Trabeculation
Cortical destruction
O v e r a l l ~
Other diagnostic tests include:
-Bone scans
Narrow Wide
Yes
Rare
Geographic
provides insight on multiple sites of involvement
Increased upIake of the nucleotide in bone reflects the
hypermetabolic osteoblastic activity
-Computerized tomography
No
Usual
Permeative or Moth-eaten
helps to detennine more precisely the location and extent of involvement of the tumor
-Magnetic resonance imaging
also helps to detennine the location and extent of involvement of the tumor, however, better
in assessing
the soft tissues and tumor characteristics.
-Laborntory studies
Alkaline phosphatase(blood and urine)
Complete blood count
Chest x rny
61
-Biopsy
age and gender specific studies may include
serum protein electrophoresis(SPEP)
urine protein electrophoresis(upEP)
prostate specific antigen(pSA)
thyroid function tests(1Frs)
liver function test (LFf)
carcinoembryonic antigen(CEA)
lncisional: cutting into the lesion to remove a sample for pathology evaluation
-required for malignant bone lesions
-carries risk of spreading lesion by lymphatic or
blood seeding
-complications are minimized with careful incision
planning, strict hemostasis, minimal dissection,
avoidance of neurovascular structures and tight wound closure
Excisional: removal of entire lesion (done for benign tumors)
Common Tumors of the Distal Leg and Foot:
BENIGN TUMORS:
1. Osteoid osteoma
-benign osteoblastic lesion clmacterized by a well demarcated core(nidus)of usually less
than 1 cm. and a distinctive surrounding zone of reactive bone formation.
-age: 10-25 years (rare>30 years) males>females
-location: femur 32% tIbia 24% . foot 11%
-presentation: point tenderness over the lesion, nocturnal pain, local soft tissue swelling in
the foot, the lesion usually appears at the junction of the anterior mid-third
of the talus or OS calcis, salicylates may completely relieve symptoms by prostaglandin
inlubition
-radiographic foatures: lesion is located most commonly in the
cortex. The lesion has a radiolucent nidus with a striking
thickening of adjacent cortical bone and periosteal new bone formation.
-pathologic foatures: lesion is clmacterized by varying degrees of osteoid and highly
vascular supporting osseous tissue.
-treatment: excision of the nidus and surrounding bone
2. OsteobIastoma
-benign, rapidly growing tumor that is histologically similar
to osteoid osteoma Characterized by the absence of any reactive perifocal bone formation.
-age: 20-30 years of age (9()01o are <30 years of age)2: 1 males:females
-location: diaphyseal and metaphyseal in the foot the tumor
occurs most commonly in the dorsal aspect of the anterior portion of the talus
-presentation: dull, aching, localized pain. Not noetumal
pain. Pain is not relieved by salicylates. Localized swelling
-radiographic foatures: lesions are weIl circumscnbed, r a d i ~
lucent and usually expansive with occasionally a thin shelf of reactive bone.
-pathologic foatures: tumor is hemonbagic, gritty and friable. Large lesions may show
central softening and cystic degenerntion
-treatment: cmettage and packing of the defect
3. Enchondroma
-benign hyaline cartilage grol\1h that develops within the
medullary cavity of a single bone
-age: usually manifest during 3rd or 4th decade; equal distribution between the sexes
-location: metaphyseal to diaphyseal- most occur in the small
62
\J
~
'lj
J
J
J
J
tubJlar bones in the foot, seen in metatarsals and pba1anges
-presentation: lesions develops slowly and gradually and is well established before clinical
symptom Often painless swelling is the fust manifestation. Painful lesions without
trauma sbould arouse suspicion that a malignant ttansformation is occurring.
-radiographic features: lesions are well ciIcumscribed with
distinct ares of Iarefuction-the lesion may show speckled calcification
-pathologic features: hyaline cartilage with scattered calcification
-treatment: curettage
** The syndrome of multiple enchondromas is known as OIlier's
disease. If also associated with soft tissue hemangiomas, the disoIder is known as
MafIbcci's syndrome.
4. Osteochondroma
-beDign, slow growing mushroom shaped hyaline cartilage capped
lesions. Classically arise from a growth plate in long bones,
growth ceases with skeletal maturity
-age: 2nd decade, 2: I male:female
-location: metaphyseal to diaphyseal- exostosis points away from adjacent joint -commooly seen in
the distal femur and proximal tibia
-presentation: often an incidental finding on x my most commonly a painless, slow growing
lesion - pain may becaused by impingement of smrounding anatomic structures.
-radiographic features: shaIply peduncu1ated or sessile tumor
at the level of the metaphysis that points away :from the nemby joint
-pathologic features: cortex and periosteum of the tumor are continuous with underlying
bone. Hyaline cartilage is usually 2-3 mm thick and this diffentiates an oste<K;hondroma
from a subungual exostosis which has a fibrocartilage cap. '
-treatment: excision
**less than 1% give rise to chondrosarcoma
5. Non-ossifying fibroma
age: 1st and 2nd decade
location: cortically based metaphyseal lytic lesion, eccentrically located-most common in
distal femur and proximal tlbia
presentation: usually asymptomatic unless associated with a pathologic fracture 'with
accompanying pain. swelling and'disability.
radiographic features: Lesion ,is an active and proliferating frum of fibrous cortical defect
seen in infimts and childrenLucent, eccentric lesions that may be loculated, with a sclerotic
rim
pathologic features: dense col1agen. giant cells and lipid filled histiocytes
treatment: curettage
6. Chondromyxoid fibroma
rare, benign tumor composed of chondroid, fibrous and myxoid tissues
age: 2nd to 3rd decades, male>females
location: occur in the metaphyses oflong bones offoot - 16%
presentation: usually complain oflocalized, dull, achy pain possibly swelling and
tenderness
radiographic features: lucent tumor, usually>5cm. with well-defined sclerotic borders
pathologic features: nodules of poorly fonned hyaline cartilage and myxoid tissue
delineated by fibrous septae
treatment: curettage
7. Aneurysmal bone cyst
primary tumor like lesion which initates an A V fistula and thereby creates, via hemo-
dynamic forces, a secondary reactive bone lesion
age: most occur in patients under 30 years of age, equal se..x distnbution
63
location: may affect any bone - foot-8%
presentation: mild to moderate pain as the lesion develops, patient may limp
radiographic features: small lytic lesion seen early
later, areas resembling Codman's triangle may develop, at the blowout stage the bone may
appear expanded with no shell around the lesion. Late lesions as a result of fibrous septae
and bony spicules appear loculated.
**angiography may help to define the vascular malformation
treatment: curettage and packing with bone chips
8. Simple bone Cyst (Unicameral bone cyst)
-fluid containing solitary unilocular cyst
-age: 80-90% <20 years old, 2: 1 males:females
-location: metaphyseal region of long tubular bones in juxtaposition to the epiphyseal plate
-presentation: indistinct discomfort makes the cysts presence known. In 50%, pathologic
fracture is the cause of diagnosis
-radiographic features: from its principle metaphyseal location, the cyst extends into the
diaphysis. Characteristically, they occupy a central location, its length is
greater than its width. The overlying cortex is eggshell thin but always intact.
***fallen fragment sign-radiologic finding describing a free fragment of cortical bone fallen by
gravity in the fluidcontaining cyst.
-pathologic features: serous usually bloody tinged fluid is expelled upon opening. Cavity is
unicystic with a whitish, thin glistening lining.
-treatment: curettage and packing with bone chips
9. Giant cell tumor
-uncommon, locally aggressive tumor so named because it contains multinucleated, osteo-
clast type giant cells.
-age: arise during 3rd to 5th decades
-location: adults: involve both epiphysis and metaphysis
(adolescents: confined proximally by the growth plate and are
limited to the metaphysis-most arise about the knee)
-presentation: location of the tumor near ends of bones causes
arthritis type symptoms-occasionally pathologic fracture is presenting concern.
Swelling, intermittent pain and limited range of motion also can be seen.
-radiographic features: large, lytic "soap bubble" lesions
which are eccentric may have a thin, perilesional sclerotic shell
-pathologic features: large and red-brown and frequently
undergo cystic degeneration.. Composed of uniform oval mono-
nuclear cells which are the proliferating component of the
tumor. Scattered within this background are giant cells having 100 or more nuclei.
-treatment: curettage, recurrence rate is 4O-6()OIo
10. Fibrous dysplasia
-localized, progressive replacement of bone by a fibrous proliferation intermixed with
poorly formed, haphazardly arranged trabeculae of woven bone.
-age: 2nd to 3rd decade most common
-location:monostotic-involvement of single bone
polyostotic-involves more than one bone, can be
seen with various endo-crinopathies
-presentation: symptoms depend on bone(s)involved and degree
of involvement-pain and swelling may accompmy pathologic fracture.
-radiographic features: "ground glass" appearance with a well-defined sclerotic rim -
central meta-diaphyseal in tubular bones
-pathologic features: lesional tissue composed of curvilinear
64
trabeculae of woven bone surrounded by a modeIately cellular fibroblastic proliferation.
-treatment excision or curettage in monostotic forntS.
11. Chondroblastoma
age: 2nd decade, 2:1 male:female
location: epiphyseal, eccentrically located - foot 10010
presentation: painful and due to location often lead to arthritis type symptoms with joint
effusions and limited range of motion.
radiographic features: well-defined geographic lucency that commonly bas spotty
calcifications
pathologic features: composed of sheets of compact polyhedral chondroblasts with well
defined cytoplasmic borders
treatment curettage
MAliGNANT TUMORS
1. Osteosarcoma
-ggressive mesenchymal tumor in which neoplastic cells produce bone matrix
age: most common in persons <20 years old, 2: 1 male:female
location: 80-90% arise in the medullary cavity of the metaphyseal ends of long bones but
any bone can be involved.
presentation: pain, local tenderness and swelling - sudden fracture is sometimes the
presenting syndrome - at time of diagnosis 20% of patients have demonstrable lung
metastases
radiographic features: large destructive, mixed lytic and blastic mass with penneative
margins. Periosteal reaction = Codman's triangle
treatment chemotherapy and irradiation to debulk lesion
followed by resection/amputation.
2. Chondrosarcoma
second most common matrix-producing tumor of bone behind osteosarcoma
common feature is the prodnction of neoplastic cartilage- often asymptomatic
age: most commonly seen in 40-60 year age group, 1.5: 1 male:female
location: commonly arise in the central portions of the skeleton, pelvis and shoulder
girdle, proximal femur.
presentation: painful, progressively enlarging masses
radiographic features: localized area of bone destruction punctuated by mottled
densities from calcification or ossification.
patholOgiC features: conventional chondrosarcomas are composed of malignant hyaline
cartilage. Myxoid variants are viscous and gelatinous-spotty calcifications are typically
present.
treatment: amputation
3. Fibrosarcoma
rare collagen-producing metastatic neoplasm
age: can occur at any age, however, most common in 2nd -4
ti1
decade, equal sex
distribution
location: arise in metaphysis oflong bones and pelvic flat bones - most common in femur
presentation: enlarging painful masses which may be palpable and tender often present
with pathologic fracture
radiographic features: permeative and lytic lesion that often eJ\.1ends into the soft tissue-
slight sclerosis at margins of tumor
patholOgiC features: composed of malignant fibroblasts arranged in herringbone pattern
treatment: amputation
65
4. Ewing's SarcQma
_ uncommon primary small round cell tumor that exhibits a
primitive neural phenotype
age: 10-15 years old, male>female, blacks rarely afilicted
location: arises in the diaphysis oflong tubular bones especially the femur
presentation: painful enlarging mass. Affected site is frequently tender, warm and swollen.
Pathologic fractures may occur
radiographic features: affected bones may demonstrate non-specific "onion skinning" and
lytic lesions
patholOgiC features: composed of sheets of uniform small. round cells that are slightly
larger than lymphocytes whichappear clear due to increased glycogen content.
treatment: chemotherapy and surgical resection with or without radiation
5. Multiple Myeloma
most common malignant bone tumor
age: 40-70 years old males>females
location: multiple sites, metaphysis of long bones, spine, skulL and pelvis
presentation: fever, malaise, weight loss, fatigue, anemia,thrombocytopenia and renal
failure. Pain in one or more bones that increases with weightbearing- monoclonal
gammopathy on SPEP. Proteinuria due to renal damage and characteristic Bence-Jones
Protein.
radiographic features: Yaooue radiolucent. oval lesions
METASTATIC TUMORS
-pathways of spread include:
1. direct extension
2. lymphatic and
3. intraspinal seeding
carcinomas of the breast, prostate, lung, kidney, and thyroid are most common sources
skeletal metastases are typically multifocal, however, carcinomas of the kidney and thyroid
may produce solitary lesions.
most metastases induce a mixed lytic and blastic reaction
in lytic lesions, the metastatic cells secrete substances such as prostaglandins, interleukins,
and parathyroid hormone related protein that stimulates osteoclastic bone resorption.
Carcinomas of the kidney, lung, GI and melanoma produce this type of bone destruction.
metastases that produce a sclerotic response stimulate osteoblastic bone formation
Prostatic adenocarcinomas typically produce this type of response .
...
Sn1iA".. ........ II: ... ..
AB . n..o5 ....... - ....... _ir,...,.... .......... II,..Doa_I$.5 .. ID ......
0.-.. .. _ ...
til ... , ............. .
66
Benign verses Malignant
Benign
- Resemble derivative tissue
- Automous growth rate
- Local invasion rare
- Low recurrence rate
- Small
- Cystic/fluid-filled
- Movable
Evaluation
Soft-Tissue Masses
Malignant
- Sarcoma
- Aggressive
- Rapid destructive growth
- Recurrence/metastasis
-Large
- Solid
- Fixed
- Visually inspect the lesion for edema, color, overlying skin, location and
transillumination.
- Palpate for size, consistency, mobility and tenderness/pain.
MRI - Benign verses Malignant
Benign Malignant
- Well-defined margins - Poorly defined margins
- Homogeneous signal intensity - Heterogeneous signal
- No N-V or bone involved - N-V or bone involvement
Biopsy
Definition: Removal and examination of tissue, cells and fluid from the living body.
Types of Biopsy:
1. Closed - obtain tissue percutaneously with a needle
- fine needle - done with 25-gauge needle to aspirate mass
- core needle - done with cannulated needle with inner trocar
* Closed biopsies are easy to perform and indicated for local recurrence
or infection. However, they oftentimes result in insufficient tissue
retrieval and diagnostic inaccuracy.
2. Open - tissue is obtained through a surgical incision
- excisional - removal of entire mass
- done for small subcuataneous, obviously benign lesions
- incisional - removal of a portion of mass leaving main mass in situ
- performed for suspected malignant masses
Incisional Placement:
longitudinal on extremities
length short as possible
over midportion of mass
67
Common Benign Tumors
Ganglion Cyst
well circumscribed, soft, cystic mass
usually in dorsal foot or ankle
close relationto tnndon sheath or joint
aspirate for definitive diagnosis - straw colored fluid
treatment - marginal local excision
Plantar Fibroma
Lipoma
subcutaneous thickening of plantar fascia
usually affects medial and central bands
bilateral 10-15%
treatment - wide local excision
recurrence common
most common benign tumor
subcutaneous, soft, movable mass
2 types:
- superficial - well-circumscribed, static
- deep - no margin
treatment - marginal excision
Neurofibroma
tumor of spindle cell origin
fusiform expansion of nerve
solitary or multiple
cutaneoud or deep
multiple associated with von Recklinghausens disease
treatment - excise cutaneous, very difficult to excise deep without nerve
destruction
Neurolemoma
tumor of peripheral nerve sheath
discrete, tender nodule
usually affects major nerve
treatment - blunt marginal excision
68
DEEP VENOUS THROMBOSIS AND PULMONARY EMBOLISM
I. Definitions
A OVT - blood clots which usually form in the deep venous system of the lower extremity
B. PE - a detached thrombus, usually from the deep veins in the leg (95%), which trav.el to and lodges in the
arteries of the lung
II. Promoting Factors - Vm:how's Triad
1. stasis
2. abnormalities of the vessel wall or damage to the wall
3. "hypen:oagulability"
ill. Pathogenesis I Pathophysiology
Promoting Factors (Vm:how's Triad.)
White Thrombus - nidus ofpIatelets
Red Thrombus ---->Fibrinolysis --->Resolution
(fibrin thrombus) or
Organization
PulmonaIy Embolus
-red thrombus - develops rapidly (minutes) and is very unstable at first (1t takes 7-10 days to stabilize.)
-fibrinolysis - the process by which fibrin is degraded
-organization - a 7-10 day process during which the thrombus stabilizes resulting in vessel narrowing
N. Conditions associated with risk of thrombosis
1. post partum 5. lower extremity traumaIfracture
2. ventricular failure 6. chronic deep venous insufficiency
3. polonged bedrest 7. using estrogen/oral contrnceptive
4. C3Icinoma 8. recent pelvic or lower extremity
surgery
v. Diagnosis
AOVT
1. Classical - pain, heat, swelling in the affected limb
2. PE - presents as the first sign in 70"/0 of prtients with OVI
3. Homan's Test - dorsiflexion of the foot elicits calfpain
4. PIatt's Sign - compression of calf canses pain
B. PE
1. sudden onset
2. "classic" triad (only experienced in 14% of patients)
a dyspnea
b. chest pain
c. hemoptysis (tachycardia is actually more common)
3. 85% of prtients with fatal PE have some warning sign such as prior embolic event or symptomatic
venous disease
VI. Diagnostic Tests for OVI
A Non-invasive Tests
1. Impedance Plethysmography - a rapid test to evaluate for OVT proximal to the thigh
2. Doppler Technique - an operator dependent technique which demonstrates OVI by lack of venous
compression
69
3. Radiofibrinogen - a very sensitive test for the diagnosis of thrombosis in the calYes
B. Invasive Tests
1. Contrast venography
Vll. Diagnostic Tests for PE
A Blood Gas - Pa02 < 80% mm Hg; PaC02 < or = to normal
B. Chest X-ray - 50% are normal (may see a hemidiaphragm, atelectasis, density, pulmonary wedge)
C. EKG - Tachycardia
D. Ventilation-Perfusion Scan (V/Q Scan) - a mismatch demonstrating an area of ventilation but no
perfusion suggests PE
1. Perfusion Scan - Inject technetium 99 labeled human serum albumin
2. Ventilation Scan - Inhalation of xenon 133
E. Pulmonary Angiography
1. Definitive diagnosis thus indicated when VlQ scan is inconclusive
2. Diagnostic signs are: intraluminal filling defect, an abrupt vessel cutoff, or loss of side branches
F. Catheterization of the right side of the heart and measure the pulmonary artery and right ventricular diastolic
pressure (increased pulmonary resistance)
VIII. Prophylaxis
A Subcutaneous Heparin
1. Pre-op - 5,000 u SQ 2 hours before surgery
2. Maintenance - 5,000 u SQ q 8-12 hours
3. Compression stockings
4. Intermittent pneumatic compression devices
5. Early ambulation or range of motion
B. Aspirin
1. 325mgpo qd (baby ASA81 mgpoqd)
IX Treatment
A Anticoagulation
1. Intravenous Heparin
a. Loading dose - 10,000 - 15,000 u
b. Maintenance via IV drip, start with 1,000 u /hr
(mix 25,000 u in 250cc ofD5 112 NSS)
c. Monitor PIT daily - titrate hepnin to maintain 1.5 - 2 times patient control
d Protamine sulfate reverses heparin (Ratio: 1 mgprotamine sulfate per 100 u heparin)
caution should be used there are many possible side affects of protamine and due to baparin's
short half life (112 -2 hours)
Note: Weight Based Pneumogram ofHepnin Dosage (variations exist)
Bolus 80 u/kg Heparin IV \\'ith a maintenance rate of 18 u/kglhr, check PIT in 6 hours, then if:
PIT
<35
and
36 -45
46-70
71-90
>90
BOLUS CHANGE RATE
80 u/kg (lean weight) increase 4 u/kglhr
40 u/kg increase 2 u/kg/hr
---take no action ---
decrease 2 u/kglhr
hold heparin 1 hour and decrease 3 u/kgIhr
Need to heme check stools prior to
during initiation of anticoagulation
70
2. Coumadin (warfarin)
a. Onset of action is delayed (peak effect 3-5 days)
b. Started after heparin is therapeutic
c. Dosage 2.5-15 mgfday
d Titrate dosage to 1.5-2.0 times control
e. Vitamin K reverses Coumadin
3. Lovenox
A Venous interruption operations - intracaval wnbrella balloon or wire filter placed in the inferior vena
cava below the renal veins
B. Thrombolytic therapy - Urokinase or streptokinase to dissolve clot (must be initiated within 24-48
hours)
C. Pulmonary Embolectomy
x Differential Diagnosis for DVf
A Ce1lulits
B. Computmetn syndrome
C. Venous stasis
XLMisce1laneous
A Fat Embolism
1. Usually occurs with large fractures of the lower extremity (from bone marrow fat)
2. Three organ systems with symptoms: Pulmonary (hypoxia), Cerebral (confusion), Cutaneous (petechiae)
3. Treatment -largely supportive
- N fluids, respiratory support, fracture care, steroids, and hypertonic glucose and insulin
B. Superficial Thrombophlebitis
1. Presents as a palp1ble cord along the distribution of a vein with erythema, edema, and pain locally.
2. Treatment - supportive consisting oflocal heal elevation and rest. Antiinflammatory agents may be
given.
D. Emboli secondary to endocarditis
1. Most common cause of endocarditis is Strep. Vrridans
2. IVDA- Staph. Aureus
Peripheral Vascular Disease
I. Arterial Disease:
Definitions:
Arteriosclerosis: generic term for a group of vascular diseases which cause thickening and
inelasticity of arteries, decreasing the blood supply to the tissues.
Atherosclerosis: diminished size of vessel lumen due to the formation of fibrofatty plaques along
the intimal surface of the artery.
Acute arterial occlusion: arterial embolic event usually derived from the heart (atrial fibrillation,
MI, valvular disease, PICA, CABG) which cause occlusion of small end arteries with ischemia to
corresponding tissues.
Monckeberg's medial calcific sclerosis: calcification of the media of the artery. Does not
decrease the vessel lumen but does falsely elevate ABJ's.
71
Major Risk Factors:
-Diabetes Mellitus
-Hypercholesterolemia
-Hypertension
-Smoking
Clinical Presentation:
-Acute arterial occlusion
Pain
Pallor
Pulselessness
Paresthesias
Paralysis
-Chronic arterial occlusive disease
Intermittant claudication
Minor Risk Factors:
-Obesity
-Stress
-Age
-Genetic predisposition
-Decreased exercise
location related to level of obstruction, calf most common
complain of cramping brought on by a certain amount of exercise
symptoms are reproducible and relieved by rest
RestPain
nocturnal and diffuse in foot while l)iug with legs elevated
legs placed in dependency for relief
Ischemic ulceration / gangrene
most advanced complication
genernlly occur in distal portion of the foot
ulcers look necrotic and do not bleed with debridement
Clinical Signs ofPVD:
-Color: pallor, cyanosis, rubor on dependency
-Temperature: decreased
-Quality and Quantity of skin, nails and hair:
skin: shiny, scaly, atrophic
nails: thickened, dystrophic
hair: diminished
-Edema: may be increased due to continuous dependency
Vascular Examination
-Pulses
palpate - femoral, popliteal, dorsalis pedis and posterior tibial arteries
doppler
-Elevational pallor
-elevate legs above heart for at least 30 seconds
-evaluate color and grade 0 to 4 with +4 indicating marked pallor
-Venous filling time
-after elevational pallor test have patient sit up quickly
-measure time it takes to fill dorsal venous arch
-NorrnallO-15 seconds, Significant disease 30-60 seconds
-dependent rubor may follow 2-3 minutes later
Non-invasive vascular testing
-Ankle mm index
-ankle systolic pressure / brachial systolic pressure
-quick and reliable test, offers little information about anatomic level of occlusion
-Segmental limb pressures
-systolic pressures measured with cuffs at groin, above knee, below knee, ankle and
transmetatarsallevels
-should note a gradual decrease of approx. 20mmHg down the ipselaterallirnb
72
-both limbs should be within 20rnmHg at similar levels
-medial calcinosis results in falsely elevated pressures resulting in unreliable information
Indices
1.00- 0.9
0.89 - 0.7
0.69 - 0.5
0.49 - 0.3
0.29 - 0.0
-Segmental plethysmography
normal
mild
moderate
impending gangrene
distal necrosis
-air cuff technique (Raines) utilizes same cuffs as segmental pressure measurements
-inflate cuffbelow DBP - allows small changes in extremity volume to be translated as a
pressure change which is plotted versus time (PVR- pulse volume recording)
crest- rapid vessel expansion in systole
normally <35%
dicrotic notch- due to elasic recoil
amplitude- normally 8 -12 mm, decreased in arteriosclerois
-other plethysmography techniques
impedence: measures volume changes by assessing differences in resistance
between 2 electrodes
mercury strain gauge: elastic tube filled with mercury is 'wrapped around
extremity, as tube elongates \\'ith systolic expansion resistance changes.
Photoplethysmography: sensor probe is placed on digit which contains infrared
light and a sensor. The light reflected and absorbed by tissues is related to
capillary bed volume.
Transcutaneous oxygen measurements
assesses tissue metabolism as a function of perfusion
< 20-30mmHg high correlation with dec. ability/inability to heal
e}.1remity dependency increases TcP02 values
Stress testing / Exercise Response:
ambulate on a treadmill at 100% gradient at 2MPH for 5 minutes
at completion, perform ABI and repeat every 2 minutes until pre-exam level obtained,
normal patients have no appreciable drop.
Magnetic Resonance Angiography:
avoids use of ionizing radiation and need for contast media as in arteriography
allows multiple imaging planes
consider in pts. with renal failure
Spin Echo (SE) -blood appears daIk ( low signal intensity)
Gradient Echo (GRE) - blood appears bright (high signal intensity)
Arteriography:
involves the injection of a organic iodine contrast medium in the arterial system which is
then visualized with radiographs
usually reserved for patients that may be candidates for bypass surgery
contraindicated in patients with a iodine allergy
need to stabilize Cr to <2.0
pts need to be Npo
anticoagulation given after procedure (plavix)
73
Treatment: (Conservative)
Exercise
No tobacco
Vasodilators
Trental
Treatment: (Surgical)
Balloon angioplasty - balloon catheter is fed into a localized area of stenosis and inflated to dilate
the artery.
Bypass surgery - utilizes either autogenous vein graft or synthetic arterial prosthesis (gortex) to
circumvent areas of occlusion and improve distal circulation.
Laser angioplasty - laser probe is passed percutaneously and then activaied at the site of occlusion
/ stenosis to recanalize the vessel.
Atherectomy - utilizes a high speed rotational burr to ablate stenosis and improve flow.
II. VENOUS DISEASE:
Superficial Thrombophlebitis:
-palpable cord along distribution of superficial vein \\'ith local eI)tbema, pain and edema
-treatment consists of local warm compresses, elevation, rest and anti-inflammatory medications
-discontinue heplock if on the involved e:x.1:remity
Deep Vein Thrombosis **see section on DVT**
MAGENTIC RESONANCE IMAGING
GENERAL CONCEPTS AND PATHOLOGY
1. MRI Physics
A Based on the hydrogen atom.
1. Hydrogen atom is made up of a single proton in its nucleus.
2. Hydrogen is abundant throughout our body.
3. Hydrogen has the highest gyromagnetic ratio known.
a. Precession is when a proton spins around its axis when placed in a magnetic field (Example-
atop)
b. The frequency of this precession is determined by the Lormor Equation:
co =yXj3
co = Precessional (Larmor) Frequency
y
f3 Strength of External Magnet
c. Since hydrogen bas the largest gyromagnetic ratio, it precesses at a higher frequency.
B. Atoms \\'ith an odd number of protons and neutrons in their nucleus are small, rotating magnets that
align themselves in the direction of the magnetic field
1. Nuclei in a sample tissue are randomly oriented until a magnetic field is applied
2. Bulk Magnification Vector (M) is the sum of the magnetic moments of all of the hydrogen nuclei
in a sample tissue.
C. A radio frequency is applied and potons are stimulated.
1. Resonance is a process where nuclei make transitions between low energy states (parallel to the
magnetic field) and high energy states (anti-puallel).
2. A radiofrequency (RF) pulse induces transitions between energy states and tends to decrease the
number of nuclei pointing to the main magnetic field
3. Before a 90 RF is induced:
a. Protons are in a longitudinal, relaxed state parallel to the z axis.
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b. Protons precess out of phase with one another.

J
e.
4. After a 90
0
RF is induced:
a. Protons are excited and flip into the transverse xy plane.
b. Protons precess in phase with one another.
D. After the temrination of the RF, the protons relax, radiowaves are emitted and an image is
reconstructed onto the computer. The signal produced depends on the number of nuclei present and
the time it takes for the nuclei to relax.
1. Tl Relaxation (Spin-Lattice Relaxation):
a. Time it takes for nuclei to realign parallel (assmne a low energy state) to the magnetic field.
M must return to the z axis.
b. Also called longitudinal relaxation.
c. Reflects the chemical environment of the proton. Strength in which the nuclei are bound to
the chemical backbone (i.e. water, fat).
2. T2 Relaxation (Spin-Spin Relaxation):
a. An exponential decay of the xy component ofM back to O.
b. Measures dephasing of the nuclei.
c. Also called transverse relaxation.
d Reflects the relationship of the proton to the smrounding nuclei.
II. Pulse Sequences
A Spin Echo: Utilizes a 90 excitation pulse followed by a 180
0
refocusing pulse. This is the most
common pulse
sequence used.
Spin Echo
" 1ao-
______________ __
1E

DelQCfion

1. TE crime to Echo): Time between a 90 excitation pulse and the production of a spin echo.
2. TR rome to Recovery): Time between 90 excitation pulses.
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B. TI-Weighted Pulse Sequence:
1. Short TE (l5-3Omsec).
2. Short TR (200-600msec).
3. Main focus is on 1R As TR increases, the difference in signal intensity (SI) decreases.
1. T 1 is called the FA T image. Fat displays a high
S1. lOI'JGllUOINAL iT n
2. Used for normal AN4 TOMY.
nm,,(m)
I".C!. 1.11. ""'''t .. __
C. T2-Weigbted Pulse Sequence:
1. Long TE (60-8Omsec).
2. Long TR (2000msec).
3. Main focus is on TE. _1\.5 1E increases, the difference Ll1 SI increases.
4. T2 is called the r-VATER image. The following display a high S1:
a. Fluid., edema, hematoma.
II: VQ"'-..I l1li1,....1 Ia..H... JI............",L'''-' ....
. .
b. Infection, inflammation.
c. Tumor.
5. Used for PATHOLOGY.
D. Proton Densitv (Intermediate-Weighted Pulse Sequence):
1. Short TE (20-4Omsec).
2. Long TR (l500-2000msec).
ttIl.l1. -"'-.... IIJ'JI .... .. u.r.-_
........ ............
3. Has a high signal to noise ratio (SIN).
a. SIN is the ratio between the strength of the signal coming back from the nuclei and the
intensity of the noise from the patient and the machine.
4. Good for delineating basic anatomv.
E. Fast Spin Echo:
1. Quicker than normal spin echo T2 sequence.
a. For each spin echo pulse sequence, multiple samples are used
b. Instead of one data line per phase pulse, there are several sample echoes in the train of each
TR sequence.
2. Sacrifice slight resolution for speed.
a. An increase in speed results in a decrease in phase direction resolution.
3. Slight shift in contrast due to longer TR.
a. Typically use longer TR (4000-5000), but multi-echo train still makes it faster than normal T2.
F. STIR (Short Tl Inversion Recovery):
I. A 180
0
excitation pulse followed by a standard spin echo.
2. If Tl is very short the 90
0
pulse of the spin echo will occur at a time when the Moffat is near o.
a. Any tissue \\-ith a short Tl, such as fat, will be suppressed Not specific for fat
3. Tissues with longer Tl values \\-ill be non-zero.
a. Any tissue with a long Tl, such as water, will produce a high SI.
4. Useful for evaluating edema in high lipid regions, such as bone marrow.
a. Also useful in evaluating articular cartilage because the joint fluid is bright and the cartilage is
darker.
76
5. When contmst agents that shorten Tl are used, such as gadolinium, the desired contmst
enhancement may be suppressed.
"-
lis
G. Fat Saturation:
1. Utilizes RF pulses prior to the spin echo sequence.
-
,..,
2. RF pulse centered at the lipid resonant frequency will saturate lipid protons and rotate them into
the xy plane.
a. Subsequent pulses rotate the lipid protons out of the xy plane and their resonance is inhibited.
3. Water protons are unaffected because there are differences in the resonant frequencies between
the lipid and water nuclei.
4. This technique is specific for fat, whereas, the STIR. technique is not.
5. Excellent technique to use with gadolinium to suppress high SI of fat.
H. Gradient Echo:
1. Starts with a RF pulse < 90.
a. Protons are not completely rotated into the xy plane.
b. Sufficient magnetization remains along the z axis which allows for short TR times. Shorter
TR times means shorter imaging times.
2. A short TR time does not allow the nuclei to completely dephase before the next RF is induced.
a. Common in tissues with long T2 relaxation.
3. Magnetization is "recycled".
4. Also called steady state magnetization.
5. Goodforjointimaging.
6. Bone marrow has a low SI.
I. Gadolinium:
1. Paramagnetic metal ion.
a. Chelated with DTP A to avoid side effects.
b. Shortens Tl.
2. Good to use with fat saturation.
3. Two methods of use:
a. Intravenous:
1. Quickly distributed into intracellular fluid
2. Areas with increased vascularity, such as neoplasms and inflammation, enhance rapidly
and retain contmst longer. **Cellulitis and walls of abscesses will enhance but pus will
not.
h. Intraarticular:
I. Assess cartilage integrity, such as talar dome lesions.
III. Pathologv
A. Bone Contusions (Bruises):
1. Trabecular microfracture with edema and hemorrhage.
2. Poorly defined, inhomogenous, low SI on T1.
3. High SI on T2 because of acute hemorrhage.
B. Stress Fractures:
1. Gradual and progressive resorption of lamellar bone and replacement of dense osteonal bone.
2. Characterized by local hyperemia, edema, and osteoclastic activity.
3. Tl- linear zone of decreased SI surrounded by less defined area oflower SI.
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4. T2-Jinear zone continues to have decreased SI, but surrounding edema has a higher S1.
5. STIR- increase in SI because fatty bone marrow is suppressed
6. Callous forotation has an intermediate S1.
C. Neuropathic Osteoarthropathv:
1. Difficult to differentiate from osteomyelitis.
a. Marrow signal changes without involvement of the periosteum!cortex is not suggestive of
osteomyelitis.
2. Tl- marked decrease in SI within medullary and cancellous bone.
3. T2- mild increase in SI (less than with osteomyelitis).
4. STIR- marked increase in S1.
D. Acute Osteomyelitis:
1. T 1- involvement of cortex/medullary bone shows slight areas of increased SI against background
of normally low SI cortex.
2. T2 and STIR- increased SI in the cortex/medullary portion of involved bone.
a. Reflects a decrease in the normal fat content and localized pus/edema.
E. Chronic Osteomvelitis:
1. Sinus tracts- linear areas of increased SI on T2.
2. Foci may demonstrate the "rim sign".
a. Low SI area surrounded by an area of local, active disease.
F. Soft Tissue Infections:
1. T2 and STIR sequences are preferred for detection of cellulitis and abscesses.
a. Increased SI causing distortion of superficial soft tissues is seen in cellulitis.
b. Well-marginated, homogenous, high SI collections are seen \\'ith abscesses.
c. Gas contained within abscesses display low SI on all sequences.
G. Osteonecrosis (AYN>:
1. Hallmarlc is a reactive interface.
a. A distinct layer of inflammatory fibromesenchymal tissue between viable and infarcted bone.
2. Tl- well defined line of decreased S1.
a. Represents granulation replacement offat.
3. T2- decreased SI.
4. STIR and long T2- "double rim sign" (Mitchell & Kressel).
a. Inner margin- increase in S1. Represents granulation tissue.
b. Outer margin- decrease in SI. Represents mineralization.
5. Staging System:
a. Class A- characteristics similar to fat.
1. Tl- increase SI.
2. T2- intermediate SI.
b. Class B- reflects subacute hemorrhage with characteristics of blood.
1. Tl and T2- increase SI.
c. With increasing fluid development in necrotic tissue, SI on Tl decreases and SI on T2
increases.
d During the late stages when fibrosis and sclerosis take place, there is a decrease in SI on Tl
andT2.
H. Osteochondral Lesions:
1. T 1- decreased SI within subchondral bone.
2. T2- SI may be increased
3. STIR - marlced increase in SI.
4. Gadolinium may be helpful. Will have a high SI on Tl.
1. Tendons:
1. Low SI on all sequences due to lower water content
2. T2 and STIR- optimizes the contrast between the dark tendon and the abnormal increase in water
content of the tendon
3. Classification ofPT Tendon Tears:
a. TJ!J!!U- incomplete, hypertrophy 4-5 times normal.
78
b. 'lYe!Ul- partial tears, longitudinal splitting. Tendon becomes attenuated and atrophic and
assumes a long, ovoid configuration.
c. Tvpe Ill- complete tear, retraction of ends with obvious gap. Ends may hypertrophy. (Need.
to distinguish from Type I.)
J. Soft Tissue Masses:
1. Most demonstrate low to intermediate SI on Tl and high SIon TI.
2. Certain benign lesions, such as lipoma, hemangioma, and ganglions reveal.cIwacteristic
morphology.
K. Bone Tumors:
1. Most reveal low to intermediate SI on Tl and high SI on T2.
2. Lesions with high SIon Tl contain either fat or blood.
3. Very low SI seen on T2 images in cellular, densely fibrous lesions, and in lesions containing
bone.
L. Septic Arthritis:
1. T2 and STIR- increased SI \\'ithin surrounding soft tissues as well as joint fluid is suggestive.
2. Need clinical correlation.
M. Metallic Artifact:
1. Two mechanisms:
a. Ferromagnetic objects have their own magnetic field They cannot be utilized in the MRI
machine.
b. Most orthopedic implants are non-ferromagnetic.
1. Distorts RF uniformity.
2. Causes low SI adjacent to implant but no more than 1 cm away.
N. Magnetic Resonance Angiography:
1. Most of the experience is with extra-cranial carotid and intra-cranial circulation
2. Non-invasive technique.
3. Lower extremity indications:
a. PVD.
b. DVf.
c. Neoplasms.
d Anatomic study preoperatively.
Radiology of Infection
I. Nuclear Medicine Studies:
A Technetium - 99m:
1. Most commonly administered in the form ~ c methylene diphosphonate (Tc-MDP) &
hydroxymethylene diphosphonate (Tc-HMDP).
2. Binds directly to calcium hydroxyapatite to form soluble salts. Referred to as a "bone seeking"
agent.
3. Isotope concentrates in active new bone formation due to osteoblastic activity related to bone
injury.
4. Most widely used nuclear medicine study.
5. NON-SPECIFIC - Positive Scans For
Osteomyelitis Recent Surgery
Neuropathic Osteoarthropathy Arthritis
Bone Tumors RSD
Fracture Ischemic Necrosis of Bone
79
6. Half life = 6 homs.
7. Remains positive for ex1:ended periods in cases of osteomyelitis & post-osseous surgery because
of continued remodeling and osteogenesis.
8. Increased levels of isotope in the following sites in nonnaI bone:
Cancellous bone> cortical bone
Metaphyseal bone
Periarticular regions, especially sacroiliac joints
Epiphyseal plates
Tips of the scapula
Petrous portion of the skull
Costochondral margin of the ribs
Sternum
9. Extra-skeletal sites where the isotope occurs;
Kidneys
Bladder
Nasopharynx
Oropharynx
Glandular tissue of the breasts
Lacrimal apparatus
10. Phases of Bone Scanning:
a. Angiogram (Immediate, Earlv, 1
st
phase):
After IV injection of the isotope, several images are taken 1-3 seconds apart as the
isotope travels to the extremity.
Displays arterial blood flow to the extremity.
b. Blood Pool (2
ad
phase):
Images are taken 2-5 minutes post IV injection.
Quantitatively describes "blood pool" occurring in the capillary beds & veins.
c. Delayed (3
n1
phase):
Isotope seeks bone & demonstrates the amount of osteoblastic activity present
Images are taken 2-4 homs post IV injection.
Represents the bone uptake for repair or maintenance.
d. Fourth Phase:
Images taken 5-24 homs post IV injection.
The delay in the time post injection demonstrates more bone activity and less soft tissue
activity,
There is a decrease in the sensitivity because the half-life is 6 hours.
11. Interpretation:
a. Evaluate all phases simultaneously.
b. The a n g i ~ & blood pool phases will be "hot" in both soft tissue and bone infections.
c. Use the 3 or 4th phase bone scan to differentiate soft tissue infections from bone infections.
Blood Pool 4"'Phase
Osteomyelitis focal uptake hot hot
CeUulitis diffuse uptake neg neg
Septic Arthritis diffuse uptake diffuse uptake diffuse uptake
B. Gallium -67 Citrate:
1. Localization in areas of acute inflammation & infection by binding mechanisms;
a Direct bacterial uptake by bacterial siderophore complex.
b. Lactoferrin. a plasma protein released by leukocytes.
c. Direct leukocyte labeling (only 6%).
2. Scan is taken 48-72 homs after injection of the isotope.
80
3. Like technetium, it is non-specific. It is not indicated for detection of osteomyelitis but
sequential technetium - !hum scans can be used.
4. Returns to normal after infection and inflammation have resolved.
5. Positive scan may represent:
Infection

Fractures

Inflammation

Epiphyseal plates

Surgical trauma

Neoplasms

Gout
C. Sequential Technetium -Gallium Scan:
1. 4 hour technetium bone scan followed by a 48-72 hour !hum scan.
2. Increases the specificity for infection.
3. Positive sequential Tc - Ga scan if the gallium uptake is greater than the technetium uptake.
4. Normal scan if the gallium uptake is spatially congruent but is less than the technetium scan.
Technetium Gallium
Acute Osteomvelitis + +
Septic Arthritis + +
Chronic Osteomyelitis +
Cellulitis +
D. Indium -111 Oxime:
1. WBC's are isolated from blood taken from the patient & labeled with indium -Ill. The tagged
cells are then reinjected back into the patient The scan is performed 24 hours later.
2. Highly sensitive & specific for acute soft tissue & osseous infections.
3. May not be effective in diagnosing chronic osteomyelitis because it is predominantly a
lymphocytic response & will not cause localization of indium labeled neutrophils.
a. Acute & subacute osteomyelitis = neutrophil response = + scan.
b. Chronic osteomyelitis = predominantly lymphocytic = neg scan.
4. Can be helpful in differentiating oSteomyelitis versus osteoarthrOpatllY.
5. Halflife = 67 hours.
6. Intetpretation:
a. (+) Scan - Presence of indium labeled WBC's
- Higher uptake than surrounding bone
- Acute osteomyelitis
b. (-) Scan - No localization of indium labeled WBC's
- Chronic osteomyelitis, osteoarthropathy
7. False positives may occur with:
a. Aseptic soft tissue and bone inflammation such as periostitis secondary to Charcot changes.
b. Hyperemia & hypervascularity which may or may not be associated 'With inflanlmation
such as fractures, arthritis, inflammatory bone disease.
E. Technetium - 99m - HMPAO Leukocytic Scintigraphy:
1. Developed in order to have a tagged WBC study which is technically easier & with less radiation
than indium. This allows for more radioactive material to be used & increased anatomical
contrast.
2. Tagging molecule = Hexylmethyl propylene amine oxime.
3. Performed by obtaining 50ml of whole blood and spinning off WBC's then taggingllabeling
them. 2ml of the preparation is then reinjected. The scan is performed 3 hours later.
81
4. May show advantages over other nuclear medicine studies in diagnosis of early osteomyelitic
changes; ho",-ever, it is non-specific and any area of inflammation will be hot
5. A negative scan can rule out a septic process with high precision (94%).
6. A positive scan may not discern septic from aseptic inflammation with sufficient accuracy.
Positive predictive value = 620/0. Note - a subtraction technique is available and may yield
higher results.
II. Magnetic Resonance Imaging:
Please refer to the MRI General Concepts & Pathology Section for basic principles.
A Cellulitis:
1. Increase signal intensity (SI) on T2-weighted & STIR images.
2. Diffuse, infiltrative pattern throughout subcutaneous tissues.
3. On Tl-weighted images, a decrease in SI occurs due to the inflammatory process infiltrating
& replacing normal high SI for subcutaneous fat.
B. Abscesses:
1. Increase in SI on T2 & STIR images.
2. Localized,. well-demarcated, relatively homogeneous signal
3. Can add contrast agent, such as gadolinium, to improve contrast between normal tissue &
pathological lesions.
4. Note- If abscess is filled with necrotic tissue or purulence, instead of inflammatory fluid, the
SI decreases.
C. Osteomyelitis:
1. T2 preferred over STIR image for detection of osteomyelitis.
2. Increase SI on T2 & decrease SI on TI.
3. Detects changes in the medullary canal, cortex, and periosteum.
Must have changes in both the medullary canal & cortex to be indicative of
osteomyelitis.
D. Chronic Osteomyelitis:
1. Opposed to acute osteomyelitis, where the cortex & medullary canal are destroyed, they are
being remodeled in the chronic state.
2. Cortical changes are more extensive than the marrow & are low SI on T2.
3. Areas of active infection can still be seen as increase SI on T2 contrasted against lower SI on
thickened surrounding bone. This is known as the "rim sign".
The rim of low SI reflects fibrous tissue surrounding focal, active disease.
4. "Healed" osteomyelitis displays an increase in SI on T1. This represents the infiltration offat
back into the marrow after resolution of the infection.
E. Septic Arthritis:
1. Joint fluid is best detected with T2 & STIR images.
2. To differentiate septic arthritis from non-infectious effusions, an increase of SI of surrounding
soft tissue must also be seen.
F. Advantages ofMRI:
1. More sensitive and specific for infection than other imaging modalities.
2. Assistance in pre-operative planning;
a. Helps localize infection & determine the proximal &distal boundaries.
Particularly helpful with long bones & the calcaneus.
Helps detennine necessary level of amputation or debridement.
3. Evaluate for other possible sources of infection:
Example: Patient with cellulitis not responding to current treatment protocol. Need
to rule out abscess or osteomyelitis.
4. Monitor infectious process:
82
III. Computed Tomography (CD:
A. Basic Principles:
1. Coronal and transverse plane images only. Sagittal plane images available via reconstruction
on computer.
2. High-energy ionizing radiation.
3. Metallic implants will result in artifacts & distortion of images.
4. Windows vaJy density
Highest Density ................................................. Lowest Densitv
Cortical Bone
Calcification
Cancellous Bone
Nerve
Tendon
Ligament
B. Clinical application of CT to evaluate infection:
Cartilage
Fat
Air
1. Use of soft tissue ",indow can demonstrate abnormal soft tissue density which may represent
suppuration. reactive granulation tissue, edema. or fibrosis.
2. Can be used to evaluate plantar compartments of the foot to diagnose plantar space infections.
3. Use of the bone window can demonstrate the osseous and articular alterations.
a. Early stages of osteomyelitis is noted as an increase in the density of the bone marrow.
GOUT
b. Can be used to establish the extent of the infection & help determine the approximate
level of amputation or debridement.
Rheumatic Diseases
Gout is a metabolic disorder in which tissue deposition of monosodium urate crystals occurs from
supersaturated e}l:tracellular fluids and results in one or more clinical manifestations which include gouty
arthritis, tophi, gouty nephropathy, and uric acid calculi in the kidneys. *** Asymptomatic hyperuricemia
in the absence of gout is not a disease state.
Gout is predominately a disease of adult men with a pt>ak incidence in the fifth decade. It is the most common
cause of inflammatory arthritis in men over age 30. Gout rarely occurs in men before adolescence or women
before menopause. Serum urate concentrations rise from normal childhood mean values of 3.5-4.0 mg/dl to
adult levels during puberty in young men. In contrast urate levels remain rather constant in women until
menopause. The discrepancy in serum urate levels between the sexes during the reproductive years appears to
stem from the action of estrogens which promote renal excretion of unc acid Serum urate levels in women rise
after cessation of the menses. The disease is widely distributed amongst many races.
PURINE BIOSYNTHESIS ( KEY STEPS )
1. RAW LIMITING SlEPS
Mg2+
ribose-5-phosphate + AlP
PRPP synthetase
>PRPP
PRPP + glutamine ;:::================================;> 5 phosphonbosvl-l-amine
I amidopbospboribosyl transferase I -
83
2. SALVAGE PATHWAYS
Hypoxanthine + PRPP --------------> Inosinic Acid
HGPRT
Gaunine + PRPP > Gaunylic Acid
HGPRT
3. URIC ACID FORMATION
Hypoxanthine --------> Xanthine ------> Uric Acid
Xanthine Oxidase Xanthine Oxidase
KEY
Enzymes listed in bold print.
PRPP = phosphoribosyl pjTophosphate
HGPRT = Phosphoribosyltransferase
PATHOGENESIS
1. Gout in humans arises from the species-wide lack of the enzyme uricase which oxidizes uric acid to
allantoin.
2. In humans uric acid is derived both from the ingestion offoods containing purines and endogenous synthesis
of purine nucleotides.
3. Under steady state conditions renal excretion is the major route of uric acid disposal. The kidney accounts for
approximately two-thirds of uric acid excretion Bacterial oxidation of urate excreted into the gut is the major
mechanism of extra-renal disposal
4. Urinary uric acid excretion is the major a<ljustable mechanism for maintaining urate hemostasis. The capacity
of extra-renal uric acid disposal is greatly limited in compnison to the kidney.
5. Increased uric acid production or djminjshed uric acid excretion by the kidney operating alone or in
combination have been demonstrated to contribute substantially to the hyperuricemia of gout.
PATHOLOGY
1. Urate crystallizes as a monosodium salt in over-saturated joint tissue.
2. Decreased solubility of sodium urate at lower temperatures of peripheral structures such as toes and ears may
explain why urate crystals deposit in these areas.
3. Histopathology of tophi reveals a chronic foreign body granuloma surrounding a core of monosodium urate.
4. The inflammatory reaction around the crystals consists mostly of mononuclear cells and giant cells.
5. Urate crystals appear to be directly able to initiate and sustain intense attacks of acute inflammation because
of their capacity to stimulate the release of several inflammatory
mediators.
STAGES OF GOUT
1. Asymptomatic Hyperuricemia
2. Acute Gouty Arthritis
3. Intercritical Gout
4. Chronic Tophaceous Gout
CLASSMCATIONS OF GOUT
1. PRIMARY: refers to those circumstances in which elevated serum urate levels or urate deposition appear to
be consequences of inherent disorders of uric acid metabolism not associated with another acquired disorder
and in which gout is a prominent feature of the clinical picture.
84
2. SECONDARY: refers to those circumstances in which gout is a minor clinical feature secondary to any
number of genetic or acquired processes.
3. URIC ACID OVERPRODUCTION: approximately 10010 of patients with hyperuricemia or gout excrete
excessive quantities of uric acid into the urine. Overproduction of uric acid occurs with some frequency in a
variety of acquired and genetic disorders cbaIacterized by excessive rntes of cell and nucleic acid turnover such
as myeloproliferative and IymphoproJiferaitve disorders, hemolytic anemias, and psoriasis ( i.e. secondary gout
).
Uric acid ovetproduction can also occur secondary to inherited derangements in mechanisms of endogenous
purine biosynthesis. In both partial deficiency of HGPRT and PRPP synthetase ovemctivity early onset gout
and renal urate calculi constitute the usual clinical manifestations. Severe HGPRT deficiency is associated with
spasticity, choreoathetosis, mental retardation, and compulsive self-mutilation (Lesch-Nyham Syndrome ) ( i.e.
primary gout ).
4. URIC ACID UNDERSECRETION : the majority of ratients with hyperuricemia or gout ( up to 90 % ) show
a relative deficit in the renal excretion of uric acid VntuaIly all plasma urate is filtered by the glomerulus, with
greater than 95% of the filtered load undergoing proximal tubular resorption. Subsequent proximal tubular
secretion contributes the mgor share of excreted uric acid A diminished tubular secretory rate may contribute
to hyperuricemia, as well as increased tubu1ar reabsorption or diminished uric acid filtration.
CLINICAL FEATURES
1. Acute gouty arthritis is the most common early clinical manifestation.
2. The 1st MIP joint is involved most often and is affected at some point in 75% of patients. In approximately
10010 of patients there is never a recurrence, but up to 60% of patients experience a second attack in less than a
year.
3. The ankle, tarsal area, and knee are also commonly affected.
4. The fust episode of acute gouty arthritis frequently begins abruptly in a single joint, often during the night, so
that the patient awakens with dramatic, unexplained joint pain and swelling.
5. Affectedjoints are usually red, hot, swollen, and extremely tender. Diffuse erythema may be present which
can be confused with cellulitis or thrombophlebitis.
6. Acute attacks of gouty arthritis may be associated with high grade fever and systemic symptoms which may
be falsely interpreted as infection.
7. The most common sites for tophi are the base of the great toe, Achilles tendon, olecranon bursae, knees,
wrists, and hands.
8. Approximately 10-20% of ratients with primary hypennicemia develop uric acid kidney stones.
9. Renal disease is the most common complication of gout except for the arthritis.
RADIOGRAPIDC FINDINGS
1. The earliest changes in gout are soft tissue swelling and joint effusions.
2. A lace pattern of erosion may be seen as an early change with a fine striated pattern of periosteal reaction
along the cortex adjacent to a tophus.
3. Bony erosions tend to be round or oval with a sclerotic margin and have been described as " rat-bite erosions
", cyst-like, or
" punched-out " erosions.
4. A feature distinguishing gout from other arthritides is the presence of destructive lesions in bone that are
remote from the articular surface.
5. Many of the lesions are expmsile \\"ith overhanging margins ( Martel's sign ) that are displaced away from
the axis of the bone.
6. Generally joint spaces are preseIVed until late in the course of the disease.
7. Ankylosis andjoint subluxation may occur in very advanced cases.
8. Tophi may be "isualized "ithin the soft tissues.
85
LABORATORY FINDINGS
1. *** Demonstration of synovial fluid monosodium urate crystals is now generally considered mandatory for
establishing the diagnosis of gout as an e..xplan.ation of acute arthritis. Monosodium mate crystals are needle-
shaped and display a negative birefringence (bright yellow) when viewed under a polarizing light microscope
parallel to the axis of slow vibration marked on the polarizing microscope.
2. Synovial fluid leukocytes are elevated ( 20,000-100,000 cells per cubic millimeter) with a predomination of
neutrophils.
3. The value of serum uric acid levels in the diagnosis of acute gout is limited; levels can be normal at the time
of an acute gouty attack.
4. The ESR ( erythrocy1e sedimentation rate) is generally elevated at the time of an acute gouty attack.
5. An elevated serum WBe count may also be seen with an acute attack.
TREATMENT
ACUTE GOUT
1. COLCHICINE: a potent inhibitor of inflammation, but also a very toxic drug. The mechanism of action
appears to be interference with several steps of the inflammatory response in which neutrophils play a
central role. Intracellular interference with the organization of labile fibrillar microtubular systems
concerned with cell structure and movement may lead to micotubular disaggregation and to decreased
neutrophil motility, chemotaxis, release of chemotactic factors, and lysosomal degranulation.
Dose: 1-2 mg IV over 2-5 minutes
0.5 mg po taken hourly until pain reduction, GI toxicity, or max. dose of 8 mg
It has been suggested that the prompt response of arthritis to colchicine is diagnostic of gout, but it should be
noted that other arthropathies have been shown to respond to colchicine, and the response to colchicine may be
variable if it is started 24 hours after an acute gouty attack.
ARTHROPATHIES WHICH MAY RESPOND TO COLCHICINE ADMINISTRATION
1. Gout 7. Sweet's Syndrome
2. Pseudogout 8. Serum Sickness
3. Familial Mediterranian Fever 9. Hydroxyapatite
4. Sarcoidosis 10. Erythema Nodosum
5. Behcet's Syndrome 11. Rheumatoid Arthritis
6. Amyloidosis
The oral administration of colchicine may cause gastrointestinal toxicity in up to goolo of patients.
Nausea, vomiting, diarrhea, and cramping abdominal pain may be severe. The gradual use of small repeated
doses is meant to minimize GI toxicity. The maximum dose should not exceed 8 milligrams over a 24 hour
period
Avoidance of GI toxicity is one of the advantages of intravenous colchicine. With proper use the only
anticipated side effects are thrombophlebitis if not properly diluted and skin sloughing if extravasated.
Excessive intravenous dosages may produce bone marrow suppression, renal failure, myoplthy, disseminated
intravascular coagulation, severe hypocalcemia, cardiopulmonary arrest, seizures, and death. The maximum
daily dose should not exceed greater than 4 milligrams over a 24 hour period After intravenous therapy no
more colchicine should be given for at least 7-10 days.
2. NSAIDS: are also potent inhibitors of inflammation. The mechanism of action appears to be inhibition of
the enzyme cyc1ooxygenase. In general NSAIDS are started at the maximum daily dosages at the first sign of
an acute gouty attack and grndually tapered and continued until the arthritis has resolved. Although less toxic
than colchicine, NSAIDS may cause significant side effects involving the GI tract, kidneys, and hematologic
86
systems. Among NSAIDS most physicians prefer indomethacin for acute gouty arthriIis. Other NSAIDS with
proven efficacy include su)indac, naproxen, piroxicam, ketoprofen, tohnetin sodium. and meclofenamate
sodium.
3. Corticosteroids: genernlly not recommen<krl for parenteral use in acute gouty arthritis because the effects are
inconsistent and rebound attacks are frequent upon discontinuation. Intra-articular steroid injections are of
benefit in cotYunction with colchicine or NSAIDS, or in pItients who are unable to take colchicine or NSAIDS
due to various medical conditions.
4. Acrn : is produced by the pituitary gland and causes release of glucocorticoids from a nonna! functioning
adrenal gland. Exogenous fonns can be administered with effects similar to corticosteroids.
CHRONIC GOUT
1. COLCIllCINE : generally given as 0 . 5 ~ . 6 mg by mouth two to three times daily as a prophylactic measure.
2. ALLOPURINOL : potent inhibitor of uric acid formation by blocking the action of the enzyme xanthine
oxidase. Dosed as 300 mg po qdlbid
3. URICOSURICS ( PROBENICID, SULFINPYRAZONE ) : both increase uric acid excretion by the kidneys
and effectively lower serum uric acid levels.
*** Allopurinol, probenicid, and sulfinpyrazone should not be started during an acute gouty attack. Rapid
mobilization of uric acid and sudden changes in plasma mate levels may predispose an individual to an acute
gouty attack.
4. CHANGElNDIET
SURGICAL PROPHYLAXIS
To prevent perioperative acute gouty attacks colchicine 0.5-0.6 mg orally ti.d 3 days before and 3 days after
surgery is recommended.
DIFFERENTIAL DIAGNOSIS OF PODAGRA
1. Gout
2. CPPD Disease
3. Rheumatoid Arthritis
4. Sarcoidosis
5. Sesamoiditis
6. Infection
7. Seroneg. Spondylo-
arthropIthies
8. Osteoarthritis
9. Type n U.poproteinemia
10. Calcium Hydro}.-yapat:ite
11. Calcium Oxalate
12. Paget's Disease
13. Calcific Tendonitis
14. Trauma
PATIENTS AT RISK AND PRECIPITATING FACTORS FOR GOUT
- male patient with 1st MIP joint arthritis and hyperuricemia
- patients with a history of uric acid renal calculi
- alcoholics
- chronic renal insufficiency
- post N contrast dye
- post treatment for hematologic malignancy
- stress, trauma, or surgery
87
- medications
CONDmONS ASSOCIATED WITH GOUT AND HYPERURICEMlA
low dose salicylates
diuretics
TB medications
warfarin
nicotinic acid
- hemopoietic and neoplastic disease
- hypertension .. ischelnic heart disease .. and hyperlipidemia
- acute myocardial infurction
- diabetes mellitus
- chronic lead poisoning ( saturnine gout)
- glycogen storage disease
- sarcoidosis
- psonasLS
- chronic renal insufficiency
- sickle cell anemia and other hemoglobinopathies
- pernicions anemia and polycythemia vera
- hyperparathyroidism
- obesity
- regular alcohol consumption
-myxedema
- toxemia of pregnancy
- chronic berrylium disease
- Down's syndrome
CALCIUM PYROPHOSPHATE DIHYDRATE CRYSTAL DEPOSmON DISEASE
CPPD crystal disease, also called pseudogout, is an inflammatory process wherein crystals are
deposited in tendons, ligaments, articular capsules, synovium, and cartilage. The incidence of clinically
symptomatic disease is about one-half that of classic gout. The male to female ratio is about 1.4:1. Radiologic
studies show a steady increasing prevalence with age so that nearly 50010 of individuals have evidence of
chondrocalcinosis ( radiographic appearence of calcified cartilage) by the ninth decade of life.
CLASSIF1CATION OF CPPD CRYSTAL DEPOSmON DISEASE
1. HEREDITARY
2. SPORADIC ( IDIOPATHIC)
3. ASSOCIA1ED WITI! METABOUC DISEASE
Hyperparathyroidism
Hypothyroidism
Hemochromatosis
Hemosiderosis
Hypomagnesemia
Gout
Amyloidosis
4. ASSOCIA1ED WITI! JOINT TRAUMA OR SURGERY
CLINICAL FEATURES
1. Acute psaIdogout is marked by inflammation in one or more joints lasting for several days or more.
2. These self-limited attacks can be as abrupt in onset and as severe as true acute gout, although the average
attack is less prinful.
88
-
I
I
I
1
3. The knee is the site of almost one-half of all attacks, although involvement of nearly all joints, including the
1st MIP joint, has been noted.
4. Provocation by surgical stress, acute medical illnesses,. and tIauma can cause acute attacks of arthritis.
5. Due to both the inflammatory and degenerative features of CPPD crystal disease, it may simulate diseases
such as rheumatoid arthritis,. ankylosing spondylitis,. and neuropathic osteoarthropathy.
RADIOGRAPmC FEATURES
1. The typical appearence of punctate and linear densities in articular hyaline or fibrocartilaginous tissues is
diagnostically helpful.
2. Calcific deposits may also occur in articular capsule, ligaments, and tendons.
3. Subchondral bone cysts and hook-like osteophytes may be seen.
LABORATORY FINDINGS
1. *** The precise diagnosis of pseudogout is made by identification of CPPD crystals in joint fluid The
crystals generally have a needle-shaped or rhomboid appearence and display positive birefringence when
viewed under a polarizing light microscope.
2. Synovial fluid leukocytes may be elevated ( 1,000-50,000 cells per cubic millimeter) ,vith a predomination of
neutrophils.
3. A systemic leukocytosis and elevated ESR may be present.
TREATMENT
Unlike gout, there is no way to effectively remove CPPD crystals from the joint Acute attacks in large
joints can be treated by thorough aspiration alone or combined with injection of microcrystalline
corticosteroids. NSAIDS are often very useful. Colchicine given inuavenously is effective, whereas the
effectiveness of oral colchicine is less predictable. But both the number and duration of acute attacks can be
reduced by colchicine. It is important to note that treatment of associated diseases does not result in resorption
of intra-articualar CPPD crystal deposits.
NEUROPATHIC OSTEOARTHROPATHY
Without any appreciable e.xternal cause we may see, between one day and the next, the development
of a general and often enormous tumefaction of a limb, most commonly without any pain whatever, or any
febrile reaction. At the end of a few days the general tumefaction disappears, but a more or less considerable
swelling of the joint remains,. owing to the formation of a hydrarthus: and sometimes to the accumulation of a
liquid in the periarticular serous bursae also. On puncture being made, a transparent lemon-colored liquid has
been frequently drawn from the joint.
One or two weeks after the invasion, sometimes much sooner, the existence of more or less marked
cracking sounds may be noted, betraying the alteration of the articular surfaces which, at this period, is already
profound The hydrarthus becomes quickly resolved, leaving after it an extreme mobility in the joint Hence
consecutive luxations are frequently founcl, their production being largely aided by the wearing away of the
heads of the bones which has taken place. I have several times observed a rapid wasting of the muscular masses
of the limbs affected by the articular disorder ... Besides the wearing down of the articular surfaces ... you may
notice the presence of foreign bodies, of all the customary accompaniments of arthritis deformans ... I am led to
believe that .. they are all produced in an accidental manner, and to all appearances chiefly by the more or less
energetic movements to which the patient sometimes continues to subject the affected limbs ...
J.M Charcot, 1868
I. DEFINITION
neuropathic osteoarthropathy implies disease of nerves that leads to underlying bone and joint abnormalities
first described by J.M Charcot in 1868
II. PATHOGENESIS
Exact cause is still unknown, but both neurovascular and neurotraumatic theories exist and may both play a
crucial role in the development of this disorder
89
Neurovascular Theory ( French Theory ) : damage to trophic nerve centers with an alteration in the
sympathetic control of blood flow to bones and joints leads to persistent hyperemia and active bone
resorption
Neurotrnumatic Theory ( Gennan Theory) : An extreme progression of degenerative joint disease
following loss of proprioception and protective pain sensation
Ill. CAUSES
Diabetes Mellitus
Syringomyelia
Tabes Dorsalis ( Lues)
Excess ethyl alcohol
Myelomeningocele
Spinal cord injury
Poliomyelitis
CMf Disease
Riley-Day Syndrome
Spina Bifida
Congenital Insensitivity
Acrodystrophic
neuropathy
Amyloidosis
Leprosy
Tuberculosis
Uremia
Pernicious anemia
peripheral nerve injury
Multiple Sclerosis
Dejerine-Sottas Disease
Tumor invading nerve
Brain injury
Intra-articular cortico-
Phenylbutazone and
indomethacin
*** Diabetes mellitus, and Tabes Dorsalis are the three most common causes of Charcot
Joints.
Specific diseases with a predilection for the lower extremity :
Diabetes Mellitus - tarsal, tarsometatarsal, and M1P joints
Amyloid netlTOplthy - ankle, tarsal joints
Myelomeningocele - ankle, tarsal joints
Acrodystrophic ne\lfO}mhy - ankle, M1P joints
Congenital insensitivtity to pain - ankle, tarsal joints
IV INCIDENCE OF CHARCOT JOINTS
** The most common cause of Charcot Joints is Diabetes Mellitus **
5-10% of JXl1ients with Diabetes Mellitus
10010 ofJXl1ients with Tabes Dorsalis
25% of JXl1ients with syringomyelia
V CLINICAL PRESENTATION
>red, hot, and swollenjoint(s)
>defonned, unstablelbypermobile joint(s)
>PAIN mayor may not be a feature owing to the degree, progression, and duration of the underlying
illness, and when present is often mild considering the amount of joint distension and destruction that
may be evident
>variable neurologic exam with decreased sensation, atrophy of intrinsic muscles, and diminished
patellar/Achilles reflexes
>variable vascular exam, but generally pulses are easily palpable
>spontaneous fractureldislocations
90
>deformity possible in all three cardinal body planes, but especially common in the sagital plane (
rocker- bottom foot)
>possible ulcerations over displaced/dislocated bony prominences
VI. RADIOGRAPHIC FINDINGS
The two classic radiologic forms are atrophic and hypertrophic arthropathy. Atrophic arthropathy is
encountered more commonly in the upper extremity, whereas hypertrophic arthropathy is encountered
more commonly in the lower extremity. The underlying disease does not determine which foml
predominates.
A'IROPIDC NEUROPATHIC OS1EOARTHROPATIIY
>extensive resorption of bone ends
>osteoporosis is present, and destruction ofbone may lead to fracturesldislocations
>no osteophytes, sclerosis, fiagmentation, or soft tissue debris is present
>tapering of the distal aspect of the bones may be present, with a "mortar and pestle" or "pencil-in-
cup " deformity
***a potential diagnostic problem which could be mistaken for cellulitis/osteomyelitis or an aggressive bone
tumor
HYPER'IROPHIC NEUROPATHIC OS1EOAR11IROPATHY
>joint space narrowing with marked bony sclerosis
>osteoporosis does not occur with this form
>fractures and fiagmentation of the articular surfaces
>a large amount of bony soft tissue debris forms and later fuses into a large, dense, well-organized
bony mass
with an integral cortex
>periosteal new bone fomlation may occur
>subluxation and dislocation proceed to destruction, malaligmnent of articular surfaces, and finally to
total >disorganization of the joint, which appears as if it were pounded by a sledge-hammer
VII. STAGES OF DEVELOPMENT
Stage I : ACUTE or DEVELOPMENTAL
joint laxity, subluxation, osteochondral fragmentation,
and debris formation.
Stage II : COALESCENCE
absorption of debris and fusion of bony fragments
Stage ill : RECONSTRUCTION
remodelling and revascularization of bony fragments
*Stages are based on pathological finding'>. **Disease course is variable and progression may be very rapid
VII DIFFERENTIAI:DIAGNOSIS
Acute septic arthritis Pigmented Villonodular Synovitis
Osteomyelitis Synovial Chondromatosis and other tumors
Apatite Crystal Deposition Disease Gout
CPPD Crystal Deposition Disease Psoriatic Arthritis
Osteonecrosis (Avascular Necrosis) Rheumatoid Arthritis
91
IX. PATHOLOGY
>multiple shards ( fragments) of bone and cartilage embedded in the deep layer of synovium are
characteristic
findings in acutely resorbed joints, bone is replaced by highly vascular retinaculum
>bone is actively resorbed by osteoclasts
>in acute stages S}novium is edematous, congested, and infiltrated with PMN's
>noninOammatory and serosanginous or hemorrllagic effusions are ftequently described
>bone and cartilage fragments as well as CPPD crystals can be identified in synovial fluid
X. 1REATMENT
Conservative
>strict cessation of weightbearing
>compression cast ( Jone's-type cast ) to control edema
>cast immobilization for :fractures ( generally 8-12 weeks )
>gradual increase to :full weightbearing based on healing
>long tenn accomadative foot wear (i.e. orthopedic shoes, custom molded shoes, AFO, PrE, CROW)
Surgical
>should not be done during the acute phase
>ulcer excision ( primary closure if possible; may require skin grafting )
>exostectomy
>saucerization
>digital stabilization
>metatarsal head resection
>Lisfranc arthrodesis
>Triple and pantalar arthrodeses
>amputation
LYME DISEASE
Lyme disease is a complex multisystem illness caused by the tick-borne spirochete Borrellia
burgdorferi. The spirochete is transmitted primarily by certain ixodid ticks ( Ixodes dammini is the principal
vector in the Northeastern andMidwestem U.S.; Ixodes pacificus is the vector in the West). The illness which
closely mimics other rheumatic diseases usually occurs in stages "With remissions, exaceIbations, and different
clinical manifestations at each stage. It was first recognized in 1975 in Lyme. Connecticut.
CLINICAL FEATURES
EARL Y DISEASE: After an incubation of 3-32 days, erythema ehronicum migrans occurs at the site of tick
bite in about 80"10 of patients. Although the lesion can occur anywhere, the thigh, groin, and axi1.la are
particulary common sites. The lesion is warm to the touch and is often prinless. Within several days after the
onset of erythema chronicum migrans, 50% of patients develop multiple secondaIy lesions which may persist
from 1 day to 14 monthes. These lesions are similiar in appearance to erythema chronicum migrans, but are
usually smaller, migrate less, and lack indurated centers. Skin involvement is commonly accompanied by low
grade fever and lympbadenoplthy.
IN1ERMEDIAlE DISEASE : GeneIally occurs approximately 1-6 monthes after the initial exposure.
Neurologic abnormalities include meningitis, cranial neuritis, motor and sensory rndiculopathy, mononeuritis
multiplex, alone or in various combinations. The most common cardiac abnormality is fluctuating degrees of
atrioventricular block Less commonly peri- and myo- carditis may occur. The typical pattern of arthritis is one
of migratory pain in joints, tendons, bursae, muscles, and bone.
LAlE DISEASE : <kcurs monthes to years after initial exposure. The most common form of chronic CNS
involvement is a subtle encepbalopathy affecting memory, mood, or sleep. Most of these patients also have an
axonal polyneuropathy manifested by either distal parasthesias or spinaVrndicular pain About 60% of untreated
patients in the U.S. develop frank arthritis. The typical plttem of involvement is brie( intermittent attacks of
monoarticular or oligoarticular arthritis in a few large joints, especially the knee.
92
LABORATORY FEATURES
Serologic testing is currently the only pI3ClicalJaboratory aid in diagnosis. IgM antIDodies peak at
approximately 3-6 weeks; IgG anb.bodies peak montbes to years after exposure. Direct blood, CSF, synovial
fluid, and skin lesion cultures are rarely positive.
TREATMENT
EARLY ADULT
Doxycycline 100 mg po bid
Tetracycline 250 mg po qid
Amoxicillin 500 mg po qid
CIllIDREN
Amoxicillin 50 tpg/lqifday in divided doses
Etythromycin 30 mg/lqifday in divided doses
NEUROLOGIC ABNOMALITIES
Ceftriaxone 2 gr/day N x 30 days
Penicillin G 20 million unitslday in divided doses
ATRIOVENTRICULAR BWCK
Intravenous anb.biotics
Corticosteroids
Cardiac monitoring
ARTHRITIS
Oral antibiotics
Intraarticular corticosteroids
NSAIDS
? synovectomy if symptoms persist > 6-12 monthes
*** During the initial 24 hours after antibiotic therapy is started, 10-15% of prtients experience a Jarisch-
Herxbeimer
reaction characterized by high rever and worsening of symptoms.
STAGE
STAGE 1 : initial
weeks of illness
STAGE 2 : weeks to
monthes after stage 1
STAGE 3 : monthes to
years after stage 1
LYME DISEASE: TIMETABLE OF A TRIPHASIC ILLNESS
SIGNS AND SYMPTOMS
constitutional symptoms
erythema chronicum migrans
recurrent skin lesions
neurologic manifestations
cardiac abnormalities
arthritis
93
RHEUMATOID ARTHRITIS
Rheumatoid arthritis is a systemic autoimmune disorder of unknown etiology. The major distinctive
feature is chronic, symmetric, and erosive synovitis of periphernl joints. The disease is known to affect multiple
organ systems in addition to the joints. The average age of onset for adults is 40 years of age, but the disease
may strike for the first time at any age. The disease tends to affect women slightly more commonly than men.
PAmOWGY
Rheumatoid arthritis is a synovial disease with secondary pathologic changes taking place in the
synovial fluid cartilage, periarticular structures, and tendons. Although data are limited, the initial pathologic
event appears to be activation and/or injury of the synovial microvascnlar endothelial cells which leads to
edema in synovial tissue and effusions within the joint cavity. Synovitis is the initial lesion. As the disease
progresses to chronic stages the synovium becomes massively hypertrophic and edematous. The formation of
proliferative and invasive granulation tissue defined as pannus leads to periarticular bone and cartilage erosions
and destruction. There is no known etiology.
CLINICAL FEATURES
SYMPTOMS
- The mode of presentation can be quite variable ( indolent, episodic, or progressive polyarthralgias ).
- Monoarticular, oligoarticular, or polyarticular joint involvement may occur.
- Constitutional symptoms such as malaise, fatigue, low-grade fever, anorexia,. and weight loss may
occur.
- Stiffness, Jmticularly after prolonged rest, is usually severe and lasts nearly 60 minutes or more.
SIGNS
ARTICULARMANlFESTATIONS
- joint swelling and periarticular tenderness
- local 'warmth over affected joints
- limitation of motion of affected joints
- symm.etry of joint involvement
- frequently affected joints include: MCPIMTP's, PIP's, wrists, knees, shoulders, hips, elbows, ankles,
midtarsal joints, and cervical spine
- tenosynovitis
- deformities ( swan neck, boutonniere, hallux valgus, hammertoes, ankle valgus, fibular/ulnar
deviation of digits )
- calcaneal erosions, plantar fusciitis, retrocalcaneal bursitis
EXTRA-ARTICULAR MANIFESTATIONS
1. Rheumatoid nodules : tend to <kvelop over pressure points. Rheumatoid nodules have chaIacteristic
histopathologic findings when biopsy is perfonned A central zone of necrosis is surrounded by
PJlisading histiocytes, fibroblasts, and DlOnocytes. The outer layer of inflammatory granu1ation
tissue is composed of lymphocytes, histiocytes, and plasma cells
2. Pulmonary : the l ~ are commonly affected by Rheumatoid arthritis. Cotnmmon complications
include:
- pleurisy with or without effusions
- diffuse interstitial lung disease
- pulmonary rheumatoid nodules
- Caplan's syndrome ( nodules with pneumoconiosis )
- pulmonary vasculitis and hypertension
94
3. Vasculitis : the most common organ systems affected are the cutaneous. nervous, gast:rointestin
and pu1monary systems. LeucocytocIastic angiitis. nail fold infim:ts. and splinter hemorrbages are
examples of dermal vermlitis which may occur.
4. CardiovascuJar : a111ayers of the heart may be involved. Pericarditis is the most common clinical
manifestation.
5. Hematologic: most patients with clinically active arthritis have anemia of chronic disease. Another
hematologic manifestation is Felty's syndrome ( triad of neutropenia, sp1enomegaly, and
Rheumatoid arthritis ).
6. Neurologic: multiple neurologic complications may develop in patients with Rheumatoid arthritis.
- myelopathy caused by subluxation of cervical vertebrae
- peripheral neuropIthies
entrapment ( i.e. tarsal tunnel syndrome )
peripheral sensory neuropathy
sensorimotor neuropathy ( may be due to vasculitis )
- autonomic dysfunction ( palmarlplantar eJythema )
7. Ocular : the eyes are also commonly affected.
- keratoconjunctivitis sicca ( dry eyes )
- episcleritis and scleritis
RADIOGRAPHIC FINDINGS
L Articular : articular manifestations ofRA tend to predominate in the small joints of the feet and wrists.
- soft tissue swelling which may be secondary to :
periarticular edema
joint effusions
hyperplastic synovitis.
- subchondral osteoporosis ( osteoporosis of juxta-articular bone is one of the cardinal diagnostic criteria for
RA).
- marginal joint erosions ( erosions at the MIP joints most commonly occur at the plantar medial aspect of the
metatarsal heads.)
- even joint space narrowing.
- joint deformities and subluxations ( marked hallux valgus with fibular deviation oftoes 2,3,and 4 ).
- arthritis mutiJans.
- subluxation of the first and second cervical vertebrae.
- late changes lead to bony ankylosis, frequently in the tarsal bones.
IL EXTRA-ARTICULAR
- resorption of the distal clavicle.
- generalized osteoporosis ( associated with disease duration and severity, menopause, physical activity, and
drugs such as corticosteroids, cyclosporin, and methotrexate ).
- stress fractures of long bones.
- Achilles' tendon thickening
- erosions may be seen at the posterior and plantar aspects of the calcaneus, and well marginated plantar heel
spurs are often present.
95
ABNORMALITIES OF SYNOVIAL JOINTS IN
RHEUMATOID ARTHRITIS
PATHOLOGIC
synovial inflammation
and fluid production
hyperemia
pannus destruction of
cartilage
pannus destruction of
"unprotected" bone at
margins of joints
RADIOLOGIC
soft tissue swelling and
widening of joint spaces
osteoporosis
narrowing of joint space
marginal bony erosions
pannus destruction of
subchondral bone
bony erosions and fonnation
of sunchondral cysts
laxity of capsule, lig-
aments, and muscular
contraction/spasm
deformity, subluxation,
dislocation, fracture,
fragmentation, and
sclerosis
THE AMERICAN RHEUMATISM ASSOCIATION 1987 REVISED
CRITERIA FOR THE CLASSIFICATION OF RHEUMATOID ARTHRITIS
1. Morning stiffness : morning stiffness in and around the joints, lasting at least one hour before maximal
improvement.
2. Arthritis of 3 or more joint areas : at least 3 joint areas have had soft tissue swelling or fluid observed by a
physician. The 14 possible areas are right or left PIP, MCP, wrist, elbow, knee, ankle, and MIP joints.
3. Arthritis of band joints: at least one area swollen ( as defined above) in a wrist, MCP, or PIP joint
4. Symmetric arthritis : simultaneous involvement of the same joint areas ( as defined in 2 ) on both sides of
the body
( bilateral involvement of PIP's, MCPs, or MTPs is acceptable without absolute symmetry ).
5. Rheumatoid nodules : subcutaneous nodules, over bony prominences, or extensor surfaces, or in
juxtaarticular regions, observed by a physician.
6. Serum rheumatoid factor: demonstration of abnormal amounts of serum rheumatoid factor by any method
for which the resuh has been positive in < 5% of normal control subjects.
7. Radiographic changes: radiographic changes typical of rheumatoid arthritis on posteroanterior hand and
wrist radiographes, which must include erosions or unequivocal decalcification localized in or most marked
acljacent to the involved joint ( osteoarthritis changes alone do not qualify ).
*** For classification pmposes, a patient shall be said to have rheumatoid arthritis if helshe has satisfied 4 of
these 7 criteria. Criteria 1-4 must have been present for at least 6 weeks. Patients \\'ith 2 clinical diagnoses are
not excluded Designation as classic, definite, or probable rheumatoid arthritis is not to be made.
96
LABORATORY FINDINGS
- elevated eI)'1:hrocyt:e sedimentation rate (ESR).
- anemia of chronic disease.
- inflammatory synovial fluid
- elevated titers of rheumatoid factors in the serum of approximately 85% of patients with RA The Iheumatoid
factors tend to correlate with severe and unremitting disease, nodules, and extIa-articular disease. The most
common rheumatoid factor is IgM antibody to IgG antibody.
SELECTED DISEASES ASSOCIATED WITH ELEVATED SERUM
RHEUMATOID FACTORS
1. SuhIcute Bacterial Endocarditis 7. Sarcoidosis
2. Leprosy 8. Liver disease
3. Pulmonary Interstitial Disease 9. Tuberculosis
4. Syphilis 10. Lyme disease
5. Rubella 11.
6. Infectious Mononucleosis
DISEASES SEEN IN ASSOCIATION WITH RHEUMATOID ARTHRITIS
1. Sjogren's Syndrome
2. Amyloidosis
3. Felty's Syndrome - classically described as a triad but may include the following:
Rheumatoid arthritis, leukopenia, leg ulcers,
lymphadenopathy, and thrombocytopenia.
TREATMENT
1. PHYSICAL MEDICINE (REHABILITATION)
Physical therapy : goals include improving muscle tone. preventing or correcting deformities, and
maintaining joint mobility and function. Physical therapy is also very important during the perioperative
setting.
Ckcupational therapy : goals include assisting patients in adapting to the activities of daily living (
ADL's), to the limitations of the disease, and supplying splints and assistive devices to aid in self care.
2: MEDICAL TREATMENT
Available medications can be considered in two groups: those that have the potential for symptomatic
reliet: and those that have the potential to modify the disease.
97
sYMPTOMATIC MEDICAL THERAPY:
Aspirin
NSAIDS
Glucocorticoids
DMARDS ( Disease Modifying AntiRheumatic DrugS ) :
ak.a SAARDS ( Slow Acting AntiRhewnatic DrugS) :
Auronofin : oral gold preparation
Parenteral gold salts
Azothioprine ( Imuran ) : oral cytotoxic purine analog
Hydroxychloroquine ( Plaquenil ) : oral antimalarial compound
Methotrexate ( Rhemnatrex ) : folic acid antagonist
Penicillamine: analog of the amino acid cysteine
3. SURGICAL TREATMENT
SOFT TISSUE SURGERY
- synovectomyltenOS}novectomy
- release of nerve entrapment
- extiIpation of rheumatoid nodules
- bursectomy
- tendon balancing/relocation
- release of joint contractures
- manipulation of joints under general anesthesia
OSJEaI'OMY
AR11IROPIAS1T +/-
- resection
- fuscial interposition
- metallic hemiarthroplasty
- plastic/silicone implant
- total joint arthroplasty
AR11IRODESIS
4. SPECIFIC PROCEDURES FOR FOOT SURGERY
Modification of procedures of Hueter and Mayo: resection of the first metatarsal head
Hoffman: resection of metatarsal heads 2,3,4,& 5
Keller: resection of the 00se of the first proximal phalanx
Gocht: resection of the 00se of proximal phalanx 2,3,4,& 5
Clayton: resection of the base of proximal phalanx and head of metatarsal 1,2,3,4,& 5
Flint and Swertnam : amputation of the forefoot
5. INCISIONAL APPROACHES TO PANMETATARSAL HEAD RESECTION
Hoffman: transverse curved plantar incision just behind the web of the toes
Fowler: resection of a plantar skin wedge
Clayton: single dorsal transverse incision
Larmon: three dorsal longitudinal incisions
- over the first metatarsal
- between metatarsals two and three
- between metatarsals four and five
Marmor: five dorsal longitudinal incisions centered over the MfP joints and extended onto the toes
98
SURGICAL CONSIDERATIONS IN PATIENTS WITH RHEUMATOID ARTHRITIS
1. Perioperative corticosteroid supplementation: A patient who has received exogenous steroids within one
year of smgery may develop sudden hypotension during surgical stress. The mechanism is based on suppresion
of ACfH secretion. Chronic steroid therapy may be associated with adrenocortical atrophy and adrenal
insufficiency. Several methods of SUAiementation can be employed.
Hydrocortisone sodium succinate 100 mg N preop
---------- 100 mgN q8Hrx24 Hr
Decrease by SOO" each day and
resume oral medications
Solumedrol 40 mg 1M pm before smgery
-----40 mg N during surgery
40 mg 1M night of surgery
20 mg 1M am and. pm POD # 1
20 mg 1M pm POD # 2 and. then resume preop routine
2. Aspirin or NSAID discontinuation: Aspirin and NSAIDS should be stopped at least 7 days prior to
surgery in order to prevent bleeding complications. Aspirin irreversibly acetylates platelets interfering with
platelet aggregation and. prolonging bleeding time. NSAID inhibition is reversible and. persists only 'while the
drug is present. Preoperative laboratory evaluation should include a bleeding time, PT, PIT, serum creatinine.
and IFf's for patients on long-term aspirin or NSAIDS.
3. Workup and prophylaxis of atlantoaDal subluxation: Atlantoaxial subluxation ( CI-C2 ) is
present in ~ " of patients with Ibeumatoid artluitis, and marked flexion of the neck during patient transport
and anesthesia may cause severe neurologic disruption ( compression of C2 netVe root, posterior column
dysfunction, or ultimately quadraparesis or quadraJmlegia ). Subaxial subluxation may be seen in up to 30% of
patients with rheumatoid arthritis. Because there is a poor correlation between symptoms and. prthologic
findings, it is advised to obtain lateral cervical spine X:rays in flexion and extension before undertaking general
anesthesia on any patient with rheumatoid arthritis > 5 years duration Frequently a soft cervical collar or other
form of cervical fixation is advised when these patients are being transported and. operated upon
4. Protection of skin : The skin tends to be vel)' thin in patients with rlleumatoid arthritis. The following
recommendations can prevent untoward damage to the skin :
a Do not shave the skin because it can be easily damaged. by a sharp razor. The use of an
electric-type I3Zor is safer.
b. The use of pJastic adherent drapes ( i.e. betadine impregnated. barriers, Op site) is
contraiudicated. because the skin may be tom when the dIapes are removed..
c. Vigorous scrubbing of the skin is also contraindicated..
5. Increased risk of infection: Owing to immunologic defects in both humo:ral and cellular mechanisms of
host defense, patients with rheumatoid arthritis have an increased susceptibility to infection The risk is
also increased in patients treated with chronic corticosteroids. It is imperative that sterile technique is
employed in performing invasive procedures such as insertion of peripheral/central venous access
devices, during prolonged surgery, and duringjoint arthroplasty with implantation with artificial joints. The
benefit of prophylactic antibiotics is v\lell recognized..
6. Delayed wound healing : Corticosteroids, penicillamine, and methotrexate may contribute to delayed
wound healing. Anatomic dissection and gentle manipulation of the skin and soft tissues will help to enhance
wound healing and decrease the risk of postoperative complications.
99
7. Temporal-mandibular and cricoarytenoid abnormalities:
50-75% of patients "'ith rheumatoid arthritis have pathology of the 1MJ's. Two main areas of concern are 1)
limitation of mandibular opening that will prevent endotracheal intubation; 2) loss of upper pharyngeal
airway space, which can result in complete airway obstruction with sedation or anesthesia. Difficult cases
may require intubation for general anesthesia by a fiberoptic intubating bronchoscope.
Arthritis of the cricoarytenoid joints is seen in up to 25% of patients with rheumatoid arthritis.
Arthritis produces progressive narrowing and fixation of the vocal cords thus compressing the airway.
Following a long procedure with endotracheal intuOOtion, extubation must be performed with great caution,
since swelling of the already compromised airnay may result in complete airn'ay obstruction in a patient who
cannot be easily reintubated For this reason, a narrow diameter should be chosen when selecting an
endotracheal tube.
5. DVT prophylaxis: Patients with rheumatoid arthritis may be at increased risk for developing a
Dvr depending on their level of incapacitation. Mini-dose heparin could be started
preoperatively on any patient undergoing surgery who may be bed ridden or incapacitated for an
extended period of time postoperatively.
OSTEOARTHRITIS
(DEGENERATIVE JOINT DISEASE)
-most common joint disease characterized by progressive loss of articular cartilage, appositional new bone
formation in the subchondral trabeculae,. and formation of new cartilage and new bone at the joint margins.
-the exact mechanisms by which primary osteoarthritis develops are unknown
-secondary osteoarthritis is applied to the disease when it appears in response to some overt local or systemic
pathology
PATHOLOGY
-in earlier stages the cartilage is thicker than normal. An increase in water content leads to swelling of cartilage
and an increase in the net rate of proteoglycan synthesis. The increase in proteoglycan synthesis is an attempt
at repair by the chondrocytes.
-with disease progression the joint surface thins and proteoglycan synthesis diminishes. The integrity of the
surface is lost and vertical clefts develop leading to exposed bone.
CLINICAL FEATURES
SYMPTOMS
-pain early in the disease occurs after joint use, particularly after prolonged activity of the joint and is relieved
by rest.
-as the disease progresses pain occurs even at rest
-stiffness, typically on arising and after periods of inacthity, is usually mild and lasts less than 15 minutes.
-muscle spasm or pressure on nerves may result in more pain than the primary joint pain
SIGNS
-asymmetric tenderness and pain onjoint range of motion
-joint en1argement primarily due to bone proliferation, spurs, secondary chronic synovitis, or effusions.
-pain on passive range of motion and crepitus
RADIOLOGIC FINDINGS
may appear normal in early stags
uneven joint space narro",ing
marginal osteophytes
subchondral sclerosis
subchondral bone cysts
possible joint mice(loose osseous bodies)
100
LABORATORY FINDINGS
-nonspecific
-synovial fluid studies reveal minimal abnonnalities
-lab studies other than rndiograpbs are helpful primarily in excluding other joint diseases
CLASSIFICATION
PRIMARY OSTEOARTHRITIS
- etiology is unknown; specific joints involved
HANDS: DIP Joints>HebeIden's nodes
PIP Joints>>>Bouchard's nodes
1st Carpo-metacaIpal joints
FEET: 1st Metatarsophalangeal joints
KNEES
HIPS
SPINE
SECONDARY ARTIlRfTIS
-applied to disease when it appears in response to some overt local or systemic pathology
1. trauma(post-traumatic joint malalignment)
2. metabolic or endocrine disorders
-ochronosis, hemochromatosis, acromegaly, Wilson's disease
3. crystal deposition disease
4. netIfOJXllhic osteoarthroJnthy (Charcot joints)
MANAGEMENT AND TREATMENT
i. GENERAL PRCXiRAM
-pnient education
-rest
-physical therapy - heatlice, exercises, gait tI3ining
-occupational therapy - splints, joint protection, assistive devices
2. DRUG TREATMENT
-analgesics(aspirin, acetaminophen)
-anti-inf1arnmatory agents(NSAIDS, intrn-articular corticosteroids)
3. SURGERY
-correction of joint malalignment
-<lebridement of loose osseous bodies and spurs
-osteotomy to redistribute joint forces
-arthrodesis
-putial or total joint replacement
PAGET'S DISEASE OF BONE (OSTEITIS DEFORMANS)
Paget's disease of bone is a condition of unknown etiology that occurs in approximately 1-4% of the
population over the age of 40. It was first described by Sir James Paget in 1877. It has variable clinical
manifestations and most cases are asymptomatic. The disease is characterized by excessive and abnormal
remodelling of bone. It is more common in males than females. Again the etiology is unknown. but most
experimental evidence supports ............ " a slowly developing viral infection of osteoclasts ", as a cause.
101
SKELETAL DISTRIBUTION
- predilection to involve the axial skeleton ( pelvis., sacnn:n,. spine. and skull ).
- also involves the long lxmes such as the femur and tibia
( lesions of the fibula are rare).
- location is similar to skeletal metastases; however the relative :frequency of tibial involvement, sparing of the
upper limb, and infrequency of rib involvement are features of Paget's disease not shared by skeletal metastases.
- bone involvement is polyostotic in most cases; may be initially or totally monostotic in 10-20% of cases.
- involvement of the foot is relatively uncommon, with the calcaneus having the highest rate of involvement (
foot involvement is noted anywhere from 3-16.3% as noted by bone scanning ).
RADiOGRAPHIC FEATURES
- features can be explained by the underlying pathologic process
STAGE I - osteolytic phase
STAGE II - mixed pbase
STAGE III - sclerotic pbase
- early stages may not be visualized on plain films depending on the amount of resorption, but bone scanning is
very helpful in detecting early osseous involvement
- late stages are usually well visualized on conventional radiographs.
- long bones display the following features :
1. INCREASED cortical width
2. INCREASE in bone length
3. coursening of trabeculae
4. bony enlargement
LABORATORY FEATURES
- elevated serum alkaline phosphatase
- increased urinary hydroxyproline
COMPLICATIONS
- osseous deformities ( bowing oflong bones., bony enlargement)
- pathologic fractures
- malignant transformation (fibro-, chondro-. osteosarcomas and Ewing's sarcoma)
- osteomyelitis
- crystal deposition
- neurologic abnormalities secondary to osseous enlargement or fracture with subsequent nerve involvement
- degenerative joint disease
- high output cardiac failure and cardiomegaly secondary to marrow expansion and increased blood volume (
steal syndromes)
TREATMENT
- symptomatic with analgesics and appropriate bracing
- calcitonin
- disodium etidronate
- mithramycin
102

The seronegative spondyl0artbr0pathies are an intetrelated group of multisystem inflammatory
disorders. As rheumatic disorders, they affect the spine, peripheral joints, periarticular structures, or all three,
and they are variably associated with cbaracteristic extra-articu1ar manifestations. The Iatter include acute or
chronic gastrointestinal or genitourinaIy inflanunation, sometimes due to bacterial infection; and, uncommonly
lesions of the aortic root, cardiac conduction system, and pulmonary apices. Most but not all of these disorders
show an increased prevalence among individuals who have inherited the Ill..A-B27 gene.
RECOGNIZED SERONEGATIVE SPONDYLOARTHROPATHIES
PAmOLOGY
1. Ankylosing Spondylitis
2. Reiter's Syndrome
3. Psoriatic Arthritis
4. Enteropathic Spondylitis
( Crobn's Disease and Ulcerative Colitis)
5. Reactive Arthritis
1. Sacroiliitis is the plthologic balJmaIk, and usually one of the earliest pathologic manifestations of
ankylosing spondylitis. The initial lesion in the spine consists of inflammatmy granulation tissue at the junction
of the intervertebral disc and the margin of the vertebIal bone. The outer annular fibers may eventually be
:replaced by bone, fonning a syndesmophyte. Progression of this process leads to the bamboo spine observed
radiographically. Similar axial plthology can occur in other spondyloartbropathies as wen. although with some
difference.
2. The pathology of peripheral joint arthritis in ankylosing spondylitis can show synovial hyperplasia, lymphoid
infiltration, and pannus formation. Similar synovial pathology can be seen in the other chronic
spondyl0artbr0pathies, although Reiter's syndrome typically shows many more polymOlphonuclear cells in
early disease.
3. Entbesitis., inflammation at sites of attachment of tendinous and ligamentous attachments to bone, is anOther
pathologic hal1matk of the spondyloartbropathies. In ankylosing spondylitis it is especially common at sites
localized around the spine and pelvis, where it may eventually undergo ossification. In the other
spondyloarthropathies, it is more common at pmpheral sites such as the calcaneal attachment of the Achilles'
tendon.
HLA-B27 ASSOCIATIONSAMONG THE SPONDYLOARTHROPATHIES
DISORDERS
Ankylosing spondylitis
( with uveitis or aortitis )
Reactive arthritis
and Reiter's syndrome
( with sacroiliitis or uveitis )
Inflammatory bowel disease
( \\'itb peripheral arthritis) not increased
( with spondylitis )
Psoriasis vulgaris
( \\'ith peripheral arthritis )
( with spondylitis )
Normal caucasians
HLA-B27 FREQUENCY,
9()O/o
nearly 100%
not increased
50010
not increased
not increased
500/0

103
REITER'S SYNDROME
Reiters's syndrome was first described by Hans Reiter in 1916. It is the most common cause of an
inflammatory oligoartllroplthy in young males. It was traditionally stated that the male to female ratio was
20: 1. but realistically the ratio is closer to 5: 1. The classic triad in Reiter's S}'ndrome consists of non-gonococcal
urethritis,. cotUWlctivitis, and arthritis. It has become clear tbat Reiter's syndrome develops in a genetically
susceptible host following a genitourinary or gastrointestinal infection. It is grouped with the other seronegative
spondyloarthropathies.
PAmOLOGY
The pathologic changes in the synovium are non-specific ( edema, vascular congestion. and infiltration with
neutrophils, lymphocytes, and sparse plasma cells ). Osteolysis and periosteal new bone formation are other
findings.
CLINICAL FEATURES
MUSCULOSKELEfAL
Arthritis typically begins one to three weeks after the inciting urethritis or diarrl1ea. Joint stiffness, myalgias.
and low back pain are prominent early features. Typically only a few joints are involved in an as}'mmetric
fashion ; the knees, ankles, small joints of the feel, and the wrists are most commonly affected. Joints are
usually only moderately swollen but tender. stiff and limited in range of motion. Constitutional symptoms are
usually mild and fever, if present, is usually low grade.
UROGENITAL TRACT
Men experience incn'2sed frequency of and burning during urination. Examination of the penis reveals meatal
erythema and edema. and a clear mucoid drainage can be expressed. Prostatitis is common and has been
reported in up to SOOIo of male patients. "Silent cystitis or cervicitis" without urethritis may be the only
urogenital involvement in females which accounts the high male to female ratio that was once reported for
Reiter's syndrome. Chlamydia t1uachomatis is a suspected pathogen for the development of Reiter's syndrome.
EYE
Up to 40% of patients demonstrate uni- or bilateral non-infectious conjuncthlitis which most often occurs early
in the course of the disease. The conjuncti,,;tis is usually mild and transient.
MUCOUS MEMBRANES AND SKIN
There are two characteristic lesions associated with this syndrome.
Balanitis Circinata : small sballow ulcers of the glans penis and urethIal meatus.
Keratoderma Blennorrbagicum : Hyperlreratotic skin lesions that begin as clear vesicles on
erythematous bases and progress to macules, papules, and then to small keratotic nodules. Lesions ftequently
involve the soles of the feet, but may involve the toes, palms, scrotum and scalp. The lesions are seen in
approximately 12-14% of patients.
GASTROIN1ESTINAL lRACT
The precipitating episode of diarrhea is often mild and transient, but may be bloody and prolonged. Enteric
infections by bacteria such as Shigella dysenteriae or fle.xneri, Salmonella enteritidis or t:yphimurinum. Yersinia
enterolitica or pseudotuberculosis, and Campylobacter jejuni may p1ay crucial roles in the development of this
syndrome.
104
HEART
In 10010 of patients with severe and long standing disease, aortic regurgitation develops as a result of
inflammation and scarring of the aortic valve and valvular cusps. Condnction defects sometimes occur early in
the course of the disease, the most common being a prolonged P-R interval.
OTHER LESS COMMON FEATURES
1. IgA Glomerulonephritis
2. Renal Amyloidosis
3. Cranial and Peripheral Neuropathies
4. Thrombophlebiti
5.Pwpura
6. Livedo Reticularis
GENERAL RADIOGRAPmC FEATURES
1. SOFf TISSUE SWELLING
Soft tissue swelling in the inteJpba1angeal joints of the toes and fingers may result in sausage-like deformities of
entire digits. Latge effusions may be encountered in the knee and ankle joints.
2. OS1EOPQROSIS
Regional or periarticular osteoporosis accompanies acute episodes of arthritis, but it is common to detect severe
cartilaginous and osseous erosions without acljacent osteoporosis.
3. JOINT SPACE NARROWING
Loss of the interosseous space is more frequent in the small articulations of the feet, bands, and wrists.
4. BONE EROSION
The most frequent sites of osseous erosion are the small joints of the feet, hands, and wrists. Erosions initially
appear at the joint margins and may later progress to involve the subchondral bone in the central portion of the
articulation. The erosions tend to be indistinct in shape and outline.
5. BONE PROLIFERATION
Bone proliferation is particularly chaIact:eristic of the seronegative spondyloarthropathies and is the most
helpful tadiographic feature in distinguishing these conditions fron Rheumatoid arthritis. Bone proliferation
may take several forms.
A Linear or fluffy periosteal proliferation may occur along metataIsa1s, metacmpals, pha1angeal
shafts, or the malleoli of the ankles. Periostitis may occur without significant articular
abnonnality. The periostitis is similiar to Hypertrophic Pulmonary Osteoarthropathy.
B. Periostitis may occur at the sites of tendon and ligament attachment to bone ( enthesitis ).
C. Intra-articular bone formation may occur about sites of osseous erosion.
6. TENDINOUS CALCIFICATION AND OSSIFICATION
These manifestations are frequent about the knee, at which site the findings can resemble Pelligrini-Stieda
syndrone ( post-tmumatic calcification of the medial collateral ligament ).
SPECIFIC RADIOGRAPmC FEATURES
1. FOREFOOT
The forefoot is affected in 40-55% of patients. Any joiny may be affected, although the 1st MIP and IP joints
are especially vulnerable. At any location osteoporosis, joint space loss, marginal erosions, as well as periostitis
of neighboring diaphyses of metatarsals and phalanges may occur. The sesamoid bones can demonstrate
significant erosions and proliferation. Subluxation and defonnity of the MIP joints may be evident,. an
105
that bas Launois's In these the degree of articular mutilation may
resemble that seen in Psonatlc and RheumatoId arthritls. or Neuropathic Osteoarthropathy.
2. CALCANEUS
The calcaneus is affected in 25-50010 of patients. Bilateral changes are frequent. Retroca1caneal bursitis creates a
radiodense shadow that obliterates the nonnallucent area between the postern-superior aspect of the calcaneus
and the Achilles tendon. ill-defined erosions on the postero-superior and posterior surfaces of the calcaneus
may be present. Posterior calcaneal spurs are rare with Reiter's syndrome, but common with ankylosing
spondylitis, Rheumatoid arthritis, and Psoriatic arthritis. On the plantar surface of the bone osseous erosions,
hyperostosis, and ill-defined spurs may develop.
3. M'KLE
The ankle is affected in 30-500/0 of patients. Soft tissue swelling, large effusions, and fluffy or linear periostitis
of the distal tibial and fibular diaphyses and metaphyses are common. Loss of joint space and articular erosions
are much less common in the ankle joint.
tKNEE
The knee is affected in 25-40% of patients. The most common abnormality is a joint effusion, although
osteoporosis, periostitis of the distal femur and proximal tlbia, and erosive changes can be detected
5. SACROILIAC JOINT
The sacroiliac joints may be affected in 40-60% of patients. Bilateral symmetric or asymmetric changes are
most commOlL
6. SPINE
Although abnonnalities of the spine occur in Reiter's syndrome, their frequency and ex"tent are less than in
classic ankylosing spondylitis and Psoriatic arthritis.
LABORATORY TESTS
*** Most laboratory tests are very non-specific for Reiter's syndrome, and the diagnosis is based on clinical and
radiographic findings.
1. Several lab tests reflect the presence of inflammation.
- Neutrophilic leukocytosis
- Elevated erythrocyte sedimentation rate
- Elevated C-reactive protein
- Normocytic anemia
- Synovial fluid is mild to moderately inflammatory and may show the presence of large macrophages that
contain nuclear debris and engulfed neutrophils ( Reiter's cells ).
2. HLA-B27 is occasionally helpful.
3. New trends will be to document the presence of a specific infection from the genitourinary or gastrointestinal
systems.
TREATMENT
1. NSAIDS
2. ROM I strengthening exercises of affected joints
3. Local corticosteroid injections
4. Topical corticosteroid and keratolytic agents
5. Su1fusa1azine
6. Immunosuppresive therapy ( methotrexate, azathioprine)
7. ? use oflong term antibiotics (investigational )
106
PSORIATIC ARTHRITIS
Psoriatic artlnitis is an inflammatory arthropathy that OCCUIS in the range of 2-6% of pltients with
psoriasis. The average age of onset is in the second decade and it OCCUIS more commonly in males. In most
adult pltients a long history of skin disease is evident, although in a few individuals, the articular abnormalities
coincide with or antedate the appearanre of skin lesions. Nail abnonnalities appear to corre1ate most closely
with articular disease.
PATHOLOGY
Pathologic changes of psoriatic arthritis are basically similar to those of Iheumatoid arthritis, 00t there
are also some pathologic chamcteristics of psoriatic artlnitis that are distinctive.
1. Synovial inflammation is encountered 00t the degree of cellular inflammation with lymphocytes
and plasma cells is much less marlred than in rheumatoid artlnitis.
2. Inf1ammatory synovial tissue ( pannus ) is prominent only on the surfilce of cartilage, whereas in
rheumatoid arthritis hyperplastic synovium is seen in both superficial and deep layers of the cartilage.
3. Bone proliferation is evident in peri-articular areas.
4. Fibrous ankylosis of the articulation may be noted as in rheumatoid arthritis, however in psoriatic
arthritis bony ankylosis is also prominent.
CLINICAL FEATURES
- variable presentation with mono-, pauci-, or poly-articular distnbution.
- virtually any articulation can be affected, although the small joints of the hands and feet are reportedly
involved in 50-75% of patients with arthritis.
- soft tissue swelling can be prominent
- nail changes are generally apparent in the same digit in which there is significant distal IP joint articular
abnormality. Nail changes include the following :
1. pitting
2. transverse ridges ( Beau's lines )
3. subungual hyperkeratosis descnbed as a whitish, waxy, greasy debris which may cause onycholysis.
4. generalized discoloration and destruction of the entire nail
5. oil spot or droplet below the nail.
CHARACTERISTICS OF PSORIATIC ARTHRITIS
- involvement of synovial joints and entheses.
- asymmetric distnbution is more common than symmetric distnbution.
- involvement of the IP joints of the hands and feet.
- sacroilitis and spondylitis with pru:avertebrnl ossification.
- bone erosion with CKljacent bony proliferation.
- destruction of phalangeal tufts.
107
GENERAL RADIOGRAPHIC FEATURES
SOFT TISSUE SWELLING
- fusiform or symmetric soft tissue swelling about involved articulation.
- " sausage-like" swelling of entire digits.
OSTEOPOROSIS
- NOT a prominent feature.
- lack of osteoporosis is a reliable sign in the differentiation of psoriatic arthritis from rheumatoid arthritis.
JOINT SPACE NARROWING AND WIDENING
- articular space may be narrowed or ~ i d e n e d
- in small joints of the fingers and toes, severe destruction of marginal and subchondral bone can lead to
significant widening of the articular space.
BONE EROSION
- erosive abnonnalities are prominent
- initially erosions predominate in marginal areas of the articulation, but as they progress central areas can also
be affected
- over a period of time it may appear as if the bones are being gnawed away or have been whittled by a pencil
sharpener.
BONE PROLIFERATION
- proliferation of bone is a striking featme and is recognized as a diagnostic sign.
- irregular excrescences create a spiculated, frayed, or " paint-brush " appearence.
- periosteal new bone formation and condensation of bone on the periosteal and endosteal surfaces of the cortex
along with trabecu1ar thickening in the spongiosa can cause an entire phalange to appear radiodense ( ivory
phalange
- Bone proliferation occurs at sites at which tendons and ligaments insert on bones ( enthesopathies ).
TUFTAL RESORPTION
- resorption of the tufts of the distal pha1anges of the hands and feet is characteristic of psoriatic arthritis.
- the eroded bone may be smoothly tapered or irregular in outline.
- the nail of the involved digit is almost always involved
SPECIFIC RADIOGRAPIDC FEATURES OF THE FOOT
FOREFOOT
- bilateral asymmetric changes predominate in the IP and MfP joints and are characterized by marginal
erosions, bone proliferation. alterations in joint spaces, and lack of osteoporosis.
- extensive destruction of the IP joint of the great toe is more chamcteristic of psoriatic arthritis than any other
disorder, although Reiter's syndrome and gout produce si.miliar but less marlred changes at this site.
- osteolysis of phalangeal tufts, phalangeal and metatarsal shafts can be encountered (arthritis mutilans ).
CALCANEUS
- erosion and proliferation of the posterior and inferior surface of the calcaneus may be present
- retrocalcaneal bmsitis creates a radiodense area acljacent to the posterosuperior aspect of the bone.
- the Achilles' tendon may be thickened and iIregular excrescences may develop at its site of attachment.
- plantar heel spurs.
- inferiorly erosions of the plantar surface frequently evoke extensive sclerosis of the surrounding bone.
- occasionally the entire inferior surface of the calcaneus becomes ebumated.
108
EXTRA-ARTICULAR FEATURES
SKIN : psoriatic skin lesions are macular or papu1ar with cbanK:teristic grey-white scales. Bleeding often occurs
at sites of scale removal ( Auspitz sign ). Lesions take munerous shapes, but are most often round and located
over extensor sur.taces.
EYE : eye jnflammatjon occms in 3O"AI of patients. F ~ include COJYunctivitis,. . iritis,. episderitis,. anD
keratocOnjunctivitis sicca.
HEART: aortic insufficiency has been reported
NEUROMUSCULAR: an associated myopathy has been ~
LABORATORY FINDINGS
- synovial fluid .from the joints is classically described as being lemon yellow. Synovial fluid analysis typically
displays 2,000-15,000 WBCc per cubic millimeter with a predomination of neutrophils. Occasional massive
effusions can have leukocyte counts in the l00,OOOImm3 :range.
- abscence of rheumatoid :fuctor in most patients
- mild anemia
- elevated ESR ( erythrocyte sedimentation rate ).
- occasionally elevated serum uric acid (related to celluJartunrover of psoriatic cutaneous lesions ).
- HLA B27 is .frequently present.
TREATMENT
1. S ~ o n of the skin dise$e may be important in helping to control the arthritis.
local application of ointments
Goeckerman regimen
PUV A therapy
topical corticosteroids
intm1esional corticosteroid injections
2. NSAIDS
3. Intm-articular corticosteroid iIijections
4. Methotrexate
5. ? Hydroxychloroquine
6. ? SulfuSalazine
7. Physical therapy
8. Surgery
9. Psycholgic support
Eoteropathic Arthritis
InflammatoI)' bowel disease is a general term that refers to both Crohn's disease and ulcerative colitis.
Both of these diseases are chronic inflammatory processes of unknown origin with distinct intestinal
distribution, histopathology and radiographic appemaDce. There is a direct causal relationship between the
intestines and the joint disease. The arthritis may be peripheral, axial or both. The rheumatologic
manifestations of these two disorders are similar but oot identical. Clinical signs of Crohn's disease usually
begin in the 2nd-3rd decades and can occur anywhere between 15-60 years old in ulcerative colitis.
109
CLINICAL MANIFESTATIONS
PERIPHERAL AR1HRITIS
-periphemI articular manifestations occur in 10-200/0 of patients (more common in Crohn's
disease) and equal male: female predilection
-the etiology of the arthritis is unknown but the close association with the activity of the bowel
disease activity suggests a common factor to both processes
-one hypothesis implicates absorption of antigenic material through damaged intestinal mucosa
and the development of a soluble antigen-antibody complex that enters the joint space to produce
synovitis
-also appears to be genetically-linked
-periphemI arthritis usually indicates active bowel inflammation
-however, the arthritic symptoms may begin before the bowel symptoms in Crohn' s disease as
opposed to ulcerative colitis, which may occur within a few years after the appearance of bowel
symptoms
-typically, the arthritis is oligoarticular or monoarticular and affects large joints (most commonly
the knees, ankles, shoulders or wrists)
-joints of the lower extremity are affected more often then the upper extremity
-asymmetric inflammation of the PIPJs of the toes is particularly suggestive ("sausage toes")
- -the arthritis is frequently accompanied by fever, prinful omI ulcerations, uveitis or skin lesions
(such as pyoderma gangrenosum in Crohn's disease and erythema nodosum in ulcerative colitis)
-the more severe the bowel disease and extra-articular manifestation, the increased risk of
periphernl arthritis
-attacks of arthritis appear abruptly and reach a peak in 48-72 hours
-these attacks are usually self-limited and resolve within sevemI weeks to several months
-recurrences are common
-Common sites ofperiphernl arthritis: knees (8-16%)
ankles (5-10%)
shoulders (2-4%)
wrists (1-2%)
-enthestopathies at the Achilles tendon and plantar fascia may also occur
EXTRASKELETAL MANIFESTATIONS
-Besides the associated bowel disease, the most common extraskeletal involvement is ocular
inflammation (uveitis) which occurs in 100/0 of patients during the disease course
-oral ulcerations, digital clubbing, hepatobiliary disease, kidney stones and amyloidosis all are
seen in about 5% of patients
-less common manifestations include pyoderma gangrenoSUlll, erythema nodosum, leg ulcers,
thrombophlebitis and anal fistula formation
RADIOGRAPmC FEATURES
-Sacroiliitis with or without higher levels of spondylitis occurs in 10-15% of patients
-this form of arthritis occurs independently of the active bowel inflammation
-symptoms and radiographic changes are indistinguishable from ankylosing spondylitis
-these changes include bilaternl sacroiliitis and thin, marginal, symmetric syndesmoph}1es (which
may ultimately lead to bamboo spine)
-the spondylitis occurs 2x as frequently in males than females and it may precede the bowel
symptoms by several years
-physical exam reveals sacroiliac joint tenderness and a decrease of lumbar spine range of motion
and restriction of chest and spinal movement
-radiographic evaluation of the periphernl arthritis usually shows soft tissue swelling and
periarticular osteopenia
-it is very uncommon to see evidence of osseous or cartilaginous destruction
110
LABORATORY FINDINGS
-only 50% have a positive 1ll.,A-B27 ifhave spondylitis
-there is no corre1ation between Ill..A-B27 and the peripheral arthritis or isolated sacroiliitis
-increased SED late, mild anemia, leukocytosis and thrombocytosis
-negative rheumatoid factor and ANA
-synovial fluid analysis usually reveals inflammatory fluid with a leucocyte count between 10,000-
50,OOO/mm3 with normal protein and glucose levels
TREATMENT
-treatment of the bowel disease usually results in the disappearance of the extracolonic
manifestations, including the arthritis
-patient education
-NSAIDs
-physical therapy
-corticosteroid injections (for symptomatic joints)
-suJfasa1azine
-methotrexate
-systemic corticosteroids
-bowel surgery/colectomy (resolves the peripheral arthritis but not the axial arthritis in ulcerative
colitis but bas no beneficial effect in Crobn' s disease)
ANKYLOSING SPONDYLITIS
Ankylosing spondylitis is a chronic systemic inflammatory rheumatic disorder that primarily affects
the axial skeleton, panwertebral soft tissues, spinal apophyseal joints. Sacroiliitis is the hallmaIk of joint
involvement. The name is derived from the Greek roots ankylos meaning "bent" and spondylos meaning
"spinal vertebrae." The disease is strongly associated with the Ill..A-B27 antigen. Clinical manifestations of the
disease usually begin in late adolescense or early adulthood. Onset after age 40 is very uncommon. The disease
bas both skeletal and extraskeletal manifestations and is three times more common in men than women.
CLINICAL MANIFESTATIONS
SKELEI'AL MANIFESTATIONS
- the most common and cbaracteristic early complaint is chronic low reck pain of insidious onset, usually
beginning in late adolescence or early adultbood.
- the second common early symptom is reck stiffness, which is worse in the morning, and is eased by mild
physical activity.
- extra-articular or juxta-articular bony tenderness due to entbesitis may be an early feature of the disease and
can be a major or presenting complaint in some patients.
- involvement of peripberal joints, other than hips and shoulders, is inftequent in primary ankylosing
spondylitis.
- mild constitutional symptoms such as anorexia, malaise, or mild fever may occur in some patients in early
stages of the disease.
- physical signs may be quite minimal in early stages of the disease, however there is often some limitation of
motion of the lumbar spine '\\ith associated spasm and soreness of the parnspinal muscles.
- the Wright-Schober test is quite useful in detecting limitation of forward flexion of the lumbar spine.
- involvement of costovertebral and costotransverse joints results in restriction of chest expansion ( nonnally no
less than 1 inch in women and 1 112 inches in men ) and breathing that becomes primarily diaphragmatic.
- direct pressure of the inflamed sacroiliac joints frequently causes pain.
- back pain and stiffness generally diminish over the years but some degree of inflammatory pain persists.
- contractures at hips and compensatory flexion of the knees favor the stooped over posture so that in advanced
cases the patient appears to be doubled up.
- sciatica-like pain may alternate from one side to another and is not significantly relieved by changes in
position.
III
EX1RASKElEfAL MANIFESTATIONS
- the most common extraskeletal involvement is acute anterior uveitis ( acute iritis ) which occurs in 25-30% of
patients at some time in the course of the disease.
- cardiovascular involvement is rare and includes ascending aortitis, aortic valve incompetence, and conduction
abnormalities.
- lung parenchymal involvement is rare and is characterized by a slowly progressive fibrosis at the uwer lobes
of the lungs.
- neurologic involvement may occur most often related to spinal :fracture/dislocation, atlantoaxial
or cauda equina syndrome. Spontaneous anterior atlantoaxial subluxation is a well recognized complication
occurring in about 2% of patients.
RADIOGRAPHIC FEATURES
1. Sacroiliac joint : Sacroiliitis is the hallmarlc of ankylosing spondylitis. Although an asymmetric or unilateral
distnbution can be evident on initial radiographic ex.am, radiographic changes at later stages of the disease are
almost invariably bilateral and asymmetrical in distribution.
2. Spine : Abnormalities of the spine can be seen in the discovertebral junction, apophyseal joints,
costovertebral joints, posterior ligamentous attachments, and atlantoaxial articulations.
3. Ankle : Rarely, changes in the ankle.can be noted in ankylosing spondylitis. The changes resemble findings
in other articulations. Periostitis is particularly characteristic in the distal medial tibia.
4. Forefoot and midfoot : Bilateral symmetric or asymmetric abnormalities of the feet, which can be evident in
approximately 15% of patients with long standing ankylosing spondylitis, show a predilection for MfP and 1st
tarsometatarsal joints, and for the IP joint of the great toe. Soft tissue swelling, diffuse joint space narrowing,
erosions with adjacent bony proliferation predominately on the medial aspect of the metatarsal heads, periostitis
of phalangeal and metatarsal shafts. and intra-articular bony ankylosis can be detected Subluxation at MfP
joint articulations consisting of fibular deviation of the toes is less frequent and less severe than in rheumatoid
arthritis.
5. Calcaneus : Although clinically manifest heel abnormalities are infrequent in ankylosing sponciylitits,
radiographic changes of the calcaneus are common. Bilateral abnormalities predominate. Well defined plantar
or posterior calcaneal spurs, or both, are a common manifestation, but are similar in appearance to those in a
"normal" population. Retrocalcaneal swelling related to bursitis, posterior calcaneal erosion, and Achilles
tendon thickening are also frequent Bony erosion and proliferation resulting in ill-defined spur formation at the
site of ligamentous attachment to bone on the inferior surface of the calcaneus may occur. Periosteal
proliferation along the entire undersurl'ace of the calcaneus is evident in a few patients.
LABORATORY FINDINGS
- there is no specific test for ankylosing spondylitis.
- HLA-B27 has a 9()O/o sensitivity among Cancasians, but is an expensive test and should not be used for routine
screening.
- up to 75% of patients have an elevated erythrocyte sedimentation rate.
- mild to moderate elevation of serum 19A is frequently observed
- synovial fluid analysis is similar to Iheumatoid arthritis.
- normocytic, hypochromic anemia may be seen.
112
HLA-B27 ASSOCIATIONS
Spondyloarthropathies
Balanitis, uveitis. etc.
Colorectal cancer
Asbestosis
Chronic inflammatory bowel disease
Lymphoblastic leukemia
Secondary amyloidosis
TREATMENT
- patient education
-NSAIDS
- snJfasaJazine ( may be useful for peripheral arthritis )
- local corticosteroid injections
- daily exeIcises
- surgical intenrention
113
PHARMACOLOGY
PHARMACOLOGY
PHARMACOLOGY
PHARMACOLOGY
PHARMACOLOGY
PHARMACOLOGY
PHARMACOLOGY
PHARMACOLOGY
PHARMACOLOGY
PHARMACOLOGY
PHARMACOLOGY
PHARMACOLOGY
PHARMACOLOGY
PHARMACOLOGY
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ANTIBIOTICS
L Penicillins
Mechanism of Action
-bactericidal
- act on penicillin binding protein to inhibit cell wall synthesis
Classification of Penicillins
1. Natural Penicillins
Penicillin G -1.2-40 million units 1M or N qd
Penicillin V - 250-500 mg po qid
Spectrum of Activity
- streptococci, nonpenicillinase staphylococci
- non penicillinase producing gonococci
- anaerobes (not Bacteroides)
2. Aminopenicillins
Ampicillin - 250-1000 mg PO, 1M, N q4-6 hr
Amoxicillin - 250-500 mg PO tid
Spectmm of Activity
- streptococci, enterococci
- gram negatives (E. coli, P. mirabilis, Shigella,
Salmonella)
3. Semi-synthetic (penicillinase resistant)
Methicillin Oxacillin Dicloxacillin
Nafcillin Cloxacillin
Spectrum of Activity
- staphylococci (not MRSA)
- streptococci
4. Expanded Spectrum (anti-pseudomonal penicillins)
Carcenicillin Piperacillin Mezlocillin
Ticarcillin Azlocillin
Spectrum of Activity
- increased gram negative (pseudomonas, Enterobacter)
- streptococci
- not active against Staphylococci
5. PenicillinlB-Iactamase Inhlbitors
ticarcillinlclavulanic acid (Timentin) - 3.1 gm N q4-6hr
piperacillinltazobactam (Zosyn) - 3.375-4.5 gm N q8hr
ampicillinlsulbactam (Unasyn) - 1.5-3.0 gm N q6hr
amoxicillinlclavulanic acid (Augmentin) - 875 mg po bid
Spectrum of Activity
- staphylococci (not MRSA)
- streptococci
- anaerobes (including Bacteroides)
- gram negatives (Pseudomonas, Enterobacter)
Adverse Reactions
- hypersensitivity -diarrhea
- neutropenia - transient elevation of LIT's
- thrombocytopenia - high sodium (especially with ticarcillin)
- myoclonic seizures
114
n. Cephalosporins
Mechanism of Action
-bactericidal
- inhibition of cell wall synthesis
Agents Available:
I" Generation ~ 1 l . 1 Creneration 3,,1 Generatioll ~ til Gl'ner.nillll
Cefazolin(Ancef)
Cephalothin(Keflin)
Cephaperin(Cefadyl)
Cephalexin(Keflix)
Cephadine(Ansper)
Cefadroxil(Duricef)
Cefoxiten(Mefoxin)
Cefuraxime(Zinacef)
Cefotetan(Cefotan)
Cefamandol(Mandel)
Cefonicid(Monocid)
Ceforamide(Precef)
Cefaclor(Ceclor)
Cefpodoxime(Vantin)
Cefuroxime axetil(Ceftin)
Spectrum of Activity
1 st Generation
- Staphylococci. Streptococci
Cefotaxime(Clafoxin)
Cizaxime(Cefuax)
Ceftriaxone(Rocepbin)
Ceftaxidime(Fortaz)
MoxaIactam(Maxam)
Cefoperazone(Cefobid)
Cefixime(Suprax)
Cefipime(Maxjphne)
- gram negatives (E. coli. P. mirabilis, Shigella, Salmonella)
- anaerobes (not Bacteroides)
2
nd
Generation
- Staphylococci (less active than 1 st generation)
- Streptococci (same as 1
st
generation)
- more gram negative (II. influenza, Proteus. Klebsiella, E.coli)
- anaerobes (cefotetan & cefoxitan active against Bacteroides)
3rd Generation
- Staphylococci. Streptococci (less active than 1 st & 2
nd
)
- Pseudomonas (ceftazadime & cefoperazone only)
-anaerobes
4th Generation
- same as earlier agents
- greater gram negative coverage (including Pseudomonas)
Adverse Reactions
- hypersensitivity (cross reactivity with PCN allergy 5-15%)
- neutropenia
- diarrhea
- bleeding
- phlebitis with IV administration
mOther B-Lactams
lmipenemlCilastatin (Primaxin) - 500 mg IV q6-8hr
Spectrum of Activity - vety broad
- most gram positive aerobes & anaerobes
- gram negatives (including Pseudomonas)
- anaerobes (including Bacteroides)
Adverse Reactions
- seizures in patients with hlo seizures
- nausealvomiting
115
Aztreonam - 1-2 gm IV q8h
Spectrum of Activity
- gram negative aerobes(Pseudomonas)
- not active against gram positive or aerobic organisms
Adverse Reactions
- no major side effects
IV. Quinolones
Mechanism of Action
- bactericidal
- inlnbits DNA gryase
Available Agents
Ciprofloxacin Lomef1oxacin
Ofloxacin Levofloxacin
Enoxacin Sparfloxacin
Spectrum of Activity
- Staphylococci (!!Qt MRSA)
- gram negative bacilli (Pseudomonas)
- Enterobacter
Adverse reactions
- GI (nausea, vomiting, diarrhea)
- insomnia
-headache
- seizures
Trovafloxacin
Sparfloxacin
- contraindicated in children -- defects in cartilage
- drug interaction with theophylline & antacids
v. Aminoglycosides
Mechanism of Action
- bactericidal - binds 30S bacterial ribosome to inlnbit protein synthesis
Available Agents
Gentamycin
Tobramycin
Amikacin
Daily Dose
3-5 mglkg q8h
3-5 mglkg q8h
15 mglkgq8h
*Check trough after third dose
Peak(uglmJ)
4-10
4-10
20-30
Trough(uglml)
2
2
10
*dosing is now being recommended for q 24 to decrease toxicity (able to do this due to
postantibiotic effect of the medication)
Adverse Effects
1. ototoxicity - irreversible
2. nephrotoxicity - reversible
3. neuromuscular blockade
Synergy with PCN
Dose Gentamycin 3mglkglday q8h or q12h
Adjust dose to 2mglkg/day in ESRD
116
VI. Sulfonamides - Trimetboprim Sulfamethoxazole (Bactrim)
Mechanism of Action
- bacteriostatic
- sulfamethoxazole ~ inlubits folic acid production
- trimethoprim ~ inhibits bacterial dihydrofolate reductase
Dosage => I DS tablet bid
- trimethoprim 160 mg/sulfamethoxazole 800 mg
- excellent oral absorption; parenteral form rarely used
Spectrum of Activity
- Staphylococci (including MRSA & MRSE)
- Streptococci
- gram negatives (pseudomanas)
Adverse Reactions
- hypersensitivity
- hemolytic anemia
- contraindicated with oral hypoglycemics & G-6-PD deficiency
YD. Macrolids
Mechanism of Action
- bacteriostatic
- binds 50s bacterial ribosome inhibiting protein synthesis
Agents Available
Erythromycin (E-mycin) - 250-500 mg po qid
Azithromycin (Zithromycin) - 500 mg 1
st
day, 250 mg qd x 4 days
Clarithromycin (Biaxin) -- 250 Dig po bid
Dirythromycin (Dynabac) - 500 mg po qd
Spectrum of Activity
- Staphylococci & Streptococci
- some anaerobes (not Bacteroides)
Adverse Reactions
- gastrointestinal (nausea & vomiting)
- hepatotoxicity
- thrombophlebitis with IV infusion
- hypersensitivity
YD. Vancomycin
Mechanism of Action
- bactericidal
Dosage
- inhibition of cell wall synthesis
- 1 gram IV qI2h[22.5(CrCI) + 150] = 24h requirement
- 125 mg po qid for C. difficile colitis only
- must monitor peaks and troughs
peak -- 15-30 mg/mL(ideal peak is betw. 30-40)
trough - < 10 mglmL(ideal trough is betw. 10-12)
get peaks!troughs after fifth dose
Spectrum of Activity
-MRSA&MRSE
- Staphylococci, Streptococci, Enterococci
- gram positive anaerobes (Clostridium, Comybacterium)
- not active against gram negatives
117
Adverse Reactions
- nephrotoxicity
- ototoxicity - reversible
- red man syndrome
- anaphylactoid reaction whereby histamine is released by mast cells
- dne to rapid IV infusion
- erythema & pruritis especially of upper torso, neck and :face
- treatment: antihistamines
IX. Clindamycin
Mechanism of Action
- bacteriostatic - inhibits translation by 50s bacterial ribosome
Dosage
- 600-900 mg IV q8h
- 300 mg po bid-tid
Spectrum of Activity
- Staphylococci, Streptococci
- anaerobes (Bacteroides)
Adverse Reactions
- pseudomembranous colitis
- diarrhea, nausea
X. Tetracyclines
Available Agents
Minocycline - 100 mg po q12-24h
Doxycycline - 100 mg po q12-24h
Tetracycline - 250-500 mg po qid
Spectrum of Activity
- Staphylococci, Streptococci
- some gram negatives and anaerobes
- rare organisms (B. burgdorferi, Actinomyces, M. Marinum)
Adverse Reactions
- gastrointestinal irritation
- rash & photosensitivity
- staining of bones and teeth
XI. Rifampin
Dosage - 300 mg po bid
Spectrum of Activity
- Staphylococci, Streptococci
-Mycobacteria
- some gram negatives (Neisseria, Haemophilus)
Adverse Reactions
- red discoloration ofbody fluids (urine, tears, contact lenses)
- skin rash
- flu-like symptoms
xn. Metronidazole (F1agy1)
Dosage
- 500 mg po tid
- intravenous -- 15 mglkg load; 7.5 mglkg q6-8h
Spectrum of Activity
- gram negative anaerobes (Bacteroides)
118
Adverse Reactions
- metallic taste/dry mouth
- antabuse reaction
- seizures in patients with bJo seizures
Surgical Propbylaxis
=:;;. Goal is to provide adequate drug level prior to and during the surgical procedure
Indications:
- prolonged surgery (>2 hours)
- use of implants (screws, k-wires, prostheses, etc.)
- trauma surgery
- immunocompromised patients
- SBE risks
Selection of Agents:
- active against most conmlon causative organism (Staphylococcus aureus)
- long half life
- intravenous administration
- antibiotic level should be maximal at incision
Specific Agents:
Cefazolin I gran1 IV
Clindamycin 600 mg IV
Vancomycin I gram IV
Miscellaneous Information
Antibiotics for MRSA
- vancomycin
- minocycline
- ciprofloxacinlrifampin
- bactrimlrifampin
Disulfiram! Antabuse Reaction
- nausea, vomiting, diarrhea
- occurs "\Vith concurrent ingestion ofEtOH and certain antibiotics
- related with the MMT sidechain present on some antibiotics
- specific drugs:
moxalactam cefomandol
cefoperazone
metronidazole
Antibiotic Associated Diarrhea
2 Types:
cefotetan
1. overgrowth of C. difficile (pseudomembranous colitis)
2. alteration of intestinal microbial population
Characteristics:
- can be caused by any antibiotics
- clindamycin is most common cause
- occurs with oral or parenteral administration
- independent of dose or duration of treatment
119
Treatment:
- discontinue antibiotic if possible
- no antidiarrheal agents (allows toxin to accumulate)
- fluid and electrolyte support
- antibiotic therapy
metronidazole 500 mg q8h
vancomycin 125 mg po q6h
ANTIFUNGAL AGENTS
Amphotericin B
Nystatin
Imidazoles
Miconazole
Ketoconazole
Triazoles
Itraconazole
Fluconazole
Imidazoles
Miconazole
Clotrimazole
Ketoconazole
Econazole
Oxiconazole
Sulconazole
Mechanism of action: FUNGISTATIC.
Terbinafine
Naftifine
Terbinafine
POLYENES
Flucytocine
Griseofulvin
Specific
Cicloprox Olamine
Haloprogen
Tolnaftate
lodochlorhydroxyquin
Nonspecific
Whitfield's Ointment
Undecylenic acid
Castellani's Paint
Binds irreversibly with ergosterol (principal sterol in the fungal cell membrane).
This results in altered membrane permeability, leakage of intracellular constituents, and
cell death. Other possible mechanisms include oxidative membrane damage and
enhancement of cell mediated immunity.
NYSTATIN (Mycostatin, Nilstat,)
cream, ointment, powder
apply to affected area BID
inhibits cell membrane sterol biosynthesis
-essentially no absorption with oral form- used to treat oral esophageal and GI
candidiasis
-indicated specifically for Candida
AMPHOTERICIN B (fungizone)
-lotion, ointment, and cream in 3% concentration
-apply to affected areas BID-QID
-derived from Streptomyces Nodosus
-active against saprophytes and yeast
-oral form poorly absorbed
120
used intravenously for potentially life threatening deep mycotic
infections/systemic fungemia
Dose: 0.25mg/kg/day infused slowly over 6 hours (important to monitor BUN/CR)
With incr. of Cr to>3.0 switch to lipophilic Amphotericin B (Amphotec)
Side Effects: GI distress, fever, chills, headaches, hypotension, hypokalemia,
hypomagnesemia, anemia, thrombophlebitis, lifer failure, renal failure
Drug Reactions:
AZOLES
Aminogylcosides & Cyclosporine: synergistic nephrotoxicity
Corticosteroids & K+ depleting diuretics: may potentiate hypokalemia,
hypomagnesemia
Imidazoles and Triazoles
Mechanism of action: FUNGISTATIC
inhibit growth of fungi by interfering with cell membrane ergosterol biosynthesis
by preventing the
14alphademethylation of lanosterol
may inhibit cytochrome c peroxidative and oxidative enzymes resulting in
increased
intracellular peroxide generation
effective against dermatophytes, saprophytes, candida and some gram positive
bacteria
many have anti inflammatory activity
SYSTEMIC AZOLES- IMIDAZOLES:
MICONAZOLE (Monistat IV)
NO oral preparation available
intravenous or intrathecal
Dose: 2003600mg/day in 3 divided doses
Side Effects: GI distress, phlebitis, seizures, tremors, anemia, hyponatremia,
thrombocytopenia, cardiac dysrhythmias
Drug Interactions: may inhibit metabolism of Sulfonolureas, Coumadin, Phenytoin
KETOCONAZOLE (Nizoral)
-well absorbed
99% bound to plasma protein
reaches skin via bloodstream and eccrine sweat glands
excreted predominantly through bile (feces 57%, urine 13%)
Indications: blastomycosis, coccidiomycosis, paracoccidiomycosis,
histoplasmosis, chronic mucocutaneous candidiasis, superficial dermatophyte
infections
Dose: 200-400mg/day for 2-8 weeks (superficial infections) 8-18 months
(onychomycosis)
Side Effects: Many! more common SE's include GI disorders.
Less common SE's: hepatotoxicity, CNS disorders (HA, dizziness), adrenal
insufficiency, gynecomastia, impotence, thrombocytopenia, anemia,
leukopenia
asymptomatic elevation in liver transaminases occur in 2-10% of patients
121
Drug Interactions: Antacids, H2 Blockers, Rifampin, Isoniazid, Phenytoin,
terfenadine, Astemizole, Chlordiazepoxide, Coumadin, Cyclosporin, Insulin,
Amphotericin B, Corticosteroids, Alcohol
SYSTEMIC AlOLES- TRIAZOLES:
-triazole ring may be responsible for increased potency, decreased toxicity, and wider
spectrum of action of these agents
ITRACONAZOLE (Sporanox)
-rapidly absorbed
-lipophilic
-only 0_2% free drug in the plasma
-"reservoir" effect- therapeutic levels persist in skin/nails/hair follicles for weeks
after discontinuation of
therapy; detected in toenails for 6 months after cessation of therapy
-hepatic metabolism-liver function tests (LFT's) should be monitored regularly
-excretion: urine (35.2%) and feces (54.1%)
-not removed by hemodialYSis
Indications: blastomycosis, histoplasmosis, asprigillosis, dermatophyte
onychomycosis
Contra indications:
-coadministration with Terfenadine, Astremizole, Triazolam, And
Midazolam
-avoid in pregnancy and in nursing mothers- dose dependent maternal
toxicity and embryotoxicity
ITRACONAZOLE (Sporanox)-continued
Dose: for onychomycosis 200mg po BID for 7 days, then first week of each
month for 3-4 months (ie. Pulse dosing)
OR
200mg/day for 3 months
for tinea pedis 100mg/day for thirty days
-clinical cure rate approx. 60-70%; mycologic cure rate approx. 74%;
approx. 15% relapse rate
Side Effects (incidence 712.5%): GI disorders, HA, dizziness, dizziness,
malaise, myalgia, rash, pruritis, fever, idiosyncratic hepatitis, vasculitis,
edema, HTN, orthostatic hypotension, hypokalemia, gynacomastia,
impotence
-elevation of LFT's in 0.3%-5% of patients- usually transient
Drug Interactions:
-decrease Itraconazole levels: Rifampin, Isoniazid, Phenobarbitol,
Carbimazepine, Phenytoin,
H2 Blockers
increases drug concentrations of: Warfarin, Digoxin, Cyclosporin, Oral
Hypoglycemics
FLUCONAZOLE (Diflucan)
-intravenous form available
hydrophilic
-more than 90% of ingested dose is absorbed
122
-only 11 % bound to plasma proteins, majority of circulating drug in free form
-no significant first pass metabolism. unlike other azoles
-primarily excreted through the kidney: unchanged (80%) metabolites (11 %)
-high concentrations in the stratum corneum and sweat
-detected in skin 10 days after cessation of therapy
Indications: vaginal and oropharyngeal/esophageal candidiasis, cryptococcal
meningitis
Dose: for onychomycosis 150-300mg/week for 6-12 months
for tinea pedis 150 mg/week for 4 months
if creatinine clearance >50mllmin then give full dose
if creatinine clearance is 21 to 50 ml/min then give half dose
if creatinine clearance is 11 to 20 mllmin then give 1/4 dose
-clinical cure rate approx_ 60%; mycologic cure rate 65%
Side Effects: GI disorders, HA, rash, increased LFT's
Drug Interactions:
-increases drug levels of: Warfarin, Cyclosporine, Theophyline, oral
hypoglycemic agents
-increases Fluconazole levels: Rifampin
-Phenytoin metabolism inhibited
TOPICAL AZOLES:
MICONAXOLE NITRATE (Micatin, Monistat)
-2% cream, aerosol, powder, solution
-apply to affected areas BID
CLOTRIMAZOLE (Lotrimin, Mycelex)
-1 % cream, lotion, solution
-apply to affected areas BID
KETOCONAZOLE (Nizoral)
-2% cream
-apply once daily
-avoid in pts with sulfite sensitivity
ECONAZOLE NITRATE (Spectazole)
-1% cream
-apply once or twice daily
-may be effective against some g+ bacteria
OXICONAZOLE NITRATE (Oxistat)
-1 % cream, lotion
-apply once or twice daily
-may be effective against some g+ bacteria
SULCONAZOLE NITRATE (Exelderm)
-1 % cream, solution
-apply to affected areas BID
CLOTRIMAZOLE AND BETAMETHAZONE (Lotrizone cream)
-apply to affected areas BID
-for more inflammatory dermatophyte and yeast infections
**stinging, burning, itching, blistering, and contact dermatitis can occur with any topical
antifungal**"
123
ALLYLAMINES
Mechanism of action: FUNGICIDAL vs. dermatophytes
-potent inhibition of ergosterol synthesis by selective inhibition of squalene
epoxidase
-lack of ergosterol can interfere with the integrity and growth of the fungal
cell wall
-squalene epoxidase inhibition causes squalene accumulation that may be
fungicidal
-weakens cell membrane and causes cell death
-effective against some gram positive and gram negative bacteria
NAFTIFINE (Naftine)
-1 % cream and gel
-apply to affected areas BID
-lipophilic- binds well to the stratum corneum and penetrates into hair follicles
-has antiinflammatory properties
TERBINAFINE (Lamisil)
Topical:
-1% cream
-apply to affected areas BID
Systemic:
-lipophilic- high concentrations found in stratum corneum, hair, and sebum
-70-80% of oral dose is absorbed
-significant first pass metabolism
-80% oral dose (metabolites) excreted in urine
-drug levels exceeding the MIC for dermatophytes persists for 2 to 3 weeks after
cessation of therapy
Indications: onychomycosis due to dermatophytes
Dose: for onychomycosis: 250 mg/day for 12 weeks
for tinea pedis: 250 mg/day for 2-6 weeks
-decrease dose in liver dysfunction and when creatinine clearance is
<50ml/min
-mycologic cure rate 70%; mycologic and clinical cure-38%; 85% pts with
no relapse
Side Effects: hepatic dysfunction (rare), GI disorders, HA, skin reactions/rash,
fatigue, loss of taste, visual disturbances, neutropenia
-avoid in pregnancy and nursing mothers
Drug Interactions: less potential for drug interactions than Azoles
-Terbinafine clearance increased by: Rifampin (100%), Phenobarbital
-Terbinafine clearance decreased by: Cimetidine (33%), Terfenadine (16%)
MISCELLANEOUS AGENTS
SYSTEMIC:
FLUCYTOSINE (Ancobon)
MOA: inhibits RNA synthesis in susceptible fungi containing the enzyme cytosine
permease
-typically used in combination with Amphotericin B
Uses: systemic mycosis, candidiasis
Dose: 50-150mg/Kg po in divided doses every 6 hours
124
Side effects: GI distress, CNS disorders (HA, dizziness), skin rash, abnormal liver
function, bone marrow suppression, renal failure, cardiac arrest, respiratory arrest
GRISEOFULVIN (Grifulvin, Fulvicin, Grisactin)
MOA: FUNGISTATIC
-inhibits cell mitosis and nucleic acid synthesis
-possibly inhibits chitin synthesis
-has anti-inflammatory properties
-effective against recalcitrant skin, hair, and nail infections caused by
dermatophytes
-not effective against candida
-reaches stratum corneum by sweating and diffusion
-not recommended in pregnancy
-contraindicated in hepatic disease and porphyria
Dose: 500mg po QD; 330-375mg po QD (ultramicrosize)
Side Effects: Many!
-more common include: GI distress, HA
-less common include: CNS disorders, urinary disorders, cutaneous
disorders, neutropenia, Arthralgias, liver dysfunction
Drug Interactions: barbiturates, coumadin, oral contraceptives, cyclosporine,
alcohol
TOPICAL:
HALOPROGEN (Halotex)
-FUNGICIDAL against dermatophytes, Candida
-synthetic 1% cream and solution
-apply to affected areas BID
CICLOPROX OLAMINE (Loprox)
-FUNGICIDAL
--blocks transport of amino acids into the fungal cell and weakens fungal cell
membrane
-effective against dermatophytes, candida and some bacteria
-1% cream, lotion
-apply to affected areas BID
-has anti-inflammatory properties
MISCELLANEOUS TOPICAL AGENTS (continued)
TOLNAfTATE (Tinactin, Aftate)
-FUNGICIDAL
-inhibits sqealene epoxidase
-inhibits growth of hyphae
-limited to dermatophytes
-synthetic 1 % gel, powder, cream, aerosol
-apply to affected areas BID
UNDECYLENIC ACID (Desenex, Cruex)
-FUNGISTATIC
-cream, ointment, powder, spray powder
-apply to affected areas BID
125
WHITFIELDS OINTMENT
-12% benzoic acid (FUNGISTATIC) and 6% salicylic acid (keratolytic)
-causes desquamation of kertinized epidermis containing fungal organisms
CASTELLANI PAINT (fuchsin, phenol resorcinol, acetone, SP alcohol40B, purified water)
-topical antifungal drying agent
-apply 1-3 times daily
LOCAL ANESTHETICS
Mechanism of Action
a. surface charge theory:
-local binds to receptor in the Na channel in nerve membrane
-Na channel is blocked
-decrease in rate and degree of depolarization
-lack of development of action potential
-conduction blockade
b. membrane expansion:
-ability of un-ionized compounds to possess anesthetic activity
-altered configuration of the membrane
-decreased diameter of the Na channel
-inhibition of Na influx / conduction blockade
c. diffusion:
-diffusion of LA depends on degree of ionization
-LA exist as uncharged molecule and charged cations
-proportion depends on pKa of LA and pH of solution
-governed by HendersolJ-Hasselbalch equation
pH = pKa + log base/cation
-as pH decreases equilibrium shifts toward cation which binds to receptor
-as pH increases equilibrium shifts toward base which causes membrane
expansion
Pharmacology
Esters and Amides
metabolism stability in sol'n allergic rx
Ester plasma esterase unstable rare(para-aminobenzoic acid)
Amide hepatiC enzyme stable very rare
Characteristics:
I.Lipid Solubility
-LA that are lipid soluble penetrate nerve membrane readily
-they have a greater potency
2.Protein Binding
-influences duration of action
-agents of short duration bind poorly
126
3.pKa
-defines the pH at which the base and cation forms are equal
-agents with a pKa closer to tissue pH have a rapid onset
4.1 ntrinsic Vasodilator Activity
-influences potency/duration of action
-inc. in vasodilator activity = inc. in vascular absorption
-less LA available for nerve blockade
Agents:
ESTERS
l.Cocaine-addictive, only vasoconstrictor, used as topical anesthetic
2.Procaine-weak potency due rapid hydrolysis, used for infiltration
anesthesia
3.Chlorprocaine-rapid onset, less toxic, used in obstetrical cases
4.Tetracaine-slow onset,inc. toxicity, used for spinal anesthesia
AMIDES
I.lidocaine-rapid onset, used in regional, topical anesth., antiarrythmic
2.Mepivacaine-used for infiltration, peripheral block, epidural
3.Prilocaine-least toxic, used for intravenous regional anesth_,
4.Bupivicaine-long duration, used in chronic pain, epidural (labor)
5.Etidocaine-rapid onset, intense motor blockade
6.Ropivacaine-rapid clearance,shorter half-life than bupiv.
Toxicity
CNS
Initial events
Tinitus
I ightheadedness
confusion
Excitation phase
tonic-clonic convulsions
Depression phase
unconsciousness
general CNS depression
respiratory arrest
Maximum Recommended Doses
Drug
mg/70kg
chlorprocaine
lidocaine
lidocaine
lidocaine
mepivacaine
prilocaine
bupivacaine
etidocaine
etidocaine
Conc.
(%)
3.00
1.00
1.50
2.00
2.00
3.00
0_75
1.00
1.50
mg/kg
PI/(Epi)
11(14)
4(7)
4(7)
4(7)
4(7)
7(8.5)
2.5(3.2)
6(8)
-(8)*
CVS
Initial events
hypertension/tachycardia
I ntermediate phase
myocardial depression
decreased cardiac output
mild hypotension
'Terminal phase
peripheral vasodilation
profound hypotension
sinus bradycardia
conduction defects
ventricular arrythmias
circulatory collapse
mg/70kg
Pl(EPI)
770(980)
280(490)
280(490)
280(490)
280(490)
500(600)
175(225)
420(560)
- (560)
Pl(EPI)
25(33)
28(50)
19(33)
14(25)
14(25)
17(20)
23(30)
42(56)
- (37)
*etidocaine 1.5 not available without epinephrine
-doses in parentheses apply when epinephrine 5ug/ml is added to solution
127
Alternative agents:
BENZYL ALCOHOL 0.9%:
Indicated with patients with amide/ester allergies
For use in short lacerations and superficial wounds
GLUCOCORTICOIDS
Glucocorticoids are the most powerful but also the most toxic class of drugs used for the
treatment of inflammatory conditions. The investigation and use of glucocorticoids began
almost fifty years ago, yet many controversies still remain regarding their clinical uses,
risks and benefits.
Glucocorticoid Structure
- cortisone is the main endogenous glucocorticoid
- structure is a 21 carbon steroid hormone
- synthesized from cholesterol
- activity depends on structure
- structure determines potency and rate of absorption
- cortisone and prednisone are inactive until converted to cortisol and
prednisolone
Hypothalamic Pituitary Adrenal Axis
- regulates cortisol secretion
- basal induced glucocorticoid release
- 20 mg/day
- diurnal - increased in evening and morning
- stress induced glucocorticoid release
- cold, exercise, infection, surgery
. HPA axis suppression => adrenal insufficiency
- due to increased endogenous or exogenous glucocorticoid
- symptoms of adrenal insufficiency
- nausea, U BP,.hyperkalemia, CV collapse
- surgical stress dosing
. for pt's on > 7.5 mg/dayof prednisone for 1 month
- hydrocortisone 100 mg IV for total 300 mg
Mechanism of Action
- work through the synthesis of other compounds
- regulates transcription and ultimately protein synthesis
- mechanism of action important because:
1. takes hours for a clinical response
2. action is indirect => causes many unwanted side effects
Metabolic Effects
=> glucocorticoids protect the glucose dependant tissues(brain & heart)
Carbohydrate Metabolism
- increase gluconeogenesis
- decrease peripheral glucose uptake
Lipid Metabolism
- increases lipolysis => insulin release and gluconeogenesis
128
Protein Metabolism
- decreases synthesis and increases breakdown in muscle
- increases free plasma amino acids
Fluids and Electrolytes
- sodium and water retention
- hypokalemia
Bone & Calcium Metabolism
- decreases intestinal calcium absorption
- inhibits osteoblast function
Connective Tissue
- decreases collagen formation
- impairs granulation tissue formation
Systemic Glucocorticoids
TherapeutiC Effects
l. Anti-inflammatory
- modulators of inflammation
- inhibit prostaglandin synthesis
- inhibits COX-2
- inhibits cytokine, adhesion molecule, chemotactic factor prod.
- decreases vascular permeability
- cellular effects
- increases # of neutrophils but decreases accumulation at sites of
inflammation
- decreases # of macrophages, lymphocytes, eosinophils, basophils
2. Immunosuppressive
- cellular> humoral
- circulating lymphocytes and monocytes decrease
- inhibit natural killer and T-cell proliferation
- effective against acute graft rejection
3. Anti-asthmatic
- inhibits lipooxygenase by promoting production of a protein called
Iipocortin
- inhibits production of leukotriene C4 &04 ~ SRS-A
- decreases bronchiole inflammation
Pharmacokinetics
- absorbed orally, intramuscularly, intrasynovially, topically
- metabolized in the liver, excreted in the urine
Dosing Regimens
1. Daily High Dose
- >15 mg prednisone daily
- life threatening autoimmune diseases
2. Pulse Methylprednisolone
- 1 gram IV over 45 minutes
- used as last resort therapy
3. Daily Low Dose
- <15 mg prednisone daily
- most common dosing schedule
- used for inflammatory arthritic processes
4. Alternate Day Dosing
- less side effects
- usually less effective
129
Drug Interactions
Increase Steroid Clearance
- phenytoin, rifampin, barbituates, carbamzepine
Decrease Steroid Metabolism
- ketoconazole, estrogen-containing oral contraceptives
Other Effects
- decrease plasma salicylate levels
increase requirement for insulin/oral hypoglycemics
Adverse Responses
Adverse responses to therapeutic uses of glucocorticoids are mainly due to
prolonged exposure to high doses_ Most adverse effects are dose related and a short
course(2 weeks) even at high doses gives a low risk_ Although threshhold doses are
varied for individual patients, studies have shown that all patients receiving 30 mg of
prednisone daily for a three month duration will experience adverse responses_
Very Common
- osteoporosis
- increased appetite
- centripetal obesity
- impaired wound healing
- increase infection risk
- HPA axis suppression
Uncommon
- glaucoma
- benign intracranial hypertension
- peptic ulcer disease
- hypokalemic alkalosis
Comparison of Various Steroids
Glucocorticoid Potency
Short Acting
Cortisone(Cortone) 0_8
Hydrocortisone(Hydrocortonne) 1
Intermediate Acting
Prednisone(Orasone) 4
Prednisolone(Delta-Cortef) 4
Methyprednisolone(Medrol) 5
Triamcinalone 5
Long Acting
Dexamethasone(Decadron) 30
Paramethasone(Haldrone) 10
Beta methasone(Celestone) 30
Frequent
- myopathy
- avascular necrosis
- hypertension
- edema
- thin, fragile skin
- cataracts
Rare
- pancreatitis
- hirsituism
- panniculitis
- impotence
Daily Dose(mg)
50 - 100
10 - 20
10 - 20
10 - 20
5 - 20
50 - 100
0_75 - 3_0
4-6
0_6 - 3
130
Local Corticosteroids
=>Maximize local effects and minimize systemic adverse effectsc:
Indications Contraindications
- rheumatoid arthritis - infectous arthritis
- gout and pseudogout - bacteremia
- seronegative arthridities - periarticular cellulitis
- acute traumatic arthritis - osteochondral fracture
- osteoarthritis - jOint prothesis
- SLE and MCTD - allergy
- tendonitis/bursitis - osteomyelitis
- nerve entrapment syndromes - bacterial endocarditis
- plantar fasciitis - several days before joint surgery
- intralesional/dermal
Adverse Responses
- postinjection flare - due to crystal deposition in the joint
- corticosteroid arthropathy - similar to Charcot osteoarthropathy
- iatrogenic infection - very rare
- tendon rupture - only if injected directly into tendonous substance
- facial flushing - more common with triamcinalone
- skin atrophy/depigmentation
- periarticular calcification - especially in DIPJ's and PIPJ's of fingers/toes
- systemic absorption
- masks signs of infection (.J... edema, erythema, calor, dolar)
Topical Steroids
Pharmacologic Actions
1. Anti-inflammatory
vasoconstriction in the skin
stabilizes lysosomal membrane
prevents conversion of membrane phospholipids to arachidonic acids
2_ Dermal Atrophy
inhibits fibroblast proliferation
inhibits deposition of connective tissue collagen
3_ Inhibits Mitoses in Epidermis
Disorders Responsive to Topical Steroids
Responsive
atopic dermatitis
erythematosis
seborrheic dermatitis
soles
lichen simplex chronicus
lipoidica diabeticorum
allergic contact dermatitis(late phases)
irritant dermatitis(late phases)
numular eczematous dermatitis
stasis dermititis
psoriasiS of face and genitalia
Disorders Less
discoid lupus
psoriasis of palms and
necrobiosis
sarcoidosis
lichen striatus
pemphigus
vitiligo
granuloma annulare
131
Potency Classes of Topical Steroids
Groups I & II
- high potency
- short term therapy
- not recommended for generalized dermatoses, chronic therapy, face of
intertriginous therapy
- Gr. I examples: betamethasone dipropionate 0.05%, clobetasol
dipropionate 0_05%
- Gr. II examples: betamethasone dipropionate 0.01%, fluocinonide .05%,
desoximetasone .25%
Groups III, IV, V
- medium potency
- recommended for trunk, extremities, scalp
- use with caution in generalized dermatoses
- Gr. III examples: triamcinalone 0.5% ointment, betamethasone 0.01 %
cream
Gr. IV examples: triamcinalone 0.1% ointment, betamethasone 0.025%
ointment
Gr. V examples: triamcinalone 0.1 % cream, hydrocortisone valerate
0.2%
Groups VI & VII
- low potency
- recommended for face, axilla, neck, groin
- Gr. VI examples: flumethasone 0.03% cream, desonide 0.05% cream
Gr. VII examples: hydrocortisone 1 % cream, dexamethasone 0.04%
cream
Topical Vehicles
1. Ointment
almost pure grease with very little water
most occlusive and hydrating
provides greater steroid effect
- use on dry rash, palms and soles; not for use on wet rash
2. Cream
grease with more water
steroid effect weaker
use for dry rash
3. Lotion
little grease with more water
- steroid effect weaker
- use on scalp, toe interspaces, axilla, groin
4. Solution
oily liquid of alcohol (propylene glycol)
steroid effect strong
- fairly drying - burns on dry, cracked skin
- use on scalp, toe interspaces, axilla, groin
5. Gel
steroid effect is as strong as in an ointment
may use under occlusion
very drying
use on scalp, toe interspaces, axilla, groin
132
SEDATIVE HYPNOTICS/SLEEP MEDICATIONS
L 1EMAZEPAM (RESTORIL )
a..ASS : benzodiazepull hypnotic
DOSAGE: 15-30 mgpoHSpm insomnia
METABOLISM: heprtic
EXCRETION: renal
WARNINGS: l. do not use during pregnancy
2. combined effects with ETOH and CNS depressants
3. potential for abuse
2. 1RIAZOLAM (HALCION )
a..ASS : triazolobenzodiazepine hypnotic
DOSAGE: 0.125-0.25 mg po HS pm insomnia
METABOLISM: heprtic
EXCRETION: renal
WARNINGS:
2. use lower doses in elderly patients
3. may cause behavioral cl1al1ges
4. combined effects with ETOH and CNS depressants
5. potential for abuse
3. FLURAZEPAM (DALMANE)
CLASS: benzodiazepam hypnotic agent
DOSAGE: 15-30 mg po HS pm insomnia
METABOLISM: hepatic
EXCRETION: renal
WARNINGS: l. do not use during pregnancy
2. combined effects with ETOH and CNS depressants
3. potential for abuse
4. do not use in children under 15 years of age
4. ESTAZOLAM (PROSOM)
a..ASS : triazolobenzodiazepine hypnotic
DOSAGE: 1-2 mg po HS pm insomnia
METABOLISM: heprtic ( I3pid in smokers )
EXCRETION: renal
WARNINGS: 1. do not use during pregnancy
2. combined effects with ETOH and CNS depressants
3. potential for abuse
5. DOXYLAMINE SUCCINAlE (UNISOM)
CLASS : ethanolamine antihistamine
DOSAGE: 25 mgpo HS pm insomnia
METABOIJSM: heprtic
EXCRETION: renal
WARNINGS: 1. should only be taken at bedtime
2. combined effects with ETOH and CNS depressants
133
6. ZOIPIDEM TAR1RA1E (AMBIEN)
CLASS : IlOn-benzodiazepine hypnotic
OOSAGE : 5-10 mgpo Hs pm insomnia
METABOLISM: hepatic
EXCRETION: renal
WARNINGS: 1. use reduced dosage with elderly
2. oombined effects with EI'OH and CNS depressants
3. potential for abuse
ANTI-PRURITUS AND POTENTIATION OF NARCOTICS
1. DIPHENHYDRAMINE (BENADRYL)
CLASS : antihistamine
ADULT DOSAGE: 25-50 po tid-qid pm pruritus
PEDS DOSAGE: 12.5-25 mg po tKkPd pm pruritus
METABOLISM: hepatic
EXCRETION: renal
WARNINGS: 1. use lower doses in children and elderly
2. additive effects with ETOH and CNS depressants
3. do not give to patients taking MAO inlnbitors
2. PROME'IHAZINE (PHENERGAN)
CLASS : phenothiazine derivitive with antihistamine, sedative, antimotion sickness, antiemetic, and
anticholinergic effects
ADULT DOSAGE: 12.5-25 mg by deep 1M injection q 6-8 Hr
PEDS DOSAGE: 12.5 mg by deep 1M injection q 6-8 Hr
METABOliSM: hepatic
EXCRETION: renal
WARNINGS: 1. contains sodium metabisuIfite ( ? allergy )
2. avoid intra-arterial injection
3. intensifies and prolongs effects of CNS depressants and sedative hypnotics
4. may inteIact with MAO inlnbitors
3. HYDROXYZINE HCL (ATARAXIVISTARIL)
CLASS: piperazine <b:ived antihistamine
DOSAGE: 25 mg po ti<k}id pm pruritus ( AT ARAX )
50-100 mg 1M q 4-6 hr pm pain ( VISTARIL )
METABOliSM: hepatic
EXCRETION: biliaIy
WARNINGS: 1. potentiation of narcotics and CNS depressants
2. do not give to nursing mothers
3. indmationlsterile abscesses at injection sites
134
ANTIEMETICS
1. CYCLIZINEHCL (MAREZINE)
CLASS : piperazine derived antihistamine
DOSAGE: 50 mg po q 4-6 hr
MET ABOUSM : hepatic
EXCRETION: renal
W ARNlNGS : 1. combined effects with ETOH and CNS depressants
2. may cause hypotension especially after surgery
2. DIMENHYDRINATE ( DRAMAMINE )
CLASS: ethanolamine antihistamine
DOSAGE: 50-100 mg po q 4-6 hr
50 mg 1M q 4-6 hr
MET ABOUSM: hepatic
EXCRETION: renal
W ARNlNGS : 1. combined effects with ETOH and CNS depressants
2. use 'with caution ifhistory of seizure disorders
3. PROCHLORPERAZINE ( COMPAZINE )
CLASS: phenothiazine derivative
OOSAGE : 5-10 mg po tid-qid
25 mg suPP pI" bid
5-10 mg by deep llvt injection q 3-4 hr
METABOUSM : hepatic
EXCRETION: renal
W ARNlNGS : L do not use in children ( symptoms similiar to Reye's syndrome)
2. strong extrapyramidal side effects
3, may cause orthostatic hypotension
4. TRIMETHOBENZAMIDE HCL (TIGAN )
CLASS : centrally acting antiemetic
DOSAGE: 250 mg po tid-qid
200 mg suPP pI" tid-qid
200 mg 1M tid-qid
MET ABOUSM: hepatic
EXCRETION: renal and biliaIy
WARNINGS: L do not use in children
2. do not use with ETOH
3. Parkinson-like sytDJXoms
4. suppositories contain benzocaine
5. PROME1HAZINE (PHENERGAN)
CLASS : phenothiazine derivative with antihistamine, sedative, antimotion sickness, antiemetic, and
anticholinergic effects
OOSAGE : 12.5-25 mg by deep 1M injection q 6-8 HI
METABOLISM: hepatic
EXCRETION: renal
WARNINGS: SEE PREVIOUS DESCRIPTION
135
6. ODANSElRONHCL (ZOFRAN)
CLASS: serotonin 5 HI -3 receptor antagonist
DOSAGE : 4 mg N pm nausea/vomitting
METABOUSM : hepJtic
EXCRETION: renal
WARNINGS : RELATIVELY NEW WITH FEW ADVERSE EFFEcrs INCLINICAL 1RIALS
? Hepatic Toxicity
LAXATIVES AND STOOL SOFTENERS
1. YElLOW PHENOLPHlHALEIN AND OC:X:USATE CALCIUM (DOXIDAN)
CLASS : irritant Jaxativelstool softener
DOSAGE : 1-2 capsule po q day up to one week
WARNINGS: (same as for COLACFJDIALOSE )
2. CASAN'IlIRANOL AND DOCUSATE SODRJM (PERICOLACE )
CLASS : irritant Jaxativelstool softener
DOSAGE: 1-2capsulespoHS
15-30 mL ( ~ ) po HS
WARNINGS: same as for COLACFJDIALOSE
3. DOCUSATE SODRJM ( COLACE, DIAWSE )
CLASS : surl3ctmt stool softener
DOSAGE: 50-200 mg po q day ( COLACE )
100 mg po q day - tid (DIALOSE )
WARNINGS: 1. do not use with mineIal oil
2. do not use with abdominal pain, nausea, or vomitting
4. CASCARA SAGRADA
CLASS : irritant laxative
DOSAGE : 325 mg po HS
5. CALCIUMPOLYCARBOPHIL (FIBERCON, FIBERALL, MITROLAN)
CLASS : bulk forming fiber laxative
DOSAGE: 2 tabs up to qid (FIBERCON )
1 tab q day - qid (FIBERAlL)
2 tabs qid or pm (Ml1ROLAN )
1. should be taken with full glass of water to prevent choking ( tablets can swell in throat if not taken with
WARNINGS at least 8 ounzes ofwater )
2. should be taken 1 hour before or 2 hOUl'S after tetIacyc1ine-like anbbiotics
6. PSYLlJUMHYDROPHlllC MUCllLOID (METAMUcn.)
CLASS; bulk forming natural thempeutic fiber
DOSAGE: avaiable in powders, pICkets, granules, and wafers
( see PDR for prescribing information )
WARNINGS: 1. patients may have an allergy to psyllium
2. contraindicated with intestinal obstruction and fecal impaction
7. SENNA CONCEN1RATE (SENEKOT)
CLASS : irritant Jaxative
136
DOSAGE: 2 tabs po q day, preferably HS
10-15 mL (syrup) po q day. preferably HS
1 tsp (granules) po q day, preferably HS
1 StJR)OSitOly pr q day, preferably HS
8. SENNA CONCENTRAlE AND DOCUSAlE SODIUM (SENEKOT-S)
a..ASS : irritant laxative/stool softener
DOSAGE: 2 tabs po q day
9. BISACODYL (DULCOLAX)
CLASS : irritant laxative
DOSAGE: 10-15mgpoqday
1 suppository pr q day
10. DON'T FORGET PRUNE JUICE !!!!
ANTIDIARRHEAL AGENTS
1. NATIJRAL BELLADONNA ALKALOIDS WITII PHENOBARBlTOL (BELLATAL )
CLASS : anticholinergi.c/antisplsmodic
DOSAGE: 1-2 tabs po tid-qid
WARNINGS: 1. additive effects with Efoo and CNS ~
2. potential for abuse
2. DICYCLOMINE HCL (BENTYL )
CLASS : anticholinergic/antispasmodic
DOSAGE: 80 mglday po in 4 divided doses
WARNINGS: 1. contrnindications :
- obstructive llIOf81hy
- obstructive disease of the GI tract
- severe ulcerative colitis
- reflux esophagitis
-glaucoma
- myasthenia gravis
- nursing mothers
2. use with caution in patients with autonomic neuropathy, hepatic or renal disease,
HIN, CAD, and CHF.
3. HYOSCYAMINE ( CYSTOSPAZ)
CLASS : parnsympatholytic agent
DOSAGE: 1-2 tabs po qid (fewer ifneeded )
WARNINGS: 1. contraindications :
-glaucoma
- obstructive llIOf81hy
- paralytic ileus
- myasthenia gravis
137
4. GLYCOPYRROLA1E (ROBINUL)
CLASS : anticholinergic agent
DOSAGE: I tab po tid
WARNINGS: 1. contraindications :
- autonomic neuropathy
- hepatic or renal disease
- ulcerative colitis
- hyperthyroidism
- hiatal hernia with esophageal reflux
5. DIPHENOXYLA1E HCL AND ATROPINE SULFA1E (LOMOTIL)
CLASS : antidiarrheaV anticholinergic agent
DOSAGE: 2 tab po qid
WARNINGS: 1. :fluid and electrolyte monitoring a must
2. do not use for antibiotic associamd diarrhea
3. may interact with baIbituIates, tIanquilizers, ETOH, and MAO inhibitors
6. KAOLIN AND PECTIN (KAOPECfATE)
CLASS : antidianheal agent
DOSAGE: capsules, chewable tabs, and liquid preps
7. LOPERAMIDE HCL (IMMODIUM)
CLASS : antidiarrheal agent
DOSAGE : 4 mg po followed by 2 mg after each unformed stool
8. PINKBISMUlH (pEPTO BISMOL)
ANALGESICS
I. Morphine sulfate
- adult dosage - 5-20mg q 4 hr SC,IM (also slow IV)
- 1O-20mg q 4 hr rectally
- pediatric dosage - 0.I-O.2mg q 4 hr SC,IM
- metabolism - liver
- excretion - kidney
- antidote - naloxone - (Narcan) - 0.4-2mg q 2-3 min IV,IM,SC up to O.lmglkg IV
MS Contin - 15,30,60,IOO,200mg in controlled release tablets with 200mg tablets only being
used in
patients with tolerance
- should titrate dose on an every 12 hoor interval starting V\-1.th 15mg q 12 hr PO
MSIR (Immediate release) - 15,30mg tablets or a solution of 5mgllml
- should titrate dose 5-30mg q 4 hr PO is a good starting point
Morphine Derivatives:
1. Oxymorphone HCL (Numorphan)
- adult dosage - 1.0-1.5mg q 4-6 hr SC,IM or 0.5mg 4-6 IV
2. Hydromorphone HCL (Dilaudid)
- adult dosage - 2-4mg q 4-6 hr PO
- 2mgq 4-6 hr SC
- 3mg q6-8 hr Rectally
138
2. Methylmorphine S04 or P04 (Codeine)
- adult dosage - 15-60mg q 4 hr PO,IM,SC
- pediatric dosage> I year old: O.5mglkg q 4-6 PO,SC
- metabolism - liver
- excretion - kidney and some liver
- antidote - narcan as above
- Compounds containing Codeine
NAME CODEINE (mg) ASA (mg) ACETAMINOPHEN (mg)
Tylenol #2 15 300
Tylenol #3 30 300
Tylenol #4 60 300
Tyl/Cod Elixir 12 120
Empracet#3 30 300
Empracet#4 60 300
Emprin#2 15 325
Emprin#3 30 325
Emprin#4 60 325
Codeine Derivatives:
1. Oxycodone HCL
- Preparations and Dosages
a. Percocet (5mg oxycodone, 325mg acetaminophen)
- 1-2 q 4-6 hrPO
b. Tylox (5mg oxycodone, 500mg acetaminophen)
-lq6hrPO
c. Percodan (4.5mg oxycodone, 0.38mg oxycodone terephthalate, 325 mg
aspirin)
-lq6PO
d Percodan Demi (pediatric)
- 112 the strength of regular percodan
- 112 tab q 6 for children> 12 years old
-114 tab q 6 for children 6-12 years old
e. Oxycontin (controlled release)
- analgesia onset within one hour
- sustained release over 12 hours
- titrate every 1-2 days, if necessary
- increase dose by 25-50% as necessary, do not increase dose :frequency
- may give oxycontin immediate release for breakthrough pain
- supplied in 10,20,40,80 mg tablets taken every 12 hours
139
2. Hydrocodone
Preparations and Dosages
NAME HYDROCOOONE (mg) ACETAMINOPHEN (mg) ASA(mg)
Lortab2.5 2.5 500
Lortab 5 5.0 500
Lortab 7.5 7.5 500
Lortab liquid 2.S 120
LortadASA 5.0 500
Lorcet 10.0 650
Hydrocet S.O 500
Vicodin 5.0 500
VicodinES 7.5 750
-- Dosages generally should not exceed 40mg of Hydrocodone
3. Propoxyphene HCLInapsylate (Darvon I Darvon-N)
- adult dosage - Darvon 65mg q 4 hr PO
- Darvon-N 100mg q 4 hr PO
or 10mglml susp at 10ml q 4 hr PO
- metabolism - liver
- excretion - kidney
- antidote - narcan as above
- Preparations:
1. Darvon compound (32mg darvon.. 389mg ASA, 324mg caffeine)
2 .. Darvon with ASA (65mg darvon, 325mg ASA)
3. Darvon-N 50 (50mg darvon-N, 325mg acetaminophen)
4. Darvon-N 100 (100 darvon-N, 650mg acetaminophen)
** May be given to codeine/morphine allergic patients
4. Pentazocine HCLllactate (Talwin I Talwin Inj)
- adult dosage - SOmg q 3-4 hr PO, 30mg q 3-4 hr IM,SC,IV
- contraindicated in children under 12
- metabolism - liver
- excretion - kidney
- antidote - narcon as above
- Preparations:
1. Talwin compound (12.5mg pentazocine, 325mg ASA)
-2tabq6hrPO
2. Talacen (25mg pentazocine, 650ng acetaminophen)
-lq4hrPO
3. Talwin Inj *(caution with SC route - may cause skin
damage Isclerosis!)
- 30mg q 3-4 hr IV,SC,IM
4. Talwin Nx *(contains Naloxone - an antagonist which
has no affect at 0.5mg PO however, it does have an narcotic antagonist affect if
given IV at this
dosage - thus preventing abuse)*
- 50mg pentaxocine, 0.5mg naloxone
- 1 q 3-4 po (may be increased to 2 tabs if needed)
140
** All Talwin products may cause withdraw due to an antagonistic affect toward morphine and
demerol regardless of the presence of naloxone
** May be used in morphine and codeine allergic patients
5. Meperidine HCL (Demerol)
- adult dosage - 50-150mg q 3-4 hr PO,IM,SC
- lS-35mg/hr IV in divided doses or slow drip
- pediatric dosage - 1.5mglkg q 3-4 hr PO,IM (single dose not to exceed lOOmg)
- metabolism - liver
- excretion - kidney
- antidote - narcan
- miscellaneous - May be given with 25-S0mg ofPhenergan or Vistiril in order to decrease the
dose and not lose effect.
** This drug should not be given to dialysis patients due to its metabolite not being dialiazable and, this
metabolite may induce seizures.
- Preparations:
1. Mepergan (2Smglml meperidine, 25mglml promethazine)
- adult - 2S-S0mg q 3-S 1M
- children - O.5mg/lb q 3-4 1M
2. Mepergan Fortis (50mg meperidine, 25mg promethazine)
- adult - 1 q 4-6 PO
6. Butorphanol (Stadol)
- adult dosage - Img q 3-4 hr IV
2mg q 3-4 hr 1M
- 1 mg puff up 1 nostril q 3 -4 hr
- pediatric dosage - contraindicated in patients under 18
- metabolism - liver
- excretion - kidney
- antidote - narcan as above
7. Non-narcotic agents with Narcotic-like pain relief
A. Ketoralac (Toradol)
- adult dosage - 60mg loading dose then 30mg q 6 hr 1M
- IOmg q 4-6 hr PO
* only for up to 5 days may this be used
* This drug is a NSAID and has all the same precautions.
** General PrecautionslContraindications for these Medications
-check: PDR if you are going to use these drugs and the following apply
1. compromised respiratory function
2. biliary tract dysfunction
3. increased CSF pressure
4. hepatic or renal disease
5. recent use of CNS depressants
6. Thyroid disease
7. recent use of MAO inhibitors
8. nursing mothers
9. be aware of acetaminophen and aspirin containing compounds and their relative
contraindications
141
NON NARCOTIC I NON NSAID
- TRAMAOOL HCL (Ultram)
CLASS: analgesic centrally acting
DOSE: 50 - 100 mgpo q 4 - ~ brs.
max dose : 400mg I day
METABOLIZED: liver
CLEARED: renal
WARNINGS: creatinine clearance< 30ml/min : dose: 50 -100mg po q 12 Ms.
cirrhosis pt. dose : 50mg po q 12 brs.
may potentiate seizure risk with other medications
associated with many GJ. complaints
NONSTEROIDAL ANTllNFLAMMATORY DRUGS
Pharmacology
With the exception of nabumetone, all NSAIDs are weak acids.
Acidic environment of stomach I proximal small iiltestine
NSAIDs - nonionized lipophilic state allowing for rapid and complete absorption.
Most NSAIDs reach peak plasma concentIations- three hours.
Steady state plasma concentrations are achieved in 3-5 half lives.
Extensively bound to plasma proteins (98-9CJOAl)
small volume of distribution. (1-2% of the drug is "free")
Patients with hepatic dysfunction may require dose alterations. .
Sulindac and Nabumetone - prodl1lgs (converted in the liver to active form)
Most NSAIDs undergo hepatic biotransformation either through the cytochrome p450 system
or glucuronide conjugation
Elimination is predominantly through the kidney although some NSAIDs can be eliminated either
partially or totally through the biliary tract (e.g .. Sulindac, Indomethacin).
patients with renal failure conjugated metabolites can accumulate and be reabsorbed and
reconverted to the active drug.
Differences in NSAID half-life generally reflect differences in renal clearance
The acidity of inflamed synovial tissue allows for increased penetration into joints and a larger
portion of unbound drug in synovial fluid
Joint concentrations ofNSAIDs will remain constant even when serum concentrations fluctuate.
Mecbanism of Action
NSAIDs possess analgesic. antipyretic, and anti-inflammatory effects.
The exact mechanism of action is not known.
Therapeutic effect is thought to be due to the inhibition of prostaglandin (PG) synthesis (yet for
many NSAIDs the dose required to suppress prostaglandin synthesis is lower than the dose needed to
produce anti-inflammatOly effects.)
Prostaglandins:
Sensitize nociceptors to the effects of bradykinin,. histamine and other substances.
Raise the set point in the hypothalamic thermoregulatory center thereby causing fever.
Effects on inflammation are not completely understood
Some PGs cause a direct vasodilation and are thought to potentiate the effects of bradykinin and
histamine on blood vessels resulting in increased vascular permeability, vasodilatation, and edema.
PGs are the byproducts of arachidonic acid metabolism
142
Arachadonic acid:
Stored in phospholipids of cell membranes
Liberated by phospholipases in response to noxious stimuli
Metabolized through cyclooxygenase or Iipoxygenase.
Leukotrienes are the endproducts of the lipoxygenase pathway,
prostaglandins, prostacyclin, and thromboxanes are the endproducts of the cyclooxygenase
pathway.
Cyclooxygenase: two distinct forms of the cycIoox-ygenase (COX) enzyme.
1. COX-l
expressed in most tissues including the GI tract. kidneys, and blood vessels.
2. COX-2
usually undetectable
induced by cells during inflammation.
Most NSAIDs inhibit the COX-l enzyme and have a similar side effect profile.
Those NSAIDs that more selectively inhibit the COX-2 enzyme (i.e.
Nabumetone, Celebrex, Viox.x) are associated with less side effects.
ARACHADONIC ACID CASCADE
PHOSPHOLIPIDS
Phospholipase A2
ARACHIDONIC ACID
Cyclooxygenase
(COX1&2)
CYCLIC
ENDOPEROXIDASES
Prostacyclin Thromboxanes
5-HPETE
Leukotrienes
143
PGta
Vasodilator
Bronchodilator
Sensitizes pain receptors
Raises set point in hypothalamic thennoregulatOIy center
Stimulates GI mucus secretion
PGF'l
Vasoconstrictor
Stimulates GI Mucus Secretion
Prostacvclin
PGI'l
Vasodilator
Inhibits platelet aggregation
Inhibits gastric acid secretion
Thromboxane
TXA'l
Promotes platelet aggregation
Adverse Effects of NSAIDs
1. Gastrointestinal
Most common side effect ofNSAIDs. (10-20,000 people each year die from NSAID induced GI
complications).
Most complications involve damage to the mucosal layer and include
indigestion
diffuse gastritis
erosions
ulcerations
severe GI hemorrhage.
Risk factors for the development of NSAID induced GI complications
prior histOIY of ulcer disease
advanced age
cigarette smoking
alcoholabuse
high dose/multiple NSAIDs
concomitant corticosteroid use.
The relationship with Helicobacter Pylori is unknown.
(NSAID induced ulcerations can be histologically distinguished from H. Pylori ulcers.
Additionally, the majority ofH. Pylori ulcers occur in the duodenum and are
symptomatic, whereas most NSAID ulcers occur in the antrum of the stomach and are
asymptomatic.)
NSAIDs have a dual insult on the GI tract- topical and systemic.
144
Topical (direct and indirect effect.)
direct effect
due to the transport of the lipophilic drug into the gastric mucosal cell where they are
converted back to the ionized form which becomes "trapped" in the cell (Ion Trapping).
The membrane permeability of the mucosal cell is then altered leading to an influx of
very acidic gastric juice back into the mucosal cell (Back Diffusion).
indirect effect
occurs from the reflux of bile containing active metabolites.
Systemic
result from the inhibition of prostaglandin synthesis.
GI prostaglandins (predominantly PGE2, PGI2) have a cytoprotective effect. They
stimulate mucus production and secretion, stimulate HC03- secretion, inhibit acid
secretion, inhibit Gastrin secretio!!, and enhance mucosal blood flow.
Various methods have been employed in attempting to decrease the incidence of GI
Side effects. Most are directed at reducing the topical effect on the mucosa and
have no systemic effect (e.g .. buffering, enteric coating, prodrugs, nonacidic
NSAIDs, administration with food). Therefore, these methods are met with limited
success. The use of cytoprotective agents (e.g .. Misoprostol, H2 blockers) has
proven to be more efficacious. Some NSAIDs are associated with less GI side
effects because they are thought to be less potent inhibitors of GI prostaglandins.
Cl1oprotective Agents
I. Misoprostol (Cytotec)-
PGE analogue
protects Born the gastric and duodenal mucosa
Side effects: Diarrhea- most common
Increases uterine contractility- AVOID in pregnancy (spont. abortion)
2. H2 receptor antagonists (Cimetidine, Ranitidine, Famotidine)
Block histamine induced release of acid from parietal cells
effective in protecting the duodenal mucosa
3. Sucralfate (Carafate)
Neutralized stomach acids
may stimulate PG synthesis
ineffective
4. Prilosec
Least Gastrotoxic NSAIDs
1. Nabumetone (Relafen)
only nonacidic NSAID
Prodrug
Selective COX-2 inhibitor
2. Etodolac (Lodine)
3. Choline Magnesium Salicylate (TriIisate)
4. Salsalate (Disalcid)
Both TriIisate and SaIsalate are nonacetylated salicylates
Less potent inhibitors ofPG's
5. Celebrex
COX - 2 inlnbitor
145
2. Renal
Prostaglandins have seveml important roles in the kidney.
regulate vascular tone
maintain GFR
enhance sodium and water excretion
stimulate Renin secretion
The effect of renal prostaglandins is negligible in normal circumstances.
Renal Side effects:
Acute Renal Failure (ARF)
Risk factors for the development of ARF include conditions that result in decreased
blood volume (liver disease, diuretic therapy, nephrotic syndrome, congestive heart
failure, sepsis. etc.). Systemic vasoconstriction occurs in these circumstances to maintain
blood pressure. Renal PGs are synthesized on demand and playa counterregu1.atory role
attenuating the decrease in renal blood flow and GFR that would otherwise occur if the
vasoconstrictive forces were left unopposed. Other risk factors in patients with normal
blood volume include contrast induced nephropathy, chronic renal failure, and advanced
age.
interstitial nephritis
proteinuria
nephrotic syndrome
abnormalities of sodium, potassium, and water homeostasis
Least Nephrotoxic NSAlDs
1. Nabum.etone (Relafen)
2. Etodolac (Lodine)
3. Sulindac (Clinoril)
4. Choline Magnesium Salicylate (Trilisate)
5. Salsalate (Disalcid)
6. Celebrex (Cox-2 inhibitor)
3. Bronchopulmonary
. asthma exacerbation.
The degree of prostaglandin inhibition correlates to the potential for inducing bronchospasm.
PGEz is a bronchodilator and stabilizes histamine stores in mast cells.
Greater leukotriene production
Theoretically, the inhibition of cyclooxygenase also funnels greater
amounts of arachadonic acid through the lipoxygenase pathway resulting
in. Many of the leukotrienes are bronchoconstrictors (L T C ~ and function
as slow reacting substances of anaphylaxes.
For this reason NSAIDs that inhibit both the cyclooxygenase and
lipoxygenase (Diclofenac, Ketoprofen) pathways are considered safer
agents.
Patients with nasal polyps, asthma, and nonallergic rhinitis are at increased risk to develop NSAID
induced bronchospasms.
146
4. Cardiovascular
Angina
Myocardial ischemia
Leukotriene D4 (LTD4} is a potent coronary artery vasoconstrictor. Its production may be
enhanced by NSAIDs by shunting arachadonic acid through the lipoxygenase pathway.
Can increase blood pressure through its actions on the kidney. blood vessels. and from the increased
salt intake associated with some NSAIDs.
5. Hematologic
impair platelet aggregation
inhibiting the production ofthromboxane A2 (TXA2).
Aspirin irreversibly acetylates cyclooxygenase and its effect lasts for the life of the platelet
(8-12 days). Platelets lack a nucleus and are unable to synthesize a new enzyme. All other
NSAIDs reversIbly inhibit cyclooxygenase and their effect persists for the time that effective
serum NSAID concentrations are present. Therefore. to ensure return of normal platelet
function aspirin should be discontinued 8-12 days prior to surgery. Other NSAIDs should be
discontinued 4-5 half lives prior to surgery (Piroxicam because of its long half life requires
8-10 days for complete reversal).
Blood dvscrasias - rare effects ofNSAID use
leading cause of death attributed to NSAID therapy.
Aplastic anemia
Agranulocytosis
Hemolytic anemia
Thrombocytopenia
(Aplastic anemia and agranulocytosis is more frequently implicated with Phenylbutazone and
Indomethacin use.)
6. Hepatic
A transient asymptomatic elevation in serum transaminases can occur in up to 15% of NSAID
treated patients. Possible mechanisms for hepatocellular injury include drug hypersensitivity and the
formation of reactive intermediate metabolites. Pyrazoles, proprionic acids and indole derivatives show
the greatest propensity for severe liver damage such as hepatitis and cholestasis. Diclofenac has also been
reported to be relatively hepatotoxic.
7. Central nenrous system
Headaches
Indomethacin causes dose related headaches secondary to its cerebral vasoconstrictive
effects.

Tinnitus

Confusion

Irritability

Insomnia
Dizziness
Idiosyncratic aseptic meningitis
(most likely a hypersensitivity reaction) has been associated with Ibuprofen. Tolmentin and
Sulindac used in patients with SLE or other collagen vascular diseases.
The majority of these effects are reversible with discontinuation of the drug.
147
8. Articular Cartilage
NSAIDs are very effective in treatingjoint inflammation because of their ability to gain access to
synovial fluid, however there is evidence that they may actually contribute to joint destruction. There is
conflicting information regardirig the role ofNSAIDs in preventing or producing cartilage destruction.
Through the inhibition of prostaglandins and certain inflammatory cells NSAIDs prevent cartilage
destruction. However, NSAIDs may inhibit certain aspects of cartilage repair by reducing the synthesis of
hyaluronic acid and glycosaminoglycans.
DRUG INTERACTIONS
1. WarfariD
Warfarin is highly bound to plasma proteins and is rapidly displaced by NSAIDs. The active
"free" level of Warfarin is then increased. The combination ofNSAID induced platelet inhibition and the
Warfarin induced inhibition of the coagulation system predisposes these individuals to serious bleeding
episodes (particularly GJ bleeds due to the effect ofNSAIDs on the stomach!).
2. Antiepileptic agents
Pyrazole NSAIDs interfere with the metabolism of Phenytoin producing increased plasma
concentrations and increase the likelihood of toxicity. Additionally Phenytoin and Valproic acid are
highly protein bound which can be easily displaced by NSAIDs.
3. Corticosteroids
Corticosteroids increase the rate of salicylate clear.mce and reduce its plasma concentration.
Combination CorticosteroidINSAID therapy considerably increases the risk of GI side effects.
4. Probenecid
Probenecid increases the plasma concentration of NSAIDs by reducing their renal excretion,
competing for albumin binding sites, and competing for liver glucuronidation enzymes.
5. Hypoglycemic agents
Sulfonylureas are highly bound to plasma proteins and can be displaced from their binding sites
by NSAIDs leading to a dangerous hypoglycemic event Salicylates have a hypoglycemic effect
themselves. Pyrazole NSAIDs can also inhIbit the metabolism of sulfonylureas.
6. Antihypertensive agents
NSAIDs can antagonize antihypertensive agents through several mechanisms; most cause
sodium and water retention, suppression of plasma renin, suppression of adrenal receptors, and impaired
prostaglandin synthesis.
7. Lithium
Lithium is almost entirely eliminated through the kidney and its clearance is significantly
reduced by the coadministration of an NSAID.
8. Methotrexate
Methotrexate is predominantly eliminated through the kidneys and its clearance is reduced by the
coadministration ofNSAIDs.
9. Digoxin
NSAIDs increase serum Digoxin levels by decreasing its renal clearance.
148
Dru!! Clas, A!!ent Trade Ilame H(", Dose -'LlX D'lil.\
Supplied D(l'l'
Salicylotes Enteric coated Ecotrin 81mg 4000mgfday 4000mg
325mg in divided doses
500mg
Salsalate Disalcid, 500mg 3000mgfday
Salflex 750mg I div doses
Choline Mg* Trilisate 500mg 2000-3000mglday
Salicylate 750mg in divdoses
IOOOmg
Trilisate liquid 500mgf5ml peds-5Omglkglday
Diflunisal Dolobid 250mg 500-1500mglday 1500mg
500mg in divdoses
Pyrazoles
Phenylbutazone l00mg 400mgfday 400mg
indivdoses
Indoleacetic acids
Indomethacin Indocin 25mg 75-15Omglday 200mg
50mg in divided doses
50mgsuppos
25mg/5ml susp
IndocinSR 75mg
Sulindac Clinoril 150mg 300-40Omglday 400mg
200mg in divided doses
Pyrrolacetic Acids
Tolmentin Tolectin 200mg 600-1800mgfday 1800mg
600mg in div doses; pediatr-
TolectinDS 400mg lS-3Omglkglday
Proprionic Acids
Ibuprofen Motrin,ffiU 200mg 1200-3200mglday 3200mg
Rufen, Nuprin 300mg in div doses
Advil 400mg
600mg
800mg
Childrens Motrin lOOm.glSml 20-4Omglkglday 40mglkglda
y
Childrens Advil suspension
Naproxen Naprosyn 250mg 500-1S00mgfday lS00mg
(*ec=avail in 375mg(ec) in div doses;
enteric coated) 500mg(ec) pediatric-
12Sm.gISml lOmglkglday lSmg/kg
suspension
137Smg
149
Supplied Dose
Proprionic Acids
continued Ketoprofen Orudis 25mg l00-300mglday
300mg
50mg indiv doses
75mg
Oruvail l00mg in single or
(ext release) lSOmg divided doses
200mg
Fenoprofen Nalfon 200mg 1200-3200mglday 3200mg
300mg indiv doses
600mg
Flmbiprofen Ansaid SOmg 200-300mglday 300mg
lOOmg in div doses
Oxaprozin Daypro 600mg 600-1200mglday 1800mg
or
in one or div doses 26mglkg
Phenylocetic Acids
Diclofenac Na + Voltaren 25mg
50mg lOO-200mglday 200mg
7Smg in div doses
Diclofenac ~ Cataflam 50mg
Anthranilic Acids
Meclofenamate Meclomen SOmg 200-400mglday 400mg
sodium IOOmg in div doses
Oxicams
Piroxicam Feldene lOmg IO-20mglday 20mg
20mg
Napthylalkllnones
Nabumetone Relafen 500mg IOOO-2000mglday 2000mg
7S0mg in one or two doses
Tetrahydroindoles
Etodolac Lodine 200mg 800-1200mglday 1200mg
300mg in div doses
400mg
SOOmg
Pyrrolopyrrole
Ketorolac Toradol lSmglrnJ single dose:
Tromethamine 30mglml <65yo-6Omg IM; 30mg IV
>65yo, renal failure, or
<50kg-30mg IM; lSmg IV
multiple dose:
<65yo-30mg q6h IMIIV 120mg
>65yo, renal failure, or
<SOkg- ISmg q6h IMIIV 60mg
** IV bolus >15 seconds
lOmg lOmgq6h 40mg
*Maxmun Durati on of use is 5 Days PO, IM, And IV
150
Tables and Formulas
Creatinine Clearance = (Lean kg) (140 - age) (0_85 if female)
[normal> 80] (72) (stable creatinine)
Wt=[(actual- ideal) x 40%]+ ideal body weight
Ideal Body Weight:
Start at height of 5'0" equiv_ to 1001bs_
for males add 7fbsJinch >5ft
for females add 51bsJinch >5ft
Body Surface Area CBSA) = square root of [height (cm) x weight (kg)].
[in m
2
] 3600.
Therapeutic Drug Levels
Digoxin 0_5 - 2.2 ng/ml
Gentamicin peak 4 - 6 mg/mf
Gentamicin trough 1 - 2 mg/ml
Lidocaine 1 - 5 mg/ml
Lithium 0_5 - L5 meq/mf
Phenoba rbita I 15 - 40 mg/ml
Phenytoin 10 - 20 mg/mf
Theophylline 10 - 20 mg/mf
Tobramycin peak 4 - 6 mg/mf
Tobramycin trough 1 - 2 mg/mf
Vancomycin peak 18 - 40 mg/ml
Vancomycin trough 5 - 10 mg/ml
Antidotes
Toxin Antidote
Acetaminophen
Benzodiazepi ne
N_ Acetyleysteine (mucomyst)
Flumazenil
151
Toxin
Heparin
Warfarin
Narcotics
Narcotic - Type Analgesic Comparisons
Drug Equi-Analgesic
Route Dose (MG)
(agonists)
Morphine
1M
PO
R
10
30- 60
60
Hydromorphine (Dilaudid)
1M 1.5
PO 4 - 7.5
R 6
(agonists)
Levorpha nol(Levo-Dromora n)
1M 2
PO 4
Oxycodone
PO 30
Methodone
1M 10
PO 20
Meperidine (Demerol)
1M 100
PO 300
Codeine
1M 130
PO 200
Duration
(HR)
4-5
4-5
4-5
4-5
4-5
4-5
4-6
4-6
3-4
4-6
4-6
2-4
2-4
3-5
3-5
Antidote
Protamine
Vitamin K
Naloxone
Drug Equi-Analgesic
Route Dose (MG)
(mixed agonist - antagonists)
Butorphanol (Standol)
1M 2
Buprenophine (Buprenex)
1M 0.3 - 0.6
Nalbuphine (Nubain)
1M 10
mixed agonist - antagonists)
Pentazocaine (Talwin Nx)
PO 180
Duration
(HR)
3-4
4-6
3-5
2-4
152
Relative potencies and Equivalent Doses of Corticosteroids
Approx. Equiv. Relative Relative Duration
Dose* Antiinflam. Sodium of Action
GI ucocorticoid Potency Potency Retaining T 112 (hrs)
Shortacting (s)
Cortisone 25 0.8 0.8 812
Hydrocortisone 20 1 1 812
I ntermediateacting(l)
Prednisone 5 4 0.8 1236
Prednisolone 5 4 0.8 1236
Methyl prednisolone 4 5 0.5 1236
Triamcinolone 4 5 0 12-36
Longacting (L)
Beta methasone 0.6 30 0 36-54
Dexa methasone 0.6 25 0 3654
*These dose relationships apply only to oral or intravenous administration; relative potencies may
differ greatly when injected intramuscularly into joint spaces.
Topical Corticosteroid Potency
Potency Drug
Level
High
Betanethasone
(Oiprolene. Oiprasone)
Triancinolone acetonide
(Kenalog-HP. Aristocort-HP)
Oesoximetasone
(Tropicat)
Ffuocinonide (Lidex)
ntermediate
Betanethasone
(Valisone)
Desoxinelasone
(T ropicortLP)
Desonide
(T ridesilon)
Tricmcinolone acetonide
(Kenalog, Aristocort)
Strength
0.05%
0.5%
0.25%
0.05%
0.1%
0.05%
0.05%
0.05%
Potency
Level
low
Very low
Drug Strength
Ffuocinolone 0.01%
(Synatar)
Betarnethasone valerate 0.01%
Triancioofone acetonide 0.025%
(Kenafog-LP, AristocortLP)
Hyctocortisone 2.5%
Hyctocortisone 1.00%
Hyctocortisone 0.5%
153
Substances which may discolor urine
Black/Brown/Dark
Cascara Chloroquine
Ferrous salts Ferrous sulfate
Furazolidone Methocarbamol
Metronidazole Nitrofurantoin
Quinine Senna
Methylene blue Triamterene
Blue/Green
Amitriptyline Indigotindisulfonate
Methylene blue Resorcinol
Tolonium
Drugs which may discolor feces
Black
Acetazolamide
Aminophylline
Amphotericin B
Chlorpropamide
Corticosteroids
Black
Cytarabine
Ethacrynic Acid
Fluorouracil
Hydrocortisone
Melphalan
Methytrexate
Potassium salts
Procarbazine
Tetracycline
Thiotepa
Warfarin
Aluminum Hydroxide
Amphetamine
Bismuth salts
Clindamysin
CycIcophosphamide
Digitalis
Ferrous salts
Hydralazine
Iodide containing drugs
Methyprednosolone
Phenylephrine
Prednisolone
Sulfonamides_
Theophylline
T riamcinlone
Red
AminoPyrine
Doxorubinicin
Idarubicin
Phenyl butazone
Phenoth iazi nes
Rifampin
Orange/Yellow
Daunorubicin
Ibuprofen
Oxyphen butazone
Phenytoin (pink)
Phensuximide
Senna
Acetanilid
Phenazopyridi ne
Sulfasalazine
Heparin
Rifampin
Warfarin
Green
Indomethacin Medroxyprogesterone
Yellow
Senna
Pink/Red
Anticoagulants
Barium
Oxyphenbutazone
T etracyC\ine syrup
Orange/Red
Phenazopyridine
Black/White speckling
Aluminum Hydroxide
Barium
Aspirin
Heparin
Phenylbutazone
Rifampin
Antibiotics (PO)
154
Chloramphenicol
Drug-Lab Test Interferences
Test
Serum ALT lAST
Serum Bilirubin
Serum Calcium
Urine Catecholamines
Serum Cholesterol
Serum Creatinine
Urine Glucose
Urine Ketone
CSF Protein
Serum Protein
Methylene blue
May increase results
Erythromycin
Methydopa
Ascorbic acid
Dextran
Epinephrine
Methyldopa
Rifampin
Hydralazine
Acetaminophen
Chloral Hydrate
Epinephrine
Erythromycin
La beta 101
Levodopa
Methenamine
Methydopa
Tetracyclines
Triamterene
Aspirin
Corticosteroids
Phenothiazines
Vitamin D
Cefoxitin (Jaffe method)
Flucytosine
Ascorbic acid
Cephalosporins
Levadopa
(Clinitest)
Nalidixic Acid
Levadopa
Mesna
Phenazopyridine
Salicylates
Methicillin
Phenothiazines
Sulfonamides
Phenazopyridine
May decrease results
Aspirin Heparin
Sulfisoxazole
Iodine containing Radiocontrast Media
Nitrates
Ascorbic acid
Cephalosporins
Levadopa
(Clinistix, Test-Tape)
Cytarabine
155
Urine Protein
Serum Thyroxin
Blood Urea Nitrogen
Serum Uric Acid
D r u ~ that can cause fever
Most common
Amphotericin
Cephalosporins
Halothane
Interferon
Iodides
Isoniazid
Levothyroxi ne
Methyldopa
Muromonab - CD3(OKT3)
Penicillins
Phenytoin
Procainamide
Quinidine
Streptoki nase
Urokinase
Vaccines
Vancomycin
Aminogglycosides
Magnesium Sulfate (Large IV doses)
Nafcillin
Phenazopyridine
Tolbutamide
Tolmentin
Heparin Heparin
Chloral Hydrate Chloramphenicol Streptomycin
Ascorbic Acid
Caffeine
Theophylline
Levadopa
Less common
Allopurinal
Antihistamines
Atropine
Azathioprine
Barbituraates
Benztropine
Bleomycin
Carbamazepine
Chlorambucil
Cimetidine
Cisplatinum
Clofibrate
Cytarabine
Daunorubicin
Diazoxide
Doxorubicin
Folic Acid
Haloperidol
Hydralazine
Hydroxyurea
Ibuprofen
L-Asparaginase
6-Mercaptopurine
Methoclopramide
Nifedipine
Nitrofurantoin
Paraldehyde
PGE2
Procarbazine
Quinine sulfate
Rifampin
Ritodrine
Salicylates
Streptomysin
Sulindac
Streptozoci n
Tetracycline
Triamterene
Trifluoperazine
156
Drugs Causing Adverse Hematological Effects
1. Drug Induced Aplastic Anemia
Acetazolamide Oral Antidiabetics
Antihistamines Oxyphenbutazone
Carbamazepine Penicillamine
Chloramphenicol Phenobarbital
Chloroquine Phenothiazines
Chlorothiazide Phenytoin
Gold Salts Propylthiouracil
Indomethacin Quinidine
Methimazole Sulfonaamides
2. Drug Induced Aganulocytosis
Acetaminophen Isoniazzid
Acetazolamide Levodopa
Allopurinal Lincomycin
Para-Aminosalicylic Meprobamate
Acid
B-Lactam Antibiotics Methazolamide
Benzodiazepines Methimazole
Brompheniramine Methyldopa
Carbamazepine Metronidazole
Captopril Nitrofurantoin
Chloramphenicol Oxyphenbutazone
Chlorpropamide Penicillamine
Cimetidine Pentazocine
a. Immune Hemolytic Anemia (continued)
Hydralzine Quinidine
HCTZ Quinine
Ibuprofen Rifampin
Isoniazid Sulfonamides
Levodopa Streptomyci n
Mefenamic Acid Tetracycline
Melphalan Tolbutamide
Methadone Triamterene
Clindamycin Phenothiazines
Clomipramine Phenylbutazone
Dapsone Phenytoin
Desirpramine Primidone
Doxycycline Procainamide
Ethacrynic Acid Propanolol
Ethrosuximide Prohythiouracil
Fenoprofen Pyrimethamine
Flucytosisne Quinine
Gentamicin Rifampin
Gold salts
Griseofulvin
Hydralazine
Streptomycin
Sulfa Antibiotics
Thiazide Diuretics
Hydroychloroquine Tocainide
Ibuprofen Tolbutamide
Imipramine Vancomycin
Indomethacin
3. Drug Induced Hemolytic Anemia
a. Immune Hemolytic Anemia
Acetaminophen Methyldopa
Para-Aminosalicylic Methysergide
Acid
Cephalosporins Penicillins
Chlorpromazine
Chlorpropamide
Cylophosphamide
Cytarabine
5-Fluorodeoxyuridine
5- FI uorouraci I
Hydroxyurea
6- Merca ptopu ri ne
Methotrexate
Probenecid
Procainamide
Phenytoin
Primadone
Pyrimethamine
Sulfasalzine
Triamterene
Trimethiprim
Vinblastine
157
b. Oxidative Hemolytic Anemia
Ascorbic Acid Menadiol
Aspirin Methylene Blue
Benzocaine Nitrofurantoin
Chloramphenicol Nitrofurazone
Chloroquine Phenazopyridine
Dapsone

Diazoxide
4. Drug Induced Megaloblastic Anemia
Para-Aminosalisylic Neomysin
Acid
Azathioprine
Chloramphenicol
Colchicine
Nitrofurantoin
Oral Contraceptives
Phenobarbital
5. Drug Induced Thrombocytopenia
Acetazolamide Hydrochlorothiazide
Allopurinol Isoniazid
Aminoglutethimide Meclofenamate
Para-Aminosalicylic Morphine
Acid
Amrinone Peniccilin
Cephalothin Phenyl butazone
Chlorothiazide Phenytoin
Cimetidine Procainamide
Desipramine Quinidine
Diazepam Quinine
Drug Induced Thrombocytopenia (cont)
Digitoxin Rifampin
Furosemide
Heparin
Sulfisoxazole
Trimethoprim
158
PERIOPERA TIVE MANAGEMENT
PERI OPERA TIVE MANAGEMENT
PERIOPERA TIVE MANAGEMENT
PERIOPERA TIVE MANAGEMENT
PERIOPERA TIVE MANAGEMENT
PERIOPERA TlVE MANAGEMENT
PERIOPERA TlVE MANAGEMENT
PERIOPERA TIVE MANAGEMENT
PERIOPERA TIVE MANAGEMENT
PERIOPERATIVE MANAGEMENT
PERIOPERA TIVE MANAGEMENT
PERIOPERA TIVE MANAGEMENT
PERIOPERATIVE MANAGEMENT
PERIOPERATIVE MANAGEMENT
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HOSPITAL CHARTING
Pre-operative note
32 yo BF presents for smgical correction of her plinful bunion left foot Condition has not resolved with
conservative
therapy.
PMH: IDDM, HIN (well-controlled)
Meds: insulin, procardia
Allergies: no known drug allergies (NKDA)
Social History:
Past Surgical History:
Labs: Chemistry= Na CI BUN
K CO creat
CBC = WBC hemoglobin Platelets
hematocrit
Urinalysis:
Serum HCG:
Foot x-rays:
Chest x-ray: no active lung disease
ECG: normal sinus rhythm
Glucose
PfIINR/PIT =
Impression: hallux abductovalgus defonnity left foot
Plan: 1. smgical correction left bunion defonnity as per attending
2. patient medically cleared for procedure as Dr. PMD
3. consent sigued
(Procedure reviewed with patient including risks, benefits and complications; all questions answered.)
Post -operative note
eponym: "SAPPPA HEMl PC"
S: surgeon
A assistant(s)
P: pre-operative diagnosis
P: post-operative diagnosis
P: procedure
A anesthesia (ie-general; spinal; local; IV sedation with local)
H: hemostasis (ie-ankle or thigh pneumatic tourniquet inflated to __ mmHg for __ minutes; local control)
E: estimated blood loss
M: ~ (ie-sutures; drains; fixation; bone grafts; etc)
I: injectables (ie-intra- or post-ilp local anesthesia; steroids)
P: pathology (ie-bone; soft tissue; foreign body)
C: complications
C: Condition - Stable, Fair, Guarded, Critical
Patient tolerated both procedure and anesthesia without <lpIm'ent complications and with vital signs remaining
stable throughout procedure. Patient transported from OR to RR with vascular status intact to (RIL) LE,
escorted by member of anesthesia department and podiatric surgical resident.
159
Post -op and Admission Orders
eponym: "ADC V ANDILMAX"
A: Admit to the service of Dr. Mlodzienski (podiatric Surgery)
D: diagnosis
C: condition (ie-stable)
V: vitals (ie-monitor vital signs q shift as per floor protocol)
A: activity (ie-bedrest)
N: nursing (ie-elevate left leg and apply ice to dorsum foot)
D: diet
1: insIouts
L:labs
M: meds
A: ancillary personnel (ie-physical therapy; social service)
X: x-rays
In-Patient Progress Note
2/28/95 Podiatric Surgery
6:30 am S: Patient visited at bedside; offers no complaints
Patient denies experiencing SOB, chest pain, cough, ca1fJthigh pain
Good appetite, - nausea!vomitting, - abd pain
+ void, +BM
0: T max , T presently , BP, P, R
Lungs - clear to auscultation (CT A)
Left foot - NVS intact
wound edges appear healthy, viable
wound margins approximated with sutures
- dehisence, - drainage, - purulence
- erythema, mild localized edema
Labs - wound culture left foot [collected 2127/95] MRSA sensitive to vancomycin
X-rays - no erosive changes consistent with osteomyelitis noted
A: 1. SIP I & D diabetic foot infection, wound status improving
2. IDDM, blood sugars well-controlled
P: 1. dressing change perfonne, will continue daily local wound care
2. continue IV Abx; will check peakItrough levels
vancomycin (day #5)
3. will repeat wound cultures and CBC tomorrow
Basic Pre-op Labs
Reasons for ordering labs
a) indication of infection
b) indication of anemia
c) indication of hemorrhage
Signature
d) indication of hyper- or hypoglycemic state
e) indication of renal disease
f) indicatioon of coagulopathies
g) indication of metabolic disease
160
Normal Lab Values
a) CBC with differential
WBC: 5000-10000 cellsIul
RBC: males 4.7-6.1 x 10 cellsIul
females 4.2-5.4 x 10 cellslul
hemoglobin: males 14-18!ifdl
females 12-16!ifdl
hematocrit: males 40-54%
females 37-4'1'10
mean cell hemoglobin (MCR): 27-31 picograms
mean cell hemoglobin concentration (MCHC): 33-3'1'10
mean cell volume (MeV): males 80-94 urn
females 81-99 um
platelets: 150000-450000 ul
segmented neutrophils: 41-71% basophils: 0-1%
stabs neutrophils: 5-10% lymphocytes: 24-44%
eosinophils: 1-3% monocytes: 3-7%
reticulocyte count (normal = 1.5%)
indicator of erythropoietic activity
reticulocytes are immature RBC's which still possess a nucleus
normal bone marrow responds to decrease in erythrocytes- (indicated by hematocrit value) with an
increase in production of reticu10cytes
Left shift
may be indication of infection, toxemia, hemonhage
present in the CBC when more ~ 20% segs are seen or when the total PMN count is greater than 80%
b) Chemistry
sodium: l34-149 meqIl
potassium: 3.2-5.2 meqll
chloride: 94-110 mmol
caIbon dioxide: 19-32 mmolll
BUN: 6-26 m!ifdl
creatinine: 0.4-1.5 m!ifdl
glucose: 56-124 m!ifdl
c) Coagulation Studies
PT (prothrombin time): 10 .1-l3.1 seconds
PIT (activated partial thromboplastin time): 23.5-34.3 sec
d) Urinalysis
color: yellow
appearance: clear
glucose (glu ua): negative
ketones (ket ua): negative
occult blood (oc bId u): negative
protein (pro ua): negative
nitrates (nit): negative
bilirubin (bili ua): negative
specific gravity: 1.010-1.025
pH: 5.0-7.5
leukocyte esterase (leu): negative
urobilinogen: 0.2-1.0 eu/dl
161
Interpreting the CBC with differential
key points to note include:
a) WBC count
>conelate count with differential to detennine extent of infection, left shift, elevation of a specific cell
lineage (ie-elevation oflymphocytes may indicate a state of chronic infection)
b)RBCcount
>correlate with indices (MCR, MCV, MCHC) to detennine anemic states and specific types of anemias
c) Hemoglobin
>indicates oxygen carrying GaJXlcity ofRBC to tissues; major concern in post-op healing
d) Hematocrit
>correlate with RBC count and indices to detennine anemic states
Alterations in Lab Parameters
There are numerous fuctors that can alter every aspect of the pre-op lab values. A complete listing of factors
that may alter the
various lab values can be found in any reference manual (ie-Clinician's Pocket Reference by Gomella, Braen &
OIding)
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162

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Peri-operative Complications
Fever
Oral temperature
normal range is 36.5-37.4 C (97.7-99.5), with an average temperature of 37 or 98.6
rectal temperatures are usually 1 F higher because this value is unaffected by external cooling factors
associated with evaporation that occurs when oral temperatures are measured
body temperature greater than 100.4 F during the postoperative period is a significant finding and the
etiology should be detennined
current theory states that the anterior hypothalamus is responsible for thermoregulation
most people exlubit diurnal fluctuation oftemperature with the lowest reading in the am and the
highest reading in the p.m.
Peri-operative fever
Malignant byperthermia
incidence
... 1112000 pediatric anesthetics
... 1140000 adults anesthetics
susceptible patients
... elevated CPK preoperatively (occurs in -70010 of susceptible patients)
... family histOIY (dominant inheritance) of anesthesia problems
... EKG abnonnalities
... diagnosis: skeletal muscle biopsy and in vitro isometric contracture testing in the presence of caffeine.
halothane, or both
triggering agents
... anesthetic agents (inbalational agents such as ether, halothane, enflurane)
... neuromuscular blocking agents (i.e. succinylcholine)
... stress
163
symptoms/signs
'+ rapidly progressive reaction
'+ first sign usually arrythmias
'+ masseter muscle spasm
'+ rapidly rising temperature
'+ tachypnealtachycardia
'+ profuse hyperhidrosis
'+ metabolic and respiratory acidosis
'+ dark, mottled skin
'+ hyperkalemia leading to cardiac dysrythmias
'+ elevated CPK levels
'+ excessive myoglobin release
treatment
'+ Stop the administration of anesthesia
'+ change anesthetic tubing
'+ hyperventilate with 1000/0 02
'+ correct the acidosis
'+ cool the patient
~ pack the patient in ice
~ gastric lavage with cold saline
~ cardiopulmonary bypass (in severe situations)
'+ Dantrolene sodium (dantrium)
~ skeletal muscle relaxant that prevents the release of calcium
~ intraoperative crisis
> begin at minimum dose of I mglkg by continuous rapid IV push and continue until symptoms
subside or until maximum dose of 10 mglkg has been reached
> if abnormalities reappear, then regimen may be repeated
~ postoperative crisis
> 4-8 mglkglday po in four divided doses for 1-3 day period
~ preoperative prophylaxis
> 4-8 mglkglday po in four divided doses for 1-2 days prior to surgery with last dose 3-4 hours
before scheduled surgery
> Dantrium 2.5 mglkg IV approximately 1 hour before the anticipated anesthesia
~ theory: Malignant hyperthermia is chemically induced by anesthetic agents or catecholamines
produced by stress. The sarcoplasmic reticulum within muscle contains - 3000 times the amount of
Ca ++ normally present in the sarcoplasm. In order for muscle contraction to occur, sarcoplasmic
reticulum must release Ca++ into the sarcoplasm. The sarcoplasmic reticulum then must resequester
the Ca ++ in order for muscle relaxation to occur. When malignant hyperthermia occurs the Ca++ ions
cannot be reabsorbed by the sarcoplasmic reticulum; the concentration of Ca ++ inside the cell rises
activating a series of metabolic reactions leading to the symptoms of malignant hyperthermia
Dantrolene works by preventing the release of Ca ++ from the sarcoplasmic reticulum.
Postoperative Fever
mnemonic [Wind, Walk, Water, Wound, Wonder drugs]
The mnemonic only serves as a guide to determine the possIble cause of a post operative fever. It
represents the more common etiologies of fever at a given time during the post operative period. Keep
in mind that most of the etiologies can potentially occur at any time during the perioperative period
(depending on why the patient is hospitalized and what procedures are performed).
intraoperative
'+ malignant hyperthermia
(Wind] 12-24 hours post op
'+ atelectasis
'+ post op hyperthermia
164
[Walk] 24 hours post op
'+- thrombophlebitis
'+- pulmoruuy embolism
[Water] 48 hours post op
'+- UTI
[Wound] 72 hours post op
.. post op wound infection
[Wonder dmgs] anytime post op
'+- drugfever
Other causes] anytime post op
'+- IV catheter phlebitis/infection
'+- catheter infection
'+- constipation (?etiology)
'+- benign postoperative fever (temperature increase of less that 2 F 48-52 and 72-78 hours post op
without any signs of complication)
workup
The work up of postoperative fever begins with a careful and thorough H&P. The patient should be
questioned specifically about symptoms such as SOB. chest pain. dysuria. pain at the IV site etc ..
Look to see if the patient is on any new medications (ie. low dose heparin. antIbiotics) to try and
determine if the fever may be a result of a medication Be sure to inspect all catheter sites. Laboratory
evaluation can begin with simple tests such as a CBC with differential. UA., and CXR. Blood cultures
should also be obtained if it is believed that the fever is from a septic source. It is recommended that 2
sets of blood cultures be obtained to avoid the potential of treating a contaminating organism that is
found in only one bottle
Severe intractable pain
'+- sutures too tighl
'+- constrictive/tight dressings
'+- hematoma
'+- ischemia
White toe
arterial in nature (usually caused by macremboli, arterial insufficiency, over stretching of
neurovascular bundle with toe lengthening or repositioning)
usually an acute incident, therefore the onset of ischemia is rapid and severe (no time for collateral
circulation to develop)
symptoms/signs
'+-excruciating pain
'+-pale coloration with blue mottling
'+-parasthesia
'+-pulselessness
treatment
'+-avoid nicotine/caffeine
'+-D/C ice/elevation
'+-place foot in dependent position
'+-loosen outer/inner bandage
'+-piston/rotate toe on K wire
'+-warm compresses to proximal neurovascular bundle
'+-local nerve block proximal to area to provide distal vasodilation
'+-vascular surgery consult
165
Blue toe
represents stasis from poor arterial inflow or sluggish venous outflow
etiology
'+microembolic shower
'+post op complication
~ tight dressing/cast
~ "tourniquet effect" of large volume of local anesthetic
~ poor tissue handling technique
~ impingement of tissue between bone or fixation device
~ dissecting hematoma
'+paraneoplastic digital thrombosis
'+transient vasospasm of digital vessels
~ collagen vascular diseases (rheumatoid arthritis, SLE, scleroderma)
~ Raynaud's disease or phenomena
~ acrocyanosis
treatment
'+blue toe secondary to venous insufficiency
~ toe is usually warm and may blanch with pressure (may not blanch if severe)
~ inspect dressing
~ D/C ice and elevation
~ avoid dependency
~ do not attempt to increase vascular perfusion
'+blue toe secondary to arterial insufficiency
~ toe is cold and does not blanch with pressure
~ inspect dressingIK wires
~ D/C ice and elevation
~ avoid nicotine and caffeine
~ heat to popliteal fossa or anterior groin
~ thermostat controlled heat lamp over foot with temperature not to exceed 90 F
~ vasodilators
oral (niacin, nifedipine, cyclospasmol)
nitroglycerin paste
~ if condition persists 12-18 hours, consider more xadical measures
blue toe syndrome m ~ also be seen in non-surgical settings
'+drug induced
'+anticoagulant thexapy (coumadin)
'+prednisone therapy
'+secondary syphilis
'+pheochromocytoma
'+hypercoaguable states
"polycythemia vera
'+thrombocytosis
'+coagulation disorders
'+arterioslerosis obliterans
'+thromboangiitis obliterans
.. cyanotic congenital heart disease
166
ANEMIAS
Classification
a) relative
1. pregnancy
2. nutritional deficiency
3. splenomegaly
4. macroglobulinemia
b) absolute
1. decreased red blood cell production
>disturbance of proliferation and differentiation of stem cells
-aplastic anemia
-myelodyspIastic anemia
>distw:bance of prolifeIation and differentiation of erythroid progenitor cells
-pure red cell apIasia
-anemia of chronic renal disease
-anemia of endocrine disease
-<:ongenital dyserythrocytic
>disturbance of hemoglobin synthesis (hypochromic)
-iron deficiency
-thalassemia
-idiiopathic pulmonary hemosiderosis
>distwbance of DNA synthesis (megaloblastic anemia)
-vitamin Bl2 deficiency
-folic acid deficiency
-purinelpyrimidine metabolic defects
>unknown or multiple mechanisms
-anemia of chronic disease
-sideroblastic anemia
-anemia associated with marrow infiltration
-anemia associated with nutritional deficiency
2. increased red blood cell destruction
>intrinsic abnormality
-membrane defects (ie-hereditary spherocytosis)
~ e deficiency (ie-G-6PD deficiency; porphyria)
-globin abnormality (ie-sieIde cell disease)
-paroxysmal nocturnal hemoglobinuria
>extrinsic abnormality
-mechanical
-chemical of physical
-infectious
-antibody mediated
-hyperactive macrophage system
4>loodl05S
Pre-operative Evaluation
a) hemoglobinlhematocrit (Hgb'Hct)
1. should be evaluated in all patients (especially in menstruating females) since most anemias (unless
severe) are asymptomatic
2. Hct should be above 4()0.4J (Hgb ~ 10 gm) for males and 37% for females, or elective surgery should be
delayed determine cause; repeat test to rule-out lab error
167
b) Aplastic Anemia
May be congenital (ie-Fanconi, Espren-Dameshek), idiopathic, acquired or associated \\'ith drugs,
chemical agents, radiation, infection, metabolic changes (ie- pregnancy) or immunologic factors.
Condition is characterized by the loss ofhematopoetic cells, fatty replacement of marrow and
pancytopenia. The anemia is generally normocytic and the prognosis is largely determined by severity
of associated thrombocytopenia and leukopenia Recognition and removal of cause may lead to remission.
Transfusions are usually not necesssary unless hemoglobin falls below 6-7 gmldL. Response to
glucocorticoids, androgens and immWlosuppressive agents are variable. Bone marrrow transplants are being
perfonned in patients with severe aplastic anemia with marlred bone marrow hyperplasia.
c) Iron Deficiency Anemia
The most advanced stage of iron deficiency, characterized by decreased or absent iron stores, low serum
iron concentration, low transferrin saturation and low hemoglobin concentration or hematocrit value.
May occur as a result of inadequate dietary iron intake, malabsorption of iron, chronic blood loss, diversion of
iron to fetal and infunt erythropoiesis during pregnancy and lactation, intravascular hemolysis or a
combination of these causes. The most common causes are excessive blood loss due to heavy menstrual
bleeding, multiple pregnancies or GI bleeding. In severe WlCOmplicated iron deficiency anemia, the
erythrocytes are hypochromic and microcytic, plasma iron concentration is decreased, iron binding capacity is
increased, serum ferritin concentration is low and the free erythrocyte protoporphyrin concentration is
increased
Fatigue irritability, palpitations, weakness and headache are common complaints of patients with iron
deficiency. Once it has been established that a person is iron deficient and the cause identified,
replacement therapy should be instituted immediately. Oral or parenteral treatment is required, with oral
administration being the preferred route. Unless the anemia is extremely severe, blood transfusion is not
indicated
d) Megaloblastic Anemia
A family of disorders showing characteristic abnormalities of blood and marrow caused by impaired
DNA synthesis. Deficiencies of vitamin B12 and folate accOWlt for over 95% of the megaloblastic
anemias. Anemia may be mild or severe, but because it develops slowly, few symptoms appear until the
hematocrit becomes extremely depressed When they appear, symptoms include weakness, palpitations,
fatigue, light-headedness, and shortness ofbreath. Patients characteristically show slight jaundice and
severe pallor, producing the telltale "lemon-yellow" tint
Differentiation of pernicious anemia (inability to absorb vitamin B 12 secondary to lack: of gastic intrinsic
facator) from other megaloblastic anemias is essential since treatment with B12 (cobalamin) must be
continued for the patient's life. Although correction of the hematologic abnormalities of pernicious
anemia may occur following the administration oflarge doses of folate, nemologic damage progresses and
may even be irreversible. The most helpful diagnostic tests are serum vitamin B12 and folate levels, the
Schilling urinary B 12 excretion test, and gastic analysis.
Initial therapy for pernicious anemia consists of 100-1000 ug 1M daily of cobalamin for two weeks,
followed by 100-1000 ug 1M each month for life. To correct a folic acid deficiency anemia, 1-5 mg folate
PO for 4-5 weeks is administered and usually adequate to replenish body stores and correct the anemia.
e) Sickle Cell Anemia
Sickle cell anemia was first described by Herrick in 1910 and represents the most common form of
congenital hemolytic anemia, affecting 11600 blacks (homozygotes). Approximately 8"/0 of American blacks
have the sickle cell trait (heterozygotes) and the incidence increases in areas such as Western Africa due to its
protective quality against falciparum malaria
The term "sickle cell" disorder refers to states in which the red blood cell assumes a sickle shape when
exposed to low oxygen tension. Under low oxygen tension the red blood cell sickles, causing sludging
that slows blood flow; this stasis creates greater hypoxia that perpetuates the cycle and produces pain as
well as infarction.
168
Hemoglobin is comprised of two alpha and two beta chains. Hemoglobin S represents a substitution of
valine for glutamic acid at position 6 of the beta chain Red blood cells containing this type of
hemoglobin are characterized by shorter survival and tendency to adhere to vascular endothelium,
resulting in anemia and vascular occlusion.
Nonnal:
Sickle Cell Trait:
Sickle Cell Anemia:
HgbAl=96%
HgbAl=55-75%
HgbAl=1-25%
Hgb A2=3% Hgb F=l%
HgbS=2545%
Hgb S=75-95%
Screening for hemoglobin S can be done via the "sickle cell prep", whereby the red blood cell sickling is
observable under a microscope. Positive screening tests should be followed Vl'ith hemoglobin electrophoresis to
determine the specific hemoglobinopathy. Many patients with sickle cell anemia are in good health much of
the time, but this state may be interrupted by a sudden crisis (infarctive, aplastic, hemolytic or sequestrative)
which can occasionally prove fatal.
Typica1lab findings in sickle cell anemia include:
decreasedHgb
decreased Het
normalMCV
normal to increased WBC
normal to increased platelets
increased reticulocyte count
elevated serum bilirubin
elevated serum LDH
Though all systems may be affected, the heart is frequently the site of the most prominent physical
findings. It is often enlarged to both the left and right with systolic and diastolic flow murmurs heard. Painful
ulceration ar01md the ankles characterized by "punched out" appearance with rolled edges, are not an
uncommon swquelae. Treatment generally consists of a combination ofbed rest, local wound care and
occasional antibiotics. Bony sickling can predispose to osteomyelitis, most commonly due to Salmonella
although pneumococcal and staphylococcal infection have been described.
Management of sickle cell anemia is mainly symptomatic and supportive. During painful crises maintain
adequate hydration, improve oxygenation (ie-oxygen via nasal cannula), provide analgesia (ie-morphine,
meperidine) and consider folic acid supplementation. Therapy to enhance production of hemoglobin F in these
patients is still investiWUional. There is no increased risk of using pneumatic tourniquets in patients with sickle
cell trait However, both pneumatic tourniquets and local anesthesia with epinephrine should be avoided in
patients with sickle cell anemia. If general anesthesia is necessary, an inhalational anesthetic is preferred and
adequate maintenance of oxygenation, hYdratiQll,.ventilationis essential.
BLOOD TRANSFUSIONS
Red Cell Antigens and AntIbodies: Serologic Considerations
a) tests for red cell antigens
L red cell typing is usually performed by exposing the cells to specific anti-sera, incuOOting at 37 C and
observing for agglutination.
2. the ABO and Rh types are determined for all blood donors and recipients to avoid transmission of ABO
incompatible blood and to prevent allo-imTDlmi73tion by the Rh antigen.
>tests for additional Rh antigens and antIbodies and those in other genetic systems (ie-Ken, Kidd,
Duffy) are often required when a patient has been allo-immunized
169
The ABO System
a) serum of virtually all individuals contains antibodies corresponding to the A or B antigens not present on
their red cells.
b) ABO typing is performed regularly by testing red cells for agglutination by kno\\'n anti-A and anti-B and
then by testing the serum for its ability to agglutinate knovm A, B and 0 red cells.
Blood Type Substitutions for Trnnsfusion (ABO and Rh)
a) acceptable: A or B red blood cells to AB patients, Rh-negative whole blood or rbc's to Rh-positive patients
b) usually acceptable: A or B whole blood to AB patients; 0 red cells to A, B, or AB patients
c) acceptable in emergency: Rh-positive whole blood or rbc's to-
1. Rh-negative unsensitized men
2. Rh-negative unsensitized posbnenopansal women
d) never acceptable (exception: bone marrow transplantation)
1. A whole blood or rbc's to 0 or B patients
2. B whole blood or rbc's to 0 or A patients
3. AB whole blood or rbc's to 0, A, or B patients
The Rh System
a) an individual inherits a complex balotype from each parent
b) red cells of both donors and recipients are typed by testing them with anti-D. If cell agglutination occurs,
the type is Rh-positive
>if cells are not agglutinated, patient is considered Rh-negative and is tested further for more weakly
reacting antigens
c) all Rh-negative patients should receive Rh-negative rbc's
>obviously, Rh-negative blood may be given to Rh-positive patients, but this rarely occurs since only
15% of the population is Rh-negative
d) the other Rh antigens (C, c, E, e) are much less immunogenic than D and it is impractical to match them in
donor and patient blood
Compatibility Tests
a) pre-transfusion compatibility tests include typing patient and donor red cells for ABO and Rh, screening
patient and donor serums for significant unexpected antIbodies, and reacting donor red cells with patient serum
(major crossmatch)
1. major crossmatch determines the presence of any allo-antibodies in the recipient's plasma that may
destroy donor red cells and serves as a:final verification of the compatibility of donor red cells and the
recipient's serum
2. while all transfusions must be preceded by an acceptable compatibility test, the crossmatch portion need
not be performed prior to operative procedures that almost certainly will not require transfusion
3. crossmatchlng blood 00sed on intIa-operative usage (known as MSBOS - Maximum Surgical Blood
Order Schedule) allows conservation of blood resources and contains laboratory costs
Transfusion of Red Blood Cells and Whole Blood
a) RBCs in the management of chronic anemia and acute blood loss
1. RBCs should be transfused whenever the deficiency of circulating red cell mass is too severe to be
treated conservatively
2. for immediate correction of acute and chronic anemia, tIansfusion ofRBCs should be the rule and whole
blood the exception
170
Treatment of Hypovolemic Shock
a) since restoration of tissue perfusion is of more immediate ~ than restoration of oxygen-<:arrying
capacity, immediate esaablishment of1arge IV lines and administnltion of IV fluids are required
initially.
Available prepuations include -
1. aystalloid solutions: primarily saline solutions
2. colloid solutions: produced artificially (ie-dextnm) or derivatives of plasma (ie-p1asma protein :fraction;
albumin)
3. whole blood and its components
b) the following guidelines are an aa:epIable approach to the management of these patients -
1. almost all shock. patients with hypovolemia should receive ba1anced saline solutions initially; some use
dextran in saline or pIagna protein solutions
2. shock: patients with anemia (symptomatic) should receive piCked RBCs
3. pIasma protein losses producing serum albumin levels of 2 WdL or less can be corrected via infusion of
albumin or plasma protein fractions
prior to tranfusions give patients BenadrylSO mg polTylenol650 mg po to prevent possible minor reactions
Side Affects of transfusions:
1. Fever
2. Rash (Urticaria, pruritis)
3. Hemolytic anemia
4. Respiratory distress
5. Volume overload
6. Noncardiogenic pulmomny edema
Screening Procedures to Deted Coagulation Disorders
LAB'IEST
platelet count
bleeding time
prothrombin time (PI)
partial t:brombopJastin
time(PfI)
thrombin time
PURPOSE
I
' detection of platelet deficiency
evaluation of platelet :function
evaluation of deficiencies of
factors II, V, VII, X
evaluation of deficiencies of
factors V, vm, X, XL XII
I
detection of abnormalities of
fibrinogen (factor I)
also prolonged with cim1lating
heparin and increased fibrin
degradation products
PRE- and POST-OP MANAGEMENT
The Cardiac Patient
a) Patients with cardiac disease should be evaluated by a cardiologist
b) Elective surgery should be delayed as long as necessary to bring the patient to the OR in optimal medical
condition
c) The risk of surgery is weighed against the risk of cardiovascular complications.
d) Recent MI- due to high mortality rates, surgery should be postponed at least six months if possible
e) Old MI- if evidence of old MI is found on the ECG without chest pain. a previous ECG should be
obtained for compuison
171
f) Unstable Angina
1. careful observation and postponement of non-emergency surgery
2. maximize medical therapy with nitrates, beta-blockers and calcium channel blockers
3. if medical management is unsuccessful, get an evaluation for coronary bypass surgery before the
elective non-cardiac surgery
g) Mild Stable Angina
1. may undergo minor procedures safely
2. beta-blockers and nitrate therapy should continue pre-op and be resumed post-op
h) Arrytbthmias
1. in generaL conventional anti-arrhythmic therapy should continue up to and through surgery for
pltients already under treatment
2. five or more PVC'siminute are associated with increased cardiac mortality. Their significance
remains controversial (puticularly if the patient is asymptomatic) and evaluation in terms of
frequency, complexity and overall patient clinical status should be taken into account. These patients
need to be carefully monitored and given anti-arrhythmic medications if more complex arrhythmia's
occur.
Hypertension
a) Mild to moderate hypertension is not a significant risk to the surgical pltient if:
1. diastolic BP is stable and <110 mm Hg
2. intra-operative and recovery room pressures are closely monitored and treated
b) In general, antihypertensive medications should be continued up to the time of surgery and post-operatively
c) Get potassium levels on all patients on diuretics; replace ifsennn potassium is::: 3.5 mEqIL before surgery
Congestive Heart Failure
a) Treat appropriately pre-operatively and postpone non-emergent surgery
b) Swan-Ganz monitoring is essential in patients with CHF who must undergo emergency surgery. Patients
with borderline cardiac status undergoing major elective surgery may also benefit from Swan-Ganz
monitoring.
Diabetic Patient
a) General Information
1. stress of anesthesia and operation exacerbates diabetic patient's glucose intolerance
2. to maintain nutrition and}XeVent ketoacidosis and hypoglycemia, the patient must receive a minimum
of 100 gm caIbohydratdday and adequate insulin must be continuously available. One liter of
D5W contains 50 gm of caIbohydrate.
3. this patient should have optimal nutritional status, hydIation level and electrolyte balance before surgery
4. correct ketoacidosis even ifbefore an urgent operation because of associated high mortality rate
5. hypoglycsemia is a more hazardous condition than hyperglycemia When there is no hyperketonemia,
moderate hyperglycemia (200-250 mg/dl) is not hazardous and should be expected during the early
post- operative period Marlred hyperglycemia can lead to osmotic diuresis, dehydration and
hyperosmlarity and thus, should be avoided.
6. there is evidence that high glucose levels alter leukocyte and fibroblast function, predisposing to
infection and poor wound healing. P1asma glucose should be maintained between 100-200
m ~ d l .
7. insulin requirements may fall abruptly after the infection has been adequately decompressed. Anticipate
this be decreasing the last insulin dose by one-third
b) Insulin and Glucose Schedules
1. no insulin, no glucose
>minor operations under local where there is low stress and the patient is expected to eat
after the surgery
>no insulin or glucose is given the morning of surgery and intra-operative fluids contain no
dextrose
>blood sugars are checked and regular insulin given as needed until the next morning when
the usual regimen is resmned
2. subcutaneous insulin with N glucose (most common)
>management is most convenient if procedure can be done in the early morning
172
>NFO (nothing by mouth) after midnight
>In the early moming-
-start IV fluids consisting ofD5 1/2NSS
-give approximately one-third to one-half of the patient's usual am dose ofNPH or lente
inulin
-hold regular insulin dose
>Upon completion of the operation-
<ontinue the IV fluids until the patient receives 2 liters (100 gm of glucose) in a 24 hour period
-give regular insulin every ~ hours blsed upon (fingerstick) blood glucose levels. The first
determination should be done as soon as the patient anives in the recovery room The dose
should be based on the patient's response to previous doses of insulin.
INSULIN SLIDING SCALE
blood glucose level Regular Insu1in
<200 no covemge
200-250 2 units SQ
251-300 4 units SQ
301-350 6unitsSQ
351-400 8 units SQ
>give omI fluids and food as soon as the patient's condition permits
>resume diet and pre-op daily insulin dose
>if the patient cannot be fed, start IV DSW or D10W to total 200 gm carbohydrate daily and divide
usual NPH or Lente dose into two equal doses given 12 hours apart. <bain serum glucose levels every
6 hours and cover with regular insulin as needed.
>lower dose ofNPH or Lente ifhypoglycemia occurs
c) Diabetics on Oral Hypoglycemic Agents
1. Minor Surgery
>withhold the medication on day of surgeIy
>if surgery is early in the morning and the patient is eating post-op, the omI agent is resumed
> if the surgery is delayed or the patient is expected to be NPO for many hours, start D5W N and
monitor glucose. Regular insulin is given as needed
2. Mgor Surgery
>discontinue omI hypoglycemic agent
>when possible an insulin regimen should be started several days before surgery to determine insulin
levels and to stabilize glucose levels
>NFO after midnight the day before surgery
>one-half to one-thitd intermediate acting insulin is then given on call to the OR and the patient
managed with regular insulin based on blood glucose levels determined every 6 hours
>with shorter time ftames, the om! agent is discontinued 24 hours before surgery. The patient should
be NPO after midnight and receive regular insulin as needed based on glucose levels every 6 hours.
D5W N is started the morning of surgery.
>omI hypoglycemic agents can be started when normal diet is resumed
Thyroid Disease
a) This condition is not a contra-indication to elective surgery
b) It is important to get the patient euthyroid before surgery
c) Hyperthyroid Patient
1. these patients are apt to develop hypertension, severe cardiac dySIbythmias, h}'J)erIhennia and thyroid
storm There is no apparent correlation between nature or severity of surgery to thyroid storm
2. bring to euthyroid state by (takes 1-6 weeks):
>propylthioruacil 800-1000 mg/day for 1 week then 200-400 mg/day maintenance dose or 30-40
mglday methirnazol PO
>beta-blockers (dose= 160 mglday) control tachycardia, palpitations, anxiety, etc.
3. all patients, unless contra-indicated, should receive combination of the above drugs
173
d) Hypotbyroid Patient
1. bring patient to euthyroid state (takes weeks to months). Once achieved, there is no increase in
morbidity associated with surgery.
2. L-thyroxine's long half-life allows it to be stopped during the perioperative period without problems.
3. myxedema coma should be suspected in patients who fail to awaken from anesthesia and who
manifest CO retention. .
Anemia
a) Evaluate the etiology of the anemia before proceding with any elective surgery.
b) Treatment is individualized on the basis of the etiology (Hct, Hgb, reticulocyte count, blood smears,
Coomb's test, bone marrow exams and the H & P are useful to pinpoint the etiology). A hemoglobin of 10
gmldI and a hematocrit of 30% have customarily been required to assure adequate tissue oxygenation
during surgery.
c) Each patient's requirement is based on several factors; the values listed above are just guidelines.
d) Decision for transfusion must be made weighing the benefits versus the risks
e) Factors requiring higher pre-op hemoglobin levels
1. old age
2. acute blood loss
3. coronaIY artery disease (CAD)
4. pulmonary disease
5. peripheral vascuIar (PVD) or cerebrovascular disease
6. significant blood loss expected
f) Factors making lower pre-op hemoglobin level more acceptable
1. youth
2. chronic anemia
3. normal exercise tolerance
4. no cardiac, pulmonary or cerebrovascular disease
5. little blood loss expected
g) Therapy should provide only those blood components required to correct the defect. Oral therapy (ie-iron,
folate. vitamin B12) is appropriate if the surgery is elective and can wait. Packed RBC's can be used for all
but severe hemorrhage.
Neutropenia
a) Etiology
1. drugs
2. infectious agents (especially viral)
3. preleukemia, myeloproliferative disorders
4. congenital
5. chronic rl1eumatic disease (ie-SLE, Felty's syndrome)
b) Cancellation of surgery if <1 OOOImm . Risk: of infection is marlredIy increased when granulocyte count is
<500/mm .
c) Treatment depends upon the etiology. Postpone surgery in viral or drug induced cases untilleukopoenia is
reversed.
d) Granulocyte transfusions have little indication for surgery and only used in an infected patient \\'ith a count
<500/mm
Hemostatic Disorders
a) Careful bistory is crucial because it may give the :first indication of potential hemostatic problem;
questioning
(include prior surgery, dental procedures, mucous membrane bleeding, transfusions, bruisability. epistaxis,
history
of hematomasIhemar delayed bleeding, family history)
b) Certain hemostatic problems are seen with normal routine Jabs.
174
LAB lEST PURPOSE
p1atelet count detection of deficiency
}XOthrombin time fuctor VII. extrinsic pathway
(PI) (warfurin)
partial tbrombop1astin factors vm. IX. XII
time (PIT) (heparin)
*factors V and X. prothrombin and fibrinogen are required for both Pf and PIT
bleeding time evaluation of platelet fimction
ABNORMAL NORMAL DISORDER (faaors)
PIT Pf hentopbilia (VllI)
Christmas disease (IX)
factor XI deficiency
Hageman fuctor (XII) deficiency
von Willebr.md's disease
PI' PIT factor VB deficiency
PIT & PI factors n, V, or X deficiency
dysfibrinogenem
DIC
vitamin K deficiency
broad spectrom antIbiotics
malabsorption
liver disease
PIT & Pf faaor XIII deficiency
von Willebr.md's disease
dysfibrinogenemia
Ehlers-Danlos syndrome
vasculitis
R.endu-Osler-Weber disease
replace factors as specific as possible and postpone SUIgeIy if possible
c) anticoagulants
l.coumadin
>coumadin interferes With action of vitamin K in the synthesis of factors n, vn, IX. X
>discontinue coumadin - normalization within 36-48 hIs
>vitamin K can be given but it is preferable to discontinue coumadin (SQ or oral administration 18-24
hours for nonnalization); vitamin K will interfere with post op anti-coagulation for 1 week.
>emergency swgery: discontinue comnadin and transfuse 2-4 units of fresh frozen plasma; this may
need to be repeated post-op
2. heparin
>PIT will be normal if discontinued 8 hIs before swgery
>mpid reversal may be achieved with protamine sulfilte (1: 1(0); usual dose is 50 mg N over 5 minutes
>heparin induced thrombocytopenia is fuirly common
Obesity
a) Defined as body weight> 30010 above ideal
b) Severe obesity is not rare
c) Mortality tate is 2-3 times that of the normal patient
d) Pre--operative evaluation is made more difficult because fat curtains the ~ system of interest
e) Careful questioning of previous lung disease, heavy snoring, blood prsssure, thrombopblebiti pulmon3IY
embolism are essential
f) Thorough cardiovascular and pulmonary exams are essential
g) Standard pulmoDaIy function tests, 12 lead ECG and ~ x-ray should be accomplished on all moderate to
severely obese patients
175
h) Prescribe regimen for optimum pulmonary function deep breathing and coughing exercises, incentive
spirometers and bronchodilators followed by chest percussion if needed
i) Unless contraindicated prescnbe mini-dose heparing to help prevent DVf and pulmonary embolism
j) Avoid Trendelenburg position because the weight will decrease lung volume
k) Use volume pressure monitors (ie: Swan-Ganz) in severely obese patients with cardiovascular or
pulmonary disease .
I) Use spinal or local anesthesia where appropriate
m) Consider waiting two days post-op to extubate if problems arise intra-operatively
n) Early ambulation
Steroids
a) Identify patients who will need supplemental steroids during the stress of surgery
b) Glucocorticoid deficiency may result from:
1. primaIy dysfunction of the adrenal gland
2. secondary adrenal insufficiency due to pituitary disease
3. adrenal suppression due to administration of exogenous steroid
c) Corticosteroid coverage has become a standard practice when treating patients with even suspected adrenal
deficiency who \DldeIgo surgery
d) Cardiovascular collapse is the major concern
e) An adrenal reserve test is available
1) The daily requirement of cortisone is approximately 300 rug
g) Suspect adrenal deficiency if:
1. >7.5 mg prednisone in single daily dose taken for> 1 mo.
2. any steroid in divided doses for >5-7 days
3. long acting preparations (ie-dexamethasone, betamethasone) taken for >5-7 days
4. >20 mg prednisone taken for >5-7 days
5. patient with Cusbingoid appearance
6. prolonged shock or unexplained shock or fever
h) A wide variety of steroid schedules have been proposed; no one has a distinct advantage over the other
i) example of glucocorticoid coverage
1. minor surgery/limited procedure
>m:inima1 to additional steroid coverage needed
>give regular dose with surgery and maintenance dose after surgery
2. major surgery
>hydrocortisone sodium succinate 100 mg 1M or IV every 6 hours for 24 hours to start with pre-op
medications. Use IV route if there is tissue hypoperfusion
>reduce by 500/0 daily beginning POD #1 until maintenance dose or equivalent is reached (20 rug AM,
lOmgPM)
>in patients with primmy adrenal insufficiency fludrocortisone 0.1 rug daily must be added. to
provide sufficient mineralocorticoid activity when the dose of hydrocortisone is 100 rug or less per
day >with short procedures give a single IV or 1M dose of hydrocortisone 100 mg with pre-
medications and an extra 20 mg oral dose that evening. Resume regular regimen the next
day
Renal Disease
a) The history and physical, glomerular filtration rate, serum creatinine, BUN, urinalysis, and blood chemistry
profiles \\'ill be indicators for renal disease
b) Risk of surgery is not likely to be increased if creatinine clearance is >50% normal (normal creatinine is
<2.0) The point of significant risk has not been determined
c) Regulation of volume status is critical
1. mild to moderate renal impairment: these patients are unable to concentrate their urine and are therefore,
at risk for vo1mne depletion. Observe fluids carefully and replace as needed Monitor body
weight, Jlas (ins and outs), electrolytes, and pH
2. severe renal insufficiency: these patients are at risk for volume overload and hypeIka1.emia. Monitor
fluid baJance and dialyze if necessary. Consider Swan-Ganz monitoring
3. UTI's are treated pre-operatively based on C & S results
176
4. obstructive lesions are removed or corrrected before major surgery
5. fluid and electrolyte imbalances should be corrected pre-op
6. metabolic acidosis, even though compensated should be corrected with sodium bicarbonate
7. anemia: Hgb 9 gm/dl and Hct 25% are satisfactory for tbe patient with chronic insufficiency
8. correct coagulation defects seen in chronic renal disease pnH)p
9. hemodialysis, when necessary, should be planned for the day before surgery
d) If renal function deteriorates or transfusion reaction occurs consider using an osmotic diuretic (ie-mannitol).
This may have a protective effect on renal tubular function
e) Nephrotoxic drugs must be administered carefully and in reduced doses
f) Post-operative urine output of <25 m1Ihr requires irnrnOOiate evaluation
g) Diabetic patients are particularly prone to acute renal failure after contrast dye studies
SW AN-GANZ CATHE'IER
Description
a) flexible quadruple lumen tube approximately 110 em long and scored in 10 em increments
b) lumens
l. distal (PA) lumen: ~
-records PAP, PCWP IF
~ mixed venous blood
for oxygen content analysis
2. proximal (RA) lumen:
-records RAP or CVP
3. balloon lumen
-tenninates 1 em from tip
of catheter
-when balloon is inflated,
it moves in direction of
blood flow
-the inflated balloon guides
catheter through the RA, RV
and into the pulmonary
artery where it lodges in
smaller branch
-records the pulmonary capillary wedge pressure (PCWP)
in this position
[pcWP: normally equal to the Left Atrial pressure
thus, sensitive indicator of presence of pulmonary congestion and left sided CHF]
4. thermistor lumen
-contains temperature sensitive 'Wires
-calculates cardiac output by thermodilution technique
Insertion
a) percutaneous insertion via internal jugular vein safest
b) location of catheter tip determined by recognition of characteristic pressure waveform of each heart
chamber
177
Complications of right heart catheterization
a) cardiac dysrhythmias
b) thrombosis
c) sepsis
d) pulmonary infarction
e) pulmonary valve perforation
f) knotting of catheter
g) rupture of balloon
Indications for hemodynamic monitoring
a) severely ill. hemodynamically unstable patients
b) acute cardiac conditions
(ie-complicated MI; RV infarction; mitral
regurgitation)
c) chronic cardiac insufficiency
~
. - -
, .
.
J
. -')
................. _.
~ f
(ie-constrictive pericarditis; congestive cardiomyopathy)
d) miscellaneous
(ie-acute non-myocardial infarction pulmonary edema)
Differential Diagnosis of common PA catheter readings
low RAP, low R VP: volume depletion
high RAP, high RVP: volume overload
CHF
cardiogenic shock
high PAP: CHF
cardiac tamponade
increased pulmonary vascular resistance (ic-hYJXlxia, pulmonary disease, ventilator effect of PEEP)
low PCWP: volume depletion
high PCWP: cardiogenic shock
LV failure
severe hypertension
mitral regurgitation and stenosis
volume overload
cardiac tamponade
Alcoholic Patient
a ) Screening:
l)ask: all patients: Do you drink alcohol, including beer, wine, or distilled spirits?
2)for current drinkers:
-On average, how many days per week do you drink alcohol?
-On a typical day when you drink, how many drinks do you have?
-What is the maximum number of drinks you had on any given occasion during the last month?
3)for current drinkers: (CAGE questionnaire)
-Have you ever felt that you should Cut down on your drinking?
-Have people Annoyed you by criticizing your drinking?
-Have you ever felt bad of Guilty about your drinking?
-Have you ever had a drink first thing in the morning (Eye opener) to steady your nerves or get rid of a
hangover?
b) Assessment for all patients at risk: of withdrawal: (Clinical Institute Withdrawal Assessment for Alcohol)
I )nausealvomiting
2)tactile distIbances (itching, pins and needles, burning, numbness)
3)tremors
4 )auditory disturbances
5)paroxysmal sweats
6)visual disturbances
7)anxiety
178
8)headache, fullness in head
9)agitation
lO)orienlation and clouding of sensorium.
c)Treatment for withdrawal
1)Lorazepam 2 mg q 6 x 4 doses, then 1 mg q 6 x 8 doses (additional doses as needed)
2)Propb.y1axis:
-15-30 mg SeIax tid x 3 days
-15-30 mg SeIax bid x 2 days
-15-30 mg SeIax qd x 2 days
-multivitamins 1 tablet po qd
-start NSS at determined rate with 100 mg thiamine/I mg folate x I bag (may give folate and thiamine po)
179
PRINCIPLES OF SURGERY
PRINCIPLES OF SURGERY
PRINCIPLES OF SURGERY
PRINCIPLES OF SURGERY
PRINCIPLES OF SURGERY
PRINCIPLES OF SURGERY
PRINCIPLES OF SURGERY
PRINCIPLES OF SURGERY
PRINCIPLES OF SURGERY
PRINCIPLES OF SURGERY
PRINCIPLES OF SURGERY
PRINCIPLES OF SURGERY
PRINCIPLES OF SURGERY
PRINCIPLES OF SURGERY
IPL
REGIONAL AND LOCAL NERVE BLOCKS
Goal:
Provide local anesthesia to area of insult
Maintain minimal patient movement
Maximum relief to the patient
Indications:
Surgical intervention
Diagnostic
Aspirate or soft tissue or joint
Equipment:
Needle
Diameter- small gauge (25 or 27)
Length- adequate to reach target (typically 1.5 inch)
Syringe (3ec, 5ec, or 10 ec)
Local Anesthetic (LA)
Antiseptic solution (Alcohol, Betadine, etc.)
Prep area distal to proximal
Technique:
1. Identify peripheral nerve(s) innervating region to be anesthetized
2. Dmw-up adequate amount of LA (insure pt is non-allergic)
3. Prep entry site with antiseptic solution
Joint entry requires betadine paint prep (three times)
4. Optional topical anesthetic prior to breaching integument (i.e. ethylchloride spray, topical
lidocaine)
5. Swiftly enter needle perpendicular to integument
6. Infiltrate intradermal wheal
7. Advance needle to desired neural structure
8. Biplane aspimte
** ALWAYS, ALWAYS, ALWAYS aspirate prior to iof'dtrating LA
9. Infiltrate appropriate amount of anesthetic solution
* Use least number of skin entries necessary to acquire desired anesthesia
* When redirecting needle always withdraw needle to subcutaneous layer, then follow steps 6 through 9
* Abide by OSHA regulations for handling, recapping and discarding of needle and syringe
Complications:
Direct injury to nerve trunk
LA toxicity- watch for CNS and CV symptoms
Allergic reaction
Nerve Blocks:
Popliteal
Indicated for intra and/or post -op analgesia of rearfoot and leg procedures
Tibial nerve/Sciatic nerve at the level of the popliteal fossa
Optional use of nerve stimulator for proper site infiltration is recommended
Set nerve stim. at 2.0-3.0 rnA
Enter 7-8 em proximal to popliteal skin crease, medial to biceps femoris
muscle/tendon
Advance nerve stimulator slowly until triceps surae and/or toe flexors twitch
Infiltrate approx. 30-40 ec's oflong acting LA
Ancillary saphenous nerve block may be indicated
180
Common Peroneal
Diagnostic for: assessing spastic peroneal muscles, stress inversion radiographs for
lateral ankle instability
Very superficial 1-2 cm deep to skin
Palpate fibular head and nerve
Enter laterally 2.5 cm distal to fibular head
Infiltrate approx. 3-6 cc's LA
Ankle Block
Indicated for multiple forefoot and midfoot procedures <2 hours, I&D
Total of 10-15 cc's LA
I. Posterior Tibial NenJe
Medially at the level of the malleolus bisect the tendo achilles and tibial
malleolus
Enter at the bisection infiltrate 1-2 cc's LA
Redirect needle distal anterior at 45 degrees to skin, bury needle to hub and
infiltrate 1-1.5 cc' s LA
Again, redirect distal posterior at 45 degrees to skin, bury needle to hub and
infiltrate 1-1.5 cc' s LA
2. Superficial Peroneal Nerve (lntennediate and A1edial Dorsal cutaneous)
Plantarllex the foot at the ankle joint and identify the superficial peroneal or
it's terminal branches in the distal1l3
rd
of the leg
Enter directly over nerve(s) approx. 1 cm proximal to ankle joint
Infiltrate 1-1. 5 cc' s LA
3. Deep Peroneal Nerve
1 cm proximal to ankle joint identify tendons of tibialis anterior and
extensor ballucis longus
Enter bisection T A and EHL, bury needle to hub (if tibia is encountered
retract needle 2-3mm
ASPIRATE, then infiltrate 1-2 cc's LA
4. Saphenous Nerve
Identify the Great Sphenous Vein at the anterolateral aspect of the medial
malleolus
Without exiting from DP block, redirect needle in subcutaneous plane
directly medially, just lateral to the GSV
ASPIRATE, then infiltrate 1 cc LA
5. Sural Nerve
MayoB/OCk
Palpate for nerve trunk 0.5-1 em inferior to lateral malleolus
Enter directly lateral at this level
Infiltrate 1 cc LA wheal directly over nerve
Redirect anteromedial in subcutaneous plane infiltrating 1-1.5 cc's LA
Again, redirect inferior and distally in subcutaneous plane infiltrating 1-1.5
cc's LA
Indicated for first metatarsal and hallux procedures (i.e. HA V Surg., closed reduction
fracture, etc.)
1. Deep Peroneal Nerve
Palpate the dorsal aspect of 1 sl and 2
nd
metatarsal bases
Enter interspace dorsal, raise wheal, aim plantarly burying needle to hub,
aspirate, infiltrate 1.5-2cc's LA
181
2. First Proper Digital Branch of the Medial Dorsal Cutaneous Nerve
Without exiting DP injection site redirect directly medially
Infiltrate 1-l.5 ce's LA along subcutaneous plane
3. First Proper Digital Nerve of the Medial Plantar Nerve
Enter medial to lit metatarsal through wheal, direct needle plantarly
Infiltrate 1-1.5 ce's LA along subcutaneous plane
4. Second Proper Digital Nerve of the Medial Plantar Nerve
Enter medial to 1
st
metatarsal through wheal, direct needle laterally just to
inferior 1
st
metatarsal base infiltrate 1-1.5 ce' s LA
Redirect plantar lateral in subcutaneous plane and infiltrate 1-1.5 ce's LA
Reverse Mayo BlDek
Hallux Block
1. Intermediate Dorsal Cutaneous Branch to Fourth Interspace and Lateral
Plantar Branch
Palpate the dorsal aspect of 4th and 5
th
metatarsal bases
Enter 4th interspace dorsally, raise wheal, aim
pIantarly bury needle
Infiltrate l.5 ce's LA
2. Lateral Dorsal Cutaneous Nerve (Sural Nerve)
Without exiting interspace injection site redirect, directly laterally
Infiltrate 1-1.5 ce's LA along subcutaneous plane
3. Proper Digital Branch to Fifth Digit of the Lateral Plantar Nerve
Enter lateral to 5
th
metatarsal through wheal, direct net:dIe medially
Infiltrate 1-1.5 ce' s LA along subcutaneous
Indicated for nail procedures, subungual exostectomy, etc.
Two-point stick
1. First Proper Digital Branch of the Medial Dorsal Cutaneous Nerve & First Proper Digital
Nerve of the Medial Plantar Nerve
Enter the dorsal medial aspect of the proximal phalanx base
Raise wheal, direct needle plantarly infiltrate 0.5-0.75 ce's in
subcutaneous plane
2. Deep Peroneal Proper Digital Branch to Hallux & Second Proper Digital
Nerve Branch of the Medial Plantar Nerve
DigitJ.Il Block
Enter the dorsallatera1 aspect of the proximal phalanx base
Raise wheal, direct needle plantarly infiltrate 0.5-0.75 ce's in
subcutaneous plane
Indicated for arthroplasty, amputation, nail procedures, etc.
Enter the dorsal central aspect of the proximal phalan..x base
Raise wheal, direct needle plantar medial, infiltrate 0.5 ce's in subcutaneous plane
Redirect plantar lateml, infiltmte 0.5 ce's in subcutaneous plane
Plantarly, look for cutaneous blanching and wheal formation
182
BONE HEALING
Definitions
a) osteoblasts: bone fonnation whether embryonic or through a healing process requires the presence of
osteoblasts. The osteoblast is the only cell capable of bone production. Osteoblasts are derived from precursors
located in the walls of blood vessels. These mesenchymal cells or pericytes differentiate into osteoblasts in
areas of fracture, osteotomy or growth. An adequate blood supply must be present for the cells to reach these
sites. TIle relationship between osteoblastic bone formation and a functional vascular network is a key
component to understanding bone healing.
b) osteoclasts: large multinucleated cells located in the tip of the "cutting cones", which dissolve bone matrix
fonning canals through existing bone. Responsible for bone reformation.
c) osteoid: a noncalcified organic matrix formed by osteoblasts, which contains 95% collagen and 5%
proteoglycans
d) mineralization: the process by which osteoid becomes deposited with calcium phosphate, mainly in the
fonn of crystalline hydoxyapatite. In mature bone, mineralization occurs 8-10 days after osteoid is formed.
Normal mineralization in lamellar bone occurs at the rate of 1 um per day as determined by Frost in 1%3.
e) woven bone: type of bone which fonns healing bone callus. The intercellular substance contains a
disordered three dimensional anay of collagen fibrils. Osteoid seanlS are narrow fu.d osteoblastic cell
population is dense. Woven bone rapidly mineralizes following formation. It may proliferate ridges and
trabeculae to form extensive networks.. Osteoblasts extrude matrix in all directions. Eventually remodels to
lamellar bone.
f) lamellar bone: highly o ~ e d bone laid do\\n in congruent layers with parallel collagen fibers which
change directions from one lamella to the next. Osteoblasts are highly polarized extruding matrix only in
their basal cell surfuce. Requires a flat smooth substrate in order to be synthesized.
Stages of Bone Healing
I. Inflammation: day 1 to day 3-4
initial hematoma formation around site followed by necrosis of bone margins
macrophages invade area to remove dead bone and tissue
II. Induction: day 1 -
(duration unknown)
osteoblasts or chondroblasts induced
good oxygen supply, vascularity and stability
-osteoblasts form
poor oxygen supply, vascularity and stability
-chondroblasts form
pro-ca11us develops from the maturing hematoma
ill. Soft Callus: day 4 to 4 weeks
clinical union noted with elimination of motion across site
formation of callus noted
IV. Hard Callus: 4 weeks to 4 months
callus converted to mature lamellar bone
radiographic union noted
V. Remodeling: 4 months to 2 years
Types of Bone Healing
a) Primmy (direct)
1. occurs when bone fragments are rigidly immobilized
2. stages of bone healing undifferentiated and callus formation absent
3. with rigid immobilization, framework provided by callus not necessary
4. due to the rigid immobilization., the fixation device assumes partial load applied to the bone; the result is
bone resorption due to reduced biomechanical demand
183
5. types ofprimaIy bone healing
-gap healing: hematoma fills the microscopic gaps
area is infiltrated by capillaries and osteoblastic cells. then filled with woven bone and
remodeled osteoblasts initially form IamelIa oriented 90 to the long axis of the
(fracture) site and are then rep1aced by axialIy oriented IamelIa
-contact healing: smfaces in direct contact
"cutting cones" cross interfi1ce, producing concentric pattern of new lamellar bone
"cutting cone" advances approximately 70-100 urn per day, as per research done by Schenk
b) Secondary (indirect)
1. occurs when bone is not rigidly immobilized
2. motionlinstability allow for additional hemonbage, wbich fuvors fibrocartilage formation and
ultimately callus
3. bone callus creates a framewOIk so that bone healing may occur. A layer of bigh tensile strength
connective tissue is laid down between fragments followed by granulation tissue, wbich resists
compression. This framework is repJaced by fibrous cartilage. Eventually chondroclasts remove the
cartilage and osteoblasts begin to produce woven bone
4. bone remodels in accordance to Wolffs Law, whereby bone deposition takes place on the concave side
and resorption on the convex side. Adaptation may correct some angular deformity, but cannot
correct misalignment of articular ends.
Complications of Bone Healing
1. malunion: a nonanatomic position of fracture fragments following the healing process. Malunion can
result in structural defonnity and reduced or total loss of fimction. Usually the result of poor reduction
combined with inadequate fixation.
2. delayed union: union is considered delayed when healing has not advanced at the average rate for the
location and ~ ' } ) e offracture. Prolonged casting or dynamic loading of bone may be needed to hasten
healing.
3. nonunion: the difference between delayed union and nonunion is not clear cut. The time when a given
fracture should be united cannot be arbitrarily set and depends on location, type, physical
characteristics of the patients and mode of therapy. A nonunion may not be diagnosed until there is
clinical or radiographic evidence that healing has ceased and union is unlikely. Generally a fracture of
the shaft of a long bone should not be considered a nonunion until at least 6 months after
surgery. The final status of a nonunion is the formation of a pseudo-arthrosis.
Diagnosis of nonunion
a) standard radiograph: presence of sclerotic borders or osseous void at the fracture site
b) stress fluoroscopy
manually manipulate fracture site under fluoroscope
should be virtually no movement between ends ands osseous bridging should be present
[not fully diagnostic of nonunion]
c) (fc-99m) bone scan
normal fracture healing stages on bone scan
week I-week: 4: diffuse uptake at fracture site and 3(ljoining areas of bone
week 4-week 12: biphasic pattern with uptake more localized to fractured ends of bone
week 12-2 years: coalescence stage with focal uptake at
fracture site alone
hypertropbic nonunion will demonstrate persistence of biphasic stage
atrophic nonunion "ill demonstrate low uptake activity at fracture site; may see focal uptake with
intervening void ("cold spot")
d) tomograms: help visualize presence of ttabeculation or persistent fracture line
e)Cfscan
184
f) osteomedullangiography
radiopaque dye injected on one side of fracture
if venous continuity is seen across fracture site, nonunion can be ruled out
if venous continuity present (positive test), immobilize and initiate NWB status
ifvenous continuity absent (negative test), open reduction with bone graft recommended

Based upon vascular supply and osteogenic potential
a) Hypertrophic or Hypervascular Nonuniom
This type of nonunion is capable of a biologic reaction. The ends of the fragments are viable and highly
vascularized. There are three subgroups within this category -
1. Elepbant Foot nonunion: very hypertrophic with heavy callus fonnation. Results from unstable fixation
or premature weightbearing. .
2. Horse's Hoof nonunion: mildly hypertrophic with poor callus formation. Results from moderately
umtable fixation.
3. Oligotrophic nonunion: not hypertrophic and callus is absent Results from displacement of fracture,
distraction of fragments or fixation without direct apposition of fragments.
Elephant Foot Horse's Hoof
b) Atrophic or Avascular Nonunions
This type of nonunion is not capable of a biologic reaction.
There are four subgroups within this category -
u
n
Oligotrophic
L Torsion Wedge nonunion: this type has an intermediate fragment in which the blood supply is
decreased or absent The intennediate fragment is healed to one main:fragment but not to the
other.
2. Comminuted nonunion: characterized by the presence of one or more intermediate :fragments which are
necrotic. Typically results from plate breakage and callus formation is absent
3. Defect nonunion: characterized by a loss of a fragment, usually in the diaphysis. The ends of the
fragments are viable, however, the gap is so large that bridging cannot occur. The ends
eventually become atrophic.
4. Atrophic nonunion: results when the intermediate :fragments are missing and scar tissue (which lacks
osteogenic properties) fills the void
Torsion Wedge Comminuted Defect Atrophic
185
Electrical Properties of Bone
a) Wolff: electric potentials are created under the application of stress to bone
b) Fukada and Yasuda (1950's): bone piezoelectricity bone becomes electrically polarized
when it is defonned the compte&ii.on side is electronegative with callus production and
the tensionside is electropositive
c) Freidenberg and Brighton (1960's): bioelectric potential nonstressed bone demonstrated
electronegative potential in areas of active bone growth and electtopositivepotentials in
areas ofless activity
d) Anderson and Erikson:
electrical properties and bone growth result from ''streaming potentials" [the pH difference between
collagen hydroxyapatite and the surrounding liquid medium causes an electrical gradient]
e) .AthenstaOOt: collagen fibers have asymmetrical chaIge distribution [parallel anangement of collagen sets
up a net dipole moment with growth occmring towaId the negative end of the fiber]
Tmdment ofNonunions
a) Hypertrophic nonunions - stabilization offiacture ends
b) Atrophic nonunions
I. resection of nonunion and bone graft with fixation
2. llizarov technique
corticotomy followed by distraction (to induce local necrosis and neovascularization)
compression-distraction ("accordion technique")
3. electrical stimulation
does not correct for shortening of malposition
the exact mechanism by which electrical current stimulates bone growth is unknown. In the 1970's
many investigators developed different electrical stimulating devices. All reportedly have the same
overall success rate of 80-850/0, however, the principles of good fracture management must be strictly
followed. All forms cannot induce bone growth in large gap nonunions. In general a gap larger than one-
half the diameter of involved bone is a contraindication to electrical stimulation All forms require
approximately 3 ~ months for bone healing.
types of electrical stimulation systems -
>invasive electrical stimulator
Electrodes and power pack are directly implanted in the nonunion site. This does not require patient
cooperntion to maintain, however, two opel3tions are required - one to place and one to retrieve the
unit
>semi-invasive stimulator
Percutaneous electrodes are placed at the nonunion site and are attached to an external power pack
This requires one operative procedure and patient coopeI3tion is necessary to maintain the unit.
>non-invasive stimulator
Involves the use of an externally applied pulsed electromagnetic field to induce an electrical
potential in the nonunion site. Totally noninvasive, however, requires patient to apply and maintain
the unit.
compression-distIaction
("accordion technigge")
, r
go S t ~
LJ.
1+
186
corticotomy and distraction bone pegging technique
CE':::]
~
D
graft interposition technique compressed bridging graft technique
BONE STIMULATION
Stimulation of bone to promote healing has indications for more thanjust nonunions. Currently osteogenesis is
stimulated through either electrical or mechanical (ie-ultrasound) means. Three methods are available for
electrical stimulation-
1. Faradic
2. Capacitive (ie-Osteogen by EBI)
3. Inductive - pulsed electromagnetic field; noninvasive
Although electrical stimulation has achieved promising results, research continues to define optimal treatment
parameters.
Keep in mind that electrical stimulation will not correct angular deformity, rotational deformity, shortening or
articular surfuce defect. Also. its potential for oncogenesis is still uncertain as of yet.
Tissue Effects of Electrical Stimulation
a) increased pH: promotes bone formation
1. inlnbit osteoclast resorption
2. stimulate mineral deposition in fracture rerair
b) decreased pO : enhances calcium deposition
1. stimulates optimal bone growth in vitro
2. growth plate cartilage and bone cells follow an anaerobic metabolic pathway
3. found in bone and cartilage cells in fracture callus
c) desensitize osteoclast to PfH
Indications
nonunions; delayed unions
congenital pseudo-arthrosis
enhance survival rate of bone graft
repair following resection of massive tumor
Charcotreconsttuction
AVN
187
Contraindications
uncontrolled motion
synovial pseu<krarthrosis
fracture gap > 1 em (or 112 diameter of the bone)
pregnancy
active osteomyelitis (invasive techniques)
pathologic fiacture secondary to malignant tumor
Exogen, Inc developed a different method to stimulate osteogenesis based upon low intensity, pulsed
ultrasound called SAFHS (sonic accelerated fracture healing system) therapy. This method provides a
mechanical stimulus and its low energy level differentiates it from conventional (high energy) ultrasound
utilized in rehabilitation therapy.
Possible mechanisms of action -
a) direct mechanical effect
b) increased perfusion through microvasculature
c) increased blood flow
d) indirect electro-kinetic effect
Studies involving mbbit tibial fractures have yielded 87-91% success rntes. Also, a femoral fracture study from
the Mayo Clinic concluded that the effects of the ultrasound therapy were not inhibited by the presence of an
intramedullary rod.
Electrical or ultrasound stimulated osteogenesis are options to promote healing, but are not substitutes for sound
surgical principles regarding fracture care.
Osteogen: EBl product
implantable device
OC power supply/capacitive method
generator placed in subcutaneous tissue, 8-10 em from cathode
-generator removal not mandatory
-tester available to make sure it was implanted COrrectlyflS still working
bone geposition OCQJTS in 5-8 mm radius around (cathode) wire
anock or cathode should not touch metal
"cuiable cathode wire configurations
"li ()'"?J lJ
~
-helix
-zigzag
-<hill hole (fish --y-y-ry scale)
this configuration allows greatest control in preventing contact with fixation
188
WOUND HEALING
Surgical Layers
a) skin: epidermis and dennis
b) superficial fascia
1. outer layer ~ c u l u s adiposis)
2. inner layer - thin membranous layer
All vessels, nerves and lymphatics lie between these layers
c) deep fascia
1. beneath this layer are muscles and tendons
2. the deep fascia may be continuous with the joint capsule and periosteum
d) bone
Classification of Wounds
a) clean: a non-traumatic, non-infected wound which does not enter the respiratory, alimentary or
genitourinary tracts
or the oropharyngeal cavity. Accounts for 75% of all operative wounds.
b) clean-contaminated: contains normal flora without unusual pathogenic contamination. A clean wound
contaminated by a minor break in aseptic technique is considered clean-contaminated
c) contaminated: includes soft tissue lacerations, open fractures, penetrating WOilllds and other fresh traumatic
injuries. A procedure with a major break in aseptic technique is considered contaminated.
d) dirty and infected: heavily contaminated or clinically infected prior to surgery
Types of Wound Healing
a) primary intention: initial closure of an incision "With accurately approximated wouknd edges; produces the
least amount of scarring.
b) secondary intention: healing occurs by formation of granulation tissue containing fibroblasts which close
the wound by contraction and secondary growth of epithelium.
c) tertiary intention: delayed primary closure
Phases of Wound Healing
a) substrate phase (lag phase): day 1 to day 3-4
vascular response -
increased vasodilation and permeability
hemostasis via activation of clotting cascade and formation of platelet -fibrin plug
leukocyte response (margination & emigration of WBCs)
capillary redirection toward wound edges in order to contribute to granulation tissue
inflammatory response -
PMNs predominate during the first few days
macrophages predominate by day 5
b) proliferative phase ( repair phase): day 3-4 to day 21
controlled by macrophages
fibroblasts lay down collagen; wound edges "heap up' due to collagen proliferation
new fibers and vessels bridge defect
myofibroblasts ("surgeon's cells") migrate from surrounding tissue to lay down collagen and
glycosaminoglycans
these cells have a contractile characteristic
collagen fibers initially laid down in random pattern
c) remodelling phase (maturation phase): day 21-
collagen fibers re-align along long axis of (linear) scar strongest scar has its fibers arranged in same
direction as the collagen fibers in the native surrounding dermis [ideally, original scar will be parallel to RSTL]
189
Complications of Wound Healing
a) local mctors delaying wound healing
l. incisions: incisions improperly placed within relaxed skin tension lines or made at an angle other than
perpendicular to the skin surface
2. traumatized tissue: rough handling of the wound during surgery can lead to excessive tissue damage
which will delay wound healing
3. improper irrigation: fililure to irrigate properly will allow foreign bodies to remain and delay healing
4. inadequate hemostasis: creates pooling, distention of tissues and dead spaces
5. desication of tissues: drying of tissue during surgical e.-xposure
6. infection: infection occurs if the innoculum and virulence of the organism overcame the resistance of
the host; purulence separates wound edges
7. prolonged dependency: leads to edema, which mvors sepatation of wound edges
8. local corticosteroids: large amounts delay granulation tissue, depress capillaJy proliferation and
suppress fibroblast proliferation Corticosteroids iIUected around the surgical site, and in proper
dosage, limit excessive edema formation.
b) systemic mctors that delay wound healing
1. uncontrolled diabetes mellitus
2. alcoholism: alcoholics are nutritionally depleted, especially in protein. Alcohol also reduces protein
metabolism; hypoproteinemia prolongs the lag phase and slows the onset of proliferative phase.
3. gastroiontestinal malabsorption
4. ascoIbic acid deficiency: synthesis of collagen and epithelial regeneration are dependent on ascorbic
acid
5. steroids: high levels inhibit collagen synthesis and mucopolysaccharide production
6. platelet inhibiting drugs: drugs that impair platelet aggregation include aspirin, phenylbutazone,
sulfinpyrazone, antihistamines, indomethacin, chloropromazine, tranquilizers and heparin
7. 7. anemia: hemoglobin less than 10 gmldl with a hematocrit less than 33% is considered inadequate
tissue oxygen supply for proper healing
8. hepatic disease: decreases clotting mctors and albumin production
9. obesity: unsatisfactory oxygen tissue levels and hypercoa.guability
10. age: decreased healing caused by autoantIbodies., altered proteins and diminished connective tissue
production
Wound healing agents
1. ACCU.2YME (papain-Urea Debriding Ointment)
-Papain, the proteolytic enzyme from the fruit carica papaya, is a potent digestant of nonviable protein
matter but is harmless to viable tissue. It is relatively ineffective when used alone as a debriding agent
and requires the presence of activators to s t i m ~ a t e its digestive potency.
-In Accuzyrne, papain is combined with urea (a denaturant of proteins) to bring about two actions: (1)
to expose the activators of papain and (2) to denature nonviable protein matter in lesions and thereby
render it more susceptible to enzymatic digestion
INDICATIONS AND USAGE
-indicated for debridement of necrotic tissue and liquefication of slough in acute and chronic
lesions such as pressure/decubitus ulcers., varicose and diabetic ulcers.. burns, post-operative
wounds and miscellaneous traumatic or infected wounds
-it digests all non-viable substrates found in necrosis even in the presence of infection (and it
does not harm healthy, viable tissue)
-usually see results in a few days
- 30g tubes (and store in a cool place)
-adverse reactions include skin irritation and "burning" sensation
190
ADMINISTRATION
1. clean wound with saline
2. apply Accuzyme directly to the wound and cover with a dry, sterile dressing
3. qd or bid applications preferred
-'1-. irrigate wound at each redressing to remove any accumulation of liquefied necrotic material
2. REGRANEXGEL (becaplermin)
-Regranex gel contains a recombinant hwnan platelet-derived growth factor (becaplermin) for
topical administration
-Becaplermin is produced by recombinant DNA technology by insertion of the gene for the
beta chain of platelet-derived growth factor (pDGF) into the yeast, Saccharomyces cerevisiae
-acts to promote chemotactic recruitment and proliferation of cells involved in wound repair
and enhancing the formation of granulation tissue
INDICATIONS AND USAGE
-indicated for the treatment of lower extremity diabetic neuropathic ulcers that extend into the
subcutaneous tissue or beyond and have an adequate blood supply
-used as an adjunct to good ulcer care including initial sharp debridement, pressure relief and
infection control
-it has not been evaluated for the treatment of diabetic neuropathic ulcers that do not eAiend
through the dennis into the subcutaneous tissue or ischemic diabetic ulcers
-contraindications include hypersensitivity (contains parabens) and known neoplasms at the
site of application
- 2, 7.5 and 15 gram tube sizes
-must store in refrigerator (do not freeze)
APPLICATION
1. wash hands thoroughly
2. rinse wound with saline solution or water
3. do not touch tip of tube to any surface
4. apply a carefully measured quantity ofRegranex gel to the wound (enough to cover the
surface)
5. after gel is applied, dress the wound
6. after 12 hours, remove dressing and gently rinse with saline or water
7. apply new dressing for next 12 hours without Regranex
Types of Scar Formation
a) hypertrophic scar
1. results from abnormal collagen proliferation. Buudles of collagen are laid do"n parallel to the skin
surface; ncapsuIated and stays within margins of original scar.
2. begins to neutralize and soften after approximately 18months
3. can be treated with topical steroid applications
b)keloids
1. fibrous tissue hyperplasia with fibroblasts arranged in randomly oriented parallel strands. Keloids are
devoid of seblceous glands and are non-encapsulated. The lesion extends beyond the margins of the
original scar; frequently entraps nerves and produces extreme pain
2. differential diagnosis .
dermatofibrosarcoma protuberans
rare malignant variant of dermatofibroma
continues to enlarge; no history of prior trauma
hypertrophic scar
191
3. treatment
surgical excision contra-indicated
intIa-Iesional steroid injection may cause keloid to flatten
pressure dressings helpful after surgery andIor injection
silicone gel sheeting may be effective
Skin Tension
Tension is the force that causes wounds to widen and scars to hypertrophy. Incisions must be placed in areas of
least tension to insure minimal scarring.
a) Langer's Lines
Described in 1861, thought to be a reflection of underlying muscle pull. In 1941, Cox determined new skin
cleavage lines utilizing LangeI's techniques
b) Relaxed Skin Tension Lines
Determined by Burges and Alexander in 1962. Their lines are created by underlying structures such
as muscle, tendon, bone or any st:rucWre tenting the overlying skin. An incision made perpendicular
to the relaxed skin tension lines will gap widely, whereas an incision made parallel to these lines will
remain well approximated
PRINCIPLES AND TECHNIQUES OF FIXATION
AOIASIF
a) AO: AIbeitsgemeinschaft fur Osteosynthesisfragen or The Association of Osteosynthesis
b) ASIF: Association for the Study oflntemal Fixation
c) Goals of the AO - rapid recovery of the injured limb
L anatomic reduction
2. preservation ofblood supply
3. stable internal fixation
4. early active mobilization
Principles of Rigid Fixation
PrimaIy vascular bone formation
a) consists of simultaneous remodeling and formation of new bone at the fracture site
b) bypasses fibrocartilage formation seen in secondary bone healing; new bone is intentionally formed at the
fracture margins aka-contact healing: direct reconstruction of fragment edges by haversian remodeling
c) absence of micromotion is necessary for direct haversian remodeling and for the cutting cones to cross the
fracture site and unite the ftacture
d) if motion ocaus, periosteal and endosteal callUs forms resulting in secondary bone healing
Principles of Internal Fixation
a) Interfragmentary Compression
1. static (compression remains constant)
>lagscrew
>eccentric loaded plate
>external fixation
2. dynamic compression
>tension band
implant absorbs tension and bone absorbs compression
k-wires provide rotational stability
b) splintage
1. internal
>nails; k-",lles, intIameduIlary nail
>cerclage wire; stainless steel wire
192
>neut::rn1 plating
neutralizes forces applied to the fracture site
*stress shielding: In the absence of physiologic stress, bone resorption occurs in accordance to
Wolff's Law. This causes disuse osteoporosis and possible refiacture. Recent research demonstrated
a direct correlation between the disturbance of blood supply upon application of internal fixation and
the resultant osteoporosis from revascularization of the area a few weeks later.
2. external
>e>.:ternal fixation
CONCEPTS AND TERMS OF MECHANICS
Stress and Strain
a) "stress-press, strain-gain"
Stress is the pressure that you put on a material in IbsIsquare inch. Strain is the length or a measured
deformation that results in a material after a certain stress has been applied to it.
b) Stress-Strain Curve
1. when stress is plotted versus strain, we get a load deformation curve; this curve represents a picture of
the mechanical behavior of a particular implant under a load
2. yield point
>Represents the point beyond which the material is no longer Hookian (ie-the strain of a material is no
longer proportional to the stress applied to it)
> When you pass the yield point of a material, further Jl1ll or stress causes an disproportionally larger
stretch or strain
>Beyond the yield point the material cannot return to its original shape and you have entered the range
of plastic deformation
3. Ultimate Failure Point
continued stress through the rnnge of rnnge of plastic deformation eventually leads to fuilure of the
material
Hook's Law: the amount of strain in a material tmder a load is proportional to the amount of stress
applied to it
Once the applied load is removed the material will spring back to its original shape (range of elastic
deformation). The resulting slope represents the stiffuess of the material [aka-Young's Modulus of
Elasticity or the "E" modulus]
Since implanted materials that we use are much stiffer than bone, the material absorbs the stresses and
strains instead of the bone. This is known as stress shielding and causes disuse osteopenia in the bone.
Materials
316LVM:
1. the ''L" stands for low caIbon content
193
the "VM" indicates that the base alloy was remelted in a vacuum, which reduces the number of impurities
that affect the material's physical properties
2. composition
iron and CaIbon: provide strength
chromium: anti-corrosive, but weakens alloy
nickel: restrengthen alloy;
1ll01ytxJenum:
manganese
silicon
copper
nitrogen
sulfur
phosphorous
Other Terms
a) Fatigue fililure
Failure of a material from repetitive loading and unloading. Many materials can undergo a certain
level of stress and if not exceeded, will not show any evidence of fatigue failure. Tensile stresses
cause a material to fail at its surface.
b) Creep
A pennanent deformation in a metal Bridges are built in a semi-arc to prevent creep. Creep is temperature
dependent (ie-tbe higher the temperature, the greater the creep). Creep rates at body temperature are
low, and thus, an implant in the body takes several months to :fuil from creep.
c) Viscoelasticity
The ability for a material to "flow" (ie-the material shows eIastic behavior, but also a "iscous flowing
behavior). The best example of a viscoelastic material is cartilage - cartilage molecules rearrange
themselves allowing for the acceptance of more stress.
d) Neutral Axis of Bone
When a long bone is loaded, a tension side and a compression side develops. The axis that experiences
neither tension nor compression is called the neutral axis of bone. Plates could withstand tension well, but not
bending.
Therefore, plates are placed on the tension side of the bone.
BONE SCREWS
Two types of screws: wood screws and machine screVr"S.
Wood screws have a threaded tip and predrilling is not necessary. As they are driven into bone, they crush and
compact the material This is not well tolerated by cortical bone, and therefore, their application is limited.
Machine screws have a blunt end and require both predrilling and tapping for insertion. Self tapping screws
have a fluted tip and cut a leading thread as they are driven. Almost all scre\\'S in current use are machine
screws.
194
.. \ \, }--E .-'
\\
H I
Screw Anatomy
r .....

... ;;o$ji,,,
. .
a) Head: with some exceptions, it is hexagonal. The hexagonal recess allows for most efficient
translation of torque from the screwdriver to the screw and reduces cam-out (lifting out of the
screwdriver from the screw head).
Torquing a screw too much on bone increases the pressure at the bone-screw interface,
causing hyperemia and bone resorption around the screw with subsequent loosening.
b) Land: undersurface of the head which comes in contact with the bone
c) Shank: unthreaded portion of the screw (cancellous)
d) Run-out: junction between the shank and threaded portion of screw. It is the weakest point on the
screw. The threads should cross well into the fracture otherwise screw breakage at the
run-out is inevitable as well as distraction of the fragments.
*Keep in mind that a screw could break anywhere depending upon the forces at the bone-
screw interface. However, a screw is "veakest at the run-out.
e) Thread diameter: represents the diameter of the screw
f) (ie-a 4.0 mm screw has a 4.0 mm thread diameter)
g) 1) Pitch: represents the distance between the threads. A cortical screw has a tighter pitch than a
cancellous screw, which makes it more suitable for hard cortical bone.
h) Core diameter: represents the diameter of the screw between the threads; determines the size of
the thread hole.
i) Tip: either trochar, round or fluted (self-tapping screw)
j) Axis: central line of a screw
k) Tip angle: tip to the axis
1) Rake angle: thread to axis angle
Self tapping vs. Non-self tapping screws
a) self tapping
1. pilot hole larger than with non-self tapping screws and screw threads do not penetrate as deeply into
bone
2. once pilot hole is drilled into the bone, the screw can be inserted (screwed in)
3. may have advantage over non-self tapping screws in thin cancellous bone and in flat bones (ie-skull,
pelvis)
b) must perform insertion carefully - if unintentially angled, the screw will cut a new path and destroy the
already cut threads
b) non-self tawing
1. require pre-drilled pilot hole and then cutting of screw thread pattern with a tap
2. less heat generated with insertion due to decreased resistance
Cortical and Cancellous Screws
Cortical
a) For use in hard cortical bone and function as positional (ie-hold a plate in place) or as a lag screw (ie-
threads of screw do not engage proximal cortex of fracture)
b) sequence of cortical screw insertion
glide hole, threaded hole, countersink, measure depth, tap and insert screw depth measured before
tapping to prevent the gauge from disrupting the thread pattern
195
Cancellous
a) The pitch of this screw is higher than that of the cortical screw. It is either fully or partially threaded.
Designed for soft metaphyseal and epiphyseal bone. When used in lag fashion, all the threads must cross
the ftacture of the osteotomy site.
b) sequence of cancellous screw insertion
tbreacbI hole, countersink, measure depth, tap and insert screw
Lag Screw Principles
Three conditions must exist for a screw to function as a lag
1. the near cortex must be drilled with a clea.t"aJ:la: hole or a glide hole to allow the screw to glide freely
2. the filr sur:filce must be threaded
3. when tightened, the screw head must contact the near mrf3ce or cortex so it can compress the fracture
segments
Lag screw is best positioned perpendiruJar to fracture sur13ce for maximum compression
If screw thread engages both near and far cortices, compression across fracture site will not be achieved and
gapping will ocarr across site
Malleolar Screw
Originally designed for fixation of medial malleolus
ChaIacteristics -
partially threaded
have same thread profile and pitch as cortical screws
trephine (self-cutting) tip
Cannulated Screws
These scre'\\'"S are designed to minimize complications associated '\\'ith screw insertion (ie-redirecting screws
and repeated bone penetration,. which compromise bone fixation). A k-wire is used to achieve reduction and an
i n t I a ~ e x-ray is taken to confirm placement. The k-wire then serves as a guide for the screw placement.
Avai1able in 3.0 nun, 4.0 nun, 4.5 mm, 7.0 mm sizes, 7.3 mm.
Effects of Screw Holes in Bone
a) decreases the bone's resistance to bending and to torsional forces
b) stress concentration is increased up to 1.6 times around a screw hole
c) fractures through old screw holes have been documented up to II months after screw removal; greater
incidence in diaphyseal bone since it is under greater torque moments than metaphyseal bone,
which experiences greater compressive stresses.
d) following screw removal, a 34 week period of casting is recommended
Plates
a) Description
Plates function through interfragmentary compression, buttressing and neutralization
1.1nter:fragment: Compression
>plate may perform more than one :function at the same time (ie-neutralization plate can protect lag
screw and also exert compression along long axis of bone)
>eccentric loading of bone creates tension on one side and compression on the other
if plate is applied to tension side, deformity will be prevented (with load, the plate is put under tension
and cortex opposite plate under compression) likewise, if plate is applied to the compression side,
cortex opposite plate will gM> under load
196
.1'
...
2. Buttress plates
Plate is applied to fracture site so as to prevent shift of the fragments under load
Special designs: "T", "L", "spoon". "cloverleaf'
3. Neutralization Plates
.-
Protect screw fixation. Interfragmentary screws are used to stabilize a fracture and the plate is applied
to neutralize the bending, torsional and shear forces that would otherwise jeopardize the fixation
obtained by lag screws alone.
b) Plate Sizes
1. tubular plate: tube with radius of 6 mm and thiclmess of 1 mm
2. semi-tubular (accommodates 4.5 mm screws)
3. one-third tubular (accommodates 3.5 mm screws)
4. one-quarter tubular (accommodates 2.7 mm screws)
5. posterior anti-glide plate
>used for Weber B fractures with posterior spike. The fracture has the tendency to displace superiorly
and posteriorly, which is prevented by this plate position.
>the plate can reduce the fi:acture
>no potential for the screw to go into the joint
>also recommended for osteoporotic bone
>the distal fragment does not require screws
c) LC-OCP: limited c o n t a c t ~ c compression plate
Further development of the DCP and DCU
Based upon the concept ofhiological plating
1. minimal surgical disruption of blood supply
2. improved healing in the zone covered by the plate
3. reduced risk of re-fracture following plate removal because of minimal damage to bone beneath the
plate
4. titanimn as the implant material provides optimal tissue tolerance
197
5. grooves on the undersur.face of the LC-DCP
>minimize damage at bone/plate interface, which preserves blood supply
>allows for small bone bridge beneath plate, in an otherwise weak spot
>allows for more even distribution of the stifihess of plate (more resistant to bending and torque)
6. description
>equal distance between screw holes along the plate
>screw holes symmetrical and have oblique undercuts at each end to allow for up to 40 tilting of
screw in each direction in long axis of the bone
>1Uldercuts between holes
>trapezoid cross-section
7. healing with the LC-DCP
>1atera1 undercut areas allow for bone fonnation at plate side of periosteal surface
>:fracture gap exhibits band of remodeling rather than resOIption of ftacture surface
>small amount of plate-induced remodeling
Other Forms of Internal Fixation
a) Kirschner Wires (1909) - "k-wire"
1. supply primary, supplemental and provisional fixation
2. supplementaIy: to augment screw or other wire fixation. Readily preformed with low morbidity.
When used with a screw, the k-wire affords rotational stability.
3. primary fixation: used for metatarsal osteotomies, fractures and fusions
4. provisional fixation: used intra-operatively in the reconstruction of a comminuted fracture. Also
fixation of choice in physea1 injuries.
5. the rigidity ofk-wire fixation can be increased by increasing the diameter of the k -wire and the
number of them used
6. threadedk-wires provide greater fixation per diameter versus the smooth k-wire. They tend to slip on
insertion and once insertion is started, they are harder to redirect and have lower failure threshold
compared to a smooth k-wire of the same diameter
7. Sizes (diameter in inches): 0.028, 0.035, 0.045, 0.062
b) Steinman Pins
1. considered large k-wires and function the same as k-wires
2. sizes in inches or millimeters
>5/64 to 12164 inch diameter (in 1164 increments)
> 1. 9 to 4.7 nun in diameter
3. tip design: applies to both K -wires and Steinman pins
>trochar, diamond or cut tips
cut tip has an eccentric point producing a large hole and sub-optimal fit
trochar tip allows for the least slippage on insertion, and thus, highest accuracy of placement
diamond tip has slightly less initial holding power than a trochar tip
>at acute approach angles, diamond and cut tips walle along cortical surface,
while the trochar tip penetrates
c) Stainless Steel Malleable Wire
1. monofilament from 24-30 guage stainless steel
2. used when fracture fragments are too small, osteoporotic or comminuted to be
suitable for screw fixation
3. best used in awlsion fractures and in tension band technique
4. the right angle loop configuration is the most stable loop configuration
ill
198
d) Staple Fixation
L suitable in bone with high cancellous/cortical ratio
(ie-calcaneus); the thicker the cortex, the greater the propensity of comminuting it on insertion
2. propensity to distract the fracture fragments if not properly compressed prior to application
3. manual insertion causes rocking of the staple legs and an enlarged elliptical channel for the legs as
well as, sub-optimal holding power
4. power driven staple fixation allows staple to penetrate the bone without rocking, thus improving
fixation; will need to pre-drill when used in cortical bone
5. staple size is determined by bridge width and leg length.
longer the leg length, the greater the pullout power
6. recommended application in circumferential fashion to prevent fracture gapping upon weightbearing
7. barbed staples increase staple purchase and holding power; they are hard to remove and produce a
significant defect in bone
e) Absorbable Fixation
L two types
>Biofix: composed of polyglycolic acid
>Orthosorb: composed of poly-p-dioxanone
tapered pin attached to stainless steel pin for drilling
completely eliminated within six months
gradually loses tensile strength as the bone heals
PDS histologically more inert; less rapidly degraded
2. undergo hydrolysis when placed in living tissue
3. possess much less stiffness and shear strength vs a
k-wire; 50010 decrease in holding power 4-6 weeks after insertion
4. indications: fixation of osteochondral fragments; digital fusions; metatarsal osteotomies
5. complications: late inflammatory reaction and sinus formation; adverse tissue reactions (ie-rejection,
irritation, encapsulation)
f) Herbert Bone Screw
I. originally designed for fixation of caIJlIl scaphoid bone
2. rom screw diameter; 16-30 rom length in 2 rom increments
3. screw is "headless", compared to cortical and cancellous screws; this feature allows for insertion of the
screw through articular cartilage
4. can be inserted manually or by the use of a jig
5. screw removal not normally required
6. threaded portions distal and proximal with tighter pitch proximally; the difference in pitch provides
7. compression between the acljacent bony fragments
8. composed of Titanium alloy - titanium alloy with
9. 6% aluminum and 4% vanadium
10. indications: fixation of osteochondral fragments; metatarsal osteotomies; Akin osteotomy
g) Reese Arthrodesis Screw
L designed to create greater compression across arthrodesis site
2. stainless steel screw with clockwise (right-handed) threads proximally and
counterclockwise (left-handed)
threads distally; smooth portion between the threaded segments (2.0 rom core diameter)
3. indications: hallux IPJ fusion; digital arthrodesis
41 r..
~ ~
199
h) Tension Band Concept
1. the combination of static intediagmentaI compression with the .functional loading of the part to
create a dynamic degree of interfragmentaI compression
2. two basic components:
Load Beam (osseous segment)
Tension Band Device
-+tension lmtd plate
-+dynamic compression p1ate
-+eerclage wire
3. examples in the ankle and foot
+avulsion fractures of the medial and 1ateral malleoli and 5
th
metatarsal base (although there is
some dispute with the 5& metatarsal base)
4. used for transverse and short oblique fractures but not amenable to long oblique, spiral fractures,
or comminuted ftactures
Complications ofIntemal Fixation
a) I n t r a ~ e complications
1. screw strips: longer screw; larger diameter screw; redirect the pilot hole and different form of fixation
2. screw, drill or tap breaks: hollow reamer/extraction bolt; trephine it out or leave it in
b) Post-operative complications
1. nonunion: results from poor fracture reduction. incorrect fixation or patient noncompIiance
2. infection: follow infection protocol-if internal fixation unstable, remove and replace with external
fixation device applied away from site to insure stability and maintain blood supply of osteotomy or
fracture site
c) necrosis: secondary to stripping of periosteum and/or excessive compression at fracture ends
d) breakage: usually due to inappropriate application of fixation device (ie-size; method; post-op course)
Complications of Specific Fixation Devices
a) K-wires and Steinman pins
1. skin protrusion as a possible site of pin tract infection
2. loosening - causes necrosis ofbone at pin site and most common cause of pin tract infections
3. migration - smooth k-wires are most prone to migration
mechanical motion at or near fixation site is important
bending, prompt removal. proper application and use of threaded pins reduces chances of migration
b) Monofilament wire
1. initation of tendon or overlying skin
2. shifting of fulgments on breakage of the wire
3. loss of fixation secondary to poor criteria and application
c) Staples
1. cortical shattering
2. distraction of the fracture ends
3. fracture displacement on insertion of the staple
d) Screws
1. poor reduction of fracturelosteotomy
2. screw thread across fracturelosteotomy site
3. one point of fixation
4. hitting the near cortex of adjacent bone
5. incorrect placement
6. incorrect choice or sequence of insertion
7. incorrect type, size or length of screw
8. overaggressive countersink with cortical disruption
e) Plates
1. increase in operative time secondary to extensive dissection of soft tissue and periosteum
2. initation and need for removal
3. disuse osteopenia secondary to stress shielding or revascu1arization after periosteal stripping and the
need for casting post removal
200
Bioenvironmental Properties and Reactions
a) Galvanic Corrosion: caused by two dissimilar metals in body
b) Crevice Corrosion: caused by one metal moving against another
c) Fretting Corrosion: occurs when the protective oxide layer is broken down due to micromotion. When a
metallic implant is placed in the body, the nickel from the implant reacts with its surrounding tissue
fluid fonning a protective oxide layer (passivation layer) that protects the metal from corrosion.
d) Stress Cracking: cracking of the metal due to cyclic stresses. Cracking results from corrosion. fatigue and
stress corrosion cracking.
EXTERNAL FIXATION
Classification ofEx1ernal Fixators
a) Sinlple Pin Fixators
1. utilize half pin or trnns-fixation pins with one or more longitudinal side arms
2. simple to use and versatile
3. disadvantage = the bone segments must be properly reduced prior to the application of the fixator
4. examples: AO tubular system; Wagner single half frame; the original Roger Anderson device
b) Modular Pin Fixators
1. the pins inserted into the bone are stabilized by one clanlp to which a universal joint is attached,
connecting the longitudinal rods
2. extremely versatile_ allowing movements and adjustments in variety of planes
3. disadvantage = the apparatus is complex, heavy and bulky
4. example: the Hoffman-Vidal frame
c) Ring Fixators
1. components include circular and selni-circular rings that attach to side longitudinal rods
2. pins connect the bony segments to the circular rings
3. disadvantage = bulky and difficult in gaining access to soft tissues
4. advantage: capable of adjusting in all planes and uses k-wires which can be inserted in a 360 orientation
without complicating the frame design
5. example: the classic llizarov frame
Functions
a) lengthening
b) neutralization
c) compression
Uses of External Fixation
a) open fractures
b) comminuted fractures
c) arthrodesis
d) osteotomy fixation
e) soft tissue stabilization/fixation
Configurntion
a) unilateral (one or two planes)
1. excellent wound access
2. not as stable as biplane
b) bilateral (one or two planes)
1. increased stability
2. increased chance of damage to anatolnic structures
201
Unilateral
Biodegradable Fixation
Ideal osteosynthesis device should remain firm enough for the duration of bone healing
and then lose its strength and transfer the nonnal stress to the healing bone. It should
then disappear from the body after healing is complete.
Fixation types (Currently available in U.S.)
* Screws
*Rods/Pins
Historical:
1973-84: Basic research on animals
1985: Clinical trials on humans, absorbable rods
1987: First totally absorbable self-reinforced screw used
Basic Polymers:
PGA - polyglycolide
PLLA - poly-L-Iactide
PDS - polydioxanione
* Fixation devices are produced by a self-reinforcing procedure that combines polymers
to improve strength (SR-PGA, SR-PLLA)
Bilateral
202
* Degraded by hydrolysis - eventually entering into the Kreb' s cycle and excreted in
urine, feces or expired CQ.
Loss of mechanical resistance:
SR-PGA - 30-60 days
SR-PLLA - 3-12 months
Complete absorption:
SR-PGA - 5-10 months
SR-PLLA - 15-60 months
Actual time depends on the shape, size, molecular weight and variable tissue
en"ironments of implantation.
Advantages:
1. Avoids stress shielding or stress protection osteopenia
2. Eliminates burden (Physiologic and financial) of secondary procedures for fixation
removal.
3. Does not lead to image artifacts when using MRI or CT post implantation.
4. May be left in sites of infection as implants are bacteriostatic.
Disadvantages:
1. Screws are Iadiolucent - unable to confirm fixation position with x-ray.
2. Less interfragmentary compression than with conventional screws.
3. Possible foreign body reaction.
Cortical Bone Pins
1. Allofix made by M1F TM (Musculoskeletal Transplant Foundation)
2. Studies underway using pin to augment fixation of Chevron (Austin) osteotomies
(and its modifications) and to fixate PIPJ toe fusions
3. made from cortical bone that has been turned on a lathe to varying sizes
a. 2.0 111Ill. 2.4 111Ill. 2.7 111Ill. 3.0 111Ill. 3.5 mm
b. insertion kits available corresponding to size of pin
SUTURE MATERIALS
Purposes:
a) approximate tissue until healing takes place
b) ligate vessels
c) tag fragile or important structures
Selection based on:
a) biologic and mechanical performance
b) structure to be sutured (tendon, fascia, skin, vessels, bone)
c) bacterial presence
I) contaminated 7 monofilament (nylon, polypropylene)
2) clean
203
Suture characteristics:
a) strength and thread dimension
1) varies with basic material composition and dimensions
b) most used standard. measurement
1) USP (United States Phannacopeia)
2) denotes dimension and knot pull strength
c) suture volume
1) nse of smaller sutures decreases foreign body volume but sacrifices knot pull strength
d) elongation
1) elasticity
~ return to original length with cessation of strain
~ stainless steel, braided polyester, catgut, silk:
2) plasticity
~ elongation persists with cessation of strain
~ polypropylene
3) intermediate
e) flexibility
~ posses both elastic and plastic properties
~ nylon, polyglactin 910
1) based on material and diameter of suture
~ small diameter is more flexible than large diameter
~ silk, dexon = flexible
~ nylon, catgut = stiff
f) monofilament vs. braided
1) monofilament has a low coefficient of friction and is better suited for contaminated wounds
2) braided has a high coefficient of friction, greater strength, and capillarity
g) capillarity
1) fluid and bacteria may penetrate into interstices of braided sutures
2) PMN's, macrophages too large to reach interstices(increases risk of infection)
h) coating
1) helps decrease capillarity
2) improves handling
3) reduces tissue drag
Suture needles:
a) desirable characteristics
1) made of high quality stainless steel
2) slim as possible without compromising strength
3) sharp enough to penetrate tissue with minimum resistance
4) rigid enough to not bend but ductile enough to not break:
204
b) needle anatomy
1) suture attachment
2) body
3) point
c) measurements
I Chord Length I
Needle
Point i .
1) chord length
2) needle radius
3) needle diameter
4) needle length
d) suture attachment
e)
f)
1) closed (eyed)
2) French (split or spring)
3) swaged (eyeless)
body
1)
2)
3)
point
1)
2)
3)
most common
suture attachment
directly into needle
decreases tissue damage
Needle length
straight, Y2 curved, Y4 circle, Y2 circle (most common), 3/8 circle, 5/8 circle
geometric shape
round, flat, oval, triangular
length (4mm-60mm)
blunt
used for friable tissue
tapered
useful for tissue offering slight resistance
paratenon, tendon sheath, subcutaneous tissue
cutting
conventional
+ cutting edge on concave curvature
+ cuts through dense, difficult to penetrate areas (tendon, ligament)
+ care must be taken not to "rip" through tissue
reverse
+ cutting edge on convex curvature
+ prevents needle from "ripping" through tissue (skin)
+ greater strength

A
Regular Cutting
Spatula
y
Reverse Cutting
Suture types:
a) absorbable
I) generally lose tensile strength within 60 days
2) natural
degraded by lysosomal enzymes
catgut
+ name may originate from "kitgut" meaning violin string
205
b)
c)
3) synthetic
+ made from submucosa of sheep intestine or serosa of bovine intestine
+ can be treated with chromic salts and formaldehyde for greater strength
+ stored in alcohol for preservation
+ highest tissue reactivity of all sutures
}> collagen
+ made from long flexor tendon of steer
+ primarily used in ophthalmic surgery
+less tissue reactive than catgut
}> degraded by hydrolysis
}> polyglycolic acid (Dexon)
+ braided
+ good knot-pull and tensile strength
+ very inert
+ completely hydrolyzed in 100-200 days
+ may be coated with polycaprolate for improved tissue passage, handling, knotting
+ skin and subcutaneous tissue
}> polyglactin 910 (Vicryl)
+ braided
+ 65% tensile strength remains at 14 days
+ very inert
+ completely hydrolyzed in 80 days
+ may be coated "'ith polyglactin 370 and calcium stearate for better handling
}> polydiaxonone (PDS)
+ monofilament
+ high flexibility and tensile strength
+ completely hydrolyzed in 90 days
+ very inert
+ 70% tensile strength at 14 days
}> polyglyconate (Maxon)
+ monofilament
+ resists kinking and curling
+ becomes softer as it's exposed to tissue fluid
+ completely hydrolyzed at 180 days (longest of any "absorbable" suture)
}> poliglecaprone (Monocryl)
+ monofilament
+ very pliable and inert
+ completely hydrolyzed in 90-120 days
+ 20-30010 tensile strength remains at 14 days
d) nonabsorbable
I) generally maintain tensile strength longer than 60 day
2) natural
}> silk
+ made from silk of the silk worm
+ known for superior handling properties especially when braided
+ impregnated and coated ",ith mixture of waxes and silicone
+ low tensile strength which is completely lost at 360 days (very slowly absorbable)
+ highly tissue reactive
}> cotton, linen
+ similar to silk
+ increased tissue reaction
+ very low tensile strength, weakest suture
206
3) synthetic
~ nylon (Etbilon, Surgilon)
+ possesses "memory" ( the tendency for a filament to want to straighten)
+ elastic in nature therefore well suited for retention and wound closure
+ high tensile strength and low tissue reactivity
+ monofilament and braided
+ may be used in contaminated wounds
~ polyester (Ethibond, Dacron)
+ braided
+ high tissue strength
+ low tissue reactivity
+ may be coated with silicone for smoothness, reduces tissue trauma
+ used when strong apposition of tissues is needed indefinitely
~ polypropylene (Prolene, Surgilene)
+ very inert
+ monofilament
+ better pliability and handling than nylon therefore holds knots better
+ excellent tensile strength
+ passes through tissue with minimal drag
+ often used in contaminated wounds and plastic surgery
~ stainless steel (Flexon = braided)
+ monofilament and braided
+ measured in the Brown and Sharpe (B&S) gauges and not in the USP method
+ may corrode especially at stress points
+ mild to moderate tissue reactivity
+ may fracture, fatigue, or kink
+ used for bone fixation, tendon repair. and retention sutures
Staples:
a) common uses
1) gastrointestinal anastomoses
2) wound closure
3) ligature substitute
b) better resistance to infection than wounds contaminated by the least reactive suture
c) often used to affix skin grafts
d) implementation
I) evert skin edges \\'ith two atraumatic forceps
1) deliver the staple at 60 degree angle to the skin
2) when staple assumes an upright position the top span will not be in contact with the skin - this
helps
Flattened Topspan
~ 1 ! lJ
Dimple Dimple Point
J ~
00
to prevent "cross-hatching"
STAPLE
~
~
STAPLER
207
~
a) made in a variety of forms that vary in backing and adhesive formulation
b) porous structure of adhesive and backing allows for evaporation
c) superior resistance to infection over any other wound closure technique
d) may only be used as primary closure device on wounds with minimal static and dynamic tension
e) may be supplemented with dermal sutures on the high tension skin of the extrenllties
Fibrin sealants:
a) biologic tissue adhesive
b) Derma Bond
208
I
I
I
I
FOREFOOT SURGERY
FOREFOOT SURGERY
FOREFOOT SURGERY
FOREFOOT SURGERY
FOREFOOT SURGERY
FOREFOOT SURGERY
FOREFOOT SURGERY
FOREFOOT SURGERY
FOREFOOT SURGERY
FOREFOOT SURGERY
FOREFOOT SURGERY
FOREFOOT SURGERY
FOREFOOT SURGERY
FOREFOOT SURGERY
FOREFOOT ..
F
'nRrFO()T sLrR ---ir: 1-< .
. \.J -"c.. ... j. lJ L_ \'.
r (' ....... r)c T ( .. '. r' IT) .'" .
i l) t" t-, \ J "'" l 1< . Jr". '\
J.A 'It...... __ ,_/1....--". '- ..
ACCESSORY BONES OF THE FOOT AND ANKLE
Accessory Bones
Developmental Anomalies
May be multiple in the foot
Unilateral in ~ 500;0 of cases
Most Common
Os Trigonum
Os Tibiale Extemum
Os Intermetatarseum
Os Trigonum
Near posterolateral tubercle of talus
"Interns Fracture"
When fused. - called "Trigonal Process"
More often bilateral
Frequency R:! 2.7 -7.7%
Os Tibiale Extemum I Accessory Navicular
Incorporated by T. Posterior Tendon
Typically pyramidal in shape
Fibrous or fibrocartilaginous
connection
Frequency R:! 3 - 12%
Type!
Really a sesamoid bone in T.
posterior tendon
Round
Account for 30%
Type II
Accessory ossification center in
the navicular
Separated from navicular body
by fibrocartilage
Triangular
Os Intennetatarseum
Between Medial cuneiform and base
of 1
st
and 2nd metatarsals
Projects between the 1
st
and 2nd
metatarsals
Spindle shaped - tapers distally
Usually fused to distal lateral comer
of the medial cuneiform
Frequency R:! 1.2 - 10%
Os Sustentaculi
Posterior aspect of sustentaculum tali
Rarely a distinct bone (0.47%)
uncinaI:us
Fibrous or fibrocartilaginous connection to sustentaculum tali
More common in males
Frequency R:! 2 - 3%
Os
P""Y:;;t-tI-l--.Llrtermetatarseum
Os cuboideum
seconclarium
209
Os Calcaneus Secundarious
Interval between anteromedial calcaneus, cuboid navicular. and head of talus
Located dorsal
Frequency"" 7 -11% (male); 6-7% (female)
Os Cuboides Secundarium
Interval between cuboid, navicular, talus, and calcaneus
Locatedplantar
Process can connect to cuboid
Frequency "" 1 - 3%
Os Talonavicular Dorsale
AK.A Os Supranaviculare, Pirie's Bone)
Located Dorsally an T -N joint - near midpoint
Frequency "" 15% (male); 11% (Female)
Os Intercuneifonne
Located dorsally between proximal segments of intermediate and medial cuneiforms and navicular
Wedge shaped
Frequency "'" 1%
Os Cuneo - Metatarsale - Plantare
Located plantarly between I st metatarsal and medial cwleifonn
Frequency "'" rare
Os Vesalianum
Located just proximal to the tuberosity of the 5
th
metatarsal
Must be differentiated from ossifying apophysis
Frequency z rare
Os Subtibiale
Plantar to medial malleolus
Round or angular appearance
Frequency z 4%
Os Subfibulare
Plantar to lateral malleolus
Round or c.omma shaped
Frequency z ?
Os trigonum .
tarsi" I
Talus
accessorius /
i
i
Os versalianum pedis
Anomalous os
,..talocalcaneum
Sustentaculum tali
Acessory navicular
Os tibiale externum
Processus uncinatus
Os intercuneiforme
Os
210
OSSIFICATION OF THE BONES OF THE FOOT
Bone Primary Center Secondary Center
Tibia 7-8 wks intrauterine Prox., before birth; Dista13-12 mos
Fibula 7-8 wks intrauterine Prox., 3-4yrs; Distal 9-12.5 mos
Calcaneus 3rd mo intrauterine Post., 6-8 yrs
Talus 6th mo intrauterine
Navicular 3rdyr
Cuboid Birth-6mos
Medial Cuneiform 2ndyr
Intennediate Cuneiform 3rdyr
Lateml Cuneiform Istyr
Metatarsal I 10th wk intrauterine Base,3rdyr
Metatarsal II, ill, IV 9th wk intrauterine Head, 3-4 yr
Metatarsal V 10th wk intrauterine Head, 3-4 yrs
Proximal Phalanges II-IS wks intrauterine Base, 2-Syrs
Middle Phalanges variable, after ISth wk intrauterine Base, 2-8yrs
Distal Phalanges 9-12 wks intrauterine
Sesamoids in FHB 10-12 yrs
DIGITAL SURGERY
Anatomy of the Extensor Apparatus of the Toes
a) the EDL tendon:
1. divided at the level of proximal phalanx into
three slips
2. a middle slip inserts into base of the middle
phalanx
3. medial and 1aternl slips into base of distal
phalanx
4. the combined EDB and EDL tendon has no
insertion at the baSe of the proximal phalanx
Base, 2-8yrs
mterosseous
muscle belly
Lumbrical
Fuse
14-17 yrs
17-20yrs
17-2Oyrs
17-20yrs
lS-18yrs
lS-18yrs
15-18yrs
b) EDL is held in central position on the dorsum of the toe by a fibro-aponeurotic structure extending from
MIP joint to PIP]
1. the proximal segment is a sling-like structure
2. wrnps around the capsule of the MIP joint
3. inserts at the junction of the plantar plate, deep transverse metatarsa1ligament and flexor tendon sheath
4. thus, the EDL tendon is finnly held to the plantar aspect of the proximal phalanx, not the dorsum
c) extensor wing or hood is distal segment of extensor apparatus
I. provides insertion for the lumbricales
2. 1umbrK:a1 muscle passes plantar to the deep transverse metatarsal ligament to insert into the extensor
hood
Extrinsic Musculature
Extensor Digitorum Longus
a) originates from anterior compartment of the leg
b) passes beneath e:l\.iensor retinaculum and cfu.ides into four slips
211
c) at the MIP joint., gives off expmsions
-proximal ex1ensions are vertically oriented
-distal extensions are oblique fibers and provide insertion to the lumbricales
d) inserts at the mse of the distal phalan.x
e) creates a dorsiflexory force at the metatarsophalangeal joints in s\\'ing phase of gait
f) also dorsiflexion at the ankle joint
Flexor Digitorum Longus
a) originates in the deep posterior compartment of the leg
b) divides into four slips in the second layer of the foot
c) each tendon passes plantar to the MIP joint and inserts into the distal phalan.x
d) four lumbrical muscle originates from the four tendonous slips medially
e) the quadratus plantae inserts into it's lateral portion, fonning a conjoined tendon
Intrinsic Musculature to the Lesser Digits
Flexor Digitorum Brevis
a) originates from plantar aspect of calcaneus in the first layer of the foot
b) passes plantar to the MIP joint
c) at the level of proximal phalan.x it splits to allow the long flexor to pass through
d) inserts into the base of the middle phalanx
e) functions to plantarflex the IPJ along with the long flexor; this causes a retrograde dorsiflexion at the
MfPjoint
Dorsal Interossei
a) are bipennate muscles
b) originate from adjacent sides of corresponding metatarsals
c) the first dorsal interossei originates from adjacent first and second metatarsal shafts, and inserts medially
. into the second toe
d) the remaining interossei originate from the adjacent sides of the corresponding lesser metatarsals and
insert laterally into the bases of proximal phalanges two. three and four
Plantar Interossei
a) unipennate muscles
b) originate from plantar medial aspect of metatarsal shafts
c) insert medially into the third, fourth, and fifth digits at the base of the proximal phalanx
d) the flexor digiti quinti brevis originates from the lateral plantar aspect of the fifth metatarsal and inserts
laterally into 00se of proximal phalan.x of the fifth digit
Quadratus Plantae Muscle
a) originates from interior swfuce of the calcaneus
b) inserts into the lateral aspect of the FDL tendon
c) provides porximal stability to both the lumbricals and FDL
d) straightened out the medial proximal pull of the FDL; if it loses it's mechanical advantage, adductovarus
fifth toe will result
Lumbricales
a) four in number originating from the medial aspects of the FDL tendon slips
b) travel plantar to the transvserse metatarsal ligament and insert medially into the extensor hood
c) their function in gait is theoretical at present
212
NAIL SURGERY
Nail Anatomy
Nail Plate
. overl.yiDg posterior skin
fold suzface ofpostuiorskin fold
Divided into three areas derived from three different germinal sites: dorsal nail plate - from upper nail root
matrix
intermediate nail plate - from lower nail matrix
ventIa1 nail plate - from the nail bed
Nail Bed
a) is located underneath the exposed and. concealed portions of the nail plate
b) consists of a germinative layer and a dense dermis
c) the deepest part of the dermis is fused to the periosteum of the distal phalanx
d) the concealed portion where nail growth happens is called the matrix
e) the outer limit of the matrix is a semicircular whitish area called the lunuJa
f) the hyponychium is a thickemxi portion of epidermis under the distal free edge and is continuous '\lith the
germinative layer of the nail bed
Nail Wall
a) folds of epidermis on either side of the nail and covers the nailproximally
b) at the proximal nail fold, the horny layer spreads onto a free surface as the eponychium or cuticle
Nail Groove
a) it is a furrow between the bed and the wall
b) the epidermis loses all of its layers here except the germinative layer, as it continues onto the undersurface
of the nail plate
Afatrixec/Omies
Indications:
a) onychoayptosis (ingrown)
b) onychomycosis (fungus)
c) onychauxis (thickened)
d) onychogryphosis (dystrophic)
e) onychohlysis (separated)
f) incurvated nail
Contraindications:
a) infection
b) vascular compromise
213
Partial Matrixectomy - Chemical
Phenol and Alcohol technique
a) done under local anesthesia and a digital tourniquet
b) ingro\\'n nail border is freed with a spatula or Freer elevator
c) English Anvil splitter is used to split the offending edge
d) the nail spicule is removed
e) matrix area and nail bed are curretted to remove debris
f) the posterior nail fold is curretted to remove any debris
g) phenolization is performed (89"10 pure phenol)
1. protect adjacent tissue with ointment (ie-petroleum jelly; betadine ointment)
2. apply phenol on cotton swab for 30 sec intervals x 3
3. apply alcohol on a cotton swab to wash the phenol
4. dress toe with a dry sterile dressing
Sodium Hydroxide technique
a) descnbed.first by Travers and Ammon in 1980
b) done in a similarfushion as the Phenol & Alcohol technique, but uses NaOH 10% and neutralized. with 5%
acetic acid
c) supposedly is more predictable, high success rate, low recurrence rate and less drainage with fuster healing
time
d) NaOH is applied. anywhere from 3 seconds to 3 minutes until there is visible coagulation of the nail bed
capillaries
e) after care includes soaks with saline and dilute acetic acid for 20 minl3x day for 7-10 days depending on the
drainage
Complications of putial chemical matrixectomies
a) recurrence resulting from:
1. improper application of the chemical
2. not enough currettage
3. dilution of the chemical secondary to bleeding
4. impropoer removal of the nail and matrix segment
b) cyst formation resulting from:
1. unaggressive matrix removal and cautery
2. sand allowed. beneath the posterior nail fold
Thermocautery
a) descnbed by Kobak in 1980
b) done under local anesthesia and a distal tourniquet
c) nail bolder is freed. and offending edge cut with nail splitter
d) the nail spicule is removed. and the nail fold is curretted
e) hand held disposasble cautery loop at temp. of2200 F is used for one or two seconds
f) after care is the same as for Phenol & Alcohol technique
g) advantage = no caustic chemical used with this technique
Electrodessication Partial Matrixectomy
a) described. by Vernon in 1938
b) involved. using electrocautery hyfrecator writ
c) needle ofhyfrecator inserted. under the posterior nail fold
d) the unit is set at 50 and hyfrecation is performed. in intervals of 34 seconds, until all the matrix is destroyed
e) Kerman and K1amus reported this technique to be safe and extremely effective
214
Total and Partial Matrixectomy Procedures
Winograd Partial Matrixectomy
a) described in 1929
b) one-fourth inch of the edge of the
nail along with matrix and nail
bed is removed and auretted
c) done via a linear incision down to
bone
d) a strip of the nail fold is removed
e) margins are undermined and the
incision is closed with suture
Frost Partial Matrixectomy
a)descnbedin 1950
b) a modification of the Winograd
procedure
c) transverse incision for better
visibility of the underlying matrix
d.) initially did not use sutures for
closure
e) follow-up studies on both above
procedures are promising
t) the flap created could cause avascular
necrosis of the tip
g) the technique could be modified by
using a "J"-sbapedincision
Whitney Total Martixectomy (Acisional)
a) first described in 1968
b) a spatula is used to open up the nail
distally. worlring proximally
c) the nail is removed in toto
d.) the posterior nail fold is bluntly
elevated
e) the nail matrix is secured with fon:eps
and removed in toto
t) technique does not provide full
exposure to the nail matrix
215
Whitney Total Matrixectomy
a) descnbed in 1968
b) skin incisions similar in design
to the Frost technique
c) two pamllel incisions are made
and flapped open
d) the nail is removed first and
the matrix fonows
e) the skin incisions are closed
with suture
1) this technique provides good
exposure to the matrix
g) lower recurrence rate compared
to the Acisional technique
Terminal Syme Total Matrixectomy
a) most radical procedure for
dystrophic nails
b) removes the entire nail, nail weill,
and matrix
c) close defect with plantar skin
flap after resecting the distal
half of the distal phalanx
d) acquired the name S}me because of
the plantar flap
e) disadvantages:
shortens the toe
potential slough
creates bulbous terminal stub
Zadik Total Matrixectomy
a) ,",-as first described by Quenu in 1887
b) the operation removes the nail matrix and the nail without shortening the distal phalanx
c) the eponychium is excised and the skin flap is advanced and sutured
d) the procedure should not be done in patients with PVD or uncontrolled diabetes mellitus because of
complications (ie-sloughing of the flap; increaesed risk of infection; de1ayed healing)
e) Kaplan modified this procedure by removing the nail bed completely down to terminal pha1anx
f) Owens modified the Kaplan technique removing the medial and lateral nail borders along with the
entire nail bed
216
HAMMERTOES
Hammertoe
a) most common digital deformity
b) the proximal p h a l a n . ~ is dorsiflexed and the middle pbalanx is plantaIflexed
c) this may buckle the MfP joint and make it prominent pJantarly
d) primarily caused by biomecbanical ma1function
e) shoes play a role in formation
f) long second toe has a tendency to develop hammertoe defonnity
g) may present with heloma occurring at the PlPJ or DlPJ levels
h) radiographically one sees a dorsiflexed proximal pbalanx with flexion of the middle or middle and distal
phalanges; .
-may see a "gun banel" sign
Types of Hammertoes
a) Flexor Stabilization Hammertoe
1. usually occurs in a pronated foot
2. usually in late stance phase of gait
3. pronation causes hypermobility of the forefoot
4. the flexors fire early in gait to stabilize a hypennobile forefoot
5. this causes overpowering of the interosseous muscles leading to hammering or cla\\-ing of digits
6. weak interosseous muscles secondary to a neuroplthy will allow overpowering of the long flexors
7. the most common etiology ofhammertoes
b) Flexor Substitution Hammertoe
1. occurs in the supinated foot
2. occurs in the late stance phase of gait
3. there is strnigbt contracture of all lesser toes
4. usually the triceps are weak
5. deep muscles of the leg try to substitute for the triceps
6. tibialis posterior,Flll., and FDL :fire earlier and longer causing contracture of all lesser digits
7. a high arched foot with contracted digits is the usual presentation
8. the least common etiology of hammertoes
c) Extensor Substitution Hammertoe
1. occurs in swing phase of gait
2. the EDL overpowers the lumbricales
3. see a strnigbt gorsal contracture of the MIP joint
4. occurs during propulsion, swing phase, and heel contact
5. deformity is demonstrated by having the patient dorsiflex the ankle in a non-weigbt bearing situation
6. in anterior pes caws foot type, passive pull on the EDL tendon is created; this causes dorsiflexion at
the MIP joint and passive contracture at the DlPJ by the flexor
7. also occurs in ankle equinus defonnity
8. in peripheral neuropathy and neuromuscular diseases, the lumbricales are affected and the EDL gains
advantage leading to an extensor substitution phenomenon.
CLA WTOE DEFORMITY
Clamoes
a) flexion of the middle and distal phalanges on the proximal phalanx
b) most often involve all the lesser toes including the hallux
c) usually associated with cavus foot and neuromuscular conditions
d) always associated with dorsal contracture of the MIP joint and plantar contracture of the lPJ's
e) often see hyperkeratosis and painful metatarsalgia beneath the metatarsal heads
f) early stages may be flexible and strnigbten out \\-ith the push-up test
217
g) late stages, the interphalangeal joints will flex, when the metatarsals are loaded
h) x-ray findings show dorsiflexed position of the proximal phalanx and plantarllexed position of the middle
and distal phalanges
i) a "gun barrel" sign ",ill be seen on DP radiograph
Mallet Toe
a) distal phalanx is flexed on the middle phalanx
b) no involvement at the PIPJ
c) associated with a long digit
d) extension of the joint is limited
e) difficult to manually reduce if long standing condition
f) x-ray see DIPJ contracture with evident gun barrel sign
g) surgical correction is via resection of the head of the middle phalanx
h) may need to release the plantar contracture "ia tenotomy and capsulotomy
i) splint in corrected alignment for three weeks in surgical shoe
FLOATING TOE
a) a condition in which one or more toes fail to purchase the weight bearing surface in stance phase and
walking
b) caused by a failure of the flexor mechanism to function effectively
c) [normally, weight bearing tenses the flexors and plantar fascia, which stabilize the proximal phalanx on
the metatarsal head; failure of the ray to load results in failure to load that strand of plantar fascia and
flexor cap. Result is unstable toe]
d) other causes include a short metatarsal; brachymetatarsia; iatrogenically short or excessivesly elevated
metatarsals; severe hammertoe or clawtoe deformity, dislocation of the MTP joint
e) important is the loss of the internal cubic content from within the MIP joint; this occurs with plantar
condylectomies.. metatarsal head resections, and with resection of proximal phalangeal base
f) e) correction is aimed at the cause of the floating toe (ie- brachymetatarsia, lengthen the metatarsal; base
of proximal phalanx resection, syndactyly)
g) stabilizing arthrodesis of the PIPJ, K-wire fixation and extensor release
h) surgical correction of floating toe
based on the cause of the floating toe (ie-brachymetatarsia) -ifthe cause is related to chronic adhesive
capsular release along with arthrodesis should be attempted
if the etiology is an elevated lesser metatarsal, then a plantar displacement osteotomy should be
performed
other options for floating toe syndrome include syndactylization and V-Y advancement
1. syndactyIization
salvage procedure secondary to prior surgery
ie-resection of the base of the proximal phalanx with resultant floating toe or floppy toe resection
of metatarsal head with resultant floating toe
loss of toe purchase secondary to iatrogenic causes
contraindications to syndactyIization
infected inter5Jm:e
macerated interspace
third and fourth toe syndactylization is contraindicated since these digits lie in between the lateral and
medial columns (thus, second toe is syndactylized to third toe and fourth toe to fifth toe)
218
2. v-v advancement flap
>a salvage procedure for the correction of iatrogenic floating toe
>produces a digit with no active dorsiflexion or pJantarOexion
>good reported cosmetic result
ARTHROPLASTY (ofPIPJ)
a) indicated for flexIble to semi-rigid digital deformity
b) the digit is 3JOOChed through a linear or incision
c) the incision is aciried through su1:H:utaneous tissue to the level of the EDL tendon
d) a transvesrse tenotomy is made at the level of the PIPJ
e) medial and 1ateral collateral ligaments are incised
f) the extensor tendon is retracted proximally
g) the head of the proximal pha1anx is resected
h) Kelikian push-up test is performed if defonnity is not reduced
sequential release is performed in the following manner:
1. extensor hood resection
2. extensor tendon lengthening
3. dorsal capsulotomy
4. pIantarcapsule release
5. arthrodesis
ARTHRODESIS OF THE LESSER DIGITS
a) converts the toe to a rigid lever
b) indicated where intrinsic muscle stability is compromised:
1. lack: ofMIP joint stability
2. semi-reducible or non-reducible contracture of the IPJ
3. hyperlreratotic lesion overlying the 1P joint
4. transverse plane defonnity of distal aspect of the toe
5. claw toe defonnity
6. abnonnally long toe
7. to neutmlize the long flexors and extensors
c) procedures ..
1. end-fo.end fusion
>done via a standard arthroplasty incision
>IP joint freed from soft tissue attachments
>cartilage from head of proximal phalanx resected along with the base of the middle phalanx
>K-wire driven through mic:klle and distal phalanges (exiting through tip of toe beneath the nail)
>resected smfuces aligned
>K -wire driven across site and stability is checked
>0.045 K-wire can be usedifnot crossingMIP joint
>0'<)62 K-wire can be used if crossing the MIP joint (anything smaller would break)
>main1ain K-\\'1re fixation for weeks
2. peg-in-hole fusion
>most optimum procedure for fusion of a digit
>poduces significant shortening of the digit
>difficult to perform
>dorsal cortex of phalangeal peg left intact to provide stability
219
>good bone stock is needed to perform
>although stable. needs a K-wire fixation
3. spike-in-hole fusion
>same as peg-in-hole fusion, but the proximal phalan.x is fashioned into a spike
>dorsal cortex of phalangeal spike left intact
>no great advantage over the peg-in-hole fusion
CONGENITAL OVERLAPPING FIFTH TOE
a) definition: deformity occurring at the fifth MTP joint
synonyms = overriding fifth toe
hyperextension of the fifth toe
elevated, contracted varus of the fifth toe
digiti quinti vams
b) etiology
1. usually congenital and bilateral
2. less commonly unilateral, traumatic or iatrogenic in nature
3. incidence is equal between males and females
4. three main components of the deformity
>adduction contracture
>dorsiflexion
>external rotation
c) clinical appearance
1. the toe usually appears smaller,
smaller, shortened and
flattened or "plddle shaped"
2. supra-adductus: the fifth toe over
the fourth
3. infra-adductus: the fifth toe under
the fourth
d) deforming forces
1. dorsal and medial skin is usually tight
2. in severe cases,. the skin of the web space can be contracted as well
3. medial coI1ateIallig:ament and
dorsomedial MPJ capsule are
shortened and tight
4. the EDL tendon is contracted
e) conservative treatment
1. usually reserved for children or for deformity that is not longganding
2. stretching and strapping into pIantarflexion and abduction
f) surgical treatment
1. consideration depends upon the age of the pltient and location and severity of the deformity:
>skin pIasty to lengthen dorsal-medial skin
>tenotomy, tendon lengthening or tendon transfer
>dorsal-medial capsulotomy
>ostectomy
>syndactylization of the fourth and fifth toes
>amputation
>a combination of procedures
220
g) historical surgical procedures
1. Anderson: removal of a plantar skin wedge, dorsal V-Y skin pIasty, lengthening of the EDL tendon.
fifth metatarsal head resection. and svndactvlization of the fourth and fifth toes
2. Butler: dorsal raquet incision with a J,tanta; extensor tenotomy and MPJ capsulotomy
3. Duvries: dorsal Z skin plasty, extensor andMPJ capsulotomy
4. Kaplan: plantar skin wedge plasty, extensor tenotomy, dorsal, medial and lateral MPJ capsulotomyand
partial }XOximal phalangectomy
5. Kelikian: syndactylization of the fourth and fifth toes and a proximal phalangectomy
6. Lantzounis: mainly a sagittal plane COIreCtion; it involves an MPJ capsulotomy and a tnmsfer of the
EDL tendon through a drill hole placed through the neck of the fifth metatarsal
7. Lapidus: division of the EDL tendon and transposition to the distal end of the abductor digiti minimi
tendon
8. Wilson: dorsal V-Y skin p1asty and extensor tenotomy and elongation
h) post-operative care
L compresssive dressings
2. observe neurovascular status
3. toe splinted 4-6 weeks to maintain correction
i) complications
1. recurrence
2. dehiscence
3. shortened digit
4. instability of the fifthMPJ
POLYDACTYLY
Definition: presence of an acessory, supernumerary or extra digit
a) very common congenital anomaly
b) may present as a hypoplastic digit without osseous structure or as a fully developed digit
c) can be either preaxial or medial to the second metatarsal (the axis of the foot) or postaxial
d) can form part of a SJ'lldrome or can present as a nonsyndromatic or isolated deformity
Classification
Postaxial polydactyly (fifth digit duplication) according to Temtamy & McKusick:
Type A:. characterized by a fully developed accessory digit that articulates with the fifth metatarsal or a
duplicated :fifth metatarsal
Type B: characterized by an accessory digit without osseous substance
this classification :fuils to address the range of forms between digit devoid of osseous substance and
completely duplicated
digit

;:!
I

II

221
Venn-Watson Classification of postaxial polydactyly
based upon degree of duplication fonn least differentiated to the most differentiated: soft tissue
duplication, wide metatarsal head T -metatarsal, Y -metatarsal and complete duplication
wide met
head
T -metatarsal
Preaxial Polydactyly (first digit duplication)
rarely involves the foot
Y -metatarsal
not well documented compared with preaxial polydactyly of the hand
Temtamy & McKusick classified four types in the hand
Type I - polydactyly of the first digit
Type 2 - polydactyly of a triphalangeal first digit
Type 3 - polydactyly of a second digit
Type 4 - polysyndactyly
Blauth & Olsson Classification (1988)
classification according to radiomorphologic alteIations
based upon position of duplication on both the longitudinal and transverse planes
complete
duplication
a) longitudinal: arrangement is blsaed on the duplication of a phalanx or ray from distal to proximal
and is subdivided into five types:
distal phalanx
middle phalanx
proximal phalanx
metatarsal
tarsal
b) transverse: arrangement indicates the number of duplicated rays which are then numbered with
Roman numerals medially to latern11y
permits classification of the hand and foot
accounts for special malfonnations, such as triphaJangism and multiple duplications
aids in accwate diagnosis and in developement of a surgical plan
222

PREDISLOCATION SYNDROME (Lesser MTPJ Instability)
Descriptive:
Patients usually middle age 30-50
Acute/subacute pain plantar mtpj(2
nd
most common)
Pain disproportionate to physical findings
History of increased activity, trauma, steroid injection
Sharp pain, bruise, throbbing
Gmpe-size lump beneath mtpj (bursal sac)
Stages: (not used clinically)
I. mild edema, tenderness plantar/distal joint, no change in alignment
II. moderate edema
ID. clinical deviation of digit, loss of toe purchase '''lith weight-bearing
Differential DX:
stress fracture
synovitislcapsulitis
hammertoe neuroma
metatarsalgia
Imaging:
X-ray findings
long 2nd met
altered MfPJ congruity
+ dIaw sign (vertical stress test)
1. stabilize met
hypertropbic
cortex of
involved met 2. hold prox phal parallel to met
3. translocate digit in sagittal plane
greater than 500/0=p0sitive test
Bone &an
MRl
inc. uptake in angiogram phase indicating inflammatory process
l.edema along distal slip of plantar fascia
2. thickening of plantar plate or rupture visible
3 .capsulosynovial joint effusion
Conservative Therapy:
Surgery
60-90% relief
reduce pain
stop progression
Splint/strapping
Metatarsal splint pad
Cross-ever tape method
Stabilize prox phalanx in plantar direction
Can be used as a diagnostic tool
Medrol dose packlNSAID
ultrasound, whirlpool
flexor tendon transfer
"z" lengthening ofEDL
extensor hood recession
total MTPJ capsulotomy
K-wire fixation in overcorrection
PrimaIy plantar plate repair from plantar incision
**Both the Weil and Helal osteotomy aJ
utilized to shorten the metatarsal and to aIlo'
joint decompression
Weil osteotomy (oblique at metatarsal neck from plantar-proximal to dorsal-distaI)
Helal osteotomy (oblique at metatarsal neck from dorsal-proximal to plantar distal)
Post -op splint to maintain correction
223
BRACHYMETATARSIA
Def"mition:
A short, hypoplastic metatarsal due to premature closure of the epiphyseal plate; when more than
one metatarsal is involved the condition is called brach)'metopody
Etiology:
congenital
developmental
iatrogenic
traumatic
Associated congenital anomalies:
- Down's Syndrome
- Turner's Syndrome
- sickle cell anemia
- dystrophic dwarfism
Characteristics:
unilateral or bilateral
25: I female to male ratio
4th metatarsal most common
- Albright's Congenital Osteodystrophy
- pseudohypothyroidism I pseudo-pseudohypoth)TOidism
- poliomyelitis
- myositis ossificans
usually becomes evident between ages 4-15
Clinical presentation:
short, contracted toe seen clinically
short metatarsal seen radiographically
cosmetic or psychological concern
metatarsalgia blc increased load to adjacent metatarsals
plantar callus formation
floating toe of associated affected metatarsal
overlapping toe causes:
extensor & flexor tendon contIactures
skin contracture
Conservative Treatment:
orthotics or accomadative devices
padding
Surgical Treatment ~ Soft Tissues
V -y skin plasty to relieve tension of contracted skin
Z-plasty lengthening of long extensor tendon
tenotomy of short extensor tendon
MIPJ capsulotomy (dorsal, medial, lateral release)
sectioning of deep transverse intermetatarsalligament
Surgical Treatment ~ Osseous
1. Osteotomy lengthening procedures (many options to restore metatarsal parabola):
I. single metatarsal osteotomy with insertion of bone graft
2. combined lengthening and shortening metatarsal osteotomies
3. slide lengthening metatarsal osteotomies
224
Complications of osteotomy lengthening:
lengthening too aggressive -+ neurovascular compromise
lesser MlPJ limitus
delayed union I nonunoin
resorption I collapse of bone graft
2. Callus Distraction (Callastosis)
Description
Technique in which bone lengthening can be achieved by slow distraction of the bone callus that forms
at the open ends of a surgically osteotomized bone.
First performed by llizarov on lower extremities using a circular external fixator device.
Based on the law oftension-sttess
Procedure
Advantages
living tissue when distracted slowly becomes metabolically active
anatomical dissection to the level ofbone
incision and reflection of periosteum
osteotomy or corticotomy -+ initiates callus formation
= osteotomy - through and through cut of bone
= corticotomy - cut ortex only to maintain endosteum
-+ studies show equal success with either technique
placement of external fixation device
latency period - time between osteotomy/corticotomy and distraction
= varies with each bone and patient age
= optimal latency 5 days to 2 weeks
rate of distraction (also varies with bone and patient age)
= 1 mmlday in 4 equal increments
= according to llizarov for tibial lengthening
distraction stopped when desired length is achieved
period of ossification at distraction site
fixation left in place until rndiographic evidence of osseous union
no need for bone graft
no neurovascular compromise because all structures are gradually lengthened
can gain more length than other bone lengthening procedures
can gradually lengthen soft tissue structures (tendons, skin)
Disadvantages
pin tract infections
need compliant patient
IndicationsIUses
brachymetatarsia
callus distraction Evans procedure for pes piano valgus
lengthening of medial cuneiform for metadductus
tibial lengthening or correction of angular deformity
Callus Distraction Procedure for Brachymetatarsia
longitudinal incision over affected metatarsal
anatomic dissection to level of bone
linear periosteal incision placement of external fixator pins
= 2 proximal to osteotomy (1 in cuboid or cuneiform; 1 in metatarsal)
= 2 distal to osteotomy
osteotomy/corticotomy
closure of periosteum and anatomic layers
225
placement of external fixator device (EBITM M-IOO mini external fixator most common)
begin distraction 5-14 days post-operatively
tum device ~ tum 2-3 times per day (.5 - .75 mm total length gain per day)
serial mdiogmphs - will see mdiolucent gap at distmction location
nonweightbearing recommended
osseous consolidation - then remove external fixator
LESSER METATARSAL SURGERY
Historical Review
1916 - Meisenbach: osteotomy 3 em proximal to MIP joint
1917 - Davis: metatarsal head resection
1940 -Man: resectionoftmpezoidal wedge
1948 - Borggeve: same as Mau, except performed distal
1952 - McKeever. subcapital osteotomy; telescoped, spiked end of shaft into capital piece; shortening
osteotomy
1953 -DuVries: pJantarcondylectomy
1954 - Giannestras: step-down shortening osteotomy
1954 - Rutledge & Green: removal of metatarsal head and one-tbird of the shaft
1 %5 - DuVries: metatarsal head arthroplasty and plantar condylectomy
1 %9 - Addante: osteoclasis 90 degrees to the shaft
1%9 - Wolf: dorsifle..xory osteotomy on distal metatarsal shaft
1971 - Scarlato: dorsiflexoty base wedge osteotomy or elevational osteotomy procedure
1973 - Jacoby: classic "V" osteotomy
226
Neck osteotomies (most commonly performed osteotomies for isolated tylomas)
a) V-osteotomy
1. Jacoby described the procedure
2. allows :free motion in the sagittal plane, but stable in the transverse pIane due to "wings"
b) Osteoclasis
1. performed at the level of the metaphyseal neck
2. free motion in sagittal and tIansverse planes
3. bigh incidence of pseudoarthrosis and nonunion
c) PMO (percutaneous metaphyseal osteotomy)
1. transverse osteotomy through the head. of the metatarsal
2. instability and heaIing problems similar to osteoclasis
d) DFWO (dorsifiexory wedge osteotomy)
popu1ar procedure that has spawned many similar procedures
e) V-wedge
1. also known as the Bartel wedge
2. more oblique wedge than DFWO, allowing for increased bone-to-bone contact
Shortening osteotomies (wilen tyloma may be secondary to an elongated, rather than a pJantarflexed metatarsal)
a) cylindrical osteotomies: through and through osteotomy with removal of the wedge
b) Chevron osteotomy: similar to Jacoby wxcept a second "V" cut is made proximal and the wedge is
removed
Basal osteotomies
a) EO (extensor osteotomy)
1. similar to the DFWO but done 1-2 em distal to the meIatarsal<Uneiformjoint
2. usually perfOImed to relieve an isolated IPK
b) EOA (extensor osteoarthrotomy)
same indications as the extensor osteotomy except that it is used when stabilization of the metatarsal-
cuneiform joint is desired
c) Buckholz osteotomy
1. similar indications as the above basal osteotomies
2. more oblique and proximally located apex than the extensor osteotomies descnbed above
3. the greater obliquity allows pJacement of a 2.7 mm cortical screw for fixation
4. most stable
The California (left coast) approach
Principles
a) perform surgery on only first, third and fifth metatarsals
b) will peIform smgery on all subtne:latat"W lesions
c) no surgery on second and fourth metatarsals
Philosophy
a) first and fifth metatarsals have independent axis of motion (triplanar), and thus, have significant influence
on the second and fourth metatarsals
b) the third metatarsal is the most independent ofbiomechanical and other metatarsal influence
c) arthrodesis or arthropJasty of the second and fourth digits to remove retrograde plantarfiexory forces
Surgical treatment
a) submet 2 lesion
1. address first metatarsasl deformity (HA V, hypermobility, sagittal plane position)
2. arthrodesis or arthropJasty second digit (remove retrograde force at the second MP])
b) submet 4 lesion
1. address fifth metatarsal deformity (Tailor's bunion, hypermobility, adducted fifth digit)
2. arthrodesis or artbrop1asty fourth digit (remove retrogI3de force at the fourth MP])
227
c) submet 3 lesion
1. usually due to long third metatarsal or iatrogenic transfer lesion
2. can perfonn appropriate metatarsal procedure
To Float or to Fix?
Floating philosophy
a) metatarsal will find its own level
b) weight bearing and soft. tissue binding (fibrosis) will pro"ide appropriate and stable level
c) decrease chance of transfer lesion
FL'I:3tion philosophy
a) why guess? can place metatarsal at desired location
b) difficult
c) prevent nonunion, pseudoarthrosis, etc
TAll.,ORtS BUNION
Introduction
predilection of Tailor's bunion occurs in 2: I female to male ratio
Types
six osseous pathoanatomical types of Tailor's bunion have been described:
a) rotation of the lateral plantar tubercle into a lateral position
b) increased intermetatarsal angle
c) increased lateral deviation angle
d) a large round dumbbell-shaped fifth metatarsal head
e) arthritic changes rresulting in exostosis fonnation at the fifth metatarsophalangeal joint
f) any combination of the above conkditions with the first three being the most common
Etiol0R.v (as described by Root)
a) abnormal STJ pronation
b) uncompensated forefoot or rearfoot varus with a pronating foot
c) congenital plantarflexed fifth ray
d) congenital dorsiflexed fifth ray
e) idiopathic condition caused by absence of transverse head of the adductor hallucis into the fifth MIP joint
Radiographic Evaluation
Intermetatarsa1 Angle: Buckholz & Fallat method, which takes into consideration the lateral bowing present
within the fifth metatarsal
a) represented by the angle between formed between two lines -
>line drawn aqjacaent and parallel to the medial proximal surface of the fifth metatarsal shaft
>line bisecting the long axis of the fourth metatarsal shaft
b) normal value is 6.47 degrees
c) pathological value is 8.71 degrees (bunion defonnity)
Lateral Deviation Angle: Buckholz & Fallat method, which takes into consideration the lateral bowing within
the fifth metatarsal
a) represented by the angle formed between two Iines -
>line bisecting the head and neck of the fifth metatarsal at the articular surface
>line drawn adjacent and}malleI to the medial proximal surface of the :fifth metatarsal shaft
b) normal value is 2.64 degrees
c) pathological value is 8.05 degrees
228
c) submet 3 lesion
1. usually due to long third metatarsal or iatrogenic transfer lesion
2. can perfonn appropriate metatarsal procedure
To Float or to Fix?
Floating philosophy
a) metatarsal will find its own level
b) weight bearing and soft. tissue binding (fibrosis) will provide appropriate and stable level
c) decrease chance of transfer lesion
Fixation philosophy
a) why guess? can place metatarsal at desired location
b) difficult
c) prevent nonunion, pseudoarthrosis etc
TAU,OR'S BUNION
Introduction
predilection of Tailor's bunion occurs in 2:1 female to male ratio
Types
six osseous pathoanatomical types of Tailor's bunion have been described:
a) rotation of the lateral plantar tubercle into a lateraI position
b) increased intermetatarsal angle
c) increased lateral deviation angle
d) a large round dumbbell-shaped fifth metatarsal head
e) arthritic changes rresulting in exostosis fonnation at the fifth metatarsophalangeal joint
f) any combination of the above conkditions with the first three being the most common
Etiology (as described by Root)
a) abnonnal STJ pronation
b) uncompensated forefoot or rearfoot varus with a pronating foot
c) congenital plantarflexed fifth ray
d) congenital dorsiflexed fifth ray
e) idiopathic condition caused by absence of transverse head of the adductor hallucis into the fifth MIP joint
Radiographic Evaluation
Intennetatarsal Angle: Buckholz & Fallat method, which takes into consideration the lateral bowing present
\Vithin the fifth metatarsal
a) represented by the angle between fonned between two lines -
>line drawn adjacaent and parallel to the medial proximal surface of the fifth metatarsal shaft
>line bisecting the long axis of the fourth metatarsal shaft
b) nonnal value is 6.47 degrees
c) pathological value is 8.71 degrees (bunion defonnity)
Lateral Deviation Angle: Buckholz & Fallat method, which takes into consideration the lateral bowing ,,;thin
the fifth metatarsal
a) represented by the angle fonned between two lines -
>line bisecting the head and neck of the fifth metatarsal at the articular surface
>line drawn aljacent and parallel to the medial proximal surface of the :fifth metatarsal shaft
b) nonnal value is 2.64 degrees
c) pathological value is 8.05 degrees
228
Intermetatarsal Angle Lateral Deviation Angle
Historical Review
1949 - Harris & Davis: first to descnbe "bunionette" deformity
proposed simple lateral condylectomy
1951 - Hohman: transverse osteotomy of metatarsasl neck without fixation
1953 - Dixon: prominent fifth metatarsasl head due to splaying
treatment consisted of wearing "ider shoe or excision lateral condyle and bursa
1956 - Leliever: felt Tailor's bunion was due to three mecbansims
1. supernumerary bone
2. increased intermetatarsal angle
3. cross-legged sitting position (tailor's)
1959 - Brown: fifth digit and metatarsal resection to narrow foot
1959 - Do Vries: bunion due to three reasons and recommended lateral condylectomy
1. hypertrophy of soft tissue overlying metatarsal head
2. congenitally wide fifth metataI5al head
3. lateral bo'wing of the fifth metatarsal
1961 - Ambrey: lateral condylectomy or metatarsal head resection if a submet lesion existed
1969 - Yaney: base osteotomky to decrease the 1M angle and head remodeling
1971 - Sgarlatto: talked about lateral bowing of fifth metatarsal
1971 - GeIbert: base wedge osteotomy using binge axis
1974 - Leach & Igou: reverse Mitchell
1974 - Rapapport: base wedge osteotomy and arthroplasties
Surgical Approach
based upon radiographic rersults from 1M and lagteral deviation angles
a) high 1M angle: procedure should be some type ofbasal osteotomy
b) nonnal 1M and high lateral deviation angle: procedure should be an osteotomy at the metatarsal neck
c) all nonnal angles: if tailor's bunion is present, then resection of the lateral surfuce of the fifth metatarsal
head is performed
d) surgical procednres:
1. ostectomy
2. reverse Hohman
3. reverse Wilson
4. reverse Austin
5. reverse Offset-V
6. adductory rose wedge
osteotomy
7. fifth metatarsal head
resection
8. joint arthroplasty
229
IMPLANTS
Indications:
a) eliminate pain
b) regain or retain motion spacer)
c) correct deformity
Historv:
a) 1962 - Seeburger
1) used durallium for his hemi 1
st
MIPJ implant
2) functioned to cover a necrotic 1
st
metatarsal head
b) 1965 - Downey
1 ) total (ball and socket)
c) 1973 - Sutter
1) double barrel stem with an external dacron mesh jacket
d) 1974 - Feder and Feder
1) ulnar head prosthesis used at 1 s[ metatarsal head
2) madeofsilicone
3) repeated by Karp ('74) and Freed ('79)
e) 1978 - Calman-Nicolle
1) total implant made of polypropylene
2) hinged in the middle with an arm into metatarsal and phalanx
f) 1982 - Swanson
1) total finger implant design made of silicone
2) dacron mesh impregnated into prosthesis
3) redesigned an earlier version of a total finger implant by Neibauer and Cutter
h) 1983 - Sgarlatto
1) used at the PIPJ and DIP! for hammertoe deformity
BiomateriaIs:
a) stainless steel
1) may cause resorption of bone
2) steel may corrode
b) Silicone
1) low elastic modulus (returns to normal form after a physiologic load)
2) does not have potential for corrosion
3) soft tissue response (fixation by encapsulation)
4) may cause detritus synovitis (chard of silicone in synovium causes chronic inflammation)
5) bone response
c) pol)'methylmethacrylate
1) bone cement used to hold implants in place
2) exothermic reaction while mixing may cause A VN
d) titanium, cobalt, polyethylene
Implant design I function:
a) hemi - Y2 of the joint
1) indication is arthritis on one side of joint
2) Swanson great toe - concave head with a long stem
3) Weil modification great toe - 15 degree DASA to compensate for abnormally high
PASA; shorter, tapered stem
230
4) Sutter - with or without internal or external dacron mesh
5) Titanium - biocompatable; titanium oxide coating resists corrosion
6) Implant should be wider than stump of remaining bone
b) total - both sides of joint
1) one component total
+ Swanson - central "U" hinge with opening dorsally; no angulation
+ Sutter - proximal stem angled 15 degree dorsally to accommodate for metatarsal
declination angle -7 LaPorta
- neutral or 15 degree angle with plantar angle on distal side-? Lawrence
+ Sgarlatto similar to Swanson
2) two component totals
+ Koenig - ti1anium proximally (plantar lip replaces metatarsal condyles);
polyethylene distally; NO transverse stability
+ Bioaction & Kinetic - metatarsal component = cobalt chrome; pba1angea1
component = ti1anium with polyethylene covering; NO transverse stability
231
Host Response:
a) materials must be biochemically inert, durable, non-irritating, non-toxic, hypoallergenic, non-
carginogenic, non-pyogenic, and handle physiologic stress
Indications:
a) hallux valgus with subluxation, hallux rigidus (should not be used as sole procedure if IM angle is
greater than 14 degrees)
b) revisional surgery
c) rheumatoid, DID, gout
d) osteochondral fracture. intra-articular fracture
e) hammertoe, cIa-wtoe, mallet toe
Surgical Technique:
a) maintain length of metatarsal and proximal phalan:x
b) all require some reaming of the medullary canal
c) maintain capsular integrity
Radiographic Analysis:
a) check: alignment and position in the medullary canal
b) the initial x-ray may show some separation between implant and bone
1) normal until the 3
rd
month
Complications:
a) material failure
1) intrinsic (metatarsal head irregularities, stress fractures)
2) extrinsic (eccentric placement, inadequate bone resection, or soft tissue release)
b) microfragmentation
I) initial abrasion of stem during implantation
2) head abrasion at bone/implant interface -7 grommet used as Cl D CQJ
metal interface to protect implant from being eroded by 0
bone .. '
c) juxta-articular bone cysts
d) frozen toe
1) due to proliferation of bone secondary to DID
e) intramedullary fibrous hyperplasia
1) secondary to aseptic necrosis from enlarged metatarsal head or proximal phalanx base
f) infection
1) acute (40010 of infections) within 5-7 days to a month post op
+ contamination during surgery
+ hematogenons spread
+ contiguous spread from hematoma, sutures, etc.
2) delayed & late (60% of infections) within 1 month to 2 years post op
+ "time lapse" effect -7 bacteria enter at time of surgery and proliferate when
the environment is optimal
3) treatment
+ removal of implant
+ synovectomy
+ bone grafting of cysts
+ fusion of joint ( dramatically shortens toe)
+ prophylactic antibiotics -7 staph. epi.
+ vancomycin
+clindamycin
232
LOWER EXTREMITY AMPUTATIONS
I. General Concepts
A Disarticulations - done in children because it preserves the epiphyseal plate allowing full limb
growth
B. Amputation length - in general the longer, the better both physically and mentally
C. Gait velocities decrease with more proximal amputations
D. Complications are the rule with difficulties in healing, prosthesis fitting, rehabilitation, and
possible additional amputations
II. Indications for Amputations
A. Trauma (crushing, mutilating)
B. Malignant neoplasia
C. Uncontrollable infections
D. Arterial vascular diseases leading to gangrene
E. Severe deformities (non reconstructable)
III. Amputation Statistics
A. 33% of patients having unilateral amputation \\-iIl have the contralateral limb amputated after
3 years
B. 33% survival rate 5 years post-op Below Knee Amputation
IV. Lower Extremity Amputations
A Hemipelvectomy (malignancies and failed Above Knee Amputations)
B. Hip Disarticulation (malignancies and failed Above Knee Amputations)
C. Above Knee Amputation (AKA)
D. Knee Disarticulation
E. Below Knee Amputation (BKA)
F. Proximal Symes Amputation
G. Pirogoff Amputation
H. Chopart Disarticulation
I. Lis Franc Disarticulation
J. Tenninal Symes Amputation
K. Ray Resection
L. Transmetatarsal Amputation (IMA)
M. Digital Amputation
N. Guillotine (open amputation at any level which requires granulation or delayed surgical
closure)
IV. Principles of Amputation
A. site must withstand friction from prosthesis I shoes which makes plantar skin more ideal for
weightbearing flaps
B. scars should not adhere to bone
C. avoid unnecessary procedures to improve cosmetic outcome
D. tendon balancing
E. amputation site should be free from cellulitis, lymphangitis, and edema
F. flaps should be under no I minimal tension
G. adequate hemostasis to avoid a pabulum
v. Proximal Symes Amputation
A. total foot amputation that may be used in healthy patients \\-ith severe foot trauma
B. medial and lateral malleoli are resected
C. preservation of the calcaneal fat pad as a posterior I plantar flap to use for weight bearing
surface
D. dog ears are revised at second stage of procedure to prevent ulceration
E. high rate of complications with prosthetic fitting and distal ulceration
233
VI. Pirogoff Amputation
A modification of proximal Symes that preserves the calcaneus for length of limb
B. fusion between calcaneus and tibia
C. high rate of complications with fusion and prosthetic fitting
VII. Chopart Disarticulation
A preserves a long plantar flap if needed
B. high complication rate, especially equinovarus deformity (TAL or achilles tenotomy
recommended)
C. prosthesis recommended
VIII. Lis Franc Disarticulation
A preserves a long plantar flap if needed
B. medium complication mte, especially equinovarus deformity (TAL or achilles tenotomy
recommended)
C. prosthesis recommended
D. do not leave articular cartilage and plane remaining uneven joint surfaces because uneven
cartilage surface at incision site delays healing and can lead to pressure points
IX. Transmetatarsal Amputation
A Most commonly used proximal foot amputation
B. metatarsals transected at dista1113 in a smooth parabola with the second being the longest,.
and the cuts of the metatarsals should be angled distal-dorsal to proximal-plantar with
metatarsall angled proximal-medial to distal-lateral, and metatarsal 5 angled proximal-lateral
to distal-medial
C. must have long plantar flap
D. ankle foot orthosis (AFO) and custom molded shoes with toe filler and rocker bottom are very
beneficial in rehabilitation
E. low complication mte (TAL or achilles tenotomy and possible anterior tibial tendon transfer
to lateral stump for tendon balancing
X. Terminaf Symes Amputation
A removal of all or part of a toe
B. flaps used for closure
1. fish mouth (mostly done on hallux)
2. long plantar
3. side to side
4. racquet
C. remove cartilage (receives its' nourishment from synovium) if disarticulating
234
INTERMETATARSAL NEUROMA
aka Morton's Neuroma
" ... a peculiar and painful affection of the foot"
- Thomas G. Mortoo 1876
HISTORY
1845
1876
1883
Durlacher. L
Morton, TG
HoadIey,AE
Original description of disease
Etiology: Compression oflateral plantar nerve between '" & 5
th
Metatarsal
heads; recommended surgical excision ~ r '" me/head
First to excise third interdigital nerve
1897 Jones & Tubby Etiology: A communicating branch blw medial and lateral plantar nerves was
compressed hili' the '" metatarsal head and the ground
Etiology: Secondary to stretching of r & '" interdigital nerves under deep
transverse inJennetatarsalligament; also :r interdigitai nerve is larger
because of additional fibers from lateral plantar nerve rommunicating branch
Etiology: Ischemic origin to nen>e lesion
1940
1948
1951
Betts, W
Nissen,Kl
Mulder,JD Etiology: Weakness of the transverse arch of the forefoot results in
hypennobility of the metatarsals alJowing the interdigital nerves to become
imtated and inflamed with jib1'QUS
1963 Kopel/& Etiology: Entrapment neuropathy of the interdigital nerve secondary to trauma
Thompson
PATHOGENESIS
~ Truly unknown?
~ Most likely etiology is an entrapment neuropathy secondary to stretching and irritation of the
interdigital nerve as it passes under inferior to the deep transverse intermetatarsailigament with
repetitive dorsiflexion at MTPJ during ambulation
HISTOPATHOLOGY
The term "neuroma" is a misnomer, it is not a tumor or mass out growing from a nerve
~ Sclerosis and edema of epineurium
~ Thickening and hyalinization of endothelial vessels in and around the nerve
~ Thickening and fibrosiS of epi-.peri-, and endoneurium
~ Demyelinization of nen'e fibers
DIFFERENTIAL DIAGNOSIS

Abnonnal Metatarsal Parabola

Metatarsus Proximus

Freiberg's Infarction

Vascular Ischemia

Plantar Fat Pad Atrophy

Hypennobile Metatarsals

Capsulitis

Ganglion c.yst

MFP Joint Synovitis

Occult Fracture

Tarsal Tunnel Syndrome
CLINICAL EVALUATION
Presentation characteristics
~ FemaleMale
~ Third to seventh decade

Neuritis

Epitheloid C.VSl

Rheumatoid Nodule

Radiculopthy

Synovial Cyst
~ Most common interspace involved is the 3rd, closely followed by 2nd
~ First and fourth interspace are rare

Traumatic Bursitis

Foreign Body

Metatarsal Stress Fracture

Pre-Dislocation Syndrome (PDS)
~ Multiple interspace involvement rare <4% (Thompson & Deland, FAI, Jan 1993)
235
Gradual onset of symptoms present many months prior to office visit
)- Symptoms
y Forefoot burning pain
);. Aggravated 7th ambulation, squatting, and tight shoe gear
y Sharp stabbing pain
Pain radiating to involved digits
y Reliefby rest and massage
Signs
y
,. Reproducible pain with lateral compression of forefoot
y Sullivan's sign (Splaying of digits)
y Pain between and just proximal to metatarsal heads
Palpable intermetatarsai mass
y Alulder's Click
ADmCTIVE CLINICAL MEASURES
1. R.adiograpIry
To RIO osseous or arthritic pathology
2. Magnetic resonance imoging (MRl)
Best seen on TJ -weighted images as focal area of decreased signal intensify
Good for determining extent of lesion
3. UlJrasonography (US)
Rely on ability to interpreter
Up to 98% sensitive
4. Electromyograph (EMG)/ Nerve tXlnducIion velocity (NCV)
Not routine diagnostic procedures
Used for atypical presentation
RIO more proximal neural pathology
CONSERVATIVE TREATMENTS
Y Provides good temporary relief of symptoms in 20-50010 cases
Y Generally poor long-term effectiveness
1. Diagnostic local anesthetic block to interdigiml space
2. Wide-toe shoe box
3. Padding and/or strapping ("Cookie pad")
4. Orthotics
5. Physical therapy
6. Ionophoresis, phonophoresis
7. Metatarsal bar
8. Corticosteroid injection(s)
Y SURGICAL TREATMENT
, Offers best def"mitive treatment
Y Effective in 70-100% of cases in the literature
Incisional Approach
1. Dorsal
A Longitudinal (McKeever 1952)
Provides good exposure to interdi.gital nerve
Y Avoids weight bearing scar
Approx. 3 em incision bIw metatarsal heads
Y Transect deep transverse intermetatarsalligament (DTIL)
236
B. Web-space (McElvenny 1943)
~ Incision through the web-space extending 1-2cm dorsally
~ Proximal exposure can be difficult
~ Allows for early weight-bearing
~ Avoids weight bearing scar
2. Plantar
Use large gauge suture
A Longitudinal (Hoadley 1893)
~ Approx. 3cm incision bisecting metatarsal beads
~ Nerve is very superficial from this approach therefore, excellent visualization of
nerve
Less dissection
~ Preserve DTIL
~

Can transect nerve more proximal
No residual dead Space therefore, decreasing
opportunity for hematoma fonnation
~ Best approach for "re-do neuroma" or "stump neuroma"
B. Transverse (Nissen 1948)
Procetb,,es:
~ 2-3cm curvilinear incision over interspace(s) just proximal to plantar digital sulcus
~ Option for multiple interspace neuroma
~ Less potential for hypertrophic scar formation vs. longitudinal
~ More potential to disrupt plantar fat pad
~ Increased risk of compromising perpendicu1ar uaversing superficial neurovascular
1. Neurectomy
~ Excision of the interdigital nerve and its concomitant branches
~ Most commonly peIformed surgical procedure
~ Dorsal or plantar approach
~ Identify and expose all nerve branches prior to resection
~ 80-85% good results
2. Epineurolysis
~ InteIdigital nerve is freed form surrounding soft tissue structures, without excision of
. nerve
DTIL: (a) remains intact, (b)is 1Iansected or (c) is transected and repaired
~ Preserves sensation to the interdigital space
~ Addresses etiology of entrapment neuropathy
~ Results:
~

Dellon . A- trQ1lsected DTIL; 80% complete relief
Guthier, G- ttansected DTIL; 83% excellent, 14% improved
~
exceHent
POST -OPERATIVE COURSE
~ Compressive dressing
Diebold et aI.- follow-up Dl1L released; 92.5%
~ Use of a drain may be considered with excessive bleeding
~ Ice QI1.d elevation for 72 hours
~ Pain medication
~ Parliai weight bearing to heel with crutches in surgical shoe
~ Suture removal 2 weeks dorsal incision and 3 weeks plantar
~ Return to regular shoe gear at 2-3 weeks
237
POST-OP COMPLICATIONS
y Hematoma
);> Stump neuroma (with neurectomy)
y Recurrence (with epineurolysis)
yEdema
y Digi tal contracture
~ Wrong interspace addressed
);> Hypesthesia
ALTERNATIVE TREATMENTS
~ Incisional scar
y Wound dehiscence
y Injection
y Hyperkeratotic lesion
y Paresthesia
~ Anesthesia
y S7dn sloughing
1. C02 LASER
2. Endoscopic decompression for intermetatarsal neuroma (EDIN)
y Described by Barrett & Pignetti JFAS 1994
3. Cryogenic denervation
4. Percutaneous electrcoagulation
RECURRENCE
y Rate is approximent(v 20%
~ Eti%gv
Wrong diagnosiS
Wrong interspace
Poor surgical technique
Failure to divide the transverse metatarsal ligament
Incomplete removal
Transect common plantar digital nen'e too distal
., Treatment
y Conservative- same as original, but more likely to fail
>- Surgical- resection of nerve or stump
Mann and Reyno/ds- 81 I)/{)()j pis. had seventy-jive to one hundred percent relief
238
ANATOMY OF THE FIRST METATARSAL PHALANGEAL JOINT
Ligaments (9)
1. medial sagittal hood
2. Iateral sagittal hood
3. medial sesamoidal
4. Iateral sesamoidal
5. intersesamoidal
6. medial col1ateral
7. Iateral collateIal
8. plantar fuscia (slip inserts into Iateral sesamoid)
9. transverse metatarsal ligament
Sesamoids
a) two in number
b) artiaJ1ate in the grooved smface of the
first meIafaISal head
c) crista of the first metatarsal head
separntes the two bones
d) fibrous pJantar pad anchors each
11 sesamoid to base of proximal phalanx
e) held securely in place by medial
sesamoidal, intersesamoidal, lateral
sesamoidal ligaments and the plantar
filscia
f) muscles and ligaments of the sesamoid
complex:
Musdes(7)
1. extensor hallucis longus
2. extensor hallucis brevis
3. abductorhallucis
4. adductor hallucis (combined insertion)
5. (2) flexor hallucis brevis (medial and
1ateral heads)
6. fle.xor hallucis longus - as it travels
through the groove of sesamoids
7. Extensor Capsu1aris
(the ligament splits into superior and inferior slips; this accommodates the adductor hallucis
tendon to insertion at base of the proximal phalanx)
239
BLOOD SUPPLY TO THE FIRST RAY
1. dorsalis pedis artery
2. ttansverse plantar arterial arc
3. first plantar metatarsal artery
4. first dorsal metatarsal artery
5. branches of the first dorsal metatarsal artery
6. medial division branch of the first plantar metatarsal artery
7. 1ateral division branch of the first plantar metatarsal artery
8. hallucal branch - medial plantar artery fOIming cruciate anastomosis
9. cruciate anastomosis
1) medial branch of the first plantar metatarsal artery
2) lateral branch of the first plantar metatarsal artery
3) hallucal branch from medial plantar artery
4) first plantar metatarsal artery
10. descending portion of the first dorsal metatarsal artery
11. common plantar haIlucal artery
12. medial and 1ateIal hallucal arteries with transverse anastomotic branch
13. transverse anastomotic branch
14. collateral arteries of the second toe

.ll-T--............,;.


l'-----4---Hi---T.V



240
-"- ... .. ... --
)
BUNION SURGERY
RADIOWGY OF THE FIRST RAY
Metatarsus AMJdns Angle
a) measumd on a DP view
b) formed by a line perpendicular
to the bisection of the lesser
tarsus and a line Jepresenring
the lesser metataISus
c) the lesser metataISus is represen1ed
by the bisection of the dorsal
longitudinal axis of the shaft of
the second meIatarsal
d) the normal metatarsus adductus
angle is 15
e) as the foot becomes more adducted,
this angle increases and a greater
chance exists for abductus deformi1;r
at the first MIP joint
Metatarsal Prolusion Distance
a) measured on a DP view
b) Iepleseuts the distance between two art:S
and demonsttates the length between
the first and second metatarsals
c) a positive millimeter distance is used to
indicate that the first metatarsal is
longer than the second metatarsal
d) a negative millimeter distance is used to
indicate that the first metatarsal
is shorter than the second metatarsal
e) normal range of the metatarsal protrusion
dist;lJJre is +/- 2 mm
f) ideally, the length of the first metatarsal
should be about the length of the tbiId
metatarsal
Metatarsal Split Distance
a) measures the split between the first
and second metatarsals
b) measured from the most lateIal aspect of
the first metatarsal base to the medial
cortex of the second metatarsal
c) measurement must be made parallel to the
bisection of the second metatarsal
d) 2 mm or greater is significant
e) important in evaluating soft tissue
deforming forces at the metatarsal-
ameiformjoint
241
)
Proximal Articular Set Angle
a) fonned by a line drawn perpendicular
to effective articular cartilage
of the head of the first metatarsal
and line representing 10ngibJdjnaJ
bisection of the first metatarsaI
b) if the angle measured is greater than
7.5 adaptive changes have
taken place at the first metatarsal
head, which indicates a structural
adaptation of the articular cartilage
c) this indicates a structural deformity
and not a positional one
Distal Articular Set Angle
a) on a DP view, it is formed by a line
drawn perpendicular to the effective
articular cartilage of the base of the
proximal phalanx
b) represents structUIal adaptation of the
base of proximal phalanx on the shaft
c) abnormal Jateral epiphyseal closure at
the base of the proximal phalanx,
which causes more gIO\\th medially
with a resulting bowing of the s.baft
may alter this angle
First Metatarsophalang Joint Position
a) the joint position on a DP view is a comparison of lines representing the effective articular cartilage of the first
metatarsal head and a line Ieplesenting the effective articular cartilage at the base of the proximal phalanx
congruent joint:
a joint is said to be congruent when
the two articular swfaces are wholey
articular and the joint space is equal
deviated joint:
a joint is said to be deviated when
the lines representing the articular
surfaces intersect outside of the joint
subluxed joint:
a joint is said to be subluxed when
the lines Jeplesenting the articular
surfaces intersect inside the joint
b) a congruent first M1P joint wither represents a nonnal first M1P joint or a structural adaptation of the first metatarsal
latemlly, creating hallux abductus deformity
c) a deviated or a subluxedjoint occmring at the first MIP joint indicates a positional deformity
243
Determination of Procedure
I. angular deformities - post-op goal to get 1M angie to 0
A 1M angles up to 16 usually respond to head procaiures
B. 1M angles above 16-18 require base proa::dures
ll. increased PASA
A Reverdin
B. Peabody
C. bipJanar Austin
D. offset V with swivel
m. HA V with metatarsus adductus
A HA V deformity is accentuated in presence of metatarsusaddnchlS: however, the 1M angle may appear
IV.
Y.
VI.
B.
A
B.
A
B.
C.
A
B.
e.
D.
Normal or slightly incresed
consider distance between first and second metataIsal heads when choosing procedure
condition of the joint
Iadiographic changes
clinical exam (ie-I3llge of motion, pain, crepitus)
condition of the bone
presence of cystic degeneration
excessive sclerosis
mar.ked osteoporosis
individual patient oornmeters
age
ambulatory status
medical status
Vil.
compliance
foot type
hypermobility
elevatus
A
B.
*REMEMBER: do not treat the x-rays*
Soft Tissue Correction (capsule tendon balance procedures)
I. Silver (1923)
A resection dorsomedial eminence of first metatarsal bead
B. lateral capsulotomy and medial capsulorraphy
ll. McBride (1928)
A resection dorsomedial eminence of first metatarsal head
B. lateral capsulotomy with removal of fibular sesamoid
C. transfer the conjoined tendon of adductor hallucis and lateral bead of FHB to dorsolateral aspect of the first
metatarsal head
ill. Hiss
A resection dorsomedial eminence of first metatarsal head
B. lateral capsulotomy
C. transfer abductor hallucis from plantar to medial to the first MPJ (abductor tendon sutured into hole in base
of proximal phalanx; acts as ligament to strengthen capsule medially)
245
BUNION SURGERY
RADIOLOGY OF THE FIRST RAY
Metatarsus Addndus Angle
a) measured on a DPview
b) formed by a line perpendicular
to the bisection of the lesser
tarsus and a line lepIesenting
the lesser metatatsus
c) the lesser metataISUs is represented
by the bisection of the dorsal
longitudinal axis of the shaft of
the second metatatsal
d) the normal metatatsus adductus
angle is 15
e) as the foot becomes more adducted,
this angle increases and a greater
chance exists for abduclus deformity
at the first MIP joint
Metatarsal Protusion Distance
a) measured on a DP view
b) lepresents the distance between two arcs
and demonstrates the length between
the first and second metatarsals
c) a positive mi11imeter distance is used to
indicate that the first metatarsal is
longer than the second metatarsal
d) a negative mi11imeter distance is used to
indicate that the fust metataIsal
is shorter than the second metatarsal
e) normal mnge of the metatarsal protrusion
distance is +/- 2 mm
f) ideally, the length of the first metatarsal
should be about the length of the thitd
metatarsal
Metatarsal Split Distance
a) measures the split between the first
and second metatarsals
b) measured from the most lateral aspect of
the first metatarsal base to the medial
cortex of the second metatarsal
c) measurement must be made pmillel to the
bisection of the second metatarsal
d) 2 mm or greater is significant
e) important in evaluating soft tissue
deforming forces at the metatarsal-
cuneiform joint
241
Metatarsal Deformation Angle
a) angle fonned by the bisection of the
proximal metatarsal base and the
shaft of the first metatarsa1
b) measures any osseous defonuity of the
metatarsal shaft relative to the base
c) nonnal is 8 or less
d) greater than 8 indicates a
structural defonuity within the
metatarsal shaft
Metatarsa1-Cuneifonu Angle
a) tills angle is fonned by the proximal
first metatarsal base facet and the
medial cuneifonn distal articular facet
b) nonnal is 25 or less
c) greater than 25 implies a structural
defonuity
Hallux Abdnctus Interphalangeal Angle
a) measured on a DP view
b) represents the angle made by the
bisections of the distal phalanx and
the bisection of the proximal phalanx
c) nonnal is 0-10
d) an increase in tllls angle represents
eitIler a congeIlltal bowing of the
distal phalanx or a transverse
deviation of the distal phalanx on
tile proximal phalanx
e) may also increase when the motion at
tile first MIP joint is limited
(ie-hallux limitus or rigidns)
Hallux Abdnctus Angle
a) on a DPview, it is the angle resulting
from the bisection of tile dorsal
longitudinal axis of the proximal
phalanx and the first metatarsal
b) nonnal is 10-15
c) an abnonnally high angle indicates a
positional defonnity at the first
MIPjoint
d) this angle increases in all cases of
HA V defonuities
242
Proximal ArtiaJ1ar Set Angle
a) formed by a line drawn perpendicular
to effective articular cartilage
of the head of the first metatarsal
and line representing longitudinaJ
bisection of the first metatarsal
b) if the angle measured ~ greater than
7.5 , adaptive changes have
taken place at the first metatarsal
head, which indicates a structural
adaptation of the articu1ar cartilage
c) this indicates a structUIal deformity
and not a positional one
Distal Artiwlar Set Angle
a) on a DP view, it is formed by a line
drawn petpendicular to the effective
articular cartiJage of the 00se of the
proximal phalanx
b) represents structural adaptation of the
00se ofproximal phalanx on the shaft
c) abnonnal Jateral epiphyseal closure at
the 00se of the proximal pba1anx,
which causes more growth medially
with a resulting bowing of the shaft,
may alter this angle
First MetltarsQphaJangeal Joint Position
a) the joint position on a DP view is a comparison of lines representing the effective articular cartilage of the first
metatarsal head and a line representing the effective artiwlar cartilage at the 00se of the proximal pbalanx
congruent joint: .
a joint is said to be congruent when
the two artiwlar surfuces are wholey
articular and the joint space is equal
deviated joint:
a joint is said to be deviated when
the lines representing the articular
surfaces intersect outside of the joint
subluxed joint:
a joint is said to be subluxed when
the lines representing the articular
surfaces intersect inside the joint
b) a congruent first MIP joint wither represents a normal first M1P joint or a structnral adaptation of the first metatarsal
laterally, creating hallux abductus defonnity
c) a deviated or a subluxed joint occmring at the first M1P joint indicates a positional deformity
243
Shape of the First Metatarsal Head (seen on DP vie,,\')
a) Round
1. round first metatarsal head creates
a high degree of instability at
the first MTP joint
2. the hallux is prone to drift
laterally on a convex surface
b) Square first metatarsal head
1. provides more stable joint
configuration versus a round
first metatarsal head
c) Square with a ridge
1. represents square metatarsal head
with an oblique or central ridge
2. stable configuration; helps
prevent lateral de",iation of
the hallux
3. a compensatory hallux interphalangeus
may be seen with this
Tibial Sesamoid Position
a) measured from 1-7 relative to the
longitudinal bisection of the first
metatarsal
b) measured from medial to lateral; the
normal tibial sesamoid position is 3
c) when the tIbial sesamoid position is 4,
the sesamoid is overriding the crista
of the first metatarsal, causing DID
d) the tIbial sesamoid could dislocate past
the crista without eroding it: this
is best evaluated on a sesamoid
axial view
Metatarsus Primus Adductus Angle
a) formed by the bisections of the first
and second metatarsals longitudinally
b) represents a deviation of the first
metatarsal in a transverse plane medially
c) rectus foot type, 1M angle = 8-12
d) adducted foot type, IM angle = 8-10
e) the 1M angle could be increased in a
congenitally bowed metatarsal or a
premature closure of the medial
epiphysis secondary to trauma
f) in post-operative films. if the foot
is held supinated secondary to guarding, false positive decrease in IM angle
will be noted
g) this angle should be assessed on weigllt -bearing views
h) os intermetatarseunl found between the 00ses of the first and second
metatarsals could contribute to an increase in the IM angle and to a hallux
valgus deformity
244
IV. component procedures
A. adductor transfer
B. various capsulorraphies
1. frontal plane versus transverse plane correction
2. Washington monument
3. elliptical
4. "T" shaped
5. "U" shaped
6. inverted "L"
C. EHL tendon lengthening
D. EHB tenotomy
Phalangeal Osteotomy
1.
A
B.
C.
D.
II.
A.
B.
c.
proximal Akin
corrects for DASA
osteotomy perfomled 5-10 nml distal to MPJ
proximal osteotomy parallel to surface of the base of the proximal phal3.IL'\:
distal osteotomy perpendicular to long axis of the shaft
distal Akin
corrects for hallux abductus interphalangeus
osteotomy perfomled at distal end of proximal phalanx
fixation of either osteotomy varies (ie-absorbable pin; k-wire; screw; suture; monofilament wire)
Capital Osteotomies
1.
A.
B.
C.
II.
A
B.
C.
Austin (1974)
resection medial eminence; lateral release
osteotomy perfonned in the center of metatarsal head with 60 degree angle between the anIlS
I. unicorrectional: nonnaIizes 1M angle
2. bicorrectional: nonnaIizes 1M angle and P ASA
axis guide - utilized to lengthen .. shorten, plantarflex or dorsiflex
Reverdin (1881)
primarily used in conjunction with other procedures
by itself - only corrects hallux abductus (P ASA)
osteotomy
1. performed in metaphyseal bone
2. first cut is 1 em proximal and parallel to the articular surface
3. second cut is perpendicular to long axis of metatarsal shaft (wedge shaped with base medial)
4. lateral cortex intact
ill. Reverdin-Green (1977)
A modification: initial cut is made parnllel to the weightbearing surface being sure to exit just proximal to the
articular swfuce of the first metatarsal head
B. avoids plantar sesamoidal grooves of the metatarsal head
C. avoids scoring the sesamoid apparatus
D. sanle indications as for the Reverdin
IV. Reverdin-Laird (1977)
A modification ofReverdin-Green: lateral cortex is cut allowing lateral translation of the capital fragment
B. corrects for P ASA and 1M angle
246
V. Reverdin-Todd (1978)
A modification: proximal osteotomy is either angled to plantar-proximal (pIantarflexes capital
fragment) or dorsal-proximal to (dorsiflexes capital fragment)
B. distal osteotomy is still parallel to the articular surface and proximal osteotomy parallel to the
weightbearing surface
Neck/Metatarsal Osteotomies
I. Peabody
n.
m.
N.
v.
A same procedure as Reverdin except that the osteotomy is performed at the anatomical neck
B. disadvantages over Reverdin -
A
B.
e.
D.
A
B.
e.
D.
E.
A
B.
e.
A
B.
e.
1. poorer healing area ofbone
2. requires secure fixation or non-weightbearing status
DRATO(Smith, 1971)
distal osteotomy - perpendicular to the long axis of the first metatarsal; through and through
proximal osteotomy - angled proximal-medial to distal-lateral (to produce PASA correction)
dorsiflexes capital fragment to place the articular cartilage in a more fimctional postiion, and thus,
attenpts to increase dorsiflexion at the first MPJ
1.
2.
3.
4.
l.
2.
3.
4.
disadvantages
poor healing bone
highly unstable
requires secure fixation or non-weightbearing status
technically difficult
()ffi;et V (Vogler)
apex of osteotomy at junction (versus center of metatarsal head with Austin)
angle of winge; is less than 60 degrees
longer osteotomy allows for greater bone-to-bone contact
length of dorsal wing determines amount of swivel posSIble
advantages
can correct for 1M angle and hallux abductus
good bone-to-bone contact
ease offixation (ie-pin; screw)
patient can be weightbearing
Kalish
apex of osteotomy in center of circle around metatarsal head; as with Austin procedure (metaphyseal
osteotomy)
1.
2.
..,
.J.
long dorsal wing allows for screw fixation
unable to swivel capital fragment to correct P ASA
Scarf or Z osteotomy (diaphvseal osteotomy)
two ways to perform osteotomy
distal cut dorsal and proximal cut plantar
(avoids posSIbility of scoring sesamoid apparatus; easier to fixate)
distal cut plantar and proximal cut dorsal
similar advantages and uses to Offset V
trough effect: dorsal segment of the "Z" (cortical bone) wants to sink down into the plantar segment when
screws are tightened down
247
VI. Ludloff(1918)
A oblique osteotomy oriented dorsal-proximal to plantar-distal exitingjust proximal to metatarsal head
B. unstable osteotomy configuration
e. can swivel for PASA correction
VII. Mall (1926)
A oblique osteotomy oriented dorsal-distal to plantar-proximal, exiting just proximal to metatarsal-ameiform
joint (osteotomy exactly opposite to Ludlom
B. unstable osteotomy configuration
e. advantages:
D.
1. both Ludloff and Mau are higbly versatile osteotomies
2. the capital fragment can be elevated, depressed, lengthened, shortened, adducted or abducted
3. good degree ofbone contact is maintained r e ~ e s s of capital fragment displacement
4. the Mau osteotomy would appear easier to fixate (especially if using screws) and bave somewhat
better stability aginst the forces of weightbearing versus the Ludloff
1.
2.
...
J.
disadvantages
diaphyseal osteotomies - poor healing bone
proximal location of osteotomy demands fixation and/or non-weightbearing status
requires significant dissection about the first ray
VIII. Hohmann (1924)
IX.
A
B.
e.
D.
A
B.
e.
D.
1.
2.
3.
1.
2.
trapezoidal osteotomy (with base oriented medially) made at the level of the metatarsal neck; through and
through osteotomy
advantages
capital fragment rotated medially to correct for hallux abductus
capital fragment could also be translated laterally (1M angle correction) and/or dorsally or plantarly
shortening of the first metatarsal could decompress the MPJ and slightly increase motion
disadvantages
significant shortening of first metatarsal
unstable osteotomy; requires fixation and non-weightbearing status
original procedure performed outside capsule and medial eminence was not resected
Mitchell (1945)
oblique osteotomy similar to Hohmann, except with lateral cortical shut intact
originaly fixed with 1-0 chromic catgut
similar indications and disadvantages as Hohmann
indications: long first metatarsal
X. Wilson
A oblique osteotomy oriented distal-medial to proximal-lateral (through and through)
B. capital fragment is shifted proximally and laterally along the osteotomy
e. capital fragment can also be translated dorsally or pIantarly
D. disadvantages
1. poor healing bone
2. unstable; requires secure fixation and/or non-weightbearing status
3. produces significant shortening
248
Basal Osteotomies
PRINCIPLES OF THE BASE OS1EOTOMY
hinge axis concept
binge has an axis and anus
motion about the hinge occurs perpendicular to the axis of the hinge; keep hinge perpendicular to the
weightbearing surface so the distal segment remains parallel to the ground when osteotomy is closed
binge axis must be perpendicular to the ground in the sagittal plane, to avoid iatrogenically induced
metatarsal elevation
dorsomedial cortical hinge plantarflexes the distal segment upon closure
plantar medial cortical hinge (runs dorsomedial to plantar lateral) dorsiflexes the distal segment upon
closure
/
..
"
complications
first ray elevatus
lesser metatarsalgia
hallux varus
PROCEDURES
1.
A
B.
c.
l.
2.
3.
D.
1.
2.
3.
Transverse closing base wedge (Loison, 190 1)
osteotomy originally descnbed as being at a point just distal to the insertion of the long peroneal tendon
base lateral with medial cortical apex intact
advantages
longer lever arm allows for correction of significant IM angle deviations
good vascular bone
relatively little dissection required
disadvantages
proximal location of osteotomy (longer lever arm) demands fixation and non-weightbearing status
greater potential for disturbing blood supply about the first metatarsal
requires pttient compliance
249
ll.
A
B.
1.
2.
3.
e.
1.
D.
1.
2.
Ill.
A
B.
e.
D.
E.
Oblique closing base wedge (Juvarra, 1919)
originally descnbed as a "double oblique section of the metatarsal" perfonlled at the junction of the middle
and proximal thirds
modification:
oblique osteotomy from proximal-medial to distal-lateral
proximal cortical apex is maintained
fixation with one or two screws
disadvantages
requires more dissection than Loison osteotomy
advantages
easier to fixate
more bone-to-bone contact
Opening base wedge (Trethowan. 1921)
linear osteotomy from medial to lateral across the base of the first metatrsal keeping the lateral cortical
binge intact
fashioned the resected medial eminence into a wedge and forced it into the osteotomy site
good for maintaining or increasing length of first ray
must be cognizant of jamming at the MP]
the high level of load at the proximal aspect of the first metatarsal often causes the autograft to resorb
IV. Osteotomy (Kotzenberg)
A osteotomy oriented in transverse plane with apex proximal
V. Crescentic (Weinstock)
A osteotomy created approximately 1.5 em distal to the first metatarsal-cuneifonn joint
B.
e.
when looking at the metatarsal from dorsal to plantar, the concave portion of the osteotomy faces distally
the distal segment of the first metatarsal is rotated until the desired correction is attained
D. the dorsal segment can also be dorsiflexed or plantarflexed as necessary
E. results in less shortening than with CBWO
F. fixation and immobilization is required
G. cmplications
1. elevatus
2. difficult to fixate
3. inaccurate reduction of the IM angle
VI. Epiphysiodesis
A fuse lateral side of epiphysis during growth years
B. (allows gro\\1b on the medial side to reduce the IM angle)
Combination procedures
I. Logrescino (1948)
A double osteotomy of first metatarsal
1. for short first metatarsal: Reverdin + Trethowan
2. for long first metatarsal: Reverdin + Loison
B. advantages
1. corrects for high IM angle and deviated PASA
2. both osteotomies are placed in good metaphyseal bone
ll. 3:1
A capsule tendon balance procedure (Silver or McBride)
B. closing abductOIy base wedge osteotomy
C. proximal Akin osteotomy
250
Arthrodeses
I.
II.
A head of the first metatarsal is &shioned into a peg
B. hole is fusliioned into the base of the proximal phalanx
C. the bones are implCted and a compression screw is driven from the plantar aspect of the base of the proximal
pha1anx into the shaft of the first metatarsal
D. McKeever advised 15-20 ofMPJ extension with 15 of hallux abductus in men and 15-25 ofMPJ extension
with 25 ofbal1ux abductus in women
E. Indications
1. grossly arthritic joint in a person whom you deem. too young to have a Keller artbroplasty
2. salvage procedure after unsuccessful Keller
3. severe RA with Iateml deviation of the toes
F. Advantages
A
B.
C.
D.
1. weight-bearing function of the great toe is maintained
2. lessen the tendency to develop lesser metatarsalgia
1.
1.
2.
3.
4.
5.
6.
1.
2.
3.
4.
Lapidus (1934)
denuded cartilage offfirst
decorticated JateIal aspect of the base of the first metatarsal and the CKljacent surface of the second
metatarsal base
packed bone chips obtained from the resected medial eminence in the space between the first and
second metatarsal bases
Indications
pain on motion offirst metatarsal-cuneiformjoint
h}]JerD1Obility of the first metatarsal-omeiform joint
DID of the :first metatarsal-cuneiform. joint
velY long first ray
excessive first metatarsal elevation or plantarllexion
excessive angulation or gapping at the first metatarsal-cuneiform. joint
Disadvantages
produces marlred shortening of the first ray
comparatively long post-q> period
increased potential for distUIbing the blood supply about the first metatarsal
technically difficult
ArthropIasty oftbe First MPJ
I. Keller
A technique
1. resection of one-fourth to one-tbird ofbase of the proximal phalanx, with cut perpendicu1ar to long axis
of the shaft
2. resection of medial eminence of first metatarsal head
3. medial capsulonaphy
B. eliminates reverse buckling forces across the first MPJ
C. mainly reserved for elderly sedentaty population
D. modifications
1. EHL lengthening to help prevent retraction of toe >sesamoid removal
2. pin fixation to maintain length
3. capsule interposition at MPJ
4. reauachment of short flexor tendon to stump of phalanx to increase stability of joint function
E. complications
1. cock-up hallux
2. Jack ofpurchase power
3. shortening of hallux
4. lesser metatarsalgia
251
II.
A
B.
Stone
---;;blique ostectomy oriented dorsal to plantar leaving plantar condyle and sesamoid apparatus intact
resection of medial eminence of first metatarsal head
ill. Mavo
A excision of 5 mm of metatarsal head including the articular surfuce
B. interpose capsule and bursal tissue between the metatarsal and base of proximal phalanx
Miscellaneous
I. Opening wedge osteotomy of medial cuneifoIDl
A described for metatarsus adductus by Fowler
B. bone graft may be allogenic or autogenic
e. complications
1. overcorrection
2. nonunion
3. fracture of intermediate cuneifoIDl
Implants
simply intended to maintain space between bony surfaces
cannot correct for osseous deformity
any osseous deformity must first be corrected prior to implant use
osteotomies must be precise to prevent eccentric loading. of the implant
good bone stock is required to receive stem of implant
foreign body reaction etiher due to primary rejection or to inlplant breakdown with detritic synovitis is
possIble
patients must be made aware of short lifespan (tempotaIy nature of the implant)
I. Hemi (Swanson, 1971) [Dow Coming Wright]
II.
ill.
IV.
A originally designed to supplement the Keller bunionectomy
B. medical grade, high performance silicone elastomer
C. flat base - provides no correction for PASA
D. available in titanium as well
A
B.
A
B.
e.
l.
2.
..,
J.
A
B.
e.
HeIDi-Angled (Well modification) [Dow Corning Wright]
base is angled - having increased depth on lateral side
designed to articulate with an adapted metatarsal head (deviated P ASA)
Total Implant - Swanson Design (Dow Coming Wright)
double stemmed implant
resected surfaces ofbase of proximal phalanx and head of first metatarsal must be cut to lie flush with
implant surfuce - eccentric load distribution will lead to early inlplant failure
note:
again - the various osseous angular deformities ust be corrected prior to implant placement
total inlplants cannot be used in the presence of cystic deformation of the first metatarsal head
total joint implants available with titanium grommets which provide protective interface between bone
and implant
Total Implant - LaPorta Design [Sutter)
proximal stem is angled 15 in sagittal plane to account for first metatarsal declination
distal stem is angled 10 laterally to provide for physiological hallux abductus
binge allows for 60 of motion
252
V. Total Implant - Lawrence Design [Sutterl
A proximal stem also angled 15 in the sagittal plane
B. distal stem is not angled (neutral)
C. binge allows for 85 of motion
D. allows for bevelled phalangeal base resection in attempt to preserve plantar insertions
Two Component Total Joint Systems
1. Koenig Total Toe lBiometl
A noncemented system; the metatarsal component has a plantar ledge to help translate loading forces to
the metatarsal
B. the metatarsal component is a titanium alloy hardened with ionized nitrogen to improve wear
characteristics
C. the phalangeal component is ultrahigh molecular weiglu polyethylene (UHMW) and is available with a
titanium backing
II. BioAction Great Toe Implant IMicroAirel
A cemented system
B. the metatarsal component is cobalt chrome and angled for right and left geometry (no plantar ledge)
c. the phalangeal component is ultra high molecular weight polyethylene with titanium backing is
available angled
AUSTIN
1
Aust.in
253
MITCHELL
WILSON
/
( .... , ..
TRETHOWAN JUVARA
JUV.AJiA (MODIFIED)
~ ~ ~
OPENING BASE WEDGE CRESCENTIC
McKEEVER
LAPIDUS LOGRESCINO
3:1
254
Sf;
STONE
OPENING WEDGE MEDIAL CUNEIFORM
HEMI IMPlANT
~
~
HEMIANGLED TOTAL IMPLANT
IMPLANT (Swanson)
MAYO
PEABODY
255
REVERDIN-GREEN-LAIRD
HOHMAN
~
~ f :
o
REVERDIN-TODD
256
Juvenile Hallux Abductovalgus
Def'mition: aberration in the function or alignment of the first metatarsophalangeal joint in persons below the age
of twenty.
Incidence
-Females> males
-Significant positive family inheritance (maternal transmission)
Etiology
-Autosomal dominance with incomplete penetrance
-Biomechanical: pes planus/limb length discrepancy/STJ pronation/equinus
-Metatarsal primus varusladductus
-Neuromuscular deformitieslligamentous laxity
-High rate of recurrence
Adult vs. juvenile HA V
-Juvenile: less valgus rotation of hallux, general absence of chronic tissue reaction and degenerative joint disease,
few adaptive changes of the first MIPJ (these are general guidelines, but not always the case)
Symptoms
-Pain is not common
-Deformation of shoe gear, difficulty fitting shoes
-Concern with self image and appearance (common presentation age 11-14 y.o.)
-Reluctance to engage in physical activity
-Children <6 y.o. rarely have symptoms (usually present with concerned parent)
Staging of First MIPJ ROM
Stage I: slight alxluction of the hallux with full ROM and presence of dorsomedial irritation of prominence
Stage II: more advanced, greater transverse plane deviation, may be reduced passively with pain free and full
ROM
Stage ill: greater deviation in the alignment of the first MIPJ, ROM in defornled position is full, but defonnity is
not passively reduCIble and all attempts to DF hallux on first metatarsal when the great toe is rectus
results in "tracking" back into deformed position. This is indicative of fixed adaptive contraction
within
the first intermetatarsal space. Usually with moderate to severe lateral displacement of sesamiods
Stage IV: rare, lack of ROM, crepitus, pain in first MIPJ
Radiographs
-Metatarsus adductus/true 1M angle
-PASAlDASNdistal metatarsal articular angle (DMAA)
-Metatarsallengthlparabola
-Hallux length
-SesanlOid position
Treatment
-Conservative:
-splints, toe wedges, bunion shields, 'wider shoes
-orthoses
Surgical intervention:
-Indications:
-pain, rapid progression of deformity, severe deformity, failure of conservative treatment,
cosmetic concerns, secondary deformity of the lesser digits
257
-Goals:
-restoration, improvement, and preservation of joint function
-relief of pain
-restoration of proper forefoot dynamics
-improved cosmetic appearance offoot
-When?
-< 6 y.o. : 40-50% of total metatarsal growth remains; surgery only in severe defonnities
-6-10 y.o. : 60-80% of metatarsal length attained, physeal plate clearly defined radiographically,
surgery for severe defonnity and in cases in which significant adaptive changes have
occurred in the articular surfaces of the MTPJ on radiographs
-10-15 y.o.: ideal period; 90% of normal metatarsal length attained in most boys by age 12 and
95% in girls the same age; osseous, cartilaginous, and collagenous tissues have
relative plastic qualities that achieve excellent repair and adaptation
-Procedures:
-soft tissue: ineffective
-opening wedge osteotomy of medial cuneifonn
-Lapidus
-epiphysiodesis/epiphyseal stapling
-digital procedures: Akin
-distal first metatarsal osteotomy: Mitchell, Austin, Reverdin
-crescentic osteotomy
-*closing base wedge osteotomy*
HALLUX LIMITUS
Definition
a) hallux limitus: decrease in the range of motion at the first MTP joint
b) halllLX rigidus: absence of motion at first MTP joint
c) nonnal first MTP joint ROM: dorsiflexion = 65-75
plantarflexion = 40
Etiology
a) hypennobile first ray
b) immobile first ray
c) excessively long first ray
d) first metatarsal elevatus
e) degenerative joint disease
f) neoplasms
g) trauma
h) septic arthritis
i) iatrogenic
(ie<orrecting functionally adapted joint with soft tissue release; failure to correct dorsiflexed
first metatarsal or abnoramlly long first ray, over aggressive medial capsulorraphy; displacement of
osteotomy; etc)
j) neuromuscular disorders
k) systemic arthritides (ie-RA; psoriatic; gouty arthritis)
1) osteonecrosis secondary to avascularity of metatarsal head
m) foreign bodies (ie-implants)
258
Classification of Hallux Limitus
a) primary vs seamdary
1. primaIy hallux limitus
>occurs in adolescent patients and is associated with a long first metatarsal
>congenitally long first metatarsal
2. secondaIy hallux limitus
>occurs in older patients
>usually caused by DID, trauma, septic arthritis and systemic arthritides
b) structural vs functional
1. structural hallux limitus
>dorsiflexion of first MIP joint is decreased when the forefoot is both loaded and unloaded
2. functional hallux limitus
>dorsiflexion of first MIP joint is decrreased only when the forefoot is loaded
Clinical Findings
a) symptoms
1. gradual onset of pain and limitation offirst MPJ ROM
2. pain localized to dorsal aspect of first MIP joint
3. pain experienced with ambu1ation and prolonged weigbtbearing
b) physical examination
1. dorsal or dorsomedial prominence of first MPJ
(aka-dorsal bunion)
2. hallux position is most commonly rectus
3. tenderness with passive dorsiflexion of hallux
4. test the first MP] dorsiflexion with the forefoot loaded and unloaded
5. excessive hallux IPJ dorsiflexion associated with:
-EHLspasm
-ganglion cyst or adventious bursa associated with EHL tendon secondruy to irritation from shoe gear
-plantarmedialIPJ hyperkeratotic lesion
(aka-pinch callus)
6. check sesamoid mobility:
>load the first ray and palpate the sesamoid apparatus while dorsiflexing the MPJ
>arthrodesed or fibrosed sesamoids prevent normal and any MPJ dorsiflexion
7. antalgic, apropulsive gait with an early heel-off
Radiographic Findings
a) nonuniform joint space narrowing
b) flattening of the first metatarsal head
c) osteophytes on first metatarsal head and base of proximal phalanx (aka4rsal flag sign)
d) subchondral sclerosis
e) loose bodies (joint mice) within the first ray
f) first metatarsal elevatus (lateral view)
1. proximal phalanx articulates with the plantar aspect of the first metatarsal head
2. bisection of the first metatarsal is superior to the talar bisection {lateral view)
g) positive metatarsal protrusion distance
Surgical Management of Hallux Limitus
a) ol:!iectives
1. removal of osteophytic spurring
2. creration of slack in the fle.xor apparatus
3. shortening of an excessively long first metatarsal
259
4. plantarflexion of an ele\ 'ated first metatarsal
5. reorientation of first metatarsal head articular surface
b) joint presen'ing procedures
1. cheilectomy (aka-:ioint remodeling)
>removal of osteophytic proliferation on the first metatarsal head or base of the proximal phalanx
2. Kessel & Bonney
>dorsiflexory osteotomy ofbase of the proximal phalaILX
3. Regnauld (aka-Mexican hat procedure; enclavement;
auto-implant; joint decompression)
>base of proximal phalanx is resected and fashioned into a peg then reinserted into the proximal phalanx
>LaPorta modification utilizes the resected proximal phalangeal base as the hole and the distal component
of the phalanx as the peg
4. Hoillruum type procedure
>indicated for long first metatarsal etiology
5. Waterman
>dorsiflexory osteotomy of the first metatarsal head
>through-and-through osteotomy 0.5 em proxiam1 to the articular cartilage which converts plantarflexory
ROM to dorsiflexoI)' ROM
>increases joint ROM by reducing the internal cubic content of first MfP joint
6. modified Waterman
>dorsiflexory wedge osteotomy of the first metatarsal head leaving plantar articular cartilage intact
7. Waterman-Green
>shortens and plantarflexes the first metatarsal
>involves two osteotornies -
-trapezoidal wedge wider medially perfOIDled in dorsal to plantar direction, 0.5 cm proximal to
articular cartilage
-oblique, transverse osteotomy (through and through) 45 to the trapezoid which avoids the plantar
articular cartilage
8. Youngswick modification of the Austin procedure
9. dorsal "V" osteotomy
10. plantarflexory wedge osteotomy
>Van Ness [transverse osteotomy]
>plantar closing wedge osteotomy
II. Cotton
>opening wedge osteotomy of the medial cuneifurm
(dorsal based wedge plantarflexes first ray)
12. reverse Cotton
>plantar based wedge osteotomy of the medial cuneiform
to dorsiflex first ray
13. Lambrinudi
>plantarflexory wedge osteotomy of the base of the first metatarsal to correct metataraI elevatus
14. sagittal Logriscino
>Waterman + Lambrinudi
c) Joint destructive procedures
I. Keller arthroplasty
>resection of one-third of the base of proximal phalanx
2. Implant arthroplasty
>totaI or herni-implant (with or "Without grommets)
>must surgically address IDlY first metatarsal deformities for implant to succeed
3. Stone
>dorsal to plantar wedge resection of one-fourth of first metatarsal head
260
4. Mayo
>excision of 5 mm of first metat:ar5al head including the articular surface
5. McKeever arthrodesis
>fusion of metatarsa1-phaJangeal joint
6. Lapidus arthrodesis
>fusion of metatarsa1-cuneiform joint
Post-Operative Management
a) biotm::banicaJ
1. orthotics
2. ptdding; aa:ommodative devices
b) continuous passive motion
1. excellent form of therapy which should be started immediately after surgery
2. hallux CPM machines available
c) intermittent active motion
1. most oommon type of therapy
2. usually instituted after one week of immobilization post-operntively
3. patient is instructed to stabilize proximally (first metatarsal) and to gently dorsiflexJp1antarllex to tolerance for a
few minutes daily
d) there is no substitution for recognizing the etiology of the deformity and correcting the problem; not just performing
surgety to "soothe" symptoms

Cl'
CHEILECTOMY
KESSEL & BONNEY

REGNAULD

eo
WATERMAN
MODIFIED WATERMAN
WATERMAN-GREEN
R
YOUNGSWlCK
DORSAL V OSTEOTOMY

....
conON
261
~ ~ ~
'-lAN NESS
PLANTAR CLOSING WEDGE
(LAMBRINUDI)
JUVARA (MODIFIED)
~ A-::::\
~ ~ q ~ ~
HOHMANN TYPE OSTEOTOMY
HALLUX VARUS
Definition
a) deviation ofthe hallux at the first metatarsophalangeal joint
COMBINATION
(HOHMANN + WATERMAN)
b) may exist as a transverse plane deformity of hallux adductus or present as an adductus, varus and malleus deformity
Classification
a) congenital hallux varus
1. primaIy: an isolated deformity
2. secondary: associated with equinovarus deformity
b) acquired hallux varus
1. static: muscle balance undistUIbed
(ie-metatarsal osteotomy)
2. dynamic: muscular imbalance (ie-adductor transfer)
Etiology
a) excessive resection of the medial eminence with disruption of the sagittal groove
b) medially sublu..xed tibial sesamoid
c) excision of the :fibular sesamoid
d) overzealous medial capsulorraphy
e) medial malposition of the sesamoid apparatus after adductor tendon transfer
f) muscular imbalance through disruption of both the adductor hallucis and lateral head ofFHB
g) overcorrection of the intermetatarsal angle by osteotomy
h) overcorrection of the proximal articular set angle (PASA)
i) aggressive post-operative bandaging and splinting
Symptoms of Hallux Varus
a) histOIY ofHA V surgery
b) unable to wear conventional shoe gear comfortably
c) prin present along medial aspect of hallu..x secondary to shoe pressure
d) prin along the medial aspect of the arch secondary to muscle contracture
e) pain at the first MPJ with or without shoe gear
262
Clinical Signs of Hallux Varus
a) adducted position or varus rotation of the hallux
b) contracture at the IPJ or involving the EHL or abductor hallucis tendons (cocked-up hallux)
c) pain on palpation of abductor hallucis
d) pain and crepitus at the first ray
e) hallux limitus or rigidus
Radiographic Signs of Hallux Varus
a) hallux adducted at the first MPJ
b) staked head offirst metatarsal with a peeking tIbial sesamoid
c) absent fibular sesamoid
d) previous osteotomy of the first metatarsal
e) reduced or negative 1M angle
f) negative proximal articu1ar set angle
g) arthritic changes at the first MPJ and/or IPJ of the hallux
Correction of Hallux Varus
a) conservative
1. abductovalgus strapping and splinting
b) surgical
I. soft tissue release
>medial capsulotomy
>JateI3l capsulorrnphy
2. dynamic soft tissue procXldures
>abductor hallucis tendon transfer
>retransfer adductor haIlucis tendon laterally
3. osseous procedures
>correct abnormal 1M angle or PASA (ie-reverse Austin)
4. joint destructive procedures
>arthroplasty (ie-Keller,. KeUer with implant)
>arthrodesis (ie-McKeever)
c) step-wise surgical approach
1. total soft tissue release at the first MPJ
2. medial capsulotomy
3. tibial sesamoidectomy (if30-500Al of the tIbial sesamoid is peeking medially)
4. address abductor hallucis as a deforming force (t:mnsfer of abductor ballucis to the pIantar-JateI3l flexor
apparatus and Iateral base of the proximal phalanx)
5. osseous correction
>determine the level of the osseous deformity
>revise the previous first metatarsal osteotomy
>if the 1M angle is negative, must reverse the overcorrection with apploptiate osteotomy
(ie-reverse Austin, reverse Offset Y, reverse CBWO)
6. arthroplasty of the first MPJ for severe deformity and for non-functional joint SlII'fuces
>Keller
>Keller with berni-implant or total implant
>Keller with fusion of hallux IPJ
7. arthrodesis of the first MPJ
>McKeever
>Lapidus
263
REARFOOT SURGERY
REARFOOT SURGERY
REARFOOT SURGERY
REARFOOT SURGERY
REARFOOT SURGERY
REARFOOT SURGERY
REARFOOTSURGERY
REARFOOT SURGERY
REARFOOT SURGERY
REARFOOT SURGERY
REARFOOT SURGERY
REARFOOT SURGERY
REARFOOTSURGERY
REARFOOT SURGERY
"R'EAR'FOOT ,......U'RG E'" ,
.... " ...... ... S i .
R .. EA'RFOOT SlJRGE,R,\-
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rARFOOT' S'I 'RGY'''''R'''''
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BONE GRAFflNG
Bone Graft Indications
1. Induction of new bone formation: the process of osteogenesis, the stimulation of new bone formation, is
an important characteristic of certain bone grafts. The property is useful in the treatment of delayed
unions, nonunions and arthrodesis by bone grafting techniques. .
2. Immobilization: bone grafting in combination with rigid internal fixation will aid in stabilization of
arthrodesis sites and unstable fmcture sites.
3. Defect replacement: a major use ofbone grafts are to replace Jarge segments of tr.wmatically lost or
surgically resected bone in order to maintain function and length of the affected segment.
Bone Graft Healing
In order for bone grafts to heal properly they must be placed in a vascuJar recipient bed in close contact with
surrounding bone fiagments and rigidly stabilized The graft site must be protected against external shearing
forces to insure proper healing. The means by which bone grafts are inoorporated into host tissue differs for
autogenous vet'SUS allogenic bone and for cortical versus cancellous bone, but generally involves five processes:
I. vascular ingrowth: this process usually occurs within the first or second week following grafting.
Initially hemostasis and in:t1ammatory cell infiltration occur. In allogenic grafts the bone antigenicity may
prolong the inflammatory process until host blocking antibodies can neutralize the graft antigens. Vascular
budding quickly follows the inflammatory response.
2. osteoblast proliferation: once vascular ingrowth is eslab1ished, the osteoprogenitor cells or mesenchymal
pericytes differentiate into osetoblasts and begin new bone formation.
3. osteoinduction: the process by which nonosseous tissue is induced to produce bone. The exact
mecbanism is unknown., however, Urist descnbes a bone morphogenic protein present in bone matrix
that acts as an inductor substance.
4. osteoconduction: the process in which the bone graft functions as a scaffold or conduit for migration of
new bone as it rep1aces necrotic "old" bone. Axhausen used the term creeping substitution to describe
this process.
5. graft remodeling: a process that may last for several months and results in reformation of the graft in
response to biomechanical forces in accordance with Wolffs law.
Types of Bone Grafts
1. autogenous bone grafts: autogenous grafts are considered to be superior, primarily because of cell
viability and iImmlllologic compatibility. Autogenous bone grafts are considered to be a true transplant
because the tissue is viable and will continue to survive and grow in the recipient site. Autogenous
grafts area primarily indicated for use in areas where vasculari1y is most important A disadvantage to
autogenous bone grafting is the creation of a second surgi.cal site and the formation of a bone defect in
that area. Specific types of autogenous bone grafts include:
a) cancellous autogenous bone grafts: a fragile lattice netwOIK which provides the largest amount of
viable cells and inductive morphogenic protein. The lattice provides an ideal structure for ingrowth of
new vessels filcilitating osteogenesis. Cancellous grafts are fur too fragile to lend any stability to the
graft site, however, they heal quickly and become progressively stronger and therefore more
radiodense as they heal. This type of graft is preferred for llOmmions especially avascular nonunions.
b) cortical autogenous bone grafts: a dense, compact strudure which provides strength and stability
to the graft site. Cortical grafts transfer very viable cells and incorporate slowly. Vascular
penetration takes twice as long as cancellous bone because osteoclastic resorption must precede
osteogenesis. In contrast to cancellous grafts, cortical grafts lose strength as they heal and becomes
more radiolucent. Approximately 400/0 of their strength is lost within a six week to six month period
Cortical grafts are ideal for areas where strength and stabilization are required. Cortical grafts also
allow secure attachment of fixation devices.
c) corticocancellous autogenous bone grafts: these types of grafts combine the strength of cortical
bone with the rapid osteogenic capabilities of cancellous bone. The iliac crest is a common donor site
for this type of graft.
d) free vascularized autogenous grafts: this form of graft is a segment of bone with its nutrient
artery and veins intact. Utilizing microsurgical techniques, the graft is harvested and reanastomosed
264
usually in areas of large bony defects. The most common donor sites include the nbs and the shaft of
the fibula. Incorporation of this fonn of graft, when rigidly stabilized, follows primary bone healing.
2. allogenic bone grafts: allografts are considered implants because the tissue is, for the most part,
nonviable. Living allografts are rarely utilized primarily because of immunologic incompatibility leading
to host tissue rejection and possible transfer of infectious disease. All donors must meet strict guidelines
developed by the American Association of Tissue Banks. The donor must be free from malignancy,
infection or transmiSSIble disease. The donor must also have no history of viral hepatitis, syphilis,
malaria, tuberculosis, leprosy, severe trauma, drug overdose or poisoning. Most allograft bone is
processed to reduce the risk: of disease transmission. There are several different types of allogenic bone
grafts reflecting the modification process utilized:
a) frozen allograft: this type of allograft is removed via sterile technique or sterilized following
harvesting by ethylene oxide gas, irradiation, autoclaving or prolonged antibiotic washes. Freezing is
perfonned to prevent enzymatic degradation. The temperature utilized, must be -70 C or below.
Freezing does not affect the biomechanical properties of the graft, however, little reduction of
antigenicity is accomplished
b) freeze-dried allografts: the process of freeze-drying removes 95% of the moisture in the graft.
Through a process called lyophilization, the bone is stored in a vacuum with infinite shelf life. The
process also reduces allograft antigenicity, however, torsional and bending strength is significantly
decreased The tensile and compressive strength are affected very little.
c) demineralized or decalcified allografts: this fonn of allograft was primarily designed to promote
osteoinduction while decreasing antigenicity. Urist developed the Autolyzed Antigen - Extracted
Bone Graft which strips the minerals from the bone exposing the bone morphogenic protein to induce
new bone production. This type of graft is very malleable and incorporates quickly into host tissue.
d) artificial allografts: many materials have been proposed, however, the most noteworthy is the
hydroxyaratite implant. This material is osteoconductive, but does not stimulate osteogenesis or
osteoinduction. Strength is excellent and little immunologic incompatibility is demonstrated
3. xenogenic bone grafts: not recommended for use currently, primarily because of immunologic
incompatibility leading to foreign body reaction which inhibits osteogenesis. Two commercially available
fonns of bovine bone graft are marlreted under the names Boplant and Kiel Bone.
4. 4. composite bone grafts: the combination of allogenic and autogenous bone grafts can be useful to take
advantage each graft's special properties. Autogenous bone is highly osteogenic while allogenic bone is
highly osteoinductive.
Tecbniques of Bone Grafting
1. onlay bone graft technique: described by Cambell, the technique utilizes a large autogenous cortical
bone graft to bridge a nonunion. The graft was then fixated in place with screws or wire. Prior to grafting,
the nonunion fragments were decorticated via a bone chisel. Phemister descnbed an onlay bone graft
which was not fixated and placed the graft ubperiosteally.
2. a) dual onlay bone graft technique: a modification of the onlay technique in which the nonunion is
centered between two cortical grafts. The technique was indicated for use in difficult or unusual
nonunioDS.
3. inlay bone graft technique: simply involves the formation of a slot or window in which the bone graft is
placed
4. sliding bone graft technique: originally described by Gill, the technique involved creating a graft from
the shaft of
5. a long bone approximately one-half the diameter in width. This graft was then moved forward across the
nonunion/arthrodesis site onto the recipient fragment
6. 4. Papineau bone graft technique: originally descnbed for treatment of chronic osteomyelitis and
infected nonunioDS. The necrotic bone was excised, then the wound was cleansed and allowed to
granulate. Small pieces of cancellous bone are then packed into the bone cavity and the wound is closed.
The technique was designed for rapid revascularization.
265
Deminera1ized Bone Matrix <DBM)
An autologous bone alternative
Bone matrix
O r ~ c
Collagen
Noncollagenous proteins
Bone Morphogenetic Protein (BMP)
Inorganic (mineralized)
Hydroxyappatite (calcium, phosphorus)
DBM-
Allograft bone containing only the organic matrix
Exposes non-collagenous proteins (BMP) to the osteogenic precursor cells
BMP has been shown to be osteoinductive
DBM function:
Osteoinduction
Process by which osteogenic precursor (mesenchymal) cells are stimuJated to differentiate into chondroblasts
and ultimately into osteob1asts
DBM Prodncts:
l. Grafton

Gel

Flex

Putty

Crunch
2. Dynagraft

Gel

Putty
3. Osteofil

Gel
4. AIloMatrix

Putty
Inferior Calcaneal Heel Spur and Plantar Fasciitis
Diagnosis
a) pain on palpation of the medial aspect of the inferior aspect of the calcaneal tuberosity.
b) post static dyskinesia: pain of the insertion of the plantar fuscia when first weight bearing after a period
of rest The pain is usually partly relieved by further activity.
c) x-ray: spur may or may not be present
Pathogenesis
Any or many of the following structures may be involved in pulling on the periosteum of the calcaneus. This
leads to periostitis which produces pain.
a) plantar fascia pull (most common)
b) abductor hallucis
c) flexor digitorum brevis
d) long and short plantar ligaments
266
Differential Diagnosis
a) calcaneal apophysitis
b) calcaneal fracture
c) nerve enttapment: usually the medial plantar calcaneal nerve
d) plantar fascial tear or herniation
e) avulsion injury
f) tumor
g) acromegalic fat pad alteration
h) connective tissue disorders with associated fat pad alterations or autoimmune arthritides (ie-rheumatoid
arthritis, Reiter's syndrome, psoriatic arthritis, ankylosing spondylitis)
i) infection: soft tissue or osteomyelitis
j) contusion
k) tendinitis (ie-first layer plantar musculature)
Treatment
Inferior heel spur syndrome and a plantar fasciitis are considered self-limiting entities and will resolve
without treatment However, the course of spontaneous resolution is long and the pain can be very
debilitating thus treatment is very often indicated
a) conservative
1. steroid injections
2. NSAIDs
3. padding and strapping (ie-low dye)
4. physical therapy
5. inunobilization: casting Oow priority since this treatment is also debilitating)
6. orthoses: can be used as treatment for the chronic variety as well for prevention of recurrence.
b ) ~
1. Griffith:
plantar U-shaped incision around the heel
2. Steindler:
rotates the posterior aspect of the calcaneus forward into a notch in tmderside of the calcaneus
need to do a tendo Achilles lengthening
3. Michele and Kruger:
COtmtersinking, L-shaped osteotomy of the inferior calcaneus
decreases the "high point"
4. Hassab and El Sherif:
several drill holes into the calcaneus
theory is that it reduces venous congestion of the calcaneus
5. Duvries:
resect inferior calcaneal spur through a medial incision ...... '" .... :fasciotomy
267
6. ENDOSCOPIC PLANTAR F ASCIOTOMY
Indications
-surgical alternative in patients with recalcitrant heel pain/pIantar fasciitis
-patients should have a minimum 6 month attempt of conservative care
Advantages
-faster recovery time
-less post-op pain
Technique
-PT and sural nerve block
-incision placement
-anterior & inferior to medial calcaneal tubercle based on NWB lateral x-ray
-5mm vertical stab incision
-blunt dissection to plantar fascia
-instrumentslEndotrac system
-fascial elevator
-hook probe
-slotted obturator/cannula
-handles for hook & triangle blades
-resection of medial 113 to Yz of plantar fascia
Complications
-Lateral column destabilization(most common)
-calcaneocuboid/midtarsal joint pain
-peroneal tenosynovitis
-sinus tarsi syndrome
-Medial column destabilization
-central arch pain
-intrinsic myositis
-hammertoe
-Other
-continued heel pain
-infection
-incision pain
-nerve entrapment-rare
-plantar fibroma
-MANAGEMENT OF CALCANEOCUBOID JOINT SYNDROME
-several weeks of restricted /partial weight bearing
-short leg weight bearing cast
-stretching
-night splint
-NSAID/steroid injections
-orthosis/cuboid pad
-physical therapy
-removable cast boot
-NWB short leg cast 4-6 weeks
268
METATARSAlrCUNEIFORM EXOSTOSIS
(aka-tarsal bossing; peak of Lampi ere)
Etiology
a) hypennobility of the first ray creates jamming of the first metatarsocumeifonn joint
b) jannning of the first metatarsocuneifonn joint causes dorsal osseous lipping at the joint and an arthritic
process within the joint.
c) bump pain, tendonitis of the extensor hallucis longus tendon and neuritis of the dorsal intennediate
cutaneous nerve can result from shoe pressure on the bump
Differential diagnosis
a) ganglion
b) neuroma
Treatment
a) conservative
1. padding (to take pressure off the bump)
2. change of shoe lacing (skipping islets so the shoe laces doesn't pass over the bump)
3. orthoses (prevents hypennobility of the first ray)
b) surgical
1. exostectomy: must actually make a divet in the bone to prevent recurrence
2. arthrodesis of the first MfP joint: indicated when there is significant DID, recurrence of the exostosis
or an unstable first ray
-
HAGLUND'S DEFORMITY
(Haglund's disease: osetochondrosis of the accessory navicular)
Diagnosis
a) history and physical: posterior lateral osseous bump on the calcaneus. T)'pically, females arc
symptomatic due to irritation from shoe gear.
b) differential diagnosis
1. calcaneal bursitis
2. achilles tendonitis
3. tendo Achilles calcification
4. tendo Achilles rupture
5. gout
6. tumor
7. fracture
8. connective tissue disease (ie-rheumatoid arthritis, Reiter's syndrome, psoriatic arthritis, ankylosing
spondylitis)
Pathogenesis
the osseous bump and soft tissue overlying are irritated by shoe gear causing pain.
Radiology
a) Fowler and Philip angle: measured on lateral radiograph.
1. intersection of a line tangent to the posterosuperior prominence at the insertion of the tendo Achilles
and a line tangent to the anterior tubercle and medial process of the plantar tuberosity.
2. nonnal = 44-69
3. when greater than 75 = Haglund's deformity
b) Total Angle (Vega): measured on lateral radiograph
1. the calcaneal incljnation angle can also contribute to the fonnation of a retrocalcaneal bump (Rueh)
2. the total angle is calculated by adding the calcaneal inclination angle to the Fowler and Philip angle.
3. a total angle above 90 is considered pathological
269
Calcaneal Inclination Angle
c) Parallel Pitch Lines: measured on lateral radiograph
Fowler" Phi lip .Angle

1. the first pitch line (pPL 1) is the line tangent to the anterior tubercle and medial process of the plantar
tuberosity. A perpendicular line is then drawn between the posterior lip of the talar articular facet and
the first pitch line (PPLl).
2. the second pitch line (PPL2)is dra"n parallel to the first pitch line and perpendicular to that
perpendicular line.
3. pathology is demonstrated if the bursal projection (the most superior posterior portion) of the calcaneus
projects superior to the second line.
Bursal projection touching or below PPL2 is considered nonnaL

Burnl Projec1ion
PPL2
PPLI
d) Valgus Curve of the Calcaneal Tuberosity: demonstrated on the Harris and Beath view.
Treatment
a) conservative: heel pads and shoe modification
b) surgical
l. Keck and Kelly: remove wedge from the posterior superior aspect of the calcaneus
2. Duvries: transverse resection of the bump through a lateral incision
3. Fowler and Philip:
transverse skin incision through posterior heel with a Mercedes incision through the tendo Achilles
resect bump through this incision
4. Dickenson: curvilinear medial incision from superior-medial to inferior-lateral
270
Complications
Avoid chasing the bump. With bone resection a new prominence is created The bump created should be
carefully rounded or additional bumps will be created with each resection.
Retrocalcaneal Exostosis
Retrocalcaneal Exostosis
Ensethopathy at Achilles insertion
Not Haglunds disease
Haglunds disease
Enlarged bursal peojection of the posrterior and superior calcaneus
Retrocalcaneal Exostosis- etiolog)'
Repetitive trauma / overuse
Equinus
Faulty biomechanics
Pathophysiology
Dystrophic calcification -
Haglund's deformity
Retrocalcaneal bursitis
calcification of soft tissues with normal calcium metabolism
Usually initiated by trauma which causes tendon fiber disruption. scar fomlation" hypovascularity
and ultilllately calcification
Symptoms and findings
Pain
Palpable painful bony prominence
Pain with passive ankle dorsiflexion
Swelling
Thickening of tendon
Possible Equinus
Treatment - conservative
Rest
Physical therapy - stretching
NSAID"s Cast Immobilization
Heel lifts / padding I orthotics Corticosteroid injection with cast immobilization
Treatment - surgical
1. Incisional approaches:
Transverse
Central midline longitudinal
Medial or lateral longitudinal
Medial or lateral L
Lazy S
2. Procedures:
Tendon splitting - partial detachment
Complete detachment
"V' tendon flap
Tendon advancement
Calcaneal osteotomies
271
3. Post-op course:
Immobilization - NWB 4-8 weeks
Physical therapy
Orthotics I change shoegear
Change exercise
Eauinus
Definitions
a) functional equinus: the foot cannot dorsiflex at least 10 degrees past the right angle relationship between
the foot and the leg. This degree of dorsiflexion is required for nonnal foot function.
b) classical equinus: the foot cannot dorsiflex 90 degrees in its relationship to the leg.
Types
a) gastrocnemius equinus: identified using the silverskiold test. The silverskiold test is performed by
measuring the re1ationship of the foot to the leg with the knee flexed at 90. If the equinus
relationship is demonstrated with the knee straight and not demonstrated with the knee bent at 90 ,
then a gastrocnemius equinus is present.
b) gastrosoleal equinus: this form of equinus is not resolved by performing the silverskiold test. Osseous and
pseudoequinus must be ruled out before a gastrosoleal equinus can definitively be identified.
c) osseous equinus: identified by bony abutment between the talus and the tibia anteriorly on a lateral stress
dorsiflexion radiogmph.
d) pseudoequinus: the apparent equinus is due to an abnormal forefoot to rearfoot relationship. This is a
cavus foot type.
e) combination equinus: any combination of the above.
Treatment
a) gastrocnemius recession
1. indications: gastrocnemius equinus
2. advantages: quick rehabilitation period
3. disadvantage: limited indication and limited deformity can be corrected.
4. procedures
Vulpius: "V" shaped cut through the aponeuronsis of the gastrocnemius muscle
Strnyer: tr.msverse cut through the aponeurosis of the gastrocnemius muscle
Baker: tongue and groove procedure in the gastrocnemius aponeurosis with the tongue portion proximal
McGlanuy and Fulp: tongue and groove procedure with the tongue portion distal
Silferskiold: resect heads of gastrocnemius muscle releasing them from their origin
272
c) tendo Achilles lengthening: all performed on the conjoined tendon of the gastrocnemius and soleus
muscles (tendo Achilles)
I. indications: gastrosoleal. severe gastrocnemius and combination types of equinus
2. procedures
open "Z"/closed "Z": transverse plane
Hauser: section posterior 2/3 proximally and medial 2/3 distally
White: section anterior 2/3 distally and medial 2/3 proximally
(based upon anatomical torque of tendo Achilles)
Hibbs: section the medial 2/3 proximally and then a longitudinal split in a distal direction at
the lateral end of the incision: section the lateral 213 distally and then a longitudinal split in
the proximal direction at the medial end of the incision
Stewart: for when tendo Achilles insertion is more medial than normal and contracted,
extending anteriorly on the surface of the calcaneus. An open transverse "z" was
performed. with sectioning of the medial I12 at the insertion and laterall/2 more
proximally.
Sgarlato: "Z-plasty" in frontal plane, sectioned anterior 2/3 distally and posterior 2/3
proximally
Hoke: triple hemi-section \Vith first and last sections medially and second cut laterally
c) tendo Achilles advancement: for spastic equinus (i.e. cerebral palsy)
see Murphy's triceps advancement under section covering tendon transfers
273
FLATFOOT
Flexible vs Rigid Flatfoot is evaluated by the following:
1. Active and passive range of motion of ankle, STJ. MfJ
Flexible feet have full r.mge of motion at the STJ and MfJ
2. Hubscher maneuver. passive dorsiflexion of the hallux with the patient standing creates the windlass
effect of Hicks in the flexible flatfoot
Arch elevation
Plantarflexion of first ray
Supination of rearfoot in medial arch height
External rotation ofleg
Flexible Flatfoot
Etiology:
1. Equinus
2. Congenital: talipes calcaneovalgus
3. Structmal forefoot-to-remfoot relationship
Compensated forefoot varus
Compensated forefoot valgus
Rearfoot equinus
4. Torsional abnonnalities
Adduction: metatarsus adductus, internal tibial torsion
Abduction: external tibial or femoral torsion. etc.
5. Frontal Plane abnormalities
Genu varum I valgum
6. Neural-nmscu1ar-ligamemous
Neurotrophic
Muscle imbalance
Flaccid paralysis
Ruptured tibialis posterior tendon. accessory navicular
L i ~ t o u s laxity I hypermobility: Ehlers-Danlos syndrome. Marfim's syndrome
**Note: The flexible flatfoot can eventually become rigid with the development of tarsal arthritis**
Radiology
*** Radiographic changes will reflect the primary plane of compensation (pIanal dominance)
1. Transverse plane (AP radiograph)
Talocalcaneal angle increases
Talonavicular congruency decreases (Talar head uncovering)
Normally- approx. 75% of the talar head is in contact with the navicular
Forefoot adductus angle decreases
Cuboid abduction increases
Wedge shaped navicular
2. Sagittal plane (lateral radiograph)
Talar declination angle increases
Calcaneal inclination angle decreases
Talocalcaneal angle increases
Midfoot sagging; naviculo-cuneiform breach
Talo-lst metJtarsal angle increases (negative Meary's angle)
274
3. Frontal plane (calcaneal axial, lateral radiographs)
Flearfootever.rion
Increased superimposition oflesser tarsus
Decreased first metatarsal declination angle
Decreased height of sustentaculum tali
***Note: In severe flatfoot ankle views should always be obtained to rule out ankle valgus***
Surgical Procedures
Categorized by:
Planal dominance
Osseous vs soft tissue procedures
Medial colwnn vs calcaneal procedure
Plana! Dominance:
Flefers to the primary plane of the flatfoot deformity (i.e., the plane in which is most
effected.
Although procedures are divided into the primary plane of correction, the other planes
are effected to a lesser extent, therefore all procedures provide triplaner correction
Transverse Plane
1. Evans calcaneal osteotomy
Osteotomy of calcaneus 1.5 em proximal to calcaneocuboid joint and insertion of a bone
graft lengthens the lateral colwnn and realigns the midtarsal joint
May unmask metatarsus adductus
2. Calcaneal-cuboid joint distraction arthrodesis
Also lengthens lateral colwnn
Thought to eliminate symptomatology at calcaneal-cuboidjoint created by the Evans
3. Kidner Procedure
Theoretically for transverse plane
Flemoval of prominent naviaJ1ar tuberosity or accessory navicular and transposition of
posterior tibial tendon plantarly into the naviaUar
Sagittal Plane
1. Lowman
Talonavicular fusion
Tendo Achilles lengthening
Tibialis anterior under the navicular into the spring ligament
Medial achilles tendon as accessory ligament for tenodesis of the medial arch
2. Hoke
NaviaJ1o-cuneiform fusion
Indicated with obvious fault or hypermobility at the naviaJ1o-cuneiformjoint
Can modify and fuse with plantarflexory bone graft
3. Miller
NaviaJ1o-cuneiform-first metatarsal fusion
Posterior tibial and spring ligament advancement using an osteoperiosteal flap
4. Cotton
Opening p1antarflexory wedge osteotomy of the medial cuneiform
5. Lapidus
1 st met - cuneiform arthrodesis
6. Young
Tendosuspension of the tibialis anterior through a keyhole in the naviaUar
T. anterior rerouted through the navicular (not detached from insertion)
Posterior tibial advanced under the navicular
275
7. Cobb
Hemisection ofT. anterior left intact at its insertion then reflected inferior and medial to
the tarsus and used to augment T. posterior
8. Tendo Achilles lengthening / gastroc recession
K1DNER LOWMAN
HOKE
MILLER
YOUNG
Frontal Plane
1. Orthotics
2. Chambers
Artbroereisis concept
Raises the posterior mcet of the subtalar joint using a bone graft under the sinus tarsi
3. Baker-hill
Osteotomy inferior to the subtalar joint posterior facet with bone graft
4. Selakovich
Opening wedge osteotomy of the sustentaculum tali with bone graft which restricts
abnormal subtalar joint motion
5. Calcaneal Osteotomies
Gleich: oblique osteotomy displaced anteriorly
Lord: displaces the calcaneus anteriorly, inferiorly and medially
Silver: lateral opening wedge with graft
Dwyer: medial closing wedge
Koutsogiannis: transpositional osteotomy
Straight cut performed parallel to and behind the peroneal tendons
Fragment shifted medially / can also be shifted anteriorly
Increases the supinatory moment arm of the tendoachilles
6. STJ Blocking Procedures
a) Arthroeresis
Really limits triplane motion at the subtalar joint
Plantarflexion of the talus
Transverse plane adduction of the talus
Frontal plane eversion of the calcaneus
276
Examples:
Addante: Villadot umbrella
Stapeg
Sgarlato mushroom
ValIente
MBA (Maxwell-Brnncheau)
b) Extra-articular STJ arthrodesis (EASTA)
Green-Grice arthrodesis
Extra-articular Fusion of the STJ in the sinus tarsi using bone graft
Appositional bone growth is not disturbed
Indicated in ages up to 12-14 years
FroJttal Plane FlaifDo1 Procedures
Arthroeresis Procecblres
CHAMBERS BAKER-HILL SD.AKOVICH GREEN-GRICE
Arthroeresis hnplaJl'ls
o
(spllere)
ADDANIE
~ s t3 ~
VlLADOT STA peg SGARLATO
GLEICH LORD sn.vm DWYER KOUTSOGIANNIS
Rigid Flatfoot
Etiology
Congenital
Oven:orrected flatfoot
Tarsal coalition -
Peroneal splSDl
Trauma (e.g. Lis Frnnc'sFracture I Dislocation)
Tarsal arthrosis I Charcot
Tarsal Coalition
1. Types
Syndesmosis: fibrous
Synchondrosis: cartilaginous
Synostosis: osseous
277
2. Incidence: approximately 500,4 are bilateral
Talocalcaneal (middle facet) - most common
Calcanea-navicular bar - second most common; "comma sign"
Talonavicu1ar - third most common
Clinical findings
Sudden onset of pain after increased activity
Symptoms usually occur at times re1ated to ossification of the coalition
T -N 3-5 yrs; C-N 8-12 yrs; T -C 12-16 yrs
With complete synostosis there is no acute pain because no motion occurs at that joint
Decreased STJ ROM
Progressive valgus deformity associated with bow-strung peroneal tendons behind the lateral
malleolus - peroneal spastic flatfoot Usually secondary to synovial irritation of the 81'J and
traumatic tenos}novitis; not due to a spasm of the tendon.
Radiographic findings
1. STJ coalition
I...ateralview
Irregular narrowing or absent middle :facet
Halo-effect: sclerosis surrounding the STJ caused by increased density
Late f i n d i n & , , ~
Talarbeak
Broadening and flattening of laternl taIar process
Ball and socket ankle joint
Harris and Beath calcaneal axial views
Evaluates middle and posterior facets
Standard:;:: 35,40,45 axial views
Three views determined by the angle of posterior facet declination reIative to
the weigh1bearing SUIface, 10 above and 10 below
Isherwood views
Oblique DP: anterior facet
Medial oblique: middle and posterior facets
I...ateral oblique: posterior facet
2. Calcaneon3vicu1ar coalition
Medial oblique: Anteater sign
Treatment
1. Conservative (ie-orthoses, PT, NSAIDs, BK cast)
2. Surgical
Excise the coalition
C-N bar: excise and interpose EDB muscle (Badgely)
Arthrodesis: selected joint or triple arthrodesis
Congenital Vertical Talus
Radiographic findings
Navicular dorsally dislocated on the taIar neck
Dorsiflexed, plantarflexed stress view:
Df stress - rearfoot remains in equinus
Pf stress - t-njoint remains dislocated
278
Treatment
1. Serial casting in younger patients
2. Surgical
Release soft tissue contractures
Tendon lengthening
Relocation of the T-N joint with pinning
lfnecessary, triple arthrodesis
CAVUSFOOT
Etiology
a) neuromuscular: most common cause
1. myopathy: muscular dystrophy
2. peripheral nelVe or lumbosacral spinal nelVe root pathology
>Charcot-Marie-Tooth disease
>Dejerine-Sottas's interstitial hypertrophic neuritis
>polyneuritis
>traumatic lesions of the sciatic nerve
3. anterior hom cell
>poliomyelitis
>myelomeningocele
>spinal cord tumor
4. spinocerebellar tracts
>Friedrich's ataxia
>Roussy-Levy syndrome
5. pyramidal or extrapyramidal tracts
>cerebral palsy
>extrapyramidal and spastic hemiplegia
6. cerebral cortex
>hysteria
b) other causes of cavus foot
1. infection: syphillis
2. idiopathic
3. trauma
>peripheral Den': damage
>tendon ruptures with subsequent fibrosis and contracture
4. congenital disorders
>myelomeningocele
>spina bifida
>myelodysplasia
>clubfoot
ClassifJCation
a) anterior cavus
1. metatarsus cavus: Lisfranc's joint
2. lesser tarsus cavus: lesser tarsal bones
3. forefoot cavus: Chopart's joint
4.locaJJgloballcombined
b) posteriorcavus
1. muscle weakness or spasticity of gastrocnemius or soleus
2. pseudoequinus: inadequate ankle joint dorsiflexion secondary to rigid anterior cavus deformity
279
Oinical Evaluation of the Caws Foot
a) subjective
1. age of patient/age of onset of caws deformity
2. symptoms and progression of caws foot type
-frequent inversion ankle sprains
-early futigue with arnhdation or stmding
~ a i n t of muscle weakness of the lower extremity
3. medical and fiunily history
-history of congenital spinal disorders
-fiunily histol)' of caws foot type and/or neuromusadar disorders
b) objective
1. neurological examination
-muscle and sensory testing
-assessmesnt of reflexes
<OOIdination tests
-electromyography and nerve conduction studies
2. physical examination
-test for flexible or rigid medial arch with the Kelikian push-up test
-assess ankle equinus
-evaluate calcaneal position - fixed varus?
-first ray: plantarflexed, fleXIble or rigid?
-digital deformities: flexible or rigid?
extensor substitution?
p1antar submetatarsallesions?
3. radiographic evaluation
-1ateral13diograph
decreased talocalcaneal angle
increased calcaneal incljnation angle
decreased talar declination angle
posterior break in the cyma line
''bullet hole" sinus tarsi
-AP radiograph
decreased talocalcaneal angle
increased metatarsus adductus
Principles of Cavus Foot Surgery
a) determine the underlying etiology
b) address the plane of deformity and the level at which the defonnity occurs. Examples:
>m!Ifoot varus - Dwyer
>ankle equinus - gastrocnemius rescession or TAL
>pJantarflexed first my - Jones suspension; DFWO
>rigid anterior caws - Cole; Japas
>digital clawtoes or hammertoes - DIPJ and PIPJ arthrodesis; Hibbs
c) cavus foot requires multilevel surgei)' (ie- digitslLisfranclmidfootlrearfoot)
Soft TISSUe Procedures (indicated for flexible defonnity)
a) p1antar fascial release
b) Steindler stripping: includes fascia, abductor hallucis, FDB, abductor digiti quinti and the long plantar
ligament
c) Bost and Larsen
-release of medial column joints
-release of plantar intrinsics
d) Garceau and Brahms
-resect the motor branches of the medial and lateral plantar nerves
280
Tendon Procedures
a) Jones suspension
-EHL is transferred to the neck of the first metatarsal
-hallux IPJ fusion
b) Hibbs suspension
-Steindler stripping
-long extensor tendons transferred to lateral cuneiform
c) modified Hibbs
-long extensor tendons transferred to the intermediate or lateral cuneiforms
-Jones suspension (EHL to first metatarsal with hallux IPJ fusion)
-anastomosis of the distal long extensor tendon stumps to the EDB tendons
d) Split Tibialis Anterior Tendon Transfer (ST A TT)
-transfer of lateral half of the tendon to insertion site of peroneus tertius tendon at base of fifth metatarsal
e) Tibialis Posterior Tendon Transfer
-tibialis posterior tendon is released from its insertion on the navicular and transferred through the
interosseous membrane
i] passed dOm} EDL sheath to insert in the lesser tarsus or
ii] half of tibialis posterior tendon is passed do\'\'n the peroneus tertius sheath and the other half is
passed dOm} the tibialis anterior sheath
f) Peroneus Longus Tendon Transfer
peroneus longus is released at the level of the cuboid and transferred through the intermuscular
septum, dO\,\,TI the EDL sheath and inserted into the lesser tarsus
peroneus longus may also be split in half; half anastomosed to tibialis anterior at its insertion and
the other half anastomosed to peroneus tertius
Osseous Procedures
Indicated for unreducible rigid deformity and in neuromuscular cases for stabilization of the foot: may also
require soft tissue release
a) Cole: dorsifle.xory wedge osteotomy
through the navicular-cuneiform
joints and cuboid
b) DuVries: dorsiflexory fusion
through the MTJ
c) Japas: displacement V-shaped osteotomy
through the cuboid, navicular
and medial cuneiform
d) IMyer: lateral closing wedge osteotomy
of the calcaneus
e) McElvenny-Caldwell: first metatarsal
-cuneiform fusion
f) DFWO of first metatarsal
g) triple arthrodesis
Caws Osteotomies
& a ~
Cok DuVr.res
~ .
Japas Dwyer
M.cElv.umy & ~ l l DFWO
281
TARSAL TUNNEL SYNDROME:
classically, entrapment of the posterior tibial nerve. This discussion will be limited to the classical type,
however, an anterior tarsal tunnel syndrome involving the deep peroneal nerve does exist.
Etiology:
Type A (direct)
7. local disease: usually either processes which produce edema or space occupying processes
occurring within the closed compartments under the Jaciniate ligament.
1. trauma: to the nerve itself or structures surrounding the nerve.
2. varicosities: causes venous congestion within the tarsal tunnel. Most common cause ofbilateIal cases.
3. congenital anomalies: accessory nmscles
4. os trigonum syndrome: inflammation with edema of the FHL tendon
5. abductor hallucis nmscle hypertrophy: space occupying
6. space occupying lesions within the tarsal tunnel: neurilemotl13, neurofibroma, lipoma,. ganglion.
aneurysm.
7. tenosynovitis: produces edema
8. iatrogenic: intra-operative, steroid nyections, tourniquet trauma, casting.
b) systemic disease
1. diabetes mellitus with associated neuropathy
2. inflammatory arthritides (ie-rheumatoid arthritis, ankylosing spondylitis)
3. crystal deposition diseases (ie-gout, pseudogout): producing crystals and edema within the tunnel.
4. mixed connective tissue disease (ie-SLE)
5. myxedema: synovial thickening
Type B (functional)
a) pronation: internal rotation of the leg with tightening of flexor retinaculum.
Diagnosis
a) History and Physical: neurological signs and symptoms on the plantar aspect of the foot
1. pain: shooting, burning or electric type sensation
2. burning sensation
3. symptoms worsen with prolonged weight-bearing and at night.
4. palpation of COId-Iike swelling
5. venous tourniquet test (causes symptonis to worsen due to congestion)
6. Tinel's sign
7. Valleix's points
8. sensory changes: two point tactile, pin prick and proprioception
9. diagnostic tibial nerve block: should resolve the pain temproarily
10. atrophy of the plantar intrinsic nmscles and plantar changes in sweat production (severe cases)
b) Electromyographic studies: prolonged latency as well as decreased nerve conduction Velocity support the
diagnosis of tarsal tunnel syndrome.
1. electromyography
2. nerve conduction velocity
Treatment
Conservative
a) corticosteroid injections
b) posterior ubial nerve blocks
c) immobilization (ie-casting)
d) orthosis: to prevent pronation
Smgical
a) external neurolysis: consists of releasing the laciniate ligament swgically. The ligament is not
reapproximated during closure. Recurrence rates of 5-20010 have been reported.
282
TRIPLE ARTHRODESIS
Definition: fusion of the following three joints
a) talocalcaneal (subtaIar)
b) calcaneal-cuboid
c) talonavicular
Indications
a) correct deformities
1. valgus deformity
2. varus deformity
3. flatfoot
4. caws foot
5. talipes equino varus
6. fixed equinus
7. fixed dorsiflexion
b) relief of pain
1. tarsal coalition
2. arthritis
3. ruptured tIbialis posterior tendon
4. salvage for severe calcaneal fractures
c) stability/improve motor power
1. lateral ankle instability
2. neuromuscular disorders
Fixation of Triple Arthrodesis
a) screws
b) pins
c) staples
d) external fixation
Triple Arthrodesis procedures
a) Ryerson:"classic triple arthrodesis" simple
joint resection
b) Hoke: remove head of talus, resect articular
surface and replace head
c) Haughton Dunn: remove l1a\>;cular
d) Elmslie: indicated for fixed calcaneus foot
type
e) Lambrinudi: indicated for fixed equinus foot type
f) Brewster: countersink talus
g) Grice: extra articular fusion of subtalar joint
h) dowel graft: uses dowel plugs of bone to fuse the joints
Complications
a) intra-operative neurovascular injury
b) ankle arthrosis
c) malalignment (can cause callosities)
d) malunion
e) nonunion (talonavicular joint most common)
TripJe Arthrodesis Procecl'ures
\
Naughton Dunn
Hoke
Lamltrinwli
Ebnslie
B:rews-rer
Ryerson
G:rh:e
283
TENDON TRANSFERS
Objectives
a) provide active motor power; in generaI, one grade of muscle strength is lost through tendon transfers
b) elimination of deforming force
c) produce stability
d) cosmesis
e) elimination ofbI3Cing
General indications
a) muscle imbalance
1. flexible hammertoes
2. hallux valgus
3. dorsal bunions
b) paralytic foot
I. poliomyelitis
2. Duchenne's muscular dystrophy
3. Charrot-Marie-Tooth disease
4. cerebral palsy
5. spinal cord impingement
6. sciatic nerve palsy
7. common peroneal nerve palsy ("Saturday night palsy")
8. drop foot
c) congenital deformities
I. recurrent clubfoot
2. forefoot equinus
3. flexible flatfoot
d) iatrogenic deformities
1. hallux varus
Procedures:
Jones tendosuspension procedure
a) procedure: the extensor hallucis longus tendon is transected at its insertion and transferred through a
transverse hole in the first metatarsal. The tendon is anchored by suturing it to itself dorsally.
b) indications: hallux extensus (cock-up hallux deformity) due to flexible cavus foot deformity or flexible
plantarflexed first ray.
c) 3(ljunctive procedures: fusion of the hallux interphalangeal joint to prevent an interphalangeal flexion
deformity. .
Panmetatarsal tendosuspension procedure
a) procedure: any or all the metatarsal heads can be suspended as in the Jones suspension
b) indications: flexible hammertoes
c) adjunctive procedures: digital fusions and/or transfer of the distal attached portion of the tendon to the
extensor digitorum brevis.
Kidner procedure (refer to flatfoot procedure section)
a) procedure:
resection of the accessory navicular and/or hypertrophied navicular tuberosity
transposition of the tibialis posterior tendon insertion from a more lateral navicular attachment to a more
plantar navicular attachment
b) indications: adjunctive procedure for a medial column flatfoot
c) 3(ljunctive procedures: usually performed with an osseous flatfoot corrective procedure
284
Hibbs tendosuspension
a) procedure
transection of the extensor digitorum longus tendons
b) transfer the tendons to the midfoot (usually into a trephine hole in the intermediate or lateral
cuneiform)the distal portions of the tendons are usually transferred (sutured) to the EDB tendon
c) indications: functional equinus (this gives the EDL tendon greater mechanical advantage in
dorsiflexing the foot and prevents the formation of hammertoes)
d) aq;unctive procedures: may be performed with a Jones suspension of the hallux and/or digital fusions
Tibialis Anterior Tendon transfer
a) procedure: transection of the tibialis anterior tendon at its insertion and transferring it to the
intermediate supination deformity from muscle paralysis (ie-CM1) or congenital muscle imbalance
(ier. ecurrent clubfoot). Also used to correct drop foot.
b) ru:ljunctive procedures: tendo Achilles lengthening or gastrocnemius recession to weaken the posterior
muscle group and/or fusion procedures of midfoot or rearfoot.
Split Tibialis Anterior Tendon transfer
a) procedure:
incisions are made over the tibialis anterior tendon at its insertion and between the middle and
distal thirds of the leg.
the tendon is split from its insertion to the level of the proximal incision.
the lateral half of the tendon is transected at its insertion and passed through the proximal incision
a third incision is made at the cuboid/peroneus tertius insertion area
the lateral half of the tibialis anterior tendon is passed either through the tendon sheath of the
peroneus tertius then sutured to the peroneus tertius near its insertion or, when the peroneus
tertius is absent, attached to the cuboid via tenodesis.
b) indications: flexIble varus and/or equinus deformities at the rearfoot or midfoot levels (increases
dorsiflexion and eversion)
c) aqjunctive procedures: dorsiflexory osteotomy of the first metatarsal, digital deformity correction,
calcaneal osteotomy and tendo Achilles lengthening.
Young tendosuspension (actually a transposition)
a) procedure: the tibialis anterior tendon is passed through a slot in the navicular without distwbing the
insertion. The ubialis posterior tendon must be detached from its insertion to perform the procedure.
It is reattached to the plantar surface of the navicular.
b) indications: flexible pes p1anus
c) aqjunctive procedures: other flatfoot procedures
Tibialis Posterior Tendon transfer
(a non-pbase transfer; can also cause flatfoot)
1. procedure:
incisions are made dorsally over the midfoot and over the posterior tibial muscle between the
middle and distal thin:Is of the leg. The tendon is transected at its insertion and passed through
proximal incision.
two piths for passing the tendon -
1. Ober technique: the ubialis posterior tendon is passed from the proximal incision and brought
around the medial malleolus and transferred into the lateral cuneifonn.
2. Putti technique: the tibialis posterior tendon is passed from the proximal incision and brought
t:brougb the interosseous membIane and transferred into the lateral cuneiform.
b) indications: flexIble or spastic equinus deformities
285
Peroneus Longus Tendon transfer
a) procedure:
an incision is made at the level of the cuboid where the peroneus longus tendon is identified
the distal portion of the peroneus longus tendon is pulled tight and sutured to the peroneus brevis
the peroneus longus tendon is transected just proximal to where it is sutured to the brevis
the tendon is then transferred through the intermuscular membIane to the IateIal ameiform
(alternatively the tendon can be split and attached to the peroneus tertius and the anterior tibial
tendons)
b) indications: flexible equinus (drop foot) deformity
Murphy triceps advancement
theoretically reduces the lever arm of ankle pIantarflexion by 50% 'while reducing the lever arm of
propulsion by 15%
a) procedure
transection of the tendo Achilles at its insertion
advancement of the tendon anteriorly, just posterior to the posterior facet of the subtalar joint
b) indications: spastic triceps in cerebral palsy
Tendon Function Around The Suhtalar Joint Axis
286
ANKLE SURGERY
Medial Ankle Instability Surgen-
Deltoid ligament injuries 0CC\lI' when the foot is forcibly everted on the leg. Chronic isolated deltoid injury is
rare. usually an old fibular :fracture is involved or undiagnosed tibiofibular diastasis.
a) Anatomy of the deltoid ligament
The deltoid ligament is divided into two portions, the deep and superficial deltoid ligaments. The
superficial portion is composed of the tibiocalcanealligament. The deep portion is composed of. from
anterior to posterior, the anterior tibiotalar, tibionavicular, intennediate tibiotalar and posterior
tibiotalar ligaments. Frontal plane instability is demonstrated by stress eversion mortise radiographs.
Generally 10 or greater degrees of talar tilt is considered positive and indicates rupture of the
tIbiocalcaneal and intennediate tibiotalar ligaments.
b) Surgical procedures
1. Schoolfield's procedure: the damaged deltoid ligament is detached at the origin in the tibia. The
foot is then forcibly inverted and the deltoid is sutured into the periosteum superior to the
detachment site. This effectively advances the deltoid ligament
2. Du Vries' procedure: the deltoid ligament is cfu,ided vertically and horizontally creating a cruciate
defect, which is then resutured Du Vries' suggested the resultant scar formation is strong enough
to stabilize the medial ankle.
3. Wittberger and Mallory's procedure: the procedure utilizes a split portion of the tibialis posterior
as a tendon graft to reinforce the medial ankle ligaments. Approximately 5 em proximal to the
ankle mortise one half of the tibialis posterior is harvested and split to its insertion in the
navicular. The portion of tendon is then passed inferiorly to superiorly through a drill hole in the
distal tIbia and sutured blck onto itself with the foot forcibly inverted
Lateral Ankle Instability Surgery
Lateral collateral ligament pUhology is extremely common and is caused by repetitive inversion injury to the
ankle. Chronic instability of the lateral ankle is a disabling condition which can predispose the patient to ankle
fractures, osteochondral talar dome fractures and degenerative joint disease.
a) Anatomy of the lateral collateral ankle ligament: the lateral
collateral ankle ligament is composed of three separate
ligamentous structures.. The anterior talofibular ligament is an
intracapsular structure which resists anterior displacement of the
talus within the ankle joint mortise. The calcaneofibular ligament
is extracapsular and oriented approximately 105 from the anterior CF
talofibular ligamentIt resists inversion of the talus within the
ankle mortise. The posterior talofibular ligament is a strong
intracapsular ligament which is situated in a nearly horizontal
plane. This ligament resists posterior displacement of the talus in
the ankle mortise.
b) Diagnosis of lateral collateral pathology: rupture or weakness of the ATF can be confirmed with an
anterior dJ:a\\'-er or push-pull lateral stress radiograph. An anterior displacement of2 em or greater as
compared to the contralateral limb is considered abnormal. Rupture or weakness of the CF ligament can
be confirmed utilizing stress inversion mortise radiographs. A talar tilt of 10 greater than the unaffected
contra1aterallimb is considered abnormal. Ankle arthrograms or peroneal tenography are only indicated
in acute ligamentous rupture with patients who have no prior history of ankle trauma. A peroneal
tenogram is greater than 95% accurate for detennination of acute calcaneofibular ligament ruptures.
287
c) Surgical procedures:
Procedures may be grouped into which ligament or ligaments they are designed to replace.
I. delayed primary ligamentous repair
Usually indicated in acute ligJImentous injury. In cases of chronic instability the
ligaments may be stretched and not tom Imbrication of the ligaments utilizing
nonabsorhlble suture is then peIformed.(Brostrom)
Gould modification: reinforcement of repair with extensor retinaculum
IT. anterior talofibular ligament replacement
::::> As a group these procedures reconstrud the A1F utilizing various structures usually passed
through the fibula, talus and occasionally the calcaneus following the anatomic orientation
of the A1Fligament.
>Watson-Jones procedure: utilizes peroneus brevis
>mini Watson-Jones procedure: utilizes peroneus brevis
>McLaughlin procedure: utilizes a split peroneus brevis
>Lee procedure: utilizes peroneus brevis
>Pouzet procedure: utilizes peroneus longus
>Storen I: utilizes a portion of the Achilles tendon
> Weber procedure: utilizes plantaris tendon
>Sefton procedure: utilizes p1antaris or long extensors
>Haig procedure: reinserts the A1F ligament
>Dockery, Toothaker and Suppan: utilizes split peroneus brevis and tertius
ill. anterior talofibular and calcaneofibular repIacement
::::> These procedures reconstruct the A1F and CF ligaments utilizing various structures passed
through and between the fibula, talus and calcaneus following the anatomic orientation of the
A1F and CF ligJIments.
>Elmslie procedure: utilizes fascia lata
>Christman-8nook: utilizes split peroneus brevis
> Winfield procedure: utilizes peroneus brevis
>Storen II: utilizes a free tendon graft of Achilles tendon
> Ahlgren-Larsson: a subperiosteal advancement of both A1F an CF ligaments
>Split Peroneus Brevis LateIal Ankle Stabilization:
utilizes split peroneus brevis tendon
IV. A1F, CF and PIF ligament repIacement
::::> Designed to replace all three ligaments in anatomic or near anatomic position.
>Spotoff. utilizes fuscia lata
>Rosendahl-Jensen: utilizes fascia lata
V. Extra-anatomic Lateral Ankle Stabilization
::::> These procedures reinforce the lateral ankle without following specific anatomically correct
ligamentous orientation.
>Nilsonne procedure: utilizes peroneus brevis
>Evans procedure: utilizes peroneus brevis
>Larsen procedure: utilizes peroneus brevis
>Viernstein procedure: utilizes peroneus brevis
288
Subluxated or Dislocated Peroneal Tendon Repair Procedures:
Dislocation and subluxation of the peroneal tendons is usually seen with sports injuries in which forced ankle
motion takes places while the peroneal tendons are under maximum tension.
a) Surgical procedures
1. Kelly and Watson-Jones procedure: an osteoperiosteal
flap is created in the posterior aspect of the lateral malleolus. The procedure effectively deepens the
sulcus preventing recurrent dislocation.
2. DuVries procedure: a wedge-shaped osteotomy is created in the posterior aspect of the lateral malleolus
which forms a bone graft. The bone graft is displaced posteriorly and fixated forming a bony block
to prevent dislocation.
3. Daimant -Berger: plicated and reinforced the peroneal tendon sheath.
4. Folschveiller: utilized a periosteal flap to reinforce the sheath and redirect the peroneal tendons
posteriorly.
5. Jones procedure: stabilized the peroneal tendons by reconstructing the retinacular ligament 'with a flap of
Achilles tendon.
:..---
Kelly & Wauon-Jones DUVRIES
AnierlorTalo6lndar lipmeni Repwemeni
Wabon-Jo:net
Se&.n,eial
DodsIery, Suppan,
Too1LaJser
289
-
Vieru1ein
ANKLE ARTHROSCOPY
In 1920 Takagi of the University of Tokyo was the first to view the inside ofajoint with an arthroscope. Since
that time great strides have taken p1ace in equipment and techniques which continue to develop today. The
surgical morbidity associated with arthroscopy is extremely low and the potential benefits to the patient are
high.
Arthroscopic Equipment
a) arthroscope: a lens containing, light-tnmsmitting tube which allows the transmission of a picture
to a television monitor or to the surgeon's eye. The arthroscopes of today contain GRIN
(Gradient Refractive Index) lenses. This lens is a solid relay lens rod coated with black paint
which allows the least amount oflight loss currently available. The tip of the arthroscope is
angled from 0 to 90 . The oblique angle on the tip of the scope allows for a greater field of view,
which allows the surgeon to peer around bends in joints. Arthroscopes are available in outer
diameters of!.7 mm. 2.2 mm. 2.7 mm. 3.5 mm and 4.0 mm..
b) light somt:eS: there are three types oflight sources all of which transmit light into the joint via
fiberoptic cables.
~ lamps: color tempeIatures of2900 K. least powerful
metal halide]amps: color temperature of 5800 K. intermediate power
xenon lamps: color temperature of 6000 K. which corresponds to daylight, most
powerful
290
c) cameras: two types are used. The Saticon tube camera functions very well in low light but is not
submersible for sterility. The ceo integrated-circuit cameras are submersible and have much
less bulk, but require more light.
d) hand instruments: include - trocars, obtwators and cannulas for entering joint spaces. Probes,
knives, rasps, scissors, curettes and grasping forceps or basket forceps are also used. A
very useful hand instrument is the suction punch which enables the surgeon to grasp
tissue and aspirate it from the joint without removing the instrument.
e) power instruments: motorized cutters, shavers and abrasion burrs which allow arthroscopic
debridement to procede at a much faster rate.
1) miscellaneous equipment: leg holders are padded U-shaped devices which secure the leg during
surgery. Joint distraction devices are also available.
Arthroscopic Portals of the Ankle
The ankle is divided into posterior and anterior joint cavities each with a medial, centrnl and lateral
compartment. There are five classic portals of the ankle joint. Three are located anteriorly and two
posteriorly.
I. anterior portals: anterocentral portal is placed between the extensor tendons and care is exercised
not to injure the anterior tibial artery or deep peroneal nerve. Most arthroscopic surgery may be
conducted through this portal. The anteromedial and anterolateral portals are designed for
vie\\'ing medial or lateral gutter structures and for placement of hand or power instrumentation.
ll. posterior portals: posterolateral and posteromedial portals are placed just lateral or medial to the
Achilles tendon. These are ancillary portals for examining the posterior ankle joint structures and
for reaching deep posterior lesions.
ill. accessory portals: an accessory portal is placed anywhere it is needed. TI3DS-malleolar portals
have been described.
Arthroscopic Technique
Three basic principles are involved in arthroscopic maneuvering.
1. scanning: a sweeping motion from side-to-side and up-and-down. Scanning allows a large area
to be viewed.
II. pistoning: moving the scope in and out, which allows the field of view to be enlarged or
reduced.
ill. rotation: turning the arthroscope on its axis. Allows a larger field of view due to the obliquity of
the arthroscope tip.
N.
Arthroscopic Joint Pathology
Initially the arthroscope was simply a diagnostic instrument, however with the advent of hand and
power instrumentation, the utility of the arthroscope is becoming evident.
I. synovitis: finger-like villi of hypertrophic synovium. Usually indicative of underlying joint
disorders.
ll. chondromalacia: this condition is an arthritic change in the articular cartilage causing changes in
consistency, texture,color and resilience. The affected cartilage must be debrided and the
subchondral bone exposed, which will allow fibrocarti1age formation.
ill. osteochondrallesionlfracture: classi:fied by Berndt-Hardy, these lesions are ~ and
sometimes difficult to visualize. The lesion must be resected by probing the extent of the
fracture and abrading or grasping the fiacture itself
IV. jmpingement lesions: hyalinized meniscoid bodies or bands which restrict motion and cause pain.
Easily resected with knives, graspers and/or suction pmches.
V. erosions: discrete focal areas of articular cartilage loss which may be abraded to subchondral
bone and replaced with fibrocartilage.
VI. emprgjng arthroscopic techniques: arthroscopic stapling or suturing for chronic lateral ankle
inslability and arthroscopic ankle fusion techniques are being developed.
291
ANKLE FUSIONS
Indications
a) arthrosis
b) severe angu1ar defonnity
c) irreparable acute trauma
d) bone tumor
e) chronic osteomyelitis
f) failed ankle prosthesis
g) paralytic deformities
h) salvage of avascular necrosis oftalar body
Anlde Fusion Fixation
a) screws
b) plates
c) pins
d) staples
e) external :fixation
Intra-articular Grafts
a) Hallock: bone chips
b) ChuinaId and Peterson: iliac wedge
c) Campbell: cortico-cancellous iliac graft in vertical fashion
d) Wescott: graft:from proximal tibia
e) Stauffer: salvage for failed total ankle prosthesis
cancellous bone packed around a cortical block
f) Van Gorder and Chen: tIbial bone graft into ankle joint without resection of joint surfaces
Anterior Grafts
a) GalIie: inlay grafts
b) Kennedy: allogenic grafts with staple fixation
c) Hatt: :fibu1ar spike
d) BriUain: tibial graft through hole in pJafond
Posterior Grafts
a) Carnrbill: :fish scale
b) White: iliac wedge
c) Gill: calcaneal wedge
Sliding Grafts
a) Qamer: sliding tibia
b) Soren: sliding tibia
c) Blair: sliding tibia into superior aspect of neck of talus used for avascular necrosis of talar body
Malleolar Osteotomy
a) Man:us. Balourdas and Heiple: chevron osteotomy of medial malleolus
b) Wdson: used only anterior halves of both malleoli
c) Bingold: :fibular spike through calcaneus
d) Anderson: bimalleolar resection, crushing and used for cancellous graft
e) Mead: bimalleolar
f) Goldthwait :fibula
g) Horwitz: split:fibu1a, and place half anteriorly and halflateraIIy
h) Adams: spIit:fibu1a, fix lateral half on to fusion site and medial half used for cancellous chips
i) Glissan: medial malleolus
j) Stewart and Harley: bimalleolar osteotomy preserving the outer cortices
k) Royal Air Force: :fibula
292
Dowel Fusion
a) Baciu and Filibiu: medial approach, using image intensification
b) Hone: dowel from anterior to posterior
c) Pridie: medial approach
d) Graham: cylindrical fibular graft
Internal Fixation
a) Doctor's Hospital: uses two 6.5 mm cancellous screws from tIbia into talus
External Fixation
a) Charnley
b) Muller
c) Calandruccio
bt.tra-articubr Grafls
Position of Arthrodesis
a) sagittal plane is neutral
b) valgus (0-5 degrees)
c) externally rotated (5-10 degrees)
d) posterior displacement of talus
Hallock Ckuiltard & PeiersoJl
1. counteract JK1ll of tendo Achilles
2. preserve prominence of heel
Anierior Tibial Grafis
Complications
a) intra-operative neurovascular injury
b) malunion
c) nonunion
Cramer
Hatt
Malleolar Osteo1Dmy
Posterior ArtItrodesis
If) II
~ ~
Gill
293
PLASTIC SURGERY
PLASTIC SURGERY
PLASTIC SURGERY
PLASTIC SURGERY
PLASTIC SURGERY
PLASTIC SURGERY
PLASTIC SURGERY
PLASTIC SURGERY
PLASTIC SURGERY
PLASTIC SURGERY
PLASTIC SURGERY
PLASTIC SURGERY
PLASTIC SURGERY
PLASTIC SURGERY
PLi-\STIC SURGfiR'l'
P'L}\STIC SURGER
SlJR,(} f{ '\
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PL. AS" '1T' S'lTRC---
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1
Plastic Surgery
WOUND HEALING
Healing by first intent: is the least complicated example of wound repair, and is the healing of a clean, uninfected
surgical incision, approximated by surgical sutures.
a. narrow incision space immediately fills with clotted blood containing fibrin and blood cells.
b. Dehydration of the surface clot forms the scab.
c. Within 24 hoors, neutrophils appear on the margin of the wound
d. Within 24-48 hoors, the cut edges thicken from mitotic activity of basal cells, epithelial cells from
the edges migrate along the cut margins of the dermis depositing basement membrane as they move.
These cells fuse to form a thin but continuous epithelial layer.
e. By day 3, neutrophils are replaced by macrophages. Increased granulation tissue at the incision site.
Collagen fibers are beginning to be manufactured along the margins, but do not bridge the gap. The
thin epithelial cell layer thickens.
f. By day 5, Neovascularization is maximal. Collagen fibers begin to bridge the gap. Epidermis is back
to its original thickens, and full differentiation.
g. During the second week, increased collagen and fibroblasts. Decreased to absent leukocytic
infiltration, edema, and increased vascularity. Beginnings of blanching due to increased collagen and
decreased vascularity.
h. End of first month, scar develops, increased tensile strength, maximal tensile strength achieved in
several months.
STAGES OF SKIN GRAFT HEALING
1. plasmatic stage: occurs 2448 hours following graft application. A fibrin layer is formed between the graft and host
bed which serves to anchor and allow diffi.Jsion of nutrients to the graft.
2. inoscultation stage: this stage begins at 48 hours and involves revascularization of the grafted tissue. The graft will
demonstrate a pink hue during this stage. Lymphatic drainage will be established by the fourth to fifth day.
3. reorganization stage: the process of reorganization continues for months following grafting. Connective tissue will
reorganize and regulate vascular and lymphatic flow.
4. reinnervation stage: occurs simultaneously with the reorganization stage. The process may require one to two years
to complete.
FACTORS INVOLVED IN SCAR PROGNOSIS
[Comprehensive Textbook of Foot Surgery]
Factors Effects
Age*
Race*
Body region *
Wound course and pattern**
Wound Length**
Tension**
Skin tension lines**
*Factors that are uncontrolled by surgeon
**Factors that are controlled by the surgeon
Young patients may hypertrophy
Blacks more likely to hypertrophy
Among whites: blondes have a finer
scaring than brunettes
Foot and leg heal well; related to
wound tension
(See "Tension")
Multiple small incisions heal better
than one long uninterrupted
incision
Tension hypertrophies a scar
Parallel lines give fine scars,
anti tension lines hypertrophy
294
FACTORS IN WOUND HEALING
Pre-existing disease states.
Nutritional status
Infection
pH
Oxygenation
Venous return
RESTING SKIN TENSION LINES
-History of skin lines is very extensive, and very boring.
-Basically, RSTL is recognized when a regularly shaped furrow is created upon pinching the skin area with index
finger and thumb.
-These lines are often perpendicular to the long axis of muscles and their tendons, and often parallel to the axis of
joints at the level of the joint.
-Ideal scar results can be acquired by placing incisions parallel to these RSTLs.
-You will quickly notice that placing incisions parallel to RSTLs will not provide adequate exposure to the
surgical field. This is overcome by "zig-zaging" or creating an S-shaped incision. These incisions have
become to be known as Anti tension lines.
WOUND COVERAGE TECHNIQUES
-{}pen wounds must be provided with coverage. These coverage techniques are some of the most cleverly devised
and technically challenging to do in all of surgery.
-Wound coverage should follow a step-wise approach. The simplest technique should be considered first. It
should follow this way: Direct closure -> Grafts -> local flaps -> distant flaps.
- These include direct closure, skin grafting, flaps (including musculocutaneous and free flaps), artificial skin,
cultured cells, amnikon, and xenografts.
1. Skin Grafts
This form of wound coverage involves removing varying thicknesses of epidermis and dermis from
a donor site, and delivering it to the wound or graft site.
Classified as:
a Autografts, Allografts, isografts, and xenografts.
1) autografts: a tissue harvested and applied within the same individual
2) isografts: a tissue harvested and applied within a set ofidentical twins
3) allografts: also called homografts, tissue is transferred between individuals of the same
species
4) xenografts: also called heterografts, tissue is transferred between different species.
Xenografts function only as biologic dressings and never area incorporated into the
host's tissues
b. Full or spIit(0.OO8-0.012-0.016-0.020) thickness
1) split tbiekness skin graft (STSG): also called partial thickness skin grafts. Only a
portion of the dermis is harvested. Split thickness grafts are the most commonly used free
grafted tissue. There are four types:
a) thin grafts: grafts with a thickness of 0.008-0.0 12 inches. Excellent host tissue
incorporation, however, this form of graft contracts the most.
b) intermediate grafts: grafts with a thickness of 0.012-0.016 inches. This form is
more durable and contracts less, however, host incorporation is slightly diminished.
c) thick grafts: grafts with a thickness of 0.0 16-0.020 inches. The thicker the grafted
tissue the less chance ofhost incorporation, due to greater tissue demands.
Dmability and contraction are much improved.
d) meshed grafts: this type of graft can be any thickness, but is placed through a
meshing device which fenestrates the graft with unifmnly placed incisions. This
process allows the graft to expand permitting greater surfuce coverage and prevents
seroma and hematoma from collecting beneath the graft. Interposed spaces heal by
epithelial migration from the surrounding graft tissue.
295
2) FaD thickness skin grafts: involves all of the dermis and portions of the superficial
fuscia Any superficial fuscia or subcutaneous tat harvested must be removed prior to
graft application. The primary indication for this type of graft is coverage in
weightbearing areas or flexion points. The probability of host incorporatim is much
lower than that of split thickness grafts. Donor sites usually include the inguinal or
popliteal fossa areas. Small full thickness grafts may be harvested :from the foot in the
areas of the medial arch and sinus tarsi. Donor site must be primarily closed or have a
split thickness skin graft applied.
3) Apligraf (SEE BELOW)
-Advantages: permanent coverage, technically simple, low risks, can be applied to almost any
area of the body.
-Disadvantages: increased failure rate over tendons and bone, graft contracture with split SO,
increased failure rate with full thickness due to vascularization difficulties, infection or non healing donor
site.
Instrumentation for harvesting: Hand(Blair & Humby knives)or power( electric, gas or batteried
powered dermatomes) instrumentation. Another useful device is the graft mesher. The graft mesher
serves two purposes, first it allows the graft to remarkably increase its size, and second it prevents the
biggest complication :from forming, seroma and hematomas. Another technique for preventing seroma
and hematoma build up is via pie-crusting.
Application of the graft:
a. graft must be in intimate contact with recipient tissue.
b. all excess fluid must be removed :from recipient site.
c. graft must slightly overlap the wound edges.
d. suture graft into place.
e. prevent shearing of revascularized graft by bulk dressings( cotton balls, fluffed gauze) secured
by stent tie-over dressing. Moistening dressings may facilitate dressing removal later on.
Excessive pressure must be avoided, because vascular channels can be occluded.
f. limb must be immobilized in cast or posterior splint.
g. post-operative dressings remain intact for 3-4 days.
h. Storage of skin grafts: a skin graft should be harvested and applied immediately, however, excess
skin graft may be stored in saline or anttbiotic solution soaked gauze and placed into a 0-5 refrigerator
for up to 21 days.
Postoperative Course
a. Removal of dressings 3-4 days post-op is done with great care.
b. hematomas and seromas are recognized and punctured with a No. 11 blade.
c. graft should be revascularizing and "pinking-up".
d. necrotic tissue is to be removed.
e.compression is maintained over graft for several months.
Complications of skin grafts: Any process which contacts between graft and host bed is interrupted will cause
skin graft death.
seroma: the most common cause of skin graft failure. A transudative fluid accwnulation beneath the graft
which tents it away :from the host bed. Seroma is prevented by proper application of a pressure dressing usually in the
form of a stent dressing. The technique of "pie austing" or placement of multiple, small incisions in the graft will allow
the seroma to escape the the dressing. Fluid may also be aspirated :from areas of concavity.
hematoma: similar to seroma, blood collection beneath the graft will also cause graft failure. Hemostasis of
large bleeding vessels is necessary, however, capillary bleeding is normal and required for healing. Normal capillary
bleeding may be controlled with proper fenestra tim of the graft and pressure dressing application.
infection: greater than 9()01o of all skin grafts will take when the level ofbacteria is less than 10 bacteria per gram of
tissue, however, certain organisms can destroy grafts quickly. Streptococcus pyogenes and pseudomonas pyocyanes
produce fibrinolysins which disrupt the fibrin bond and devastate the graft. Systemic antibiosis has variable results in
preparing recipient sites. Local wOWld care is far more important in reducing or eliminating infection.
296
APLIGRAF
Description: a viable, bi-Iayered, skin construct: the epidermal layer (dull, matte finish) is formed by human
keratinocytes and has a well-differentiated stratum cornewn; the dermal layer (glossy finish) is composed of human
fibroblasts in a bovine Type I collagen lattice. While the graft contains matrix proteins and cytokines found in
hwnan, Apligraf does not contain Langerhans cells, melanocytes, macrophages, lymphocytes, blood vessels or hair
follicles. Apligraf is manufactured under aseptic conditions from human neonatal male foreskin tissue.
Indications: for use with standard therapeutic compression for the treatment of non-infected partial and full-
thickness skin ulcers due to venous insufficiency of greater than I month duration and which have not adequately
responded to conventional ulcer therapy.
Contraindications:
clinically infected wounds
patients with known allergies to bovine collagen
patients with a known hypersensitivity to the components of the Apligraf agarose shipping medium
How Supplied:
sealed in a heavy gauge polyethylene bag with a 1 0% C ~ / a i r atmosphere and agarose nutrient medium
should be kept in the sealed bag at 20C-31C until use (for single use)
supplied as a circular disk approximately 75 mm in diameter and 0.75 mm thick
should be used within 5 minutes of opening
To maintain cell viability, the product is aseptically manufactured, but not terminally sterilized
Preparation ofthe Venous Ulcer Wound Bed Prior to Apligraf Application:
Wound Infection: graft should not be applied over infected or deteriorating wounds until the underlying
condition has been resolved
Bacterial Containment: Antimicrobial agents may be used during the week prior to Apligraf application to
reduce the risk of infection. Dakin's solution, Mafenide Acetate, Scarlet Red Dressing, Tincoban, Zinc Sulfate,
Povidone-iodine solution, and Chlorhexidine have been determined to be cytotoxic to Apligraf
Wound Bed Preparation: graft should be applied to a clean, debrided wound after thoroughly irrigating the
wound with a non-cytotoxic solution. Oozing or bleeding resulting from debridement should be stopped
through the use of gentle pressure. Previous ulcer treatments other than standard therapeutic compression
should be discontinued
Control of Heavy Exudation:
Heavy exudation may displace Apligraf and reduce adherence. Exudation should be minimized by appropriate
clinical treatment. If exudation persists, Apligraf should be made permeable to exudate by perforating the graft
to allow for drainage.
Suggested Technique for Application of Apligraf:
Prepare a sterile field and atraumatic instrwnents: forceps
Lift off the tray lid and note epidermal and dermal layer orientation: ApJigraf is packaged with the epidermal
(dull, matte finish) layer facing up and the dermal (glossy) layer facing down
When lifting Apligrafwith atraumatic forceps, be careful not to perforate or lift the polycarbonate membrane
beneath Apligraf
Apligraf should be placed such that the dermal layer (the glossy layer closest to the medium) is in direct
contact with the wound surface. Trim Apligraf so as to cover the wound bed with 1/8-1/4 inch margins
Secure Apligrafwith a three-layer dressing so as to assure contact to wound bed
FoUow-up: The wound should be inspected and the dressing changed at least once a week during the immediate
post application period. More frequent changes may be required on highly exudative wounds. Additional
applications of Apligraf may be necessary. The safety and the effectiveness of Apligrafhave not been established
for patients receiving greater than 5 device applications.
297
2. Skin Flaps
Skin flaps differ from skin grafts in that skin flaps retain their vascular supply.
Indications: coverage of areas with poor vascularity (ie, bone and tendon), reconstruction of full
thickness, padding over boney prominences, coverage of areas requiring an operation at a later date, and
restoration of sensation to an area. .
TermiJlology:
Flap - refers to the tongue of tissue
pedicle - refers to the base or stem of the tissue.
Classification:
A. Vascular Anatomy Classification
1. random pattern (cutaneous flaps) derive their blood supply from the cutaneous
dermal-subdermal plexus. They have no axial arteries. These are limited based on their
dimensions (lengthlbreadth ratio). The pedicle must be wide enough to support the flap.
The base should be at least as wide as the flap is long. If this is not possible, a delay
procedure can be used to increase rate of survival.
2. Dial pattern (arterial flaps) - derive their blood directly from a cutaneous artery. The
survival in these flaps are dependent on the dimensions of the artery and the length of
the territory of the artery, not on the width of the pedicle. Examples are the dorsalis
pedis flap and lateral calcaneal arterial flap.
a. Island flaps - no skin bridge
b. Free flaps - transferred from distant site. More common in Podiatry.
An example is the latissimus dorsi transfer.
B. Transposition Site classification
1. Local Oaps - adjacent to the defect.
a. Rotational flaps (rotation, transposition, interpolation)-pivot about
the pedicle.
Rotational flap - Ideally the flap should be a half circle. Movement is
in a lateral orientation. Tension is relieved by Burow's
triangle(excision of the triangle adjacent to the pivot point).
Transpositional flap - usually rectangular or square. Movement is in
an arc. Example: bi-Iobed flap, Limberg f1ap(rhomboid defect).
b. Advancement flaps - moved directly forward to cover defect, without
lateral or rotational movement. Takes advantage of skin elasticity.
Examples: V-V flap, V-V flap
2. Distant Oaps
-indirect distant flaps seldom used in podiatry.
-direct flaps - primarily taken from adjacent areas
3. Muscle & Myocutaneous Flaps
The advantage of the muscle flap is its' bulk and vascularity.
* Preoperative considerations for muscle flaps should include:
1. viable length of the muscle on the dominant vascular pedicle
2. point and arc of rotation of the flap
3. the effect of the loss of function of the muscle
4. possible size of the cutaneous segment to be transferred with the
muscle. muscles can, generally, support a cutaneous region 50% larger
than the size of the muscle belly.
Lower Extremity Coverage with muscle Oaps:
Upper 113 of leg. . . . . . . . . . . gastrocnemius/soleus
muscle bellies
Middle 113 ofleg. . . . . . . . . . gastroc/soleusIFDU
298
2. Distant flaps
-indirect distant flaps seldom used in podiatry.
-direct flaps - primarily taken from adjacent areas
3. Muscle & Myocutaneous Flaps
TIle advantage of the muscle flap is its' bulk and vascularity.
Preoperative considerations for muscle flaps should include:
1. viable length of the muscle on the dominant vascular pedicle
2. point and arc of rotation of the flap
3. the effect of the loss of function of the muscle
4. possible size of the cutaneous segment to be transferred with the
muscle. muscles can. generally, support a cutaneous region 50% larger
than the size of the muscle belly.
Lower Extremity Coverage with muscle flaps:
Upper 113 of leg. . . . . . . . . . . gastrocnemiUS/soleus
muscle bellies
Middle 1/3 of leg. . . . . . . . . . gastroclsoleus/FDU
Tibialis Anterior mbs
Distal 1/3 of leg. . . . . . . . . . soleus/peroneus
brevismbs
Heel. . . . . . . . . . . . . . . . . FDBIEDB mbs
Below medial malleolus. . . . . . .. abductor hallucis mb
Below lateral malleolus. . . . . . . abductor digiti
minimimb
Complications of muscle flaps
-surgical errors of anatomy
-traction, twisting. and transection of the vascular pedicle
-larger defect than previous defect if flap fails
SKIN PLASTIES
I. Derotational Skin Plasty
Indications: congenital clinodactyly, arthroplasty of the fifth toe.
General Principle: skin wedge must be placed perpendicular to the axis of rotation of the toe.
Also, wedge removal should only be deepened to derma1lsubQjunction, in order to preserve
neurovascua1r components - unless exposure is critical.
2. Z-Plasty
-essentially a transposition of two triangular flaps.
General Principles:
-consider the gain in length at the expense of transverse shortening.
Circumvented using multiple smaller Z-plasties.
-should be planned so that the scar is in the RSTL.
-arms of the Z should be equal.
-the angle of flap tips are ideally angulated 60 degrees(to ensure a sufficient
vascular base).
-the tip is secured using the Lambody suture(intraderma1 at tip and mattress at
slot).
Complications:
-tip necrosis due to tension, scar tissue across base, tissue undermining.
299
3. v-v & y-VPlasties
-a popular technique for skin lengthening
General Principles:
*Maintain a wide angle V, for optimal blood supply
* Apex should be proximal
* A V-V will lengthen in one plane, and the Y -V will lengthen in the
other(perpendicular) plane.
4. Redundant Skin Plasties
--certain bone removal procedures will create skin redundancy, which can cause
unacceptable cosmesis. Many of the times two semi-elliptical incisions will correct this surgical
problem.
5. Double S Incision
--use when incision is very large
6. Syndactylization
--Goal is stability. Used when one digit is flail, and the adjacent is stable.
--usually a salvage procedure.
DOG EAR REPAIR
-Dog-ear is a term to descnbe the bunched-up tissue that may develop during wound closure.
-can often be avoided by using cross hatch lines across planned incision site.
-Smaller dog-ears will flatten with time, but larger dog-ears may be cosmetically displeasing.
-These are easily rectified by extending the incision along the dog ear and allo\\'ing the flap to
rotate.
-other techniques describe cutting wedges out in line with RS1Ls
-Another measure used is the Burow's triangle.
WOUND APPROXIMATION
1. Sutures
2. Steristrips
3. Staples
advantages:
disadvantages:
ereduce incidence of infection
ereduces overall cost of surgical procedure
ereduces pt's exposure to anesthesia and tourniquet time
cosmesis
anatomicallimitations
WOUND EDGES - GENERAL PRINCIPLES
-To ensure decreased scar formation, certain general principles must be followed:
.handle tissue gently
heapproximate the tissue anatomically
.close the deep tissues to decrease tension on skin
tuse least reactive wound approximation devices
tuse the proper gauge of suture to reapproximate to remove the tension
tsubcuticular closure provides for excellent cosmetic results
.Plantar incisions will require sutures to be left in for 3 weeks, nonweightbearing
MANAGEMENT OF KELOIDS AND HYPERTROPIDC SCARS
-keloids and hypertrophic scars are benign gro\\'1hs characterized by an overabundance of collagen deposition.
-both tend to be pruritic, raised, erythematous, and nodular.
-they differ in that the keloid extends beyond the original incision site. Also, hypertrophic scars will improve in
appearance, while keloids may worsen.
300
-Keloids occur most frequently in adolescent blacks
-Very important to do a thorough history and physical preoperatively
Treatment: there are many modalities, none of which are consistently successful.
1. treatment should not begin less than 6-12 months postoperatively.
2. Surgical excision is more applicable to hypertrophic scars than to keloids. combined with one or more
Z-plasties to decrease the tension.
3. Use of nonabsorbable skin sutures with the least reactivity, ie polypropylene, surgical steel, or nylon.
Remove sutures in 7 days to minimize inflammatory reaction.
4. Strict adherence to atraumatic technique
5. Maintenance of good hemostasis
6. Postoperative irradiation and corticosteriods along scar will improve potential results. Corticosteriods
will decrease the level of collagenase inhibitors and thereby increase collagen degradation.
Triamcinolone acetonide 40 mgflOOml is the preferred drug. Care should be taken to keep the drug
within the scar, and away from the surrounding healthy tissue. Injections are preformed 3-5 weeks
apart. When used with surgery, should inject 1 month prior to surgery, and for 3-4 weeks post-op.
7. Pressure over the scar exceeding 25 mm Hg for 4-12 months. This decreases vascularity, which
thereby reduces cellular response and collagen deposition.
301
PEDIATRICS
PEDIATRICS
PEDIATRICS
PEDIATRICS
PEDIATRICS
PEDIATRICS
PEDIATRICS
PEDIATRICS
PEDIATRICS
PEDIATRICS
PEDIATRICS
PEDIATRICS
PEDIATRICS
PEDIATRICS
1 t\
II"\.
METATARSUS ADDUCTUS
Definition:
structural or positiooal medial deviation of the metatarsals in the transverse plane occurring at the
tarsometatarsal articulation.
Erroneously tenned one-third of a clubfoot deformity as coined by Kite (1950)
talipes equinovarus:
forefoot adductim at midtarsal joint
rearfuot varus
rearfoot equinus
Incidence:
111000 live births
Risk to second in fiunily 1120
4.5% 1
51
degree relatives similarly affected
No sex predilection
500"" bilateral
When willateral then left more commm than right
History:
Henke (1963)
Germ.an literature
First to mention adductim of the fore part of the foot with valgus position of the heel
Bankart (1921)
First to report in English literature
Thought deformity was due to absence of the ''internal'' (medial) ameiform bone
McCormick and BIOWlt (1949)
Coined the tenn ''Skewfoot''
Kite (1950)
Erroneously tenned "Third of a Clubfoot"
Etiology - Unknown!
Theories:
1. Genetic
2. Atavistic medial ameiform
3. Intrauterine position
Left sided cany
Prima gravida
4. Environmental
sleeping positions - belly sleeping
5. Arrest in fetal development
6. Muscle imbalance
hyperactive abductor hallucis
302
shortened muscles (Abd hall / T. Post) gain mechanical advantage over lengthened muscles
(peroneals)
7. Abnormal muscular insertions
Medial instead of plantarmedial insertion of abductor hallucis onto proximal phalanx
Tibialis anterior entirely onto 1 sI metatarsal instead of combined insertion with medial CWleifonn
Tibialis posterior primarily onto medial CWleiform instead of navicular
8. Absent medial CWleifonn
Associated Conditioos
IntemaI tIbial torsion (1 M-SOIo)
Congenital hip dysplasia (1.5-10%)
Clubfoot
Windswept deformity (Met adductus on one foot and calcaneal valgus on the other)
Subjective Concerns
In toeing
Tripping
Difficulty wearing shoes
Lateral shoe wear pattern
Bunion and hammertoes
Clinical Features:
1. Uncompensated
C - shaped foot
Convex lateral border
Concave medial border
Prominent Sth met base
Separation of great toe from lesser toes
Higharch
2. Compensated
SkewfOOt (flatfoot)
Adducted forefoot
Midfoot Iate:rally translated
Hindfoot valgus
HAV
Digital cont:ractw-es
Clinical Exam
Must determine:
1. Presence of tendon contractures / hyperactivity
LicbtbIau test: the heel is stabilized, Sth met head is braced, and lateral pressure is applied to the
medial aspect of the 151 metatarsal head ( abductory stress)
A tight abductor halIucis will appear bowstrung
2. Concomitant presence of internal tIbial Union
3. Equinus?
303
Component of clubfoot
4. Flexible vs Rigid?
If rigid then conservative therapy and soft tissue procedures are likely to full
Radiograpbic Evaluation
1. Metatarsus Adductus Angle - traditional
Normal = less than 21 degrees is a rectus foot
Pathologic = greater than 21 degrees
Consists of the longitudinal axis of the midfoot and the longitudinal axis of the metatarsals (which the
second metatarsal serves as a reference)
Line bisecting the talar head and extending distally win full medial to first metatarsal in metatarsus
adductus rather than laterally as seen in talipes equinovarus
2. Metatarsus Adductus Angle - Simplified (Engle's angle)
Utilizes the bisection of the second metatarsal and bisection of the middle ClIDeiform instead of the lesser
tarsus axis
3. Talo-1
st
metatarsal Angle-(Simons' Angle)
N=Oto-20
Line bisecting the talar head will full medial to the first metatarsal in metatarsus adductus (negative) rather
than laterally as seen in talipes equinovarus (positive)
4. Talocalcaneal angle (Kite's Angle)
N = 20 - 35 (AP)
N = 25 - 45 (Lateral)
This angle is nonnal or increased in metatarsus adductus and decreased in TEV
Bisection Points of
Lesser Tarsus
Lesser Tarsus Axis
304
Metatarsus Adductus Angle Metatarsus Adductus Angle
utilizing Engle.' s Angle
Metatarsus Adductus vs Uubfoot (lEV)
Clinical Comparison
Metatarsus Adductus Clubfoot
Adducted forefoot Adducted Forefoot
lateral navicular subluxation (or normal) Medial navicular subluxation
Hindfoot neutral or valgus
Hindfoot varus
Noequinus Equinus
Radiographic Comparison
Metatarsus Adductus
Simons' angle
Positive
Kite's angle
Normal or increased
Talonavicular relationship
Normal or lateral navicular
Cooservative Tberapy
Clubfoot
Simons' angle
Positive
Kite's angle
Decreased
TalonavicuIar relationship
Medial
1. Passive stretching and manipulation (up to 3 weeks old)
2. Serial plaster casting (up to age of ambulation )
3. Modified Furlong cast
4. Modification of sitting or sleeping positions
5. Orthotics devices
6. Shoes I Splints
Biomechanically SOlDld Biomechanically lDlSOWld
Ganley Splint Reverse last shoes
Bebax
Denis-Browne Bar

Wheaton brace
Fillauer Bar
Unibar
305
Ipos AntiaddndUs shoe
TIIREE POINTS OF PRESSURE:
1. Abduction at medial side of:first metatarsal head
2. Adduction at lateral side of cuboid
3. Inversion at heel
***Must be maintained to avoid valgus torque 00 hindfoot
The foot should be maintained in the corrected positioo for a time at least as loog as it took to gain the
desired oorrectioo
Surgical Coasiderations
1. Age
yotmger patients more amenable to soft tissue procedures
2. Has conservative therapy been attempted?
gm attempt conservative therapy up to the age of 5
3. Conamitant
'. Int tibial torsion
residual clubfoot
severe valgus with HA V and hammertoe
4. Severity of deformity
the more severe the deformity the greater the resistance to treatment and the more aggressive one needs to
be in surgery
5. Osseous maturity
6. FiexJ."le or rigid?
the two above are related- with osseous maturity the metatarsal square off and the deformity
more rigid As the deformity more rigid soft tissue procedures are less likely to achieve the desired
correction.
Forceful manipulation of the rigid foot may force the hindfoot into valgus
SurgieaI Treatment

I. 2 to 6-8 years
Soft tissue procedw-es
2. 4 to 8 years
Gray zone
Too old and too advanced osseous maturity to perform soft tissue and yet not quite
mature enough to perform osseous procedw-es
3. Ages greater than 6-8 years
Osseous procedw-es
Soft tissue procedures:
1. Heyman, Herndon and Strong procedure (1958)
procedure initially described using a transverse incision aa:oss Lisfranc's joint
three dorsal. linear longitudinal incisioos now used more commonly to avoid neuorvascu1ar embarrassment
release <bsal, interosseous and plantar ligaments along with the joint capsule
Modified HHS now more common (Kendrick et al., 1970)
306
preserve plantar lateral ligaments to prevent dorsal dislocation)
Complications:
Dorsal dislocation
Degenerative arthritis (Stark et aI., 1987)
2. Thomson procedure (1960)
Resection of abductor hallucis muscle belly and medial capsulotomy
3. Lichtblau procedure (1975)
Modified Thomson procedure
Tenotomy or partial resection of abductor hallucis plUscle
4. LaPorta and Sokoloff
Tibialis posterior tendon lengthening with talonavicular capsulotomy, usually used in conjunction with
lUJ&S or Berman-Gartland procedures
Gray Zone (Cartilaginous procedures):
1. Johnson wedge chondrotomy (1978)
Resection of laterally based chrondrotomies from the bases of metatarsals 2- 5 laterally based closing wedge
osteotomy on the first metatarsal, just distal to the epiphyseal growth plate
Osseous procedures:
1. Bankart (1921 )
Advocated excision of cuboid
2. Peabody & Muro (1933)
Excision of the bases of the three central metatarsals
Osteotomy of the fifth metatarsal
Mobilization and luxation of the first metatars<K:uneiformjoint
Correction of any abnormal insertion of the tIbialis anterior tendon
3. McCormick & Blount (1949)
Arthrodesis of the first metatarso-cuneiform joint
Osteotomies of metatarsals 2-4
Wedge resection of the cuboid
4. Fowler (1959)
Opening wedge osteotomy of the medial cuneiform with bone graft
5. Steytler & Van Dec Walt (1966)
Base wedge "V - shaped" oblique osteotomies of all the metatarsals (lateral oriented base; apex - proximal)
6. Berman & Gartland (1971)
Proximally oriented crescentric dome-shaped osteotomies of each of the metatarsals
Osteotomy made at least 6 rom distal to growth plate of 1st metatarsal
First and fifth metatarsal osteotomies fixed with Steinman pins; second, third and fourth not fixed
Popular procedure today
307
7. Modified Bennan-Gartland (actually the Steytler & Van Dec Walt procedure)
Transverse closing abductory base wedge osteotomies of all the metatarsals
Multiple fixatim techniques for all the metatarsal osteotomies
Popular procedme today
8. Lepird procedure (1982)
Oblique closing abdnctay wedge osteotomies m 1st sometimes (due to epiphysis) and sometimes the 5th
metatarsals
Rotatimal oblique base osteotomies of metatarsals 2-5
Rotatimal osteotomies should parallel the ground supporting surfilce (thus, transverse plane
motim)
Technique: medial cortical binge initially preserved for stability, the screw is placed perpendicular
to the supporting surfilce but not tightened, the medial cortex is then transected and the metatarsal
is rotated to its corrected positim and the screw is tightened
Popular procedure today
9. Brink and Levitsky (1995)
Cuneiform and wboid wedge osteotomies
performed through two incisions
Staple and K - wire fixatim
***Note: the above procedures can be performed alme or in combination ( ego Fowler and modifications of the Bankart
procedure)
Johnson osteochondrotomies
308
Berman & Gartland Steytler & Van Der Walt McCormick & Blount
Peabody & Mum Lepird
Brink & Levinsky
309
CLUBFOOT
I. Congenital:
A. Postural (Extrinsic):
1. Definition: Forefoot Adductus
Rearfoot Varus
Ankle Equinus
2. Mild, flexible defonnity with normal anatomy
3. Etiology: Intrauterine malposition
4. Prognosis: Good
5. Treatment: Conservative
B. Talipes Eguinovarus (Intrinsic):
1. Definition: Forefoot Adductus
Rearfoot Varus
Ankle Equinus
Talonavicular Subluxation
Lateral Rotation o/Talus inAnJde Mortise
2. Severe, rigid defonnity with pathologic anatomy
3. Prognosis: Poor
4. Treatment: Surgical
II. Acquired:
A. Neuromuscular Disorders:
1. Poliomyelitis
2. Meningitis
3. Cerebral Palsy
4. Spina Bifida
5. Myelomeningocele
6. Post-CVA
B. Post-Traumatic:
1. Spinal Cord Trauma
2. Peripheral Nerve Trauma
3. Tendon Laceration
4. MalINon-Union
5. Volkman's Contracture
6. Burn Contracture
Ill. Historical Review:
A. 1210 BC: wall etchings of pharaoh Siptah with clubfoot deformity
B. 1000 BC: 1
st
description of clubfoot in Indian literature
C. Greek Mythology: Greek God Hephaestus with bilateral clubfoot deformities
D. Aztecs: made splints from cactus leaves
E. 300-400 BC: Hippocrates thought etiology was intrauterine position and recommended manipulation
and bandaging
F. 6
th
- 15
111
Centuries "Dark and Middle Ages": marked those with a clubfoot deformity as the devil
G. 15
th
- 16!h Century 'The Renaissance': renewed interest in clubfoot deformity
H. 1782: Lorenz advocated achillis tenotomy for treatment
I. 1803: Scarpa believed osseous changes occurred secondary to soft tissue contractures
J. 1831: Stromeyer performed achillis tenotomy on a recurrent clubfoot
K. 1839: Little (Stromeyer's student) had a clubfoot defonnity secondary to an infantile febrile disease.
He wrote the "Treatise on the Nature o/Club/oot & Analogous Distortions"
L. Late 1800's: Aggressive, radical treatment with forcible manipulation (Thomas Wrench) and resection
of large bone wedges
M. 1933: Kite had an 88% success rate with conservative therapy consisting of gentle manipulation with
plaster of paris splinting. Kite's angle (talocalcaneal angle).
310
N. 1884 - 1969: Staged, piecemeal soft tissue release
o. 1971: Turco recommended a comprehensive, posteromedial release with temporary fixation of the
talonavicular joint
P. 1982: McCay advocated circumferential release
Q. 1985: Simons also advocated circumferential release
R 1982: Crawford developed the Cincinnati incision
IV. Incidence:
A. 2: 1 Male:Female
B. 50% Bilateral (when unilateral Right> Left)
C. Polynesian: 6.81/1000
Middle East & South African Blacks: 3.5/1000
White: 1.1211000
Asian: 0.57 f] 000
D. Most common pathologic, congenitalfoot deformity: 2.29/1000 live births
V. Etiology: IDIOPATHIC, possible factors include:
A. Extrinsic & Environmental factors:
1. Intrauterine malposition: Hippocrates 400BC
2. Common peroneal nerve palsy secondary to intrauterine position (anterior muscle weakness):
White 1929
3. Amniotic strictures
4. Diseases: Diabetes, maternal hypothermia
5. Drugs: Aminopterin, d-tubocurarine, Methotrexate
6. Radiation
7. Malnutrition
8. Viruses
9. Multiple Pregnancies
B. Intrinsic & Anatomic factors:
1. Germ Plasm Defect: malposition of head and neck of talus: Irani & Sherman 1963, & Shapiro &
Glimcher 1979. The most widely accepted etiology.
2. Arrest of fetal development at 5
th
week of gestation: Bohm 1929
3. Arterial dysgenesis: absent or underdeveloped anterior tibial & medial plantar arteries
4. Anomalous tendon insertions: plantar insertion of TP or medial insertion of achillis & PL
5. Muscle maldevelopment
6. Congenital constriction bands: Keith 1940
7. Uneven rate of bone and muscle growth: Bechtol & Mossman 1950
8. Contracted deltoid ligament: Hirsch 1960
C. Hereditary factors:
1. Autosomal Dominant
Autosomal Recessive
Sex-linked Recessive
2. Race Predilection
3. Unaffected By: Birth Weight
Birth Number
Maternal Age
4. Incidence in Twins (Idelberger, 1939): Identical: 32.5%
Fraternal: 2.')0/0
5. Incidence in Relatives (Wynne-Davies, 1973): 1
st
degree: 20-30 fold ina-ease
zDCi degree: 6 fold inaease
3td degree: no ina-ease
6. Polygenic, multifactorial inheritance with sex-linked threshold:
The number of abnormal genes must exceed the threshold Females have a higher tolerance;
therefore, it takes more genes to a-eate the deformity. Since so many genes are required, the
deformity is usually more severe in females. Males have a lower threshold; therefore, less genes
are needed to create the deformity and when it is present it is usually less severe.
311
VI. Pathologic Anatomy:
A. Talus:
1. Reduced size
2. Head & neck anguJated medial and plantar
3. Anterior & lateral deviation in ankle mortise
4. Ta1ar Declination Angle = 115 - 135 (Normal = 150)
5. Ta1ar Neck Obliquity = 50 - 65 (Nmnal = 15)
B. Calcaneus:
1. Normal shape
2. Possible undecdeveloped sustentaculmn tali
3. Anterior & middle tilcets may be one
4. Plantarmedial angulation beneath talus (equinus & varus)
C. Navicular:
1. Normal shape
2. Hypertrophic tuberosity
3. Plantarmedial subluxatioo
4. May articulate with medial malleolus
D. Soft Tissues involved in deformities:
1. Skin, filscia, retinaculmn, vinculi (Master Knot of Henry), joint capsule, ligaments, tendons,
muscles, veins & arteries, and nerves
2. Tendons & Muscles:
a. Posterior: Contracted
b. Medial: Cootracted
c. Plantar: Contracted
d Peroneals: Elongated
e. Anterior Tibial: Dorsomedial displacement
3. Ligaments:
a. Calcaneofibu1ar: Cootracted
b. Posterior Talofibular: Contracted
c. Bifurcate: Cootracted
d. Interosseous: Contracted
e. Spring Ligament: Contracted
VII. Pathomechanics:
A. Lateral rotation of talus with head and neck angulated medial & plantar
B. Posterior displacement of fibula (reason for contracture of CF lig)
1. Horizontal Breach (Angle between the bisection of the rearfoot and the malleolar plane)
a. Normal = 75 - 90"
b. TEV= < 75
C. Calcaneus in varus & equinus
D. Navicular medial and plantar (may abut medial malleolus)
E. Forefoot adductioo
VIII. Clinical Evaluation:
A. History:
1. Pregnancy: Gestation, illness, drugs, tramna
2. Delivery: Duration, anesthesia, complications
3. Growth & Development: Milestones
B. General Examination:
1. Neurological: Motor tooe & fimction, reflexes, sensation
2. Back & knees
3. Skin
312
C. Lower Extremity Examination:
1. Appearance
a. "Club-like"( equinoadductovarus)
b. Small drawn-up heel
c. Adducted forefoot
d. Calf atrophy
e. Decreased foot size
2. Medial:
a. Skin: creases/furrow
b. Navicular prominent
c. Forefoot adducted
3. Lateral:
a. Skin: thin/stretched
b. Talus prominent
c. Fibula posterior
IX. Radiographic Evaluation:
A. Talocalcaneal Angle (Kite's Angle):
I. AP: Normal = 20 - 40
TEV = 15 or less
2. Lat: Normal = 35 - 50
TEV = 25 or less
B. Talo-I
5I
Metatarsal Angle:
I. AP: Normal: 0 - (-20)
TEV = 15 or more
C. Talocalcaneal Index:
1. Add talocalcaneal angles together on AP & lateral
2. Normal is> 40
D. Simons Rule 0(15:
I. Predicts presence of talonavicular subluxation using measurements on AP radiograph
a. Navicular does not ossify until about age 3
2. Talonavicular subluxation is present if:
a. Talocalcaneal Angle < 15 AND
b. Talo-l
51
Metatarsal Angle> 15
E. Positioning for Radiograph:
I. Position of maximwn correction: dorsiflexion & abduction with foot plantigrade
2. Sitting with hips & knees flexed 90
F. Sources of Erroc:
1. Poor position
2. Identification: Navicular does not ossify until about 3 years
Ossific nuclei in talus & calcaneus are eccentrically placed
G. Indications for Radiographs:
1. Determine severity of deformity
2. Monitor response to therapy
3. Iatrogenic changes
4. Intra-operative realignment
X. Conservative Treatment:
A. Performed on ALL congenital clubfeet
B. Begin immediately
C. Manipulatioo:
I. Gentle but firm 10 - 15 minutes
2. Reduce all components: Abduct forefoot
Evert Heel
Distract heel
313
D. Serial Casting:
1. Used to maintain reduction
2. Above-knee cast changed every 1 - 2 weeks
3. Continue until satisfactory correction obtained or until further correction is unobtainable
4. Bivalve last cast and use for night splints
5. Monitor therapy with radiographs every 1 - 2 months
E. Post-Reduction:
1. Night Splints
2. Prewalker Shoes
3. Orthotics
4. Stretching
F. Complications with Manipulation:
1. Rocker-bottom foot
2. Flat top talus
3. Wedge-shaped navicular
4. Dorsal displacement of navicular
5. A VN: talus, navicular, distal tibia
XI. Surgical Treatment:
A. Soft Tissue Release:
1. Comprehensive, circumferentiol release: Posterior, medial, lateral, plantar
2. Summary: General anesthesia, thigh towniquet, soft tissue release, reduction, K-wire fixation of
talonavicular joint, intra-operative radiographs, compression cast
3. Ideal Age: 3 -12 months
a. No surgery before 3 months old because you need conservative therapy to stretch the tissues
and it is also technically difficult due to the small size of the structures
b. Decrease success when age is> 3 years old
4. Incision Placement:
a. Posteromedial ([urco): decreased visualization laterally
b. Cincinnati (Crawford): Cosmetically superior however great incidence of wound dehiscence
c. Posteromedial + Lateral
5. Sequential Release:
a. Retract tarsal tunnel contents
b. TP tendon lengthening (Z-plasty): follow distal to navicular tuberosity
c. Talonavicular joint capsulotomy
d. Spring ligament
e. FDL tendon lengthening (Z-plasty): follow distal to Master Knot of Henry
f. FHL tendon lengthening (Z-plasty)
g. Superficial deltoids
h. Interosseous ligament
i. Calcaneofibular ligament
j. Achillis tendon lengthening (Z-plasty)
k. Posterior ankle joint capsulotomy (including posterior talofibular ligament)
1. Plantar fascia
B. Osseous Procedures:
1. Indications:
a. Recurrence
b. Severe, rigid deformities
c. Performed only in the child & adult NEVER on infants
314
2. Osteotomies (Ages 2 - 6 years old):
a. Lateral Column Shortening:
1. 1902 Ogston: Cuboid closing wedge
2. 1961 Evans: Calcaneocuboid joint closing wedge and arthrodesis
3. 1973 Lichtblau: Anterior calcaneus closing wedge
b. Medial Column Lengthening:
1. 1959 Fowler: Medial cuneiform opening wedge
3. Salvage Procedures:
a. Triple Arthrodesis (> 12 years old): Increases stability in severe, rigid deformities
b. Talectomy (4 - 8 years old): Used for severe, rigid deformities such as arthrogryposis &
myelomeningocele
C. Complications:
1. Wound dehiscence
2. Residual deformity
3. Navicular wedging & subluxation
4. Flat top talus
5. Rocker-bottom foot
6. Overcorrection: calcaneus, pes planovalgus
D. Residual Deformities:
1. Metatarsus Adductus:
a. Soft tissue release
b. TA tendon transfer
c. Osseous procedures
2. Rearfoot Varus:
a. Calcaneal osteotomy: Dwyer
3. Equinus:
a. Achillis tendon lengthening or tenotomy
CALCANEOVALGUS
Definition:
Clinical:
Incidence:
Etiology:
Radiograph:
Deformity identified at birth with the foot markedly dosiflexed at the ankle and valgus position of
the foot with respect to the leg.
dorsum of foot in contact with anterolateral leg ("up and out")
Severe limitation of plantarflexion and inversion
Lateral-loose skin folds below lat mall.
Medial-skin stretched and taught
most common congenital malformation
1 : 1 000 live births
more common in females
usually bilateral with one limb more severe than the other
first born of young mothers
Compression of the prima gravada with small tight uterus
External rotation & contracture of hips
Sleeping position with ext. rotated & abducted hips
(primary deforming structures = tendons of anterolateral ankle)
AP- inc. TC angle
Dec. 1N congruity with FF abduction
Medial angulation of head & neck of talus
315
CVvs. VT:
DiifDX:
Treatment:
Lat- plantarflexed talus(relative due to df foot) with respect to tarsal bones
Bisection ofh&n of talus inferior to cuboid(normal=superior halt)
Dorsifelexion of calcaneus
radiograph
CV VT(vertical talus)
Nav medial to talus
Relative PF of talus
Inc. DF of calcan
dora! to h&n of talus (if ossified)
verticaJ/PF position of talus
calc parallel with low or neg CIA
Clinical
Reducible with manipulation
Foot against antec. Leg
nonreducible
foot 9Odeg. To leg or equinus
vertical talus
Congenital medial posterior bowing of the tibia
Neuromuscular disease
conservative
surgical
Manipulation in early dx with flexible deformity
Daily passive manip.
PF & 1NV to stretcbllengthen dorsolat soft tissues
20-30x in 4 daily sessions
Serial casting
toes to tib tuberosity
correct component parts of deformity
foot held pf
if adduction
rf neutral to inv
(avoid using if as lever to cast rf in varus)
cast weekly or biweekly 3-6 months
gentle gradual persistent correction is the rule
post cast - maintain with splints(Ganley)
12-16hr/day up to 6 months
considerations
options
rigid deformity
failed conservative tx
age of patient
development of secondary arthritis
division of soft tissue structw"es
anterior ankle
peroneus tertius
EDB
EDL
AITFL
Correct valgus
Z lengthen peconeals
Divide preoneal sheath
Div lat lig of STJ
316
Correct FF abduction
Div ligg of CCJ
Section TNJ capsule
Single K-wire across MTL
AK cast 10-12 weeks
Other procedures
VERTICAL TALUS
Introduction
most rigid form of flatfoot
Calcaneal osteotomies-Evans
STJ arthroeresis
Arthrodesis
other terms: congenital rocker bottom
foot, congenital convex pes valgus,
congenital flatfoot with talonavicular
dislocation, ''Persian slipper foot"
severe cases involve cc joint, less
favorable outcome
50% occur BIL, right> left
males = females
50% occur as isolated congenital
defonnity
DitJerential Diagnosis
Idiopathic Flat foot
Paralytic Flatfoot
Flat foot in cerebral palsy
Oblique talus
Talonavicular joint subluxation with weightbearing only
plantarflexed view, total reduction of Talooavicu1ar joint
benign flexible flatfoot
requires orthotics, possible Tendo-achilles lengthening, serial casting, surgical interventioo rare
Etiology
500/0 secondary to either spina bifida, arthrogrypbosis, or a chromosomal abnormality (trisomy)
Neural tube defects - usually rigid form
Diastematomyelia, lipoma of cauda equina, sacral agenesis, myelomeningocele
Arthrogrypbosis multiplex congenita
Neurofibromatosis
Ischio-calcaneal band, rare contracture of triceps
Acquired
Cerebral palsy
Poliomyelitis
Spinal muscular atrophy
Part of clinical spectrum
Freeman-Sheldon
Smith-Lemli-Opitz
Marfan



Hurler's
DeBarsy
Nail-patellae
317


Inheritance

Pnme-belly (Eagle-Barrett Syndrome)
Multiple Pterygium Syndromes
Autosomal dominant, incomplete penetrance
Pathologic Anatomy
Wedge-shaped navicular with hypoplastic plantar segment
Severe pIantarfIexion of ankle joint
Tibia articulates with talus in posterior I13 only
Calcaneus closely approximates with distal tip of fibula and is everted and plantarfIexed
SustantacuIum tali is hypoplastic,no support for talar head
Absent anterior talar facet
Dorsal Talonavicular ligaments thickened and blend with deltoid
Superior peroneal retinaculum - attenuated, allowing peroneal subluxation
TP tendon attenuated under talar head, subluxed anteriorly onto medial malleolus
Peroneus Longus muscle is major deforming force, with increased pronatory potential
Contractures seen in:
Tibialis Anterior
Extensor Hallucis Longus
Extensor Digitorum Longus
Peroneus Brevis
Triceps Surae
Peroneus Tertius
Dislocated tendons:
Tibialis Posterior


Peroneus Brevis
Peroneus Longus
ClUUcalilppearance
Forefoot abducted and pronated, lateral clawtoes
Convex plantar surface, rocker-bottom foot
Palpable talar head medially and plantarly
Hindfoot equinovalgus
Tight heel cord
Crease over narrowed sinus tarsi
Hollow anterior to lateral malleolus is helpful sign to differentiate VI from calcaneovalgus
Gait:



Delay in ambulation is uncommon
Older children with shortened stride
Decreased balance
Pain may not appear lDltil adolescence
Radiographic Findings
Include ankle in evaluation offoot
Forced plantarflexion lateral view paramount in diagnosis
Talus, calcaneus and metatarsals all visualized in newborns
Cuboid ossifies within first month of birth
Navicular ossifies in 3 to 5 years
Resting lateral view:
Use lateral cuneiform as marker to locate navicular
Dislocation of navicular dorsal to talus, forfoot follows the navicular
Increased talar metatarsal angle
Calcaneus in equinus
318
Vertical position of talus
Resting dorso-plantar view:
Increased Kite's angle (talo-calcaneal angle)
Increased talar metatarsal angle
Severe VT will present with dislocated calcaneal-cuboid joint
Osteochondritis of the navicular (Kohler' s disease) may sometimes occur
Classifications
Dupont Institute - Aksu & Kumar
Group I - Supple foot that resemble calcaneovalgus
Group II - Rigid foot, part of a syndrome
Group III - VT associated with Trisomy 13 - 15 or 18
Group IV - VT associated with neuromuscular disease such as spina bifida
Wenger & Rang
Teratogenic - bilateral stiff as seen in arthrogryphosis
Neurogenic - muscle imbalance, more supple - as seen in spina bifida
Acquired - malposition in utero - as seen in children with no other major problems
Coleman
Type I - absence of associated calcaneal-cuboid joint dislocation
Type II - presence of calcaneal-cuboid dislocation
Treatment
Goals:
Plantargrade foot with balanced distribution of weight between hindfoot and forefoot
Re-establish normal anatomical relationship between hindfoot and forefoot
Restoration of medial column competency
Conservative tberapy(Casting) is aimed at stretching soft tissue structures in preparation for surgical
intervention
Casting (forefoot in plantarflexion) - start at birth and continue for 3 to 4 months
Surgical approach:
Cincinnati incision
mid-dorsal incision
medial arch incision
Surgical treatment may be performed in two stages(forefoot correction followed by hindfoot correction)
Lengthen contracted and dislocated tendons
Capsulotomy of talo-navicular and ankle joints
Capsulotomy of calcaneo-cuboid joint in severe cases
Tendo-achilles lengthening
Maintain alignment of talo-navicular and ankle joint with Kirshner wires
Release of calcaneo-fibular ligament to allow dorsiflexion of the talus
Release of taIo-calcanealligament to allow reduction
Tendon transfer (PB, TA) to talar head or neck has been described
Subtalar or Triple arthrodesis in severe cases, older patients or if above mils
319
TORSIONAL DEVELOPMENT I DEFORMlTIES OF THE LOWER EXTREMITIES
TRANSVERSE PLANE DEFORMITIES
Femur
Antetorsion I retrotorsion
lllp malposition / contractures
Tibia
Internal / external tibial torsion
Knee malposition / contractures
Foot
Metatarsus Adductus
SUBJECfIVE CONCERNS
In Toe I Out Toe
Tripping I Falling
Clumsy Gait
KneePain
Knock Knees
Bowlegs
IN TOEING
1-3 Years
Internal Tibial Torsion
Metatarsus Adductus
>3Years
Internal Femoral Torsion
PATHOPHYSIOLOGY
Heredity
Intrauterine Position
Persistent Fetal Alignment
Persistent MaIposture in Postnatal Life
Sleeping I Sitting Positions
Iatrogenic
TERMS
Torsion:
The act or process of twisting; turning or rotating about an axis
Version:
The act or process of turning or changing direction
Ante
Prior to I Before
In front of
Retro
Backward
Located behind
PODIATRIC TERMS
Version
Rotation at the joint level
Torsion
Rotation about the long axis of a bone
IN
Antetorsion
Retroversion
our
Retrotorsion
Anteversion
320
ORTHOPEDIC TERMS
Version
Angular difference between the transverse axis
of each end of a long bone
Torsion
Present when the version is abnormal or
excessive
PODIATRIC
Femoral Retroversion
1
.'
,..,
.......
.. ,
.. .
. ,.,. ....... .
.......
ORTHOPEDIC
PODIATRIC
Femoral Anteversion
Antetorsion (16)
Normal ( ~ 1 2 )
Retrotorsion (6)
INTERNAL FEMORAL TORSION
(Femoral Antetorsion)
Internal Deviation

....
...

FEMORAL .ANTEVEBSION - transverse plane angle between head/neck and femoral condyles
Birth
Normal: ~ 40 degrees
Range: 31-52 degrees
Adult
Normal: ~ 8-16 degrees
321

Range: 7-28 degrees
45
40
35
- Anteversion
30
25
20
15
lD
5
0
Birth 1 3 5
V-.
7 9 15 Adult
TIBIAL VERSION - transverse plane angle between tibial plateau and plafond (ankle axis)
Fetus
.:. Internal/Medial
Infant
.:. +/- Neutral
.:. Normal: 0 - 7 Degrees
Child
.:. Slightly External/Lateral
Adult
.:. Lateral/External
.:. Normal: 20 - 30 degrees
30
25
20
15
10
5
0
-5
Birth 1 3
TORSIONAL PROFILE
.:. Foot - Progression Angle
5
.:. Medial Hip Rotation in Extension
.:. Lateral Hip Rotation in Extension
.:. Thigh - Foot Angle
.:. Transmalleolar Axis Angle
- Tibial Version
7 9 11 15 30 50 70
Years
322
.:. Foot Configuration
90
80
70
.....
.....
.....
60
"
.....
"-
.....
50
"-
--
40
30
20
10
0
Birth 1 3 5 7 9
Years
FEMORAL ANTEVERSION - Measurement
Clinical
.:. Netter method
Patient is placed Prone
Palpate Gr. Trochanter - Femur
Internally rotate the leg - Knee bent
until Gr. Trochanter is the most
prominent laterally
Measure angle between tibia (leg) and
vertical
Radiography
.:. Magilligan technique
.:. Dunn technique
Both are not often used
Computed tomography / MRI
.:. Best Methods
TIBIAL TORSION - Measurement
Clinical
.:. Thigh - foot angle
.:. Second metatarsal
.:. Transmalleolar axis
Radiography
.:. Hutter and Scott Method
Computed Tomography
Ultrasound
--Internal
---- External
11 20 30 50 70
......
t ....
11.." DO
INTERNAL FEMORAL TORSION
.:. In-toeing> 2-3 years
.:. Medial rotatation of thighs
.:. Patellae turned inward
.:. Int rotation> Ext rotation
INTERNAL FEMORAL POSmON
.:. Shortened or Spastic Medial Hamstrings /
Adductors
.:. Contracture of Hip Capule
Pubocapsular
Illiofemoral
.:. Gait Analysis
Increased Adduction - Late Midstance
TIBIAL TORSION
Internal
.:. Failure of normal external rotation to occur
External
.:. Concomitant Internal Femoral Torsion
Miserable MaJalignment Syndrome
.:. Iatrogenic post treatment for ITT or 1FT
ADULT
323
TIBIAL'IORSION - Treatment Considerations
.:. Usually resolves by age 3
.:. 4% of adults have unresolved lIT
1 % Incapacitating
.:. Greater and Faster Correction?
FUNCTIONAL EFFECTS OF TORSIONAL ABNORMALITIES
Internal Deviations
Prior to Age of Self Awareness:
.:. Decreased Angle of Gait
.:. Supination
Beyond Age of Self Awareness:
.:. Conscious Pronation
.:- Pronation
External Deviations
.:. Heel Contact Pronation
TREATMENT - TORSIONAL ABNORMALITIES
CONSERVATIVE TREATMENT
.:. Passive Stretching and Manipulation
.:. Change Sitting / Sleeping Habits
.:. Serial Long Leg Casting
.:. Bars
Denis-Browne
Ganly Splint
Counter Rotation System (CRS)
.:. Braces
.:. Wheaton Telescoping Brace
.:. Orthotics
SURGICAL MANAGEMENT
Indications
.:. Child> 8 years old
CONSERVATIVE TREATMENT - Seguale
.:. Recurrence
.:. External Tibial Torsion
.:. Chondromalacia of the Patella
Miserable malalignment syndrome
:Long Term Effects Unknown
SURGICAL MANAGEMENT
Femur
.:. Rotatinal Osteotomies
Multiple Locations
.:. Illizaorv
Tibia .:. Significant Functional Disability
:Severe Cosmetic Deformity .:. Proximal or Distal Rotational Osteotomy
324
EMERGENCY MEDICINE
EMERGENCY MEDICINE
EMERGENCY MEDICINE
EMERGENCY MEDICINE
EMERGENCY MEDICINE
EMERGENCY MEDICINE
EMERGENCY MEDICINE
EMERGENCY MEDICINE
EMERGENCY MEDICINE
EMERGENCY MEDICINE
EMERGENCY MEDICINE
EMERGENCY MEDICINE
EMERGENCY MEDICINE
EMERGENCY MEDICINE
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EMERGENCY MEDICINE
ANAPHYLAXIS
Introduction
Anaphylaxis according to Dorlands is a manifestation of immediate hypersensitivity (type I) in which
of a sensitized individual to a specific antigen or hapten results in life-tbrea1ening respiIatory distress. usually
followed by vascular collapse and shock and accompmied by urticuria. pruritus and angioedema.
Anaphylactoid is a reaction similar to anaphylaxis but it is not immullologically precipitated and thus occurs
after the initial e.xposure. Anaphylaxis means lack of protection due to immunization. Your body creates an
antibody that will not defend you from certain antigen. but "in cause a reaction.
Pathophysiologic Mechanism
The susceptible person has an initial exposure to an antigen or a hapten which produces a specific sensitizing
antibody or reagin. This reagin is kept within circulatory IgE immunoglobulins. These antigen specific 19E
comple.xes bind \\'ith mast cells and Imophils; Upon re-exposure to the antigen, bridging occurs between the
antigen alld the sensitized 19E complexes that have developed on the surfaces of the mast ceslls and basophils.
This bridging causes a change in the cells causing a decrease in cyciic AMP. leading to degrnnulation and a
release of pbarmocoJogically active mediators such as histamine. SRS-A serotonin. bradykinin and also
chemotactic factor for cosinophiIs neutrophils and p1atelcts.
The above mentioned mediators except for histamine and SRS-A are thought to have added effect on
anaphylaxis, but it is histamine and SRS-A that are the true causes of the anaphylactic reactions.
Histamine is thought to be a truYor mediator of anaphylaxis of man. Histamine causes bronchial oonstriction.
increased capillary penneability and vasodilation. Slow-reacting substance of anaphylaxis causes constriction
of bronchial smooth muscle. Histamine and SRS-A aJong "\\ith the other above mentioned mediators arc
responsible for the manifestations of anaphylaxis. These manifestations are what we see clinically and what
must be recongized so that treratment can be instituted immediately.
There is no universal pattern or step-by-step process of anaphylaxis. The manifestations of anaphylaxis are
listed below: with any reaction. not aJI the manifestations may occur and those that do may not appear in any
order.
1. Cutaneous: erythema pruritus. urticaria and angioedema (usually of the eyes. lips or tongue)
II. Respiratory failure: two types
A) Upper airway obstructions 0\\1ng to edema of the larynx and/or epiglottis which can cause acute
distress and death by suffocation.
B) Lower airway bronchoconstriction which leads to limited airflow that is not relieved by endotracheal
intubation, leading to a problem of gas e.xchange and hypoxemia and hypercarbia.
III. Cardiovascular: probably the most severe reaction which leads to hypotension. arrhythmias and cardiac
arrest
Signs and symptoms
The typical manifestations of anaphylaxis aIC that the patient complains of a sense or aura of uneasiness.. and
becomes agitated and flushed Reaction can occur "\\ithin 1 to 15 minutes or several hours after exposure to
antigen. Symptoms progress to palpitations. paresthesias. pruritus, coughing. sneezing. urticaria and difficulty
breathing. Cardiovascular collapse can occur concomitantly "With respiratory distress or in its absence.
Unrecognized, anaphylaxis can lead to shock and ultimately death
Causes
The causes of anaphylaxis and anaphylactoid reactions are infinite. The most obvious and important
precipitants are: narootic anaJgesics. local anesthetics (more prevaJent with esters than arnides), antibiotics (ie-
penicillin and sulfonamides). antifungaIs (ie-amphotericin) and radiopaque dye. Cross reactivity between drug<;
is equally important (ie-ccphaJosporins should not be prescribed to a penicillin aJIergic pltiellt).
325
Treatment
Because of the dire consequence of anaphylaxis/anaphylactoid reaction, quick recognition and immediate
intervention is tantamount. Inullediate treatment consists of 0.3 ml epinephrine (1:1000 dilution) given
intramuscularly, whether the clinical picture is generalized pruritus, laryngeal edema, bronchospasm or
hypotension. Further treatment includes the use of a tourniquet, placing the patient in a recumbent position,
monitoring vital signs, establishinglmaintainingan airway. ox-ygen. etc.
Key Points
-difference between anaphylaxis and anaphylactoid reactions
-anaphylaxis is type I hypersensiti"ity (inunediate)
-drug of choice is 0.3 ml 1M epinephrine (1: 1000 dilution)
-patient history of allergic responses to drugs. foods. etc.
APPROACH TO CHEST PAIN
There are many causes of chest pain. All complaints of chest pain should be taken seriously. Empiric
treatment should be started immediately. if there is any suspicion of a cardiovascular or respiratory event.
I. History of trauma and/or reproducible prin with palpation
-most likely musculoskeletal in origin
II. CardiovascuIar and/or Respiratory etiology
a) begin ox-ygen - 5 Umin
b) monitor vital signs
c) appropriate STAT consuItation with internist or cardiologist when possible (if event occurs in hospital)
d) transfer patient to Intensive Care or Cardiac Care Unit
e) examine for shock. increase in venous pressure. pulmoruuy edema
Ill. Shock. Hypotension. Increased venous pressure and/or Pulmonary edema
A) treatment
1.) insert Iarge bore IV
2.) obtain arterial blood gas STAT
3.) obtain ECG and chest x-ray
4.) examine patient
5.) insert urinaIy catheter and monitor fluid status
B) differential diagnosis
1.) myocardial infarction
2.) pulmonary embolism
3.) acute heart fuilure
4.) pericaIdial effusion
5.) others: cardiac tamponade, tension pneumothorax.. aortic dissection, leaking aortic aneurysm
IV. Acute distress from pain or dyspnea "ithout shock. hypotension. increased venous pressure and/or
pulmonary edema
A) treatment
1.) history and physical
2.) insert IVandinfuseD5W
3.) obtain arterial blood gas
4.) obtain ECG - correct severe arrhytlunia
5.) N morphine 2-5 mg every 10-20 minutes
B) differential diagnosis
1.) all those listed in the above section
2.) cardiac. respiraIOJ),. abdominal and musculoskeletal causes
326
ELECfROCARDIOGRAM
L Basics
A) EKG paper
1.) usually run at 25 mm/sec
2.) thin 1 mm box = 0.04 sec
3.) thick 5 rom box = 0.2 sec
B) Components
L) P wave: represents atrial contraction
2.) QRS complex: represents ventricular contraction
3.) T wave: represents ventricular relaxation
4.) P-R interval: not to e.xceed 0.2 sec
5.) QRS complex: should be less than or equal to 0.12 sec
ll. Rate
A determined by pacemaker
1.) sinus atriwnnode (SA node)
a) normally the pacemaker
b) normal rate = 60-100 beats/minute
c) sinus bradycardia = less than 60 beatslminute
d) sinus tachycardia = greater than 100 beatslminute
2.) ectopic pacemaker
a) either atrium
b)AVnode
c) either ventricle
B. how to determine the rate by quick estimation count the number of thick (5 mm) lines between two R
waves each thick line is given a value in succession
-300. ISO, 100.75.60.50
III. Identifying arrhmthymias
A) determine the rate
B) identify tbe pattern or regularity of tbe arrhythmia
I.) premature beats (ie-a beat earlier than e.xpected)
2.) speeding up or slowing down of the r h ~ t h m
3.) presence of any pauses
4.) total irregularity or chaos
C) recognize and define atrial activity
1.) identify the P wave
2.) P wave may change iftbere is an ectopic pacemaker in either atrium. bowever a P wave will be present
and the QRS complex will be nonnal
3.) ectopic A V node pacemaker may have an inverted P wave or no P wave
D) recognizing ventricular activity
if ectopic pacemaker is in the ventricle then QRS comple.x will be greater than 0.12 sec and P wave will be
absent
E) determine relationship of atrial to ventricular activity
1.) normal l:l, fixed
2.) prolonged 1:1, fixed
3.) multiple P waves to QRS complexes
4.) P waves and QRS complexes unrelated
327
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328
COMATOSE PATIENT
Initial management to ensure maximal recovery and avoid further damage.
I. Asses ABC's
II. Obtain blood for STAT analysis
A) toxic substance screen
B) electrolytes, glucose. calcium. BUN & creatinine
C) liver function tests
Ill. ~ which may improve patient's status and will not bann
A) glucose (ampule ofD50) - consider h:ypoglyoemia until proven otherwise
B) thiamine - give it with glucose to avoid precipitating acute Wemicke-Korsakotr syndrome
(encephalopathy) in thiamine ~ c i e n t patient
C) corticosteroids - decrease cerebral edema
D) mannitol - osmotic agent to reduce an elevated intracIanial pressure
E) naloxone 0.4-2.0 mg IV - reverse DaIOOtic overdose
F) valium 5-10 mg IV - stop seizure activity
G) flumazenilIV - reverse benzodiazepi.ne overdose
IV. Normalize metabolic abnonnalities and body temperature
SHOCK
General management of shock
1. Recognize the presence of the shock state
2. Identify the probable cause of the shock state.
3. Early intervention - treatment of shock is directcd toward restoring cellular and organ perfusion with
adequately oxygenated blood, rather than merely restoring pulse and blood pressure: therefore,
vasopressors are contra-indicated in hypovolemic shock.
The goal of treatment i ~ to re.Uore organ perfusion
Signs of Shock
1. Tachycardia: earliest sign of shock.
infant 160: preschool 140: school age 120: adult 100
2. Respiratory rate: when tissue perfusion decreases, ox-ygen tension decreases and cells switch to anaerobic
metabolism. Lactic acid is then produced which induces a metabolic acidosis. Respiratory rate will
increase causing a transient respiratory alkalosis. Tachypnea represents another early sign of
shock.
3. Capillary filling: capillary f"dling \\-ill decrease cansing cold extremities. Normal capillary filling is 1-2
seconds. This sign is not considered a criteria in the h}'J1Olhennic (Iltient.
4. Pulse Pressure: the difference between systolic and diastolic pressure. This value \vill reduce as the
patient enters the shock state. A narrowed pulse pressure is considered less than 20 mmHg. The
phenomenon is primarily related to a rise in diastolic pressure because catecholarnines released during the
shock state increase peripheral resistance.
5. Change in memaI status: often subtle in the early stages of shock. htitiallyanxiety may be expressed as
fright or hostility. In the late stages the mental status may degrade to unresponsiveness and eventually lack
of consciousness.
6. Fall is systolic pressure: this does not occur until a significant amount of blood is lost. usuall:r between
1500-2000 ml. Requires immediate interventiOlL
329
7. Drop in uriruuy output: usual urinary output in the adult is 20-30 mJ/hOUT. Urinal)' output is only affected
in severe shock states. Once fluid replacement has been initiated urinary output may be used
as a gauge of effectiveness. Urinary output should be 50 mllhoUT for adults.. 2 mlJkg/hoUT for infants
and I rnlIkglhour for pediatric JDtients.
8. Hematocrit (hemoglobin concentrntion): a massive blood loss may produce a minimal acute decrease in
hematocrit. A low hematocrit suggests significant blood loss or anemia, however a normal or near normal
hematocrit does not rule out a significant blood loss. Therefore. hematocrit is an unreliable measure of
blood loss
Types of Shock
* All patients in shock are treated initially as though they were in hypovolemic shock*
I. Cardiogenic shock: a shock state induced by myocardial dysfunction. In the trauma patient this fonn of
shock is common, second only to hypovolemic shock. Characterized by increased CVP pressure and
a history of chest trauma. Causes include cardiac tamponade (muffled heart sounds. engorged neck veins).
tension pneumothorax. cardiac contusion. air embolism and myocardial infarction (rarely).
2. Neurogenic shock: in general, isolated head trauma does not cause shock. Head and spinal cord injuries
may produce hypotension secondary to loss of S}mpathetic tone, however this only compounds the effects
of hypovolenria. Characterized by hypotension without the classic signs of shock and \\1de pulse
pressure.
3. Septic shock: shock due to infection is uncommon in trauma. however should be considered with
penetrating wounds of the abdomen where bowel contents are spilled. Characterized by mild tachycardia
\"ann skin fand a "ide pulse pressure.
4. Hypovolemic shock: defined as an acute loss of ciIt:ulating blood. The normal adult circulating blood
volunte is ']010 ofbody weight or in a 70 kg man. approximately 5 liters. In children the blood volume is 8-
9% of body weight or 80-90 mlJkg. Once hypovolemic shock is suspected immediate aggressive fluid
resuscitation must begin.
5. Factors that alter vascular dynamics:
a) JDtient age - the older the JDtient the more difficult) they have in tolerating and compensating for
hemorrhage.
b) severity of injury - special attention to anatomic location.
c) time Iap;e - the tinte between occurrences of injury and treatment is significant
d) prehospital therapy - fluid replacement or use of MAST (military antishock trousers) or PASG
(pneumatic antishock garments).
Classes of Hemorrhagic Shock
1. Class I ltemorrhage: a loss of 15% of blood volwne or 750rnl. No measurable signs of shock. are
demonstrated with the exception of minimal tachycardia. Without therapy the body will compensate for
the volume loss within 24 hours, however crystalloid fluid replacement is suggested.
2. Class IT hemorrhage: a 15-30% volume loss or 750-1500 mIs. Characterized by tachycardia, tachypnea,
decreased pulse pressure. Systolic pressure and urinary output usually remain stable. Patient may
ex-perience ~ e CNS changes. The majority of patients in this stage of ltemorrhage may require blood
transfusion eventually, however, are easily stabilized with crystalloid fluid
3. Class ill hemorrhage: a 30-40% blood loss or 1500-2000 mIs. This class of hemonbage presents the
classical signs of shock (ie-marked tachycardia tachypnea. change in mental status and fall of systolic
pressure). At least 30% of blood volwne must be lost before the systolic pressure drops. Treannent
requires immediate crystalloid fluid replacement and eventual transfusion. The decision to immediately
transfuse is based on the patient's response.
330
4. Class IV hemorrhage: more than 40",4. volume loss OT 2000 mls. This degree of exsanguination is
immediately life- threatening. Characterized by the classic signs of shock, negligible urinary output and
unobtainable diastolic pressure. Immediate fluid and blood replacement and surgical
intervention to stop the hemorrhage is warranted
Loss of 50% of blood volume results in loss of consciousness, pulse and blood pressure.
Soft tissue fluid loss
Ma:ior soft tissue injuries and fractures affect the circulation in m"O ways-
L blood loss: a fractured tibialhumerus can lose up to 750 ml of blood. Femurs can lose 3 units
(1500 mI) and the pelvis can lose 6 units (3000 mI) of blood
2. inflammatory edema: consists of plasma and e.macellular fluid
Roughly 25% of fluid fowtd at the ifYured area is circulating volume. Therefore the 3: 1 rule of fluid
replacement is indicated For example, most patients in hemorrhagic shock will require 300 ml of
electrolyte solution fOT each 100 ml of blood volume loss.
Initial management of hemorrhagic shock
1. Airwaylbreathing: restoring blood volume does nothing unless the blood being circulated is oxygenated
Maintenance of arterial oxygen tension at least 95% PI02 or better is necessary.
2. Hemorrhage control: bleeding from arterial wowtds is controlled with direct pressure. Internal bleeding
requires surgical evaluation immediately.
3. Gastric decompression: the GI tIact stops functioning in the tramnatized prtienL The danger of aspiration
with fatal sequela exists.
4. Vascular access: must be obtained promptly using large bore 16 gauge or larger catheters. If peripheral
access annot be obtained a saphenous vein cutdown is performed before a CVP is considered The
cutdown is quicker and with less complications.
5. Initial fluid therapy: crystalloid isotonic electrolyte solutions are used for resuscitation only. Ringers
Iactate is first choice followed by normal saline. Normal saline is not preferred due to the potential to
cause hypochloremic acidosis especially in renally impaired patients. The initial bolus in adults is
1-2 liters and 20 ml/kg in children.
6. Blood replacement: once the decision to begin tIansfusion has been made, three types of blood are
available depending on the urgenCy of the patient's condition.
fully crossmatched blood : preferred, however, usually takes one hour to prepare.
type specific (saline crossmatched): compatible \\-ith ABO and Rh blood types but minor
antlbodies e.xist. Available within 10 minutes.
type 0 negative blood: reserved for use in patients with exsanguinating hemorrhage. Rh
negative mctor is suggested to avoid future sensitization.. especially women of childbearing
years.
Blood wanners should be used with blood and crystalloid fluids to prevent hypothennia. A 160
micron filter should be used to filter microscopic clots. All other filtering devices should be
avoided because they do not allow rapid fluid administration.
7. Pewnatic Antishock Garment (pASG): this de\ice raises systolic pressure by increasing peripheml
resistance and myocardial afterload. The device is a prehospital therapy designed to buy time.
Only two in-hospital indications exist
severe pelvic fracture with continous hemorrhage and hypotension
patients in-route to the OR with intra-abdominal trawna and severe hypovolemia
Contra-indications
uncontrolled hemorrhage outside the confines of the garment
pulmonary edema
suspected OT kno\,\TI rupture of the diaphragm
left ventricular dysfunction
respiratory distress: necessitates the deflation of the abdominal compartment
331
The device cannot be removed until the patient has been adequately managed and is stable or when
there is adequate preparation for immediate surgical intervention. The deflation process is graduaL
begirllling with the waist compartment and proceeding to each leg cOlllfwtment. Air is released until
a 5 mmHg drop in blood pressure is noted.
Complications in treatment of hypovolemic shock
A) Age the older patient has difficulty compensating and tolerating hypotension from hcmorrhage.
B) Athletes: this group of patients have pulse rates of 50 and increases in blood volunle by 15-20%. Cardiac
output increases 6 fold and stroke volume by 50%. Assessment of this patient is difficult.
C) Medications: beta-adrenergic receptor blockers and calcium channel blockers significantly alter the
paticnt's hemodynamic response to hemorrhage.
D) Hypothemua: temperature is extremely important to record in tile suspected shock patient.
E) Pacemakers: heart rate remains constant in these patients until blood loss causes myocardial failure. This
group should be monitored by CVP pressure.
F) Continued hemorrhage: if hemorrhage cannot be controlled by initial treatment immediate surgical
intervention is requi.red
G) Fluid overload: once the patient management is completed the risk of fluid overload is minimized by CV'P
monitoring or pulmonary wedge pressure. A pulmonary wedge pressure is technically difficult to
perfonn in the emergency room setting, therefore CVP pressure can be employed much more simply
=> Central venous pressure monitors only the right hearl'S ability to accept fluid The precise
measure of cardiac function is tlle relationship between end diastolic ventricular volume and
stroke volume. Therefore right heart pressure to cardiac output as determined by CVP pressure is
indirect and insensitive estimate of cardiac function. however. it is useful for gross evaluation of
tlle clinical situation
-a minimal rise in tlle initial low CVP values indicate need for further fluid
replacement.
-a declining CVP value indicates continued hemorrhage.
-an abrupt elevation in CVP value suggests replacement is too much or too rapid and
cardiac function is comprontised
H) Acid-Base balance: the initial respiratory alkalosis gives way to metabolic acidosis of a mild fonn in tlle
early stages of shock and does not require treatment. In prolonged late stage shock a severe metabolic
acidosis can occur. This is treated only witll increased fluid not bicmb Bicarbondate therapy is indicated
whcn tlle pH drops below 7.2
n Recognition of other problems: when the patient fails to respond properly to tllerapy. consider other causes.
1) Constantly re-evaluate the patient.
332
TRAUMATOLOGY
TRAUMATOLOGY
TRAUMATOLOGY
TRAUMATOLOGY
TRAUMA TOLOGY
TRAUMATOLOGY
TRAUMATOLOGY
TRAUMATOLOGY
TRAUMATOLOGY
TRAUMATOLOGY
TRAUMATOLOGY
TRAUMATOLOGY
TRAUMATOLOGY
TRAUMATOLOGY
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FRACTURE MANAGEMENT
Initial Assessment
Extremity trauma is rarely Jife-threatening, but associated injuries can be potentially serious. Certain injuries and
combinations of injuries to the skeleton may be pennanently disabling if not properly recognized
L Primary Survey: life-threatening conditions are identified with this exam
AirwaY maintenance with cervical spine control
and ventilation
with hemorrhage control
Qisability: quick neurologic check using the A VPU method
A alert
V: responds to visual stimuli
P: responds to stimuli
U: unresponsive
of patient, remove all clothing
2. Secondary Survey:
The secondary survey is a head to toe evaluation of the tIauma patient, which does not begin until the primaIy survey is
complete and the patient is stabilized Each region of the bocJy, beginning with the head and ending with the feet. must be
thoroughly examined. Special procedures such as laboratory studies and radiographic examinations are conducted in this
survey.
3 History:
Information concerning the cause of the injury will help determine the direction and strength of the defonning forces. A
history can be obtained at any time during the evaluation of the patient, but cannot interfere with the primary and
secondary survey.
4 Definitive Care Phase:
In this phase, all the patient's injuries are managed This phase includes comprehensive management, fracture
stabilization and any necessary operative intervention, as well as stabilization of the patient in preparation for appropriate
transfer to a fucility that can provide a higher level of medical care.
Fracture Assessment
Fractures are generally classified into two major groups, open or closed fractures. Any obvious or suspected fracture near
a wound should be assumed to be an open fracture, even if the fracture cannot be seen in the wound
1. Life-threatening fractures
crush injuries of the pelvis and abdomen
traumatic amputations of the arm, foreann, thigh or leg massive open long bone fractures
2. Limb threatening injuries
vascular injuries with or without fracture
crush injuries
compartment syndromes
dislocation of major joints
open fractures
3. Associated or occult fractures
333
In the podiatric assessment of a trauma patient occult fractures are easily overlooked. Certain types of accidents and/or
fractures have associated injury pattenlS.
=> Compression fractures - this t)-pe of fracture is most commonly seen in a patient who has fallen from a height and
landed on their feet Calcaneal fractures are associated with tibial plateau fractures and vertebral body fractures.
Spinal radiographs are required on all 'jumpers".
4. Neurovasuclar injuries
Assessment of neurovascular status is the first step in evaluation of extremity injury.
a) vascular injuries: vascular injuries disrupt the integrity of the vessel wall, with bleeding or thrombosis resulting
in impairment of distal circulation and ischemia. Bone is an extremely vascular organ. Fractures involving long
bone and pelvis can result in hypovolemic shock. The pelvis can lose six units of blood, the femur three units and the
tibia one and one-half units. Dopplers and angiograms provide the most accurate means of vascular evaluation.
b) comautment syndromes: a compartment syndrome occurs when the interstitial pressure rises above that of the
capillary bed., local ischemia of nerve and muscle occurs. Compartment syndromes take several hours to fonn. The
patient may have excellent pulses, however, the pain the patient is experiencing is out of proportion to the injury
sustained Cannulation and measurement of compartment pressure is diagnostic. Pressures greater than 30 mmHg are
indicative of compartment syndrome. Prompt fasciotomy is necessary.
c) nerve injury: injury to nerves may represent actual division of the nerve or a physiological disruption. In general,
stretch injuries have a poor prognosis compared with compression injuries.
d) amputations: patients with amputations require rapid assessment and consultation with a specialized center.
The amputated part should be cleansed of any gross debris and wrapped in a sterile towel moistened with saline and
placed in a crushed ice cooler and the patient shonld then be transferred to a center capable of microvascular re-
anastomosis. Amputated parts remain viable from 4-6 hours at room temperature or up to 18 hours if cooled
properly.
Oassifications of Closed .Fractures
Rockwood and Green devised a classification system based on fracture mechanism which help determine subsequent
treatment.
1. Direct Trauma: closed fractures caused by direct blows of varying velocity
a) Tapping :fractures: low velocity blow which results in no comminution and little soft tissue damage
b) Crush:fractures: high velocity blow which creates extensive soft tissue injmy and comminution
2. Indirect Trauma: closed fractures resulting from forces acting at a distance to the fracture site
a) traction:fractures: transverse avulsion fracture at the site oftenckm or ligament attachment
b) angulation fractures: transverse fracture caused by bending forces on a long bone. The convex side
transversely fractures while the concave side splinters
c) spiral :fractures: an oblique:fracture 45 to the long axis ofbone, caused by rotational forces
d) compression fractures: result from impaction of the shaft into the soft cancellous bone
e) angulation and axial compression fractures: cause transverse fractures with butterlly fragment
f) angulation and rotation fractures: cause oblique fracture lines
334
Treatment of Closed Fractures
Prior to definitive treatment, the primary and secondary survey must be completed. The neurovascular and tendon
function are first priority.
1. Contra-indications to closed reduction
=> no disp1acement
=> no reduction is possible due to comminution
=> reduction cannot be held by external immobilization
=> traction forces produced the fracture
=> open fracture
2. Indications for open reduction
=> closed reduction technique have failed to approximate fragments
=> articular surfiIce involvement, anatomic reduction is necessaty
=> traction force fractures resulting in large avulsion fi:actures
3. Technique of closed reduction
=> anesthesia is necessaIy to prevent patient muscular guarding; guarding causes excessive reductive force to
be used resulting in greater tissue damage
=> review of fracture mechanism is necessary to understand proper reductive movements
=> slow, steady traction applied along the axis of the bone with counter-traction applied by an assistant
=> restorntion oflength
=> correction of rotatory deformity
=> apposition of bone fragments
=> correction of angulational deformity
=> application of Jones compressive dressing
* tissue swelling usually peaks approximately 6-8 hours following injury
=> timely application of a compressive dressing will reduce soft tissue edema
=> evaluate neurovascular status
=> following a 3-4 day course of elevation with compressive dressing application, a "hard" cast may be applied
Fractures in Children and Adolescents
Children's bones react much more quickly to fi:actures than those in the adult Within a few days, the fragments are joined
by callus. Reduction of the fractme is easiest within the first 24 hours.
1. Indications for operative or nonoperative treatment:
In general. closed reduction is preferred for children's fractmes. The healing capacity of growing bone is
considerable and pseudarthrosis seldom occurs. Malunion may be corrected by subsequent growth. Operative
treatment should be considered when closed reduction fails or surgery will prevent a poor result
2. Aims of fracture treatment in children
a) prevention of malunion: the ability of bone to spontaneously correct post-traumatic deformity
decreases with age. Anatomic reduction is indicated in the adolescent.
b) prevention of growth disturbances: setmation of the epiphysis heals perfectly following precise
reduction. If closed techniques cannot precisely reduce the epiphysis, operative reduction is
recommended Excessive longitudinal growth is regularly seen following fracture of the diaphysis. It is
compensated for by allowing the fractme to unite with slight initial shortening.
335
DIGITAL AND SESAMOIDAL FRACTURES
Pedal digital and sesamoidal fractures are not incidental. trivial injuries. The sequela from mistreatment of these fractures
can result in long tenn J:Xlinful disability.
Hallux fractures: Considered to be the most common fracture in the forefoot. Most hallux fractures occur at the distal
phalanx and result from a stutbing injuIy or a crushing injury from a heavy oqject falling on the toe. Crushing injuries
cause comminution of the distal phaiaIL'{ and are often associated with subungual hematoma due to a lacerated nail bed.
Pressure caused by the hematoma can damage the nail matrix if not relieved within 6-12 hOUTS. If the hematoma involves
more than 25% of the nail plate, avulsion of the entire nail plate should be considered. If a nail bed laceration is noted
upon removal of the nail plate, the injury should be treated as an open fracture.
Sesamoid fractures: Usually caused by repetitive, high-impact activities or by crushing injury to the foot. Sesamoid
fracture must first be differentiated from a bipartite or multipartite sesamoid
Findings supporting a diagnosis of sesamoid fracture-
>fracture line usually jagged, irregular or uneven
>large space between fragments is consistent with fracture
>anatomical1y abnormal fragment positions indicate fracture
>bone callus formation is suggestive of fracture
>multipartite sesamoids are usually larger than nonna!
>contralateral views demonstrate no evidence of similar findings on the uninjured foot
>iffurther diagnostic studies necessary, Consider technetium 99-mdp bone scan, dorsiflexion stress radiographs of
the first MIP joint CT scans or MRI
=> Fracture of the tIbial sesamoid may be more common due to greater load during gait.
Lesser digital fractures: Fracture to the fifth digit due to night walking is the most common lesser digital fracture. The
proximal phalanx is usually affected, demonstrating an oblique or spiral oblique pattem
Treatment
Hallux fractures: Comminuted tuft fractures usually respond to immobilization in a weightbearing cast or surgical shoe.
Intra-articular condylar fractures may respond to conservative management (NWB cast immobilization), but may require
ORIFdepending on the size of the fracture fragment. If conservative therapy fails, surgical excision may be necessary.
Sesamoid fractures: Conservative management consists of cast immobilization (with extension to end ofhalllL'<) NWB
for 4-6 weeks. Surgical shoe pad::Jed to alleviate pressure under the first metatarsal head and "W-alking cast are other
options, but may be more appropriate for sesamoiditis than for fracture management. In some cases of severe injury
surgical excision of the affected sesamoid and long tenn management with functional orthoses may be required
Lesser digital fractures: If nondisplaced, support via buddy splint and avoiding narrow toed shoes is usually adequate. If
displaced, reduction is required This reduction may be maintained with a simple buddy splint, percutaneous K -wire, or
modified cast. Severe injuIy may necessitate ORIF or excision of fracture fragments.
336
Jabss' Classification of First MTP Joint Dislocation Injury
~ dorsal dislocation of the proximal phalanx and sesamoids with the intersesamoidalligarnent intact. The
JDC'clwnism of injwy is hyperextension of the hallux.
=> Treatment: open reduction
Type ITA: dorsal dislocation of the proximal phalanx and the sesamoids with rupture of the intersesamoidalligament.
=> Treatment: closed reduction
Type lIB: dorsal dislocation of the proximal phalanx and the sesamoids with transverse fracture of one of the
sesamoids.
=> Treatment closed reduction
Type IIC: dorsal dislocation of proximal phalanx and sesamoids with complete disruption of the intersesamoidal
ligament and transverse fracture of either sesamoid
=> Treatment: open reduction
Type II variant: dorsal dislocation of proximal phalanx with complete disruption of sesamoid-plantar pIate
complex and separation of previous bipartite tIbial sesamoid
=> Treatment: closed reduction
J ahss' Classification of First MTPJ
Dislocation Injury
Type I Type lIA
Type lIB
METATARSAL FRACfURES
Classification of Metatarsal Fractures: these injmies share the same classification as long bones, which have been
descnbed by Salter.
=> site: diaphyseal, metaphyseal, epiphyseal or intra-articular
=> extent: complete or incomplete
=> configuration: transverse, oblique, spiral or comminuted
=> relationship of fracture fragments to each other: shifted sideways, angu1ated, rotated, distracted, overriding or
impacted
=> complicated or uncomplicated
*Gudas further classified metatarsal fractures into intemal metatarsal (2,3,4) and external metatarsal (1,5) fractures.
He suggested that further consideration be given to the external metatarsals due to the effects of extrinsic muscles
and independent ranges of motion.
337
Treatment of metatarsal fractures: treatment varies according to the metatarsal involved anatomic location of the
fracture as well as degree of displacement. Sagittal plane defonnity must be minimized in order to prevent subsequent
metatarsalgia and/or frncture of the adjacent metatarsals.
Diaphyseal frnctures: treatment varies by the amount of displacement. Nondisplaced fractures are generally placed
in a nonweightbearing cast. Displaced frnctures require attempted closed reduction followed by cast inmlobilizatio11.
Should the reduction 110t be maintained in a cast, open reduction with internal fixation is required.
MetaphYseal fractures: usually transverse in nature, these f:rnctures can be managed conservatively \vith a cast.
Unstable fragments, however, may require intemal fixation.
F'IF"IH METATARSAL BASE FRACTURES
Radiologic Classification (after I.M Stewart) as translated from Courrier des Pedicures Romands bv Miss M Soufflet, MChs
~ : supra-articular f:rncture occurring at the metaphyseal-diaphyseal junction
>this injury corresponds to a true Jones frncture mechanism - vertical and transverse forces act upon a
fixed foot that cannot invert
nonunions common due to the dynamic forces of soft tissue attachments, the fifth metatarsal's independent
range of motion and vascular supply to fifth metatarsal
=> Treatment=if nondisplaced, 6-8 weeks NWB immobilization
surgical repair in competitive athletes and in cases when conservative therapy fails consist of ORIF with
pins, screws, plate with screws, wire or bone graft with plate fixation
~ : intra-articular avulsion fracture with one or two fracture lines
Type III: extra-articular avulsion fracture in which the peroneus brevis tears a small fragment from the
styloid process
=> Treatment for avulsion fractures involves conservative therapy as outlined above and tension band wiring if
surgical intervention is required
Type IV: intra-articular, comminuted fracture
Type V: e>..1ra-articular avulsion fracture of the epiphysis in children
338
Fifth Metatarsal Base Fracture Classification
I
II ill IV
v
Stewart Classification from: Jones's Fl3Cture: Fl3Cture of Base of Fifth Metatarsal by IMStewart, MB, FRCSE
Clinical Orthopedics, 1960. This is the preferred classification.
Type I A TypeIB
339
TypeilA
n
Type lIB
Classification of Fifth Metatarsal Base Fractures from 51 cases
Cases
Fracture at the ction of shaft and base (JONES) - T I A 8
Comminuted - T I B 6
Fracture of the IIA 11
With Joint involvrnent - T 21
Stewart Classification from: Jones's Fracture: Fracture of Base of Fifth
Metatarsal by I.M.Stewart, ME. FRCSE, Clinical Orthopedics, 1960.
TARSOMETATARSAL JOINT FRACTURE I DISLOCATION
FractUre/dislocation to this joint is rare and difficult to diagnose. The configuration of the joint is extremely stable due
to a recessed second metatarsal base and strong plantar/dorsalligaments.
Two classification systems based upon radiographic appearance are most commonly employed-
A) Quenu and .Kuss
:::::> Homolateral: fractureldislocation with all the metatarsals displaced in one direction corresponds to Type A Hardcastle
classification Isolated: involvement of a single metatarsal, usually dislocation of the first metatarsal
=> Divergent: fractureldislocation which forces the first metatarsal medially and the lesser metatarsals laterally
340
B) Hardcastle
Type A total incongruitylhomolateral
=> total incongruity of the entire tarsometatarsal joint
=> with displacement in the sagittal or transverse p1anes
Treatment =
closed reduction if non-disp1aced
ORIF if severe
stabilization with 2 K-wires is common, but depends on the stability of the
tarsometatarsal joint (ie-one wire medially ~ :first metatarsocuneifonn joint and one
wire JateraI1y across fifth mecatarsocuboid joint)
Type B: partial incongruity
partial displacement involving partial incongruity of the joint complex in either sagittal or transverse
planes or both
B 1 - medial dislocation
=> displacement of the first metatarsal in iso1ation or in combination with displacement of the lesser
metatarsals
B2 -lateral dislocation
=> first metatarsal unaffected
Treatment =
surgical stabilization of joint complex
closed reduction, depending upon severity
Type C: divergent
divergent displacements involving partial or total incongruity of the joint
the first metatarsal is displaced medially and any combination of the lateral four metatarsals are
disp1aced laternlly in the sagittal or transverse p1anes or both
lateral plantar artery is compromised
Cl - partial displacement
C2 - total displacement
Treatment =
=> surgical repair due to instabili1y of joint complex
(ie-three or more K-wires)
Type A
TypeBl
341
TypeB2
TypeC
MIDFOOT FRACfURES (CUNEIFORM, CUBOID AND NAVICULAR)
Cuneiform and Cuboid Fractures
Isolated fractures of the cuneiforms or cuboid are rare and usually caused by direct impact trauma. Fractures to these
bones can also occur as associated injuries with tarsometatarsal frnctures, fifth metatarsal base fractures and navicular
fractures.
Oassification of cuneiform and cuboid fractures
1) avulsion fracture
2) body fracture (simple, comminuted or crush)
3) fracture with dislocation
Treatment: these injuries usually respond to cast immobilization since the bones are strongly bound by intertarsal
ligaments and surrounding bony structures. If avulsion fracture does not respond to conservative therapy, surgical
excision offiagment should be considered.
342
NAVICULAR FRACTURES
Watson..Jones classification
I1mJ: tuberosity fracture Type II: dorsal chip fracture
Type m: fracture of the body with or without displacement
Treatment: treatment varies acoording to location
The tuberosity fractures are usually satisfactorily managed with cast immobilization. Pull of the tibialis posterior can
delay or prevent healing, necessitating the surgical excision of the fragment Chip fractures respond well to casting. Body
fractures, depending upon the degree of displacement, will require closed reduction and frequently open reduction with
internal fixation.
TALAR FRACfURES
The talus is almost wholly artiadar and has a unique blood supply which predisposes it to severe post-traumatic
COmplications including crippling arthritis, delayed OT nonunion and avascular necrosis. Fractmes of the ta1ar head are
frequently seen in sudden dorsiflexmy force injuries, however, usually have a good prognosis with cast immobilization.
Due to the large amount of artiadar surface, bloocJ. can only supply the talus through three main sources: through the
neck, through the sinus tarsi, through the tarsal canal and through the medial side of the body. The three main arteries
which supply the talus, in order of significance, are - the posterior ti.biaI, anterior tIbial and peIforating peroneal. Hawkins
sign is frequently used to ~ the viability of the talus following fractureldislocation; it appears as a subchondral
radiolucency on the AP view of the ankle approximately 6-8 weeks after injury and occurs when no avascular necrosis is
present. It has been postuJated that Hawkins sign is caused by disuse osteopenia or vascular congestion, which suggests
maintenance of blood supply to talar body.
343
Hawkins Classification of Talar FractureJDisJocations
nondisplaced vertical fracture oftalar neck
body of the talus retains its nonnal position in the STJ and ankle joint
Type II: vertical fracture of the talar neck with STJ subluxation or dislocation
Type ill: vertical fracture of the talar neck with STJ and ankle joint dislocation
all three sources of blood supply are disrupted
Type IV: vertical fracture of the talar neck with STJ, ankle and talonavicular joint dislocation
all three sources of blood supply are disrupted
Ha\>vkins Classification ofTalar Neck Fractures
II
INCIDENCE
OF AVASCULAR INCIDENCE OF
TYPE NECROSIS STJ AR1HRlTIS
I
II
ill
IV
20%
40010
100%
100%
rare
60-75%
100%
100%
Berndt-Hardv Classification of Talar Dome Fractures
small area of subchondral bone compression
Stage II: partially detached osteochondrnl fragment
Stage ill: completely detached, osteochondral fragment
Stage IV: displaced osteochondral fragment
Treatment:
ill
stage I
stagell
medial stage ill
observe, immobilize. NWB
cast immobilization, NWB
8-12 weeks cast immobilization
lateral stage ill
stage IV
::::> small lesion - excise fragment
dril1/curette subchondral bone
early ROM exercises
surgical intervention
surgical intervention
cast immobilization NWB 2 weeks, then
PWB4weeks
:::::> large lesion - ORIF
:::::> arthroscopy - recommended to remove loose bodies
pneumonic = ''DIAL-A-PIMP'
N
344
dorsiflexion-inversion causes an anteroIaternllesion
shallow, wafer shaped lesion
pIantarflexion-inversion causes a medial posterior lesion
deep, cup shaped lesion
Anterolateral
Lesions
44%
KEY
Fractures
""'-
Posteromedial
Lesions
56?/o
Miscellaneous TaJar Fractures: fractures of the talar head are frequently seen in sudden dorsiflexory force injuries,
however, usually have a good prognosis with cast immobilization. Areas of ligamentous attachment such as the dorsal
taJar neck and medial talus are sites of avulsion chip fractures. These, too, respond well to conservative therapy. The
lateral taJar process is a common fracture site, referred to as a Shephard's fracture and must be properly immobilized to
prevent prolonged pain due to delayed or nonunion.
Snepoen classification of talar body fractures
Group I: transchondraI or compression fracture of taJar dome
(including osteochondritis dessicans of talus)
Group II: coronal, sagittal or horizontal shearing fractures involving the entire taJar body
~ coronal or sagittal fracture
IA: nondisplaced
ill: displacement of trochlear articular surface
Ie: displacement of trochlear articular surface with associated subtalar joint dislocation
ID: total dislocation oftaJar body
Group II: Type I
IA
IB Ie
Tvpe II: horizontal fracture
ID
345
IIA: nondisplaced
lIB: displaced
Group II: Type II
ITA
Group ill: fracture of the posterior tubercle of talus
Group N: fracture ofIateral process of talus
Group V: crush fracture oftalar body
ITB
Group ill
Group IV
Group V
346
CALCANEAL FRACTURES
~ Calcaneal :fractures account for approximately (i()O/o of all major tarsal injuries and 1-2% of all diagnosed fractures.
~ Calcaneal fractures are arguably the most disabling of pedal fiactures.The most oommon mechanism of injury is a
fall from a height of as little as two feet The talus is driven through the calcaneus. cteating fracture lines of three
types - avulsion, oompression and shear. Asc;ocjated ftactures of the tibial plateau. femur, hip and lumbar spine must
also be considered
Diagnosis: patients oompJain of severe pain upon weightbearing and will usually give a history of a fall from a height
Characteristic ecchymosis may occur below the medial and lateral malleoli as well as extending to the plantar aspect of
the heel. referred to as "Mondur's sign".
Radiographic examination should include the following views:
-dorsop1antar view: assessment of calcaneocuboid joint
-laternl view: assessment of anterior beak. tuberosity and posterior filcet
-axial view: demonstrates lateral cortical bllge and the presence of a superomedial fmgment
-Broden I view: assessment of posterior filcet
~ central beam is cephaJad; 90 footlleg angle with foot and leg internally rotated 45; radiographs taken at 10,
20, 30, 40 angles.
(central beam is caudal with Broden II views)
Radiographic measurements: interpretation of subtalar joint depression is oommonly derived from the measurement of
two angles formed on the laternl view
1) Bobler's Angle (Crucial Angle: Angle of incidence): formed by a line joining the highest point on the
posterior articular SUIfiJce to the most superior point of the calcaneal tuberosity and a line joining the high point
of the posterior articular SUIfiJce to the high point on the anterior beak
Normal=20-40
Injury causing depression of the subtalar joint will cause this angle to decrease.
2) Gissane's Angle (Critical Angle): angle formed between the anterior laternl cortical shelf and the posterior
margin of the posterior fucet
Normal= 120-140
Injury causing depression of the subtalar joint will cause this angle to increase.
Gissane's Angle
347
Oassification of Calcaneal Fractures
Many classification systems have been suggested, however, no one system completely integrates mechanism with
treatment. Two commonly used systems will be descnbed which group calcaneal fractures into extra- and intra-articular
fractures.
Rowe Classification
Type IA: fracture of medial tubercle
Tvpe IB: fracture of sustentaculum tali
Type IC: fracture of anterior process
IA IB
Ie
Type ITA: avulsion fracture of posterior superior calcaneal process
Type DB: avulsion fracture of posterior beak. with involvement of tendo Achilles
d II A - Beak Fracture
~ I 1 B - Avulsion Fracture
Type ill: extra-articular fracture through body of calcaneus
Type IV: intra-articular fracture through body of calcaneus without joint depression
348
~ : commjrnrted, intra-articu1ar fiacture through body of calcaneus with joint depression
I t5?J<QJ1
Essex-1opresti cJas;e:ification of intra-articuJar gdgmeaJ fractures
This c1as<;ification system is commonly utilized to describe Rowe IV or V fractures. Both the tougue andjoint depression
types contain a primary and secondaIy fiacture line. The primaIy fracture line runs from superior to inferior, extending
from the apex of Gissane's crucial angle to the plantar aspect of the calcaneal body. The seoondaIy ftacture line is
determined by the direction of foICe - vertical directed foICe creates tongue type and anterior directed foICe creates joint
depression fractures. Further evaluation of articu1ar disruption through cr scan may be necessary
Type A:. Tongue type
=> talus carries the foICe into the
subtalar joint
=> sharp spur of talus is driven
inferiorly into the crucial
angle, splitting it along
the lateral cortex
=> secondaIy fiacture line extends
to posterior border of the
tuberosity
Type B: Joint Depression Type
=> primary (sagittal plane) fracture
divides calcaneus into medial and
lateral fragments
=> the medial :fragment includes the
sustentaculum tali and medial
portion of posterior facet of STJ
=> the lateral :fragment includes the
lateral portion of posterior facet and
remaining body of calcaneus
=> the lateral talar process acts like a
wedge causing sepmIlion and
depression of (lateral portion)
posterior facet into body of calcaneus
=> lateral wall fiacture occurs with
lateral cortical extension or with distal
extension into calcaneo-cuboid joint
349
Treatment:
=> calcaneal fracture treatment varies according to the location of the fracture and articular surface involvement.
tuberosity fractures: usually this type of calcaneal :fracture is minimally displaced and responds to cast immobilization.
Occasionally, closed and possibly open reduction is necessary.
sustentaculum fractures: these fractures involve portions of the anterior and/or middle :fucets. If nondisplaced cast
immobilization and non-weightbearing status is required Displaced fractures require closed or open reduction
techniques.
anterior process fractures: these fractures are usually caused by an inversion mechanism about the ankle. This injury
responds well to cast immobilization. If chronic pain results, the fragment may be excised
posterior beak fractures: should the Achilles tendon insertion run through or above the :fracture line, plantarflexory
power will be compromised Open reduction with cancellous lag screw or tension band fixation followed by
casting is indicated
eAm-articular body :fractures: usually little or no joint depression \\ill occur and the injury will respond "ill to non-
weightbearing cast immobilization.
intra-articular body :fractures: always involve joint depression to some degree. Several methods of reduction have been
suggested in the literature-
1. immobilization with early weightbearing
2. skeletal traction or Bohler clamp reduction
3. primary subtalar joint or triple arthrodesis
4. open reduction with internal fixation via the medial approach as described by McReynolds
5. open reduction with internal fixation via the lateral approach with bone grafting as descnbed by Palmer
6. extemal fixation (ie-llizarov technique)
350
Syndesmosis Sprains
-can range from minor strains to complete rupture ( diastasis) of the syndesmotic
ligaments
Anatomy:
-anterior inferior tibiofibular ligament (AITF)
-posterior inferior tibiofibular ligament (PITF)
-posterior inferior transverse ligament
-interosseous ligament
-interosseous membrane
Mechanism of injury:
-forced external rotation of the foot with simultaneous internal rotation of the leg
-hyperdorsiflexion with forceful external rotation
Classification of Syndesmotic Diastasis
-latent diastasis: ankles that appear normal on routine radiographs but experience ankle
mortise widening with stress external rotation radiographs
-frank diastasis: syndesmotic separation visible on plain radiographs
*deltoid ligament most likely concominantly ruptured with ankle diastasis
Symptoms:
-marked, generalized edema
-pain out of proportion for isolated lateral ankle sprain
-ecchymosis
-tenderness over the AITFIPITF that may extend proximally over the interosseous
membrane
-limited ankle ROM
-inability to perform toe raise
-toe to heel ambulation
Special Tests:
-anterior drawerltalar tilt to rio ATF/CFL involvement
-palpation of the syndesmotic ligaments
-passive dorsiflexion of the foot (this wedges the wider anterior talus in the ankle mortise
causing separation of the tibia and fibula)
-external rotation of the foot on a neutral ankle with the knee held at 90 degrees
-"squeeze test" (manual compression of the tibia and fibula above the level of the calf)
*these test are considered positive if they result in pain within the syndesmosis*
Adjunctive Imaging:
-plain radiographs (need to rio fracture)
-stress external rotation radiographs (look for ankle mortise widening/increase in medial
clear space)
-arthrography
-MRI
351
Treatment:
Conservative: these patients take a longer time to rehabilitate then medial/lateral ankle
sprams
-immobilization with gradual progression to protected weightbearing
-physical therapy to include ROM, proprioreceptive training, strengthening
-return to normal activities with protective bracing for the first 3-4 months
Surgical:
-consider in complete tibiofibular diastasis or with continued ankle instability
-transsydesmotic screw fixation
Possible Sequelae:
-continued pain/instability
-heterotopic calcification (usually causes no long term functional disability)
352
ANKLE FRACTURES
The mechanism by which an ankle fracture occurs must be fully understood in order to restore anatomic alignment of the
joint. Ramsey found that experimentally 1 mm lateral ta1ar displacement within the ankle mortise decreased tIbiotaJar
contact by as much as 42%. Yablon found that division of the and/or lateral malleolus leads to greater
ankle instability than sectioning of medial structures. He, therefore, concluded that anatomic reduction of the lateral
malleolus is the key to restoration of ankle stability in bimaI1eolar fractures. The work: of these as well as that
of the A-O form the basis of our current understanding of ankle fractures.
Eponyms descrIbing ankle fractures
Pott's (Dupuytren's) fracture: bimalleolar fractnre
Cotton's fracture: trimalleolar fracture
Bosworth's fracture: lateral malleolar fracture with ankle displacement
Maisonneuve fracture: proximal fibular fracture
Volkmann's fracture: posterior malleolar (tIbia) fracture
Tillaux fracture (tubercle avulsion fracture of the anterior lateral tIbia
Wag$ffe fracture: avulsion fractnre of the anterior medial fibula
Classification of Ankle Fractures
Classification
This classification system descrIbes 95% of all ankle fractures and allows one to predict the degree and severity of
ligamentous injury based upon the type of osseous injury. Each type of fracture is descnbed by two terms. The first
describes the position of the foot at the time of injury and the second descrIbes the direction the talus was driven by the
injuring force.
Sutrination-Adduction
Stage I: transverse avulsion fracture of the lateral malleolus or lateral ligament rupture
Stage II: vertical fracture of the medial malleolus
Pronation-Abduction
Stage 1: transverse avulsion fracture of medial malleolus or deltoid ligament rupture
Stage II: rupture of Al1F and/or PITF ligaments
Stage ill: short, oblique fracture of the lateral malleolus
Sutrination-Eversion
Stage I: rupture of Al1F ligament
Stage II: spiral fracture of the fibular malleolus
Stage ill: rupture ofPITF ligament or Volkmann's fracture
Stage N: rupture of deltoid or avulsion fracture of medial malleolus
Pronation-Eversion
Stage 1: rupture of deltoid ligament or avulsion fracture of tIbial malleolus
Stage II: rupture of the Al1F ligament or avulsion fracture (Tillaux or Wagstaffe)
Stage ill: high fibular fracture (Maisonneuve)
Stage N: rupture of the PITF ligament or Volkmann's fracture
Pronation-Dorsiflexion
Stage I: vertical fracture of tIbial malleolus
Stage II: fracture of the anterior tibial lip
Stage ill: supramalleolar fibular fracture
Stage N: transverse fracture of posterior tIbia, level with
proximal aspect of the anterior tIbial fracture
353
Supination-Adduction
! . '\
Stage I Stage II
Supination-Eversion
Stage I Stage II Stage III
Stage IV

Stage I
Stage II
Stage III
354
Pronation-Eversion
Stage II Stage III Stage IV
Pronation-Dorsiflexion
Stage I
Stage II
Stage III
Stage IV
Danis-weber classification
This system represents a surgical classification based UJXln the level of the fibular fracture and its relationship to the
syndesmosis
fibular fracture begins at or below the syndesmosis
corresponds to supination-adduction classification
fibular fracture begins at the syndesmosis
corresponds to and pronation-abduction injuries
fibular fracture begins above the syndesmosis
corresponds to injwy
355
Treatment of Ankle Fractures
The A-O group suggests that exact anatomic reconstruction of the ankle mortise is necessary for perfect guidance of the
talus. Elegant retrospective studies performed by Bauer indicate supination-eversion stage n fractures with less than 2
mm displacement are stable and do not lead to post-traumatic arthrosis when treated conservatively rather than surgically
reduced.
Ankle joint integrity depends upon:
I) Correcting length of the fibula in its position within the :fibular notch
2) Integrity of the tibiofibular ligaments
The surgical correction of ankle fractures requires the use of A-O screws, plates and/or tension band principles. Distal
fibular fractures may be repaired with lateral buttress plates or posterior anti-glide plate technique. Weber C fractures of
the fibula require fixation of the :fibula to the tibia, which
facilitates repair of the interosseous membrane.
TIBIAL PLAFOND FRACfURES <PILON FRACTURES)
A pilon fracture is the result of direct impact of the talar trochlea against the distal ubial articular surface. The soft
cancellous metaphysis of the distal tIbia is compacted, creating a large void when length is restored.
AlIgower Oassification - based upon the amount of comminution
~ :fissure fracture without significant displacement
~ : :fissure fracture with significant articular incongruity
Type lli: compression fracture with significant displacement of the weightbearing cancellous segments of the
metaphysis
I
\ ~
''-OV
II ill
356
Treatment of Pilon Fractures
Treatment frequently involves a combination of internal and external fixation techniques. The A-O suggest four step
method for adequate surgical reduction-
-Step 1: reoonstruction of the fibula
-Step 2: reoonstruction of the tibial articular swface
-Step 3: bone graft the metaphyseal deficit
-Step 4: buttress plate the tIbia
PHYSEAL FRACTURES
Physeal fractures are injuries involving the physis or epiphyseal growth plate. These are often incorrectly referred
to as epiphyseal fractures, which descnbe fractures of the epiphysis of the bone.
Anatomy and Physiology
Each long bone may be divided into epiphysis, metaphysis and diaphysis. The epiphyseal complex refers to epiphysis and
thephysis.
The physis is the radiolucent cartilaginous plate with a characteristic arrangement of cells that progress from resting
chondrocytes to ossified bone.
Three zones of the physis:
1. Growth zone
=> most important zone of the physis
=> relatively strong area aqjacent to the epiphysis
=> consists of predominantly intercellular matrix with germinal cells or dividing chondrocytes
2. Zone of Cartilage Cell Degeneration (zone of maturation)
=> h)pertrophy of chondrocytes followed by calcification and degeneration
=> weakest area of the phyusis because of the loss of inten:ellular matrix and intracellular substance
3. Zone ofPrimaIy Bone Formation (zone of transformation)
=> vaScuIar ingro\\th occurs followed by ossification and remodeling
=> adjacent to the metaphysis
Zone ofRanvier:
=> consists of fibrous tissue and osseous ring of Lacroix (osseous Ring of Lacroix is an extension of the
metaphyseal cortex)
=> provides structural support to the physis and appositional gro\\th
Blood Supply
Epiphysis: epiphyseal arteries form a vascular plexus and extend to supply the germinal cel1s of the physis
Metaphysis: metaphyseal arteries via the nutrient arteries of the diaphysis
Perichondrium: perichondral vessels
by epiphyseal, metaphyseal and perichondral vessels
The result of interruption of the blood supply to the physis will differ according to the vessel damaged.
-epiphyseal vessel damage leads to permanent growth disturbance
-metaphyseal vessel disruption results in transient slowing of growth
-perichondral vessel damage has no adverse effects on longitudinal growth
357
Differences between Child and Adult Injuries
~ The physis is tbe weakest area, relative to bones and ligaments in children. This results in fracture patterns that differ
from those in adults.
=;> Ligaments are relatively stronger than bones in children. Therefore, ligamentous injuries in children are uncommon.
~ Certain pbyseal injuries will cause growth disturbance if the germinal cells of the growth zone and/or the epiphyseal
blood supply are damaged
Regarding ankle joint injuries-
l. -before 8 years of age the pbysis represents a relatively weak structure that is less resistant to tensile forces,
compared to bone and ligaments
~ separation of the physis is more likely since the ligaments with high tensile strength insert below the physis
of the ankle joint
~ ligamentous or osseous injuries are rdrely seen in this age group
2. -at 10 years of age the union between the epiphysis and metaphysis strengthens. Separation of the physis usually
involves a .fracture
3. -after 15 years of age the fracture pattern resembles those occurring in adults
Classification svstems
Epiphvseal Fractures
(:fracture of the epipbysis without involvement of the physis)
1. Avulsion at ligament attachment
2. Compression fracture of epiphysis
3. OsteochondIal fracture
Phvseal Injuries
The two types of physeal injuries are separation and fracture
1. Separation of physis:
~ Most frequently occurs along the metaphyseal border of the physis in the region of the zone of primary bone
fonnation and the degenerating cartilage cells
~ Qx:urs at the weakest area of the physis and is a result of shear forces
=> There is no damage to the epiphysis, its blood supply or to the growth zone of the physis and, thus,
prognosis is good
2. Fracture of physis:
~ Involves a fracture at the articular epiphyseal surl3ce that continues through the physis
~ Injury results from axial compression and bending forces
~ Damage occurs to the epiphysis, the growth zone ofphysis and possibly the eipphyseal blood supply. Thus,
prognosis is worse
Complications ofPbyseal Injuries
Common complications include:
1. Angular deformity due to premature partial physeal closure
2. Limb-Iength discrepancy due to premature complete physeal closure
3. Joint incongruity with seconda.ty post-tIaumatic osteoarthritis
The most common reason for growth distwbance is bony bridging
This callus bridge formation between the epiphysis and metaphysis is the strongest stimulus to premature closure of a
growth plate
358
Ao pbyseal iniory classification
T:we A: good prognosis
::::::> NO injury to growth zone of physis
::::::> NO injury to epiphyseal vessels
::::::> good prognosis with adequate
reduction
T:we B: doubtful prognosis
::::::> Injury to growth zone
::::::> Potential injury to epiphyseal vessels
::::::> Usually serious sequelJae if treated
incorrectly
Salter-barris classification of pbyseal injuries
Type!:
::::::> sepuation of pbysis without damage to the germinal cells or epiphyseal
blood supply
::::::> results from a shearing force
::::::> diagnosis by clinical suspicion of localized edema and point tenderness
along the physis
Treatment: usually possible to obtain adequate results with closed reduction
TypeR:
::::::> partial separation of physis with a metaphyseal fragment
U
C::J
* Thurston-Holland sign=metaphyseal fragment produced by a lateral displacement force
Treatment: usually closed reduction will give adequate alignment
* if displacement is unacceptable, ORIF may be needed
ie-4.0 cancellous screw parallel to the physis; parallel small smooth k-wires approximately 90 to physis
short leg cast NWB 4'() ,,'eeks
359
TypeID:
=> fracture of epiphysis with partial physeal separation intra-articular fracture
Treatment: lor 2 screws (4.0 or 3.5 nun) parallel to physis
short leg cast NWB 4-6 weeks
Tll.LAUX FRACTIJRE (transitional fracture)
=> represents a Salter-Harris m of the distal tibia
=> most commonly occurs at age 13-14
=> physiologic closure of the distal tibia physis begins at its midpoint and progresses medially. the lateral
half of the physis closes approxiIuately 18 months later at age 14-18
=> external rotatory force may canse AITF ligament to avulse the anterolateral quadrant of tIbia with the
Type IV:
open lateral physis goal is anatomic reduction to restore joint congruency
=> premature closure of physis is not a concern because there is limited growth potential
=> only case when a screw may be placed across an open physis
=> follow ORIF with short leg cast NWB 4-6 ",eeks
=> fracture of epiphysis. partial physeal separation and fracture of metaphysis
Treatment: commonly unstable and will require ORIF to obtain acceptable reduction, smooth joint smface and
adequate reduction to prevent bony bridging and growth distwbance
short leg cast NWB 4-6 weeks
TripJane fracture ofjmJde: combination of Salter-Harris n and Salter-Harris ill
=> fracture lines run in three planes and require multiple x-ray views to clarify fracture pattern
=> cr scan will help evaluate extent ofinjury and fragmental patterns (2 or 3)
Treatment: same as for Salter-Harris IV injury
360
Type V:
=> crush injury of the physis
=> may be misdiagnosed as a Salter-Harris I
=> prognosis is worse because bony bridging may lead to
partial or complete premature p h ~ closure and
growth distuIbmce
Type VI:
=> avulsion of perichondral ring
(modification by Rang)
TypeVll:
=> avulsion fracture of epiphysis without involvement of
physis
(modification by Ogden)
Guide to treatment of pbyseal injuries
Rang Modification
8
1. Bilateral films for comparison to he1p recognize physea1 separation.
2. Multiple views in different planes to avoid missing diffiadt fracture lines which may be obscured by overlapping bones.
3 . X-ray the joint above and the joint below if clinically indicated to rule out additional fractures.
4. <lJtain post-reduction x-rays to assess anatomic position after reduction and to clarify fracture patterns.
<lJtain cr scans to assess artiadar congruency and the extent of injmy.
5. Treatment is determined by:
-type of injury
-degree of damage to physis, epiphysis and its blood supply
-skeletal age of patient
-potential growth ofbone remaining
-degree of intra-artiadar damage
~ of closed reduction
6. The key to successful treatment ofphysea1 injuries is dependent on REMODELING
Remodeling will generally help:
* child with 2 years or more of growth remaining
* fracture near the ends ofbone
* deformity in the plane of joint motion
Remodeling will not help:
* displaced intra-artiadar fracture
* fracture in middle of long bone that is grossly shortened, angu1ated or rotated
* displaced fracture with axis of displaacement at right angle to plane of motion
* displaced ftacature crossing physis at right angle
7. Generally all physeal injuries should be followed for 6 months to 1 year for potential complications of growth
di.stmbance.
8. Effects of compression on the physis:
-increase in pressure along an axis parallel to direction of growth may inhibit or arrest longitudinal growth
-screws or threaded pins placed across the physis will cause compression and lead to prematme physeal closure
361
-small smooth k -wires should be placed 90 to the physis or near the margins of the physis to decrease the incidence
of growth disturbance
Summaty of Classification ofPhyseal Injuries
Salter & Harris )1 ( \ )v
1963 t:J t17t:t
Aitken
1936
A.O.
Rang
1969
Poland
1898
OPEN FRACTURES
Gustillo classification
Type I: wound less than I em long
B ffi !;)o




t3Gb&
little soft tissue damage; no sign of crushing injury
simple. transverse or short oblique fracture with little comminution
Type IT: wound greater than I em long
no extensive soft tissue damage; slight or moderate crushing injury
moderately comminuted fracture; moderate contamination
Type m: extensive soft tissue damage; high degree of contamination; severely comminuted fracture
associated with high velocity trauma
type InA - soft tissue covemge of bone is adequate (despite flaps, lacerations, soft tissue destruction)
severely comminuted fracture from high energy trauma

type IIIB - extensive injury to or loss of soft tissue requiring local or free flap for coverage after adequate debridement
associated with periosteal stripping and exposure ofOOne, massive wound contamination and fracture comminution
type me - any open fracture associated \\'ith an arterial injury that must be repaired
Open Ii'adures associated with arterial. injuries that DIIL'It be repaired have m amputation rate of25-9O"/o.
362
Absolute indications for primary amputation
>Type me injwy acoompanied by disruption of the posterior ubial nerve
>Type me iIYmY with loss of soft tissue, massive contamination, severely comminuted segmental fracture or
massive loss ofbone that wiUlikely result in significant impairment offunction
Relative indication for amputation
>Type me iIYmY that is untreated for 8 hours or more
Antibiotic therapy
Type I: single dose of 2.0 gm cephalosporin on admission and 1.0 gmevery 6-8 hours for 48-72 hours
Type n & m: single dose of2.0 gm cephalosporin andanaminoglycoside (1.5 mglkgbodyweight) on admission
continue this regimen of cephalosporin and aminoglycoside (3-5 mgIkg body wt) for 48-72 hrs.
add 10 million units Penicillin if fi:mn injwy
According to the liternture, infections are largely due to gram negative bacteria. Previous studies had implicated gram
positive Ol"fiInisms-
Treatment Protocol:
1. Initial evaluation in Emergency Department
-history & physical. wound inspection and cultures. tetanus prophylaxis. temporary stabilization
2. Debridement with copious irrigation in OR
a) repeat debridement in 48-72 hours
b) debridement may need to be repeated with types IIIB or C to achieve clean. stable wound
3. Stabilization offracture
4. Antibiotic Therapy
5. Coverage and closure ofwound
-delayed primary closure 5-7 days after injury with types I & n
TYPE RAlE OF INFECTION RAlE OF AMPUTATION
I 0-2%
II 2-7010
IlIA 7010 00/0
IIIB 10-50010 16%
me 25-50010 42%
363
Avascular Necrosis
Definition
Death of bone marrow and trabecular elements secondary to repeated interruptions or a single
massive interruption of the blood supply to the bone.
Etiology
Atraumatic:
- alcoholism - hyperlipidemia
- hypercorticalism - hemoglobinopathies
- obesity - hyperuricemia
- infection - pancreatitis
- pregnancy
Traumatic:
- fractures/dislocations
- iatrogenic
Signs & Symptoms

Progressive
Acute joint pain
Occasional spasm






Radiographic
Aggravated by weightbearing; relieved by rest
Limitation of motion
Continuous joint pain
Joint destruction
Not for early diagnosis
Focal subchondral demineralization
Radiolucency surrounded by radiodensity
Subchondral collapse/stress fracture
Total joint destruction
Treatment
Early Stages
Late Stages
GOAL => prevent subchondral collapse
TotalNWB
Electrical bone stimulation
NSAID's
GOAL => alleviate pain
Conservative -- patellar tendon weightbearing brace, NSAID's
Surgical - arthrodesis procedures, bone grafting procedures
364
COMPARTMffiNTSYNDROME
*** SOOIo of cases occur in the lower extremity
Etiologies
a) fractures
b) crush injuries
c) musculoskeletal surgeIY
d) hematoma
e) arterial emboli (rare)
f) infection
Pathogenesis
a) increased tissue pressure: increase in net force per unit area on the vessel wa1ls
b) increased venous pressure
c) decreased arteriovenous gradient
d) decreased local blood flow and oxygenation
Diagnosis
a) the six P's
I. pain: the most important sign. The pain is usually out of proportion to what one would expect for the
clinical situation. This is often one of the first signs since nerves are the most sensitive tissue to
ischemia The pain is exacerbated by putting the muscles in the compartment at passive stretch.
2. paresthesias: followed by hypoesthesia and anesthesia; these are reliable indicators.
3. paralysis: a late finding
4. pressure: tenseness of the compartment envelope.
Second most important sign; can be measured via a wick catheter. An intracompartmental
pressure of greater than 30 mmHg is considered to be diagnostic of compartment syndrome;
however, some believe that irreversible damage doesn't occur until 45 mmHg.
5. pink: routinely have good capillary refill, except in cases of major arterial disease.
6. pulses: routinely present except in cases of pre-existing major arterial disease.
b) timing of signs, symptoms and tissue damage: the disease progresses rapidly, thus patients should be
monitored every 30 minutes.
30 minutes paresthesias
2-4hours functional muscle changes
3 hours post-ischemic swel1ing
4-12 hours irreversible muscle deterioration begins
over 12 hours contracture formation
24 hours onset of myoglobinuria
Treatment
a) remove all casts and dressings
b) keep limb at heart level; do not elevate. Elevation creates more ischemia and interferes with venous
drainage.
c) hydration (prevents deleterious effects of myoglobinuria)
d) surgical decompression via fasciotomy: individual compartments can be decompressed if not all
compartments are involved Often all four compartments and decompressed The wound is not closed,
but packedopen.
I. single incision: through an incision at the peroneal compartment all four compartments can be
decompressed
II. double incision: through an anterolateral incision the anterior and lateral compartments can be
decompressed Through a posteromedial incision both deep compartments can be decompressed.
365
ill. Four compartments
a) anterior: along with the deep posterior compartment are the two compartments most
commonly involved in compartment syndrome.
b) lateral
c) deep posterior: along with the anterior compartment are the two compartments most
commonly involved in compartment syndrome.
d) superficial posterior
Sequela
a) Volkmann's contracture of muscle
muscle ischemia muscle necrosis muscle contrncture
b) renal fuilure: secondary to myoglobinuria
Osteochondritides
Definition:
A group of related disorders, which are thought to be due to a disturbance to the ossification center
of the bone. It may affect both the primary and secondary ossification centers during the time of
developmental activity.
Clinical Findings:
pain
swelling
symptoms increase with activity
Radiographic Findings:
lucency
fragmentation
collapse of articular surface
Names of Specific Osteocbondritides:
Theiman Phalanges
Freiberg Metatarsal heads
Islen 5
th
metatarsal base
Buschke Cuneiforms
Kohler Navicular
Lance Cuboid
Sever
Osgood-Schlatter -
Blount
Kohler
Calcaneus
Tibial tuberosity
Tibial epiphysis (proximal)
Patella
366
GUNSHOT WOUNDS
Theory of Wounding Capacity
Kinetic Energy (KE)
m=mass
v=velocity
-velocity is more important than
-energy imparted on impact determines extent of injury
High velocity == >2000 ftlsec
==> -requires emergent radical wound debridement
==> -military battlelhuntingaccidents
==> -<:avitation effect
KE==
* energy of bullet exceeds expansile capacity of tissue
* a vacuum is created pulling debris into the wound
Low velocity == <2000 ftlsec (majority of pedal gunshot wounds)
==> -consists of bullets weighing 100-300 grains
==> -entry port sometimes not enough energy for exit
==> -occur at short ranges

2
==> -no cavitation; expaI1Slble capacity of tissue exceeds energy of bullet
Management
-A,B,C'sistabilize patient
-detailed foot and ankle exam
-Tetanus
-vascular status
-neurological status
-muscle testing
-entry/exit wounds, laceration, skin slough
-ROM, pain, crepitus, deformity
-presence of foreign bodies
-radiographic studies
0.5ml toxoid if previous immunization
250 units of tetanus immunoglobulin + 0.5ml of toxoid if no previous
immunization
Fracture
-any fracture associated with external environment is considered open
-bullet not heat sterilized / wound considered contaminated / potentially infected
-adhere to principles outlined by Gustillo for open fractures
-if> 8 hr considered infected
-most LV are type I
-antibiotic recommended (cephalosporin) for 3 days or until infect. subsides
-open reduction
-fractures that require intraarticular reconstruction/rigid fixation to stabilize
Surgery
-debridement
-gross contamination/necrosis
-intraarticular
-neurovascular destruction
-compartment syndrome
-prophylactic antibiotics
-not essential for wounds not grossly contaminated
-determined by clinical appearance of each individual wound
-most L V injuries not cause devitalized tissue at distance from wound tract
367
-extreme debridement may not be necessary
-cleansing of wound
-3 L saline or 10 % povidine iodine
-excise exposed muscle and fascia
-avoid probing of missile tract
-foreign bodies removed only if excessive dissection not required
-bullets not excised unless superficial and palpable
-complicated exploration avoided unless vital structure threatened
-closure
-depends on degree of surgical intervention
-small wounds left open allow to granulate
-surgical debridement Gustillo I&II <8m can close primarily
-any question leave open until no sign of infection (3-7 days)
SOFT TISSUE TRAUMA(General)
General guidelines for evaluation of lower extremity soft tissue trauma.
1. Primary survey: assess airway, breathing and circulation
2. Secondarv survev: check for life threatening injuries and associated injuries (ie-spinal fractures, etc)
3. Obtain a historv
PMH;. Meds; Allergies; PSH; Family history: Social history
Female -last menstrual period
tetanus status
time food/drink last ingested (in case of emergency surgery)
mechanism of injury and time of occurrence
estimated blood loss
initial treatment
4. Phvsical Examination
vitals: temperature, pulse, respiration, blood pressure
vascular: pulses; capillary filling time; skin temp; edema
if pulses nonpalpable - Doppler, arteriogram
neurologic: sensory; motor, deep tendon reflexes
musculoskeletal:
evaluate for muscle or tendon damage
ROM; palpation
muscle strength testing
x-rays if fracture or foreign body suspected
wound evaluation: dimensions (width, depth, length)
signs of infection (ie-edema, erythema, calor, pus, etc)
wound classification:
clean = less than 6 hours post trauma
contaminated = greater than 6 hours post trauma
debris and necrotic tissue present
extensive soft tissue damage or loss increases the possibility of infection
infected = clinical signs of infection
significant gross contamination
Wound care guidelines for soft tissue trauma
1. Tetanus immunization status
2. Cleanse surrounding skin with betadine or Hibiclens solution
3. Exploration:
inspect for foreign body and debris
inspect for deep tissue damage (ie-tendon laceration, joint involvement)
inspect for vascular damage
368
4. control small vessel bleeding by the following-
apply gentle manual compression
elevation of the limb
electrocoagulation with bovie
band tie or suture ligature
thrombin (protein substance that clots fibrinogen of blood)
SUIgicel (a sterile absorbable knitted 13bric of after saturated with blood, the Surgicel
swells into a ge1atinous mass which accelerntes clotting)
Gelfoam(absOIbable sterile ge1atin absorbs many times its weight in blood within its mesh
and functions as a hemostatic agent)
5. Take deep cultmes (aerobic, anaerobic); gram stain
6. Debridement and IIIigation
dilute betadine, Hibiclens solution, saline or lactated Ringer's solution
use syringe and blunt needle or N catheter to create pulsating lavage
7. Decision planning for wound closure is guided by:
a) contaminated wound versus infected wound
1. signs of infection [clinical infection = >10 -lO orgsIg tissue or one suture+ 10 oqg tissue]
2. hours post injury
3. mecbanism of injury and innoculum
4. (ie-rusty, dirty nail puncturing through a sneaker vs. clean kitchen knife vs. animal or human bite)
5. degree of tissue damage or loss
b) natma1 defense mechanisms
host resistance depends on medical history (ie-diabetes, long term steroid therapy, etc)
immune response (ie-AIDS, leukemia, etc)
c) genemIly primary closure can be performed on
clean wounds
contaminated wounds converted to clean wounds by copious irrigation and debridement (if
questionable, pack wound open)
d) infected wounds require
culture and gram stain
local wound care with JECking
empiric antibiotic theI3py until culture results -evaluate wound in 2-3 days for progress
delayed closure when indicated or secondary intention healing
7. Prophylactic vs TheIapeutic Antibiotic TheIapy
prophylactic antibiotics should be given within the first 3 hours of contamination for effectiveness
-clean and contaminated wounds require adequate debridement and irrigation, not prophylactic antIbiotics
-one exception is human bites, which have a high risk of infection
therapeutic antibiotics are indicated for established clinical wound infections
8. Tetanus prophylaxis
tetanus prone wound: greater than 6 hours post injury
greater than 1 em depth
bum, frostbite, crush or missile injury
stellate woWld, abrasion or avulsion of skin
devitalized, ischemic tissue
contaminants feces, saliva)
Tetanus Prophylaxis
wound
tetanus prone
non-tetanus prone
immune status
uncertain<5 yrs
Td+TIG
Td
last tetanus booster
6-lOyrs
Td Td
no Td
*Td = tetanus and diphtheria toxoid adsorbed dose: 0.5cc 1M
*TIG = tetanus immune globulin (human) dose: 250 U 1M
369
CHRONIC REGIONAL PAIN SYNDROME (REFLEX SYMPA mE TIC DYSTROPHY)
Misnomer
RSD and Sudeck's atrophy are not interchangeable. Sudeck's atrophy is pathognomonic for the second stage of
RSD. which includes specific osteolysis
Etiology
usually triggering factor is trauma
severity of trauma has little correlation to severity of symptoms
ankle sprains, pes valgo planus, neuroma, injections. tourniquets. poliomyelitis. infection
Phases
LA,. cold/vasoconstrictive phase (2-6 weeks)
decreased temperature of affected foot
hyperalgesia present
skin mottled by patches of pallor on a pinkish-blue backdrop
ill: the classically described initial phase; "sweaty-vasodilatory phase" (2-6 months)
increased warmth to foot
hyperalgesia still present
foot color changes to red coloration
greatest likelihood of remission in this phase
II: hallmark of Sudeck's atrophy osteoporosis visible radiographically
osteolysis is in a "spotty" pattern
Sudeck's atrophy die to hyperemia, increased intramedullary pressure, and decreased pH. Not due to disuse!
skin is taut and glossy with a brawny coloration
poor likelihood of reversing syndrome
ill: dead phase (6-12 months)
foot is pale and wax-like
marked joint stiffness
marked osteoporosis
T reatrnent:
local anesthetic blocks into areas ofpain (trigger points)
1ENS units
surgical sympathectomy
supportive
physical therapy; analgesics: anti-inflammatories
calcitonin therapy
TRAUMATIC NERVE PATHOLOGY
Nerve Anatomy
endoneurium surrounds a single nerve fiber
perineurium surrounds a bundle of nerve fibers (fascicle)
epineurium surrounds a large nerve (multiple fasciculi)
Seddon Classification of Nerve Injurv
Neuropraxia: least severe
nerve contusion/compression
conduction deficit without axonal damage
Axonotmesis: Wallerian degeneration (degeneration of axon distal to injury)
axon damage without endoneurial tube damage
reversible; muscle wasting may occur
Neurotrnesis: most severe
partial or complete severance of nerve with complete disruption of endoneuria! tubes
irreversible unless surgically repaired
370
Feature Neuropraxia Axonotmesis
Pathologic
Anatomic continuity Preserved Preserved
Essential damage Myelin sheath distortion Wallerian degeneration
with endoneurial tube
preservation
Clinical
Motor paralysis Complete Complete
Muscle atrophy Very little Progressive
Sensory paralysis Usually spared Complete
Autonomic paralysis Usually spared Complete
Recovery
Quality Perfect Perfect
Rate of recovery Rapid; days to weeks 1-2 mm/day
March of recovery No order According to order of
innervation
Treatment
Surgical repair Not necessary Usually not necessary
Seddon "s. Sunderland Classifications
SUNDERLAND
Type/Degree First Second Third
SEDDON
Sunderland Classification
First degree - equivalent to Neuropraxia.
Neurotmesis
Maybe lost
Complete disorganization
Complete
Progressive
Complete
Complete
Imperfect
1 -2 mm/day (if surgically
repaired)
According to order of
innervation
Essential
Fourt
h
Fifth
Second degree - corresponds with axontmesis with axon disruption but not endoneurial tube disruption.
Third degree - form of axon tmesis or neurotmesis and incorporates axon and endonuiraI tube disruption with
intact perineurium.
Fourth degree - encompasses physical disruption of fascicles and perineurium with intact epineurium.
Fifth degree - true neurotmesis, complete disruption of the nerve trunk
Nerve surgerv
neurolysis: lysis of adhesions
external neurolysis (detach adhesions outside of nerve)
internal neurolysis (enter epineurium to detach adhesions)
neurorrbaphy: resection with end-to-end anastomosis
neurectomy: nerve resection
nerve grafting
37i
Surgical treatment of traumatic neuromas
Note: Numerous procedures and devices have been devised to prevent stump neuroma (the most common
complication with neurectomy) The follo",ing is a small list of what has been attempted. None have been
consistently reliable
Inhibition of Axonal Regrowth
PhYsical Containment
+ Chemical Treatment
Alcohol
Phenol
Formaldehyde
Nitrogen mustard
Pepsin
Hydrochloric acid
Iodine
Gentian violet
Steroids
+ Cauterv
Electrocoagulation
Laser
Radiofrequency current
Cryosurgery
+ Ligation
Types of Nerve I n j u ~ ; Based on Etiology
Cause o/Injury Neuropraxia
Cuts and lacerations
Fractures
Missiles +
Traction +
Compression + (momentary)
Thermal +
Ischemia +
a+, frequent; , occasional: -, infrequent

+
+
+
+ Synthetic Containment
Silicone caps
Rubber
Plastic
Lucite
Polyethylene
Collodium
Cellophane
Metallic foil
Tantalum
Glass
Nerve glue
+ Physiologic containment
Epineurorrhaphy
Nerve grafting
Translocation away from Painful Stimuli
Excision and retraction
Implantation into muscle
Implantation into bone
En bloc translocation
Axonotmesis Neurotmesis
+

+
+
+ (prolonged)
+
+ +
372
Quantitative Sensory Testing (QST)
Conceived by neurologists in order to provide a non-painful method to measure peripheral
nerve function
Measures cutaneous pressure perception with the use of a pressure-specifying sensory device
(PSSD)
Pressure Specifying Sensory Device (PSSD)
Designed to measure the threshold for perception of pressure stimuli on the surface of the
human body
Provides a threshold measurement throughout a continuous range of applied pressures
Consists of 2 metal prongs with hemispherical tips that measure the distance between the tips
ofthe prongs as well as the amount of cutaneous pressure required for perception of the tips
Able to measure one-point moving, one-point static, two-point moving, and two-point static
over a particular piece of skin
Pressure threshold measured in g/mm2
Patient recordings compared to normative data
Indications

Diabetic neuropathy

Tarsal tunnel syndrome

Heel pain

Cubital tunnel syndrome

Morton's neuroma

Sural nerve entrapment

Carpal tunnel syndrome
373
ACEITLLESTENDONRUPTURE
Diagnosis:
stabbing type pain of posterior ankleJIeg
tenderness and palJXlble defect in the Achilles tendon which increases with dorsiflexion
decreased active plantarflexion and weakness of plantarflexion of the ankle joint against resistance
apropulsive gait with a "ball-like" contracted calf muscle
Thompson's test- with the patient lying in a prone position, the gastroc-soleus complex is squeezed to
assess plantarflexion of the ankle joint

positive test = decreased to no plantarflexion of the ankle joint relative to the contralateral foot
false negative = the long flexors, tibialis posterior and peroneus longus provide motion at the ankle joint
Differential Diagnosis:
achilles tendonitislbursitis
partial rupture of gastrocnemius
mnligonfractwreoftheadcaneus
traumatic hematoma of the lower leg
Pathogenesis:
Rupture commonly occurs 2-6 cm proximal to its insertion at an area of decreased vascularity (Lagergren
& Lindholm)
Predispogng factors: collagen vascular diseases (ie-gout, RA)
long term systemic steroid therapy
load steroid injection
Treatment
Conservative:
Indicated for partial tears, sedentary older patients and non-surgiad candidates
higher incidence of re-rupture compared to surgiad treatment
gravity equinus casting:
long leg cast with knee flexed at 20 or SLC; ankle joint placed in gravity equinus for 6-8 weeks
followed by SLC weight-bearing with reduced amounts of equinus to eventual heel lift in shoegear
Surgical:
a) primary reprir with suturelimplant
I. Ma and Griffith: percutaneous suture reprir with nonabsorbable suture on a straight needle
2. E n d - ~ E n d anastomosis with nonabsorbable suture
3. Implants (absorbable polymer carbon fiber compogte - Parsons et al)
4. Pull-out wire techniques
5. Fascial reinforcement
a. Bugg and Boyd: modified Bunnell pull-out wire suture in combination with three fascia lata strips
b. Lynn: reinforcement of end-to-end anastomogs with the plantaris tendon; plantaris is detached
from its insertion and fanned out to form a membrane
c. Silverskiold: central strip of gastrocnemius aponeurosis is flapped distally over the defect
d Lindholm: two outer strips of gastrocnemius aponeurogs are flapped distally to reinforce the
tendon repair
6. Tendinous reinforcement
a. Bosworth: a strip of gastrocnemius tendon is freed proximally, flapped distally and passed
through the proximal and distaI tendon stumps to join the ruptured tendon
b. Teuffer: peroneus brevis is detached from its insertion, placed through a drill hole in the adcaneaI
tuberosity and passed proximally along the ruptured tendon for reinforcement; its is also sutured
to itself to produce a dynamic loop.
374
Achilles Tendon Primary Repair Techniques
MA &: GRIFFITH
BUGG&BOYD
SILVERSKIOW UNDHOIM BOSWORTH
LIGAMENTOUS ANKLE INJURIES
Diagnosis
a) history
1. what happened? how long ago?
2. where does it hurt? ( point with one finger)
3. what treatment have you done? can you walk on it?
4. mechanism of injury
5. past medical history, social history
6. current medications, if any
7. allergies
b) physical exam
1. vascular status (pedal pulses; cft)
2. senoory/ neurologic status
3. edema, erythema, ecchymosis, calor, dolor
4. palpation
lateral foot
dorsolateral foot
lateral ankle - anterior talofibular l i ~ e n t
calcaneofibular l i ~ e n t
posterior talofibular l i ~ e n t
medial ankle - deltoid l i ~ e n t s
posterior ankle
lateral malleolus
high fibula (Maisonneuve fracture)
medial malleolus
5. radiographic exam
DP and oblique of the foot
lateral of the foot and ankle
AP, mortise, and oblique of the ankle
6. stress inversion
normal depends on which study must compare to opposite limb
LYNN
TEUFFER
positive usually greater than lO for double ligament injury (ATF and CF)
375
7. anterior drawer
greater than 4 mm is positive for ATF tear
several ways to measure anterior drawer
8. peroneal tenogram
infiltrate dye into peroneal tendon sheath
CF lig. in intimate contact with lateral ankle joint capsule and deep aspect of peroneal tendon sheath
mortise and lateral ankle x-rays
normal study = dye stays within tendon sheath
positive study for CF ligament rupture = dye extravagates into the ankle joint
several authors describe a normal communication between peroneal tendon sheath and ankle joint
(approx. 2%)
9. ankle joint arthrography
dye injected into the ankle joint
positive study = dye extravagates into soft tissues
diagnostic for ATF ligament rupture
less accurate than tenogram for CF lig. rupture
10. MRI - able to evaluate soft tissues (ie-ligaments)
Associated fractures
a) fifth metatarsal base
b) anterior process of calcaneus
c) dorsal lateral calcaneus (EDB a"u}sion)
d) lateral talar process
e) Shephard's fracture (posterior talar process)
f) osteochondral fracture of the talar dome
g) avulsion fracture oflateral malleolus (usually associated with dislocation of peroneal tendons)
h) high fibula (Maisonneuve fracture)
i) medial malleolus
j) Salter-Harris I in children
Oassifications of Lateral Ankle Ligamentous Injuries
a) Leach
first degree: partial or complete tear of ATF ligament
second degree: partial or complete tear of ATF and CF
third degree: partial or complete tear of ATF, CF and PTF ligs
b) O'Donoghue
first degree: ligament stretch with minimal disruption
second degree: partial ligament disruption with joint instability
third degree: complete ligament disruption
c) Dias
grade I: tmtial rupture of CF ligament
grade 2: ATF ligament rupture
grade 3: ATF, CF anellor PTF ligament rupture
d)Henry
group 1: tender over A TF lig.; negative anterior drawer:
taIar tilt < 5
group 2: moderate injury; tender over ATF and CF ligs.; negative anterior drawer, talar tilt < 15
group 3: severe injury; lateral ankle swelling and pain; positive anterior drawer, talar tilt > 15
group 4: chronic problem; positive anterior drawer;
talar tilt > 15
376
Treatment
a) conservative
I. rest, ice, compression. and elevation
2. Unnaboot
3. Gibney boot
4. Jones compressive dressing with -
5. Aircast
posterior splint AO splint
eggshell cast
6. degree of weight bearing depends on severity of injury
b) surgical
I. primaIy repair of tom ligaments
usually reserved for a combined ATF and CF lig. tear
2. lateral ankle stabilization procedures
VASCULAR TRAUMA
Categories
a. blunt trauma: artery is crushed or contused resulting in hemorrhage; may cause compartment S)'ndrome
b. penetrating tmuma: i e ~ e p laceration, gunshot wound
Treatment:
stop active bleeding by gentle manual compression; elevation of limb may further compromise the
ischemic foot
assess DP and Pf pulses; if the major vessel in the vicinity of the wound is nonpalpable, you must assume
Vascular injury until proven otherwise
if pulses nonpalpable, auscultate with the Doppler; determine ankle/brachial index
even with pulses the extremity should be monitored for compartment syndrome
if vascular status is compromised or questionable, get a vascular consult; arteriogram may be required to
evaluate the extent of the injury
NAn.. BED INJURIES
All require x-rays to RIO distal phalanx fracture
Subungual hematoma
involving <25% of nail bed
dIain hematoma using #11 scalpel blade, 18 gauge needle, rotary ball burr or sterilized paper
clip
involving >25% of nail bed
skin p-ep, nail avulsion to RIO nail bed laceration
Nail bed laceration
a. skin prep and nail avulsion
b. wound care
c. primary repair with absorbable suture within 7 days post injury to avoid scar formation
of nail bed
d prevent nail bed and proximal nail fold contact in order to avoid nail deformity, use
Adaptic, Vaseline impregnated gauze or Xeroform to maintain space
*if nail bed laceration noted with underlying phalangeal fracture, treat injury as an open fracture"
377
Rosenthal Classification of Digital Injury
Level of tissue loss
zone I: distal to bony phalanx
zone II: distal to lunula
zone III: proximal to distal end oflunula
Plane of tissue loss:
dorsal oblique
transverse
plantar oblique
axial (tibial or fibular oblique)
central (gouging)
Treatment:
zone I:
Rosenthal Classification of
Digital hJjuries
~
~
~
Central

distal digital amputation with nail bed avulsion
",ithin zone I without exposed bone, allow to granulate in by secondary intention healing
tissue loss> 1 em , skin graft on acute or delayed OOsis (ie-full thickness skin graft on digital tip;
reverse dennal graft to:fill large nail bed avulsion defect)
zone II:
local (adjacent) pedicle flaps are indicated
(ie- Atasoy plantar V-Y advancement graft; Kutler type V-Y advancement graft for toe
reconstruction)
zone III:
nail bed augmentation
ablate remaining nail bed if too much has been lost
generally not amenable to nail bed reconstruction
primary amputation is usually performed with attempt to preserve distal IPJ and distal tendon
function
PUNCTURE WOUNDS
I. Foreign body injuries
a) plantar foot wounds may be contaminated with dirt, grass, sock or shoe material
b) pin/needle
diagnosis: standard x-rays
removal by the following methods
-triangulation with needles placed at 90 angle to isolate the foreign body's depth
-visualization under C-arm fluoroscopy
-hand held electromagnetic metal locators emit a higher pitch sound wave near metal objects
~ o n follows clinical signs of inflammation, abscess or hemorrhage
c) wood toothpicks/splinters
diagnosis: xeroradiography, standard x-rays, CT (most reliable)
d) glass
diagnosis: standard x-ray can pick up tinted or glass containing lead
378
2. Complications ofpuncture wounds
a) cellulitis: Staph aureus >50% of cases
Staph epi, streptococcus, E. coli
b) abscess
c) osteomyelitis: Pseudomonas aeruginosa approx. 90 of cases usually wounds 3-4 wks old
3. Treatment of puncture wounds
a) tetanus status
b) x-rays
c) wound care with removal of foreign body; pack wound open
surgical debridement and lavage if it penetrates the joint
d) antibiotics if infectedlcellulitic, if deep wound extends to bone or if penetrates the joint
e) if infected puncture wound does not respond to anbbiotics, there is probably a foreign body present
BITE WOUNDS
Dog and Cat Bites
common pathogens: Pasturella multicida (facultative gram neg rod)
Staph. aureus, alpha-hemolytic streptococcus
treatment:
1. tetanus prophylaxis
2. Rabies prophylaxis
Dog/Cat: >if animal is healthy and available for observation, no treatment unless animal develops rabies
>rabid animal, suspected or unknown status:
give rabies immune globulin and IIDCV (human diploid ceU vaccine)
if animal is negative, stop prophylaxis
3. Wound care: explore to rIo tendon laceration, joint damage
4. Antibiotic therapy: controversial
-some advocate prophylaxis because animal bites are high risk and highly contaminated
-recommend Augmentin (ifPCN allergic, give Erythromycin)
only use antIbiotics if clinically infected
Human Bites
Common pathogens: anaerobes (ie-Bacteroides fragilis)
Eikenella corrodens (gram neg rod)

Treatment:
1. follow guidelines for wound care
2. if injury >6 hours old, pack wound open and foUow-up in 2-3 days
3. AntIbiotics
oral: Augmentin
parenteral: Unasyn, Timentin
prophylaxis advised because human bites are highly contaminated wounds and at high risk of infection
BURNS
Classification
By depth:
first degree = erythema
second degree = blistering
third degree = destruction of epidermis, dennis and skin appendages: anesthetic
fourth degree = destruction of fat, muscle and bone
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Or.
partial thickness: first or second degree
full thickness third or fourth degree
By extent of bum: o/ototal body surface area (BSA)
nile of nines -
head 9% chest/abdomen 18%
arm 9% back 18%
groin I % leg 18%
Treatment:
I. remove burning agent
2. ABC's and treat associated injuries
3. tetanus status
4. assess vascular status.
-observe for vascular compromise with circumferential burns, edema and eschar
-circumferential eschars may require escharotomy
5. wound care:
immediately cool the area with water or saline
blister care
debride ruptured blisters
intact blisters may be left undisturbed for 24-36 hours to provide biologic wound coverage and to
prevent tissue necrosis
topical agents (for burns >20% BSA)
silver nitrate
silver sulfadiazine (Silvadene);
bacitracin:
neomycin
mafenide acetate
Xeroform dressing
reconstruction for third or fourth degree burns with skin grafts is indicated
6. Antibiotics
-prophylactic antibiotics are not recommended because it may result in superinfection with
Pseudomonas or yeast
common pathogens of infected bums
Staphylococcus
Streptococcus
Pseudomonas
Proteus
COLD INJURIES
Immersion foot
injury to tissue due to a combination of wet and cold
Frostbite
injury to tissue due to freezing
frostbite classification
L hyperemia
2. blisters
3. necrosis
4. necrosis and tissue loss
treatment
tetanus status
rewarm limb rapidly at temperature of 104-108 for 15-20minutes: may require narcotic analgesics.
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FROSTBITE
L Definitions
A Frostnip: pallor and numbness of the affected tissues; mildest form; warming results in freedom
from epidermal or dermal damage
B. Chilblain/pernio: chronic vasculitis of the dermis that is provoked by repeated exposure to cold
temperatures above freezing in high humidity
C. Trencbfoot: occurs when feet are exposed to wet conditions and temperatures between 0-20 degrees
celsius
D. Frostbite: occurs when skin and subcutaneous tissues exposed to thenna! stress freeze with
tempemtures < 2 degrees celsius
II. Who is at risk?
-males between ages 20-50
-altered mental status
*psychiatric disorders
*alcohol abuse
*headinjwy
-homeless
III. Predisposing Factors
-environmental temperatures
*low tempemtures
*moisture
*windchill
*duration of exposure
-Miscellaneous
*motor vehicle problems
*improper clothing
*fatigue
IV. Pathogenesis
Direct freeze
-elderly
-malnourished
-military personnel
-outdoor sports enthusiasts
*skiers, runners, climbers
-laborers in cold environment
-host factors
*alcohol abuselhomeless
*psychiatric illness
*malnnourishment
*PVD/atherosclerosis
*smoking
*chronic liver/renal disease
*Raynaud's disease
-extracellular ice crystal formation followed by intmcellular ice crystal formation with cell membrnne
damage
-increase osmotic pressure in interstitium causing water to be dmwn out of cells, intracellular
dehydmtion, and cell death
-denaturing of lipid protein membrnne
Indirect Injwy (vascular and inflanunatory changes)
-"Hunting Reaction": alternating vasoconstriction and vasodilation
-persistent vasoconstriction leading to hypoxia, acidosis, increased blood viscosity
-capillaries, arterioles, and venules thrombose
-release of inflammatory mediators: prostaglandin PGF2 and thromboxane A2
-vasoconstriction, platelet aggregation, and blood vessel thrombosis
V. Clinical Presentation
Predictors of Poor Outcome: Favorable findings:
-sensation to pinprick -small vessicles with dark blood fluid
-skin that indents with pressure -nonblanching cyanosis
-normal skin color -skin that feels "wooden" to touch
-large blisters filled with clear fluid -skin that does not indent \"ith pressure
-infection
-delay in seeking medical attention
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VI. Diagnosis
-physical examination
-conventional radiography
-lxme scintigraphy
-angiography
-digital plethysmography
-doppler flow studies
VII Treatment
-University of Chicago Protocol
-rapid rewarming in wann water at 104-108 degrees F for 15-30 minutes (patients presenting 24 hours
post injury are not rewanned)
-white blisters are debrided with application of topical aloe vera every 6 hrs
-hemorrhagic blisters are left intact with application of topical aloe vera every 6 hrs
-affected part is elevated with splinting as indicated
-analgesia as indicated
-ASAJibuprofen
-daily hydrotherapy
-physical therapy
*definitive amputation is delayed until clear demarcation of gangrene (early debridement only
indicated with uncontrolled infection)
VIII. Sequelae
-cold insensitivity -tissue loss
-hyperhydrosis -vasospastic attacks
-intrinsic muscle atrophy -hyperesthesias
-color changes in integument -chronic pain
-arthritis -pinneal calcification
-growth plate abnormalities -squamous cell carcinoma
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