Neoplasm of Musculo Skeletal

Neoplasm like lesion

Osteochondroma
An abnormality of growth direction and remodeling in the metaphyseal region of long bones in growing
children. The lesion consist of an outgrowth of bone and cartilage that forms a prominent tumor, in the
sense of local swelling or lump.

Clinical feature
Osteochondroma is usually seen in young person. The lesion always arises in the metaphyseal region.
The most common site are those most active in growing:
 Upper end of humerus
 Lower end of femur
 Upper end of tibia
Osteochondroma are not painful, but may interfere with surrounding soft tissue, such as tendon or nerve.
If it grows large enough, it may interfere with joint function.

Radiographic examination
Radiographic examination can only reveal the bony part of osteochondroma, therefore it always appear
larger clinically than radiographically.

Pathological feature
The protruding lesion always points away from the nearest epiphyseal plate. The lesion consist of normal
bone capped with cartilage. Osteochondroma has its own epiphyseal plate that grows and stop at the
same time as the neighbouring epiphyseal plate. A synovial bursa of the friction develop between the
osteochondroma and soft tissue.
There are 2 types of osteochondroma:
 Pedunculated/Stalked type – Long with narrow base
 Sessile type – Short with broad base
Only 1% of osteochondroma turns malignant (usually into osteosarcoma). Transformation is suspected if it
becomes larger and symptomatic in adult life.

Treatment
Surgical excision if it interferes with joint function, or for aesthetic purposes.
Osteoid Osteoma
A reactive bone lesion characterized by persistent pain. It develops in children and adolescent, particularly
boys. It can occur in any bones except the skull. Predilection sites are bones of the lower limb, especially
femur and tibia.

Pathological feature
The lesion consist of a small round nidus (nest) of osteoid tissue surrounded by reactive bone. It doesn’t
continue to grow and seldom grows more than 1cm.
If it grows in cancellous bone – There is little reactive bone
If it grows in cortical bone – Reactive bone is out of proportion

Clinical feature
Mild and nagging pain, most noticeable at night. Relieved by mild analgetics or NSAIDs.
If it is near a joint – synovial effusion might interfere with joint motion
Local muscle atrophy may ensue
If it develops in the vertebrae – Painful scoliosis

Radiological examination
Radiological examination shows a radiolucent nidus surrounded by reactive bone.
Scintigraphy is useful in diagnosis

Treatment

The persistent pain usually necessitates surgical excision.

The nidus and a narrow margin of surrounding reactive bone need to be excised to prevent recurrences.
To minimize incision and excision, a percutaneous CT guided insertion of guide wire directly into the nidus
and ablating it by overdrilling, cauterization, laser coagulation, and cryotherapy.
After the procedure, the remaining reactive bone will gradually disappear.

Osteoblastoma
A big osteoid osteoma. It tends to develop in the vertebrae, flat bone with little sclerosis. Consist of
osteoid. It is usually painful. Treated with surgical excision followed by bone graft on the surgical defect.
 True Neoplasm

Osteosarcoma
An extremely malignant neoplasm of the bone that arises from primitive cells of metaphyseal region of
long bone in young individual.
It is the second most common neoplasm of the bone.
It affects mostly children, adolescent, and young adult.
Predilection sites are those most active in growth, such as: upper end of humerus, lower end of femur,
upper end of tibia and fibula, and pelvis.
In old person, it might be caused by complication of Paget’s disease.

Pathological feature
Osteosarcoma grows rapidly and is locally destructive. Some are osteosclerotic, some are osteolytic.
Osteosarcoma erodes the cortex of metaphyseal region and predisposes it to pathological fracture. It
continues to grow and lifts the periosteum. Reactive bone forms in the angle between the bone and
elevated periosteum. The most common site of metastases is the lung.

Radiological examination
Codman’s triangle forms between the bone and elevated periosteum.
Sunburst appearance – A combination of reactive bone and neoplastic bone deposited along blood vessels
that radiates through the neoplasm from cortex to the elevated periosteum.

The most accurate diagnosis is by MRI. Scintigraphy is useful in detecting skip lesions. CT-scan of the chest
to detect lung metastases.

Clinical feature
Progressive pain – initially mild and intermittent, becomes severe and constant.
It may interfere with joint motion. A diffuse tumor mass develops rapidly and is usually tender. The
overlying skin is warm because of increased vascularization. Superficial veins are dilated, best seen under
infrared. Serum ALP is elevated.

Treatment
 Chemotherapy (Methotrexate, Adriamycin, Doxorubicin, Cisplatin, Ifosfamide)
o Neo-adjuvant
o Adjuvant
 Surgical operation:
o Limb-sparing procedure (If no skip lesion)
o Amputation / disarticulation
Prognosis
Combination of chemotherapy and more effective surgical procedure have resulted in 5-years survival rate
of >70%.
Ewing Sarcoma
A rapidly growing malignant neoplasm that arises from primitive cells of the bone marrow in young person,
usually in the medullary cavity of long bones.
It is 5% of all bone cancer.
It develops in children, adolescent, and young adult.
Predilection sites are: femur, tibia, ulna, and metatarsals.

Pathological fracture
Beginning within the medullary cavity, ewing sarcoma perforates the cortex of the shaft and elevates the
periosteum.
Microscopically, it is characterized by poorly differentiated round cells of marrow origin with intercellular
glycogen as detected by means of periodic acid schiff stain.
Ewing sarcoma grows so rapidly that it often outgrows its blood supply resulting in necrosis of the central
area of the neoplasm.

Radiological examination
Onion skin appearance from the repeated elevation of periosteum and consequent reactive bone
formation.
CT, MRI, and scintigraphy are all required for staging.

Clinical feature
Pain and local tenderness. Pain is very progressive.
A diffuse soft tissue mass is palpable and tender.
Systemic manifestation of bone necrosis such as fever, leukocytosis, and elevated sedimentation rate.
Avascular necrosis from diminished supply.
Metastases to lung and other bone.

Differential diagnosis
Chronic osteomyelitis
Eosinophilic granuloma

Gold standard
Surgical excision and histological examination
Treatment
Neoadjuvant chemotherapy and radical surgical resection (limb-sparing procedure / amputation), followed
by adjuvant chemotherapy with or without radiation.

Prognosis
With proper treatment, 5-years survival rate is >50%.
Multiple Myeloma
A widespread multicentric neoplasm that arises from plasma cells of hematopoietic tissue of the bone
marrow.
Usually affects person > 50 Y.O.
Predilection sites are: spine, pelvis, ribs, sternum, and skull.
The most common neoplasm of the bone. (>50% of case)

Pathological feature
Rapid destruction of bone with little reactive bone formation.

Clinical feature
Pain, Pathological fracture.

Diagnosis
High gamma globulin in serum.
Bence Jones protein in urine.
Elevated ESR and anemia.

Gold standard
Aspiration biopsy of bone marrow from the iliac crest or sternum.

Treatment
Open reduction and internal fixation (ORIF) with bone cement on pathological fracture.
Chemotherapy.
Bone marrow transplantation.
Spinal brace for patient with vertebral fracture.
Chondrosarcoma
A slow growing malignant neoplasm that arises from normal bone or malignant change from benign
neoplasm such as osteochondroma.
Usually affect person > 30 Y.O.
The third most common neoplasm of the bone (After multiple myeloma and osteosarcoma).
Predilection sites are: pelvis, shoulder girdle, and proximal end of long bones.

Pathological feature
Histologically, the lesion consist of poorly differentiated cartilage cells with relatively few mitotic figures.

Radiological examination
Patchy calcification within the cartilage, best seen with CT-scan.

Clinical feature
A large cartilaginous mass slowly develops. Metastases develops late.

Treatment
Complete removal of neoplasm by limb-sparing procedure or amputation.

Prognosis
35% cured in high grade malignancy
80% cured in low grade malignancy
 Infection

Acute Osteomyelitis
A rapidly developing infection of the bone and its marrow from either blood-borne bacterial infection of
secondary to trauma.

Incidence rate
Hematogenous osteomyelitis is primarily a disease of growing bones. Therefore it affects children, boys 3x
more likely than girls.
Predilection sites are: femur, tibia, fibula, humerus, radius, ulna and affect the metaphyseal region of bone.

Etiology
90% of acute hematogenous osteomyelitis are caused by staphylococcus aureus. Some are caused by
streptococcus and pneumococcus.
Port d’entrée is usually the skin, secondary to scratches, abrasions, pimples or boils. It can also be caused
by respiratory tract infection, secondary to nose or throat infection.

Pathogenesis and Pathology

Initially a small focus of bacteria forms with hyperemia and edema in the cancellous bone and its marrow
of the metaphyseal region of long bones. Intraosseus pressure rises causing severe and constant pain.
Pus forms, and intraosseus pressure rises even more compromising local circulation, leading to vascular
thrombosis and bone necrosis.
It destroys the bone by osteolysis. It enters the bloodstream causing septicaemia, manifested by fever,
anorexia, and malaise. It then penetrates to the periosteum; separates and elevates the periosteum
causing subperiosteal abcess.
In a few days, it penetrates the periosteum causing a cellulitis, and eventually soft tissue abcess. If it
continues into a joint, it can cause septic arthritis. If it continues near a joint but outside of joint, it can
cause sterile synovial effusion.
The compromised local circulation of bone causes an area of bone necrosis. This may vary in extent from a
small spicule to an entire shaft. This will eventually be separated to form a sequestrum (a separated
fragment of infected bone).
Extensive new bone formation from the deep layer of elevated periosteum forms an enveloping bony tube
(an involucrum), that maintains the continuity of the involved bone.
Clinical Feature
50% of the time there’s history of previous trauma and pre-existing bacterial infection elsewhere.
Severe and constant pain near the end of long bone.
Local tenderness and unwillingness to use the affected limb.
Systemic manifestations such as fever, anorexia, and malaise.
Soft tissue swelling after a few days.
During the first week, there’s no radiological evidence.
After the first week, there’s radiological evidence of bone destruction in metaphysis and reactive new
bone formation from periosteum.
During the first week, scintigraphy and MRI maybe of value.
WBC and ESR are elevated.

Treatment

 Bed rest & analgetic

 IV fluid
 Local rest by splint or traction to reduce pain, retard spread of infection, and prevent soft tissue
contracture
 Antibiotic treatment
 If local and systemic manifestation doesn’t improve after 24 hours of treatment; Surgical
decompression by drilling of bone to evacuate the pus and reduce intraosseus pressure. Obtained
pus used for culture. Post-operatively, local continuous saline infusion and antibiotics with drainage
for a few days.
 Antibiotic for 3-4 weeks. Stop only when ESR approach normal level
Prognosis
4 most important factors:
Time interval between onset and treatment (Best in first 3 days)
Effectiveness of antibiotics
Dosage of antibiotics
Duration of antibiotics

Complication
Early: Late:
 Death from sepsis  Chronic Osteomyelitis
 Abcess formation  Pathological fracture
 Septic arthritis  Joint Contracture
 Local growth disturbance
Chronic Osteomyelitis
An osteomyelitis that persist and become chronic or recur at a later date because of inadequate treatment.

Pathogenesis
Infected bone separates from the living bone forming a sequestrum. Bacteria survives and multiply within
the sequestrum. As a result it became the source of either persistent or recurrent infection.
Brodie’s abcess - An infection within cancellouse bone, walled off by fibrous tissue

Clinical feature
Pain, swelling, tenderness, and loss of function in the involved bone.
There might be one or more sinuses.
Radiological finding: sequestrum.

Treatment
Sequestrectomy
Antibiotics (Local and systemic)
Saucerisation of abcess cavity

Complication

 Joint contracture
 Pathological fracture
 Amyloid disease
 Epidermoid carcinoma
Septic Arthritis
Rapidly progressive infection in a synovial joint. Affects children, newborn infants are particularly
susceptible. Most affects hip and elbow joint.

Etiology
Most commonly caused by spread of osteomyelitis.
Most frequently by Staphylococcus aureus.

Pathogenesis
Infection of synovial joint causes destruction of articular cartilage. It is caused either by PMN leukocytes or
bacteria. As the joint fill with pus, fibrous capsule softens and stretches and may cause dislocation. The
increase of intra-articular pressure can cause avascular necrosis.

Clinical feature

 Irritability in infant; Pain in the region of involved bone.

 Reluctance to move the affected joint; Pain when moved.
 Fever, muscle spasm, and tenderness.

Diagnosis

 Elevated ESR.
 Needle aspiration of joint and culture.
 Radiological examination
o Soft tissue swelling in the first week
o Dislocation usually in second week
 Narrowed cartilage space when articular cartilage is destroyed

Treatment

 Antibiotic
 Local treatment of the joint by removal of pus and irrigation of the joint by arthrotomy or
arthroscope
 If the joint is dislocated – Reduce and immobilize in stable position

Complication
Early: Late:
 Death by septicaemia  Degenerative joint disease
 Destruction of joint cartilage  Fibrous ankylosis
 Dislocation  Bony ankylosis
 Avascular necrosis
Tuberculous Osteomyelitis
Always secondary to tuberculous infection elsewhere in the body.
Usually affects children. Most commonly develop in the vertebrae.
It may also develop in the epiphysis and spread to joint causing tuberculous arthritis.
In children it can involve the shaft and phalanx.

Tuberculous Spondylitis (Pott’s disease)

>50% of all bone and joint tuberculosis. Begins during early childhood.
Most common site is lower thoracic and upper lumbar vertebrae through Batson’s plexus of paravertebral
vein.

Pathogenesis

 Bone destruction in anterior part of vertebral body.

 Segments of bone becomes avascular and produce tuberculous sequestrum.
 Tuberculous granulation tissue penetrates the thin cortex of the vertebral bodies producing para-
vertebral abcess.
 Destruction of bone anteriorly leads to progressive kyophosis.

Clinical feature and Diagnosis

 Back pain
 Reluctant to sit up, stand up or bend forward
 Locan deep tenderness and muscle spasm
 Systemic manifestation with tuberculosis infection elsewhere (Lung/Urinary tract)
 Elevated ESR
 Tuberculin test (+)
Confirm diagnosis with Aspiration of paravertebral pus and studied microscopically.
Closed punch biopsy or open surgical biopsy reveals histological picture of tuberculous infection, such as
hystiocytes and giant cells.

Radiologic examination

 Osteolytic in anterior part of vertebral body

 Regional osteoporosis
 Intervertebral disc narrowing
 Paravertebral abcess
Treatment

 Anti TB drugs
 Local rest of the spine on a turning frame or in a plaster bed
 After 1 month of drug therapy and rest, operate to evacuate pus, removal of sequestrum, and
fusion of involved segments by anterior interbody fusion using autogenous bone graft
 Spinal brace / cast

Complication

 Paraplegia of active disease

o Result either from extra-dura pressure (TB pus, sequestra) or from direct involvement of
spinal cord by tuberculous granulation tissue.
 Paraplegia of healed disease
o Result either from gradual development of bony ridges that impinge the spinal canal or from
fibrosis of granulation tissue.
 Cold abcess
Fracture
A structural break in continuity of bone, epiphyseal plate or cartilaginous joint surface.

Fracture description (SEC FEC)

 Site (1/3 distal, medial, proximal)

 Extent (Complete / Incomplete)
 Configuration (Transverse, oblique, spiral, comminuted)
 Relationship of fracture fragments to each other (Displaced / Undisplaced)
o (Translated, angulated, rotated, distracted, overriding, impacted)
 Relationship of fracture to external environment (Open / Closed)
 Complication (Uncomplicated / Complicated - Local or Systemic)

Diagnosis of fracture

 Patient history
o Mechanism of injury
o Localised pain (Stable? Aggravated by movement?)
o Decreased function
 Physical examination
o Look (Inspect)
 Swelling
 Deformity (Angulation, rotation, shortening)
 Abnormal movement at the fracture site
o Feel
 Sharp localized tenderness at the site of fracture
o Move
 Aggravation of pain and muscle spasm during the slightest passive movement
Look and feel for less apparent injuries on the same limb as well as the brain, spinal cord, peripheral
nerves, major vessels, skin, thoracic and abdominal viscera.

Diagnostic imaging
Radiolucent splint can be used to avoid unnecessary pain and further soft tissue injury
Rule of 2:

 2 limbs – for comparison

o Include entire length of bone with 2 joints at each end to allow assessment of angulation
and rotation
 At least 2 projections (AP & Lateral)
o + oblique for small bones, ankle, vertebrae, pelvis
 2 occasions
o Some fractures are not easily visible after trauma
 CT and MRI for spine and pelvis
Bone healing
Cortical bone
1. Initial effect of fracture
 Fracture hematoma on the fracture site
2. Early stage of healing from soft tissue
 External callus from deep layer of periosteum
 External callus contain thick enveloping mass of osteogenic tissue
 Internal callus from endosteum
3. Stage of clinical union
 When movement no longer occur at the fracture site, but has not regained original strength.
Radiographic examination shows callus formation, but fracture line is still apparent.
4. Stage of consolidation / radiographical union
 When all the immature bone and cartilage of the temporary callus have been replaced by
true lamellar bone. At this stage remodeling occur under the effect of wolff’s law.

Cancellous bone
1. Formation of internal callus
 Internal callus fills the open spaces of the spongy cancellous fracture surface whenever
there is good contact.
2. Clinical union
 Fracture healing occur at the site of direct contact between fracture and endosteal callus
3. Radiographic union
 The woven bone is replaced by lamellar bone as the fracture consolidate
Cancellous bone are more susceptible to compression fracture.

Articular cartilage
Hyaline cartilage of a joint is extremely limited in its ability to heal or regenerate.
Fracture in articular cartilage either heal by fibrous scar tissue or fails to heal at all.

Time required for uncomplicated fracture healing

 Age of patient (Related to osteogenic activity of periosteum & endosteum)

o At birth : 3 weeks
o 8 years : 8 weeks
o 12 years : 12 weeks
o >20 years : 20 weeks
 Site and configuration of fracture
o Bones that are surrounded by muscle heal more rapidly (Thicker periosteum)
o Cancellous bone heal more rapidly than cortical bone
o Epiphyseal separation heals 2x faster than cancellous metaphyseal fractures of the same
bone
 o Long oblique fracture and spiral fracture heals more rapidly than transverse fracture (larger
surface area)
 Displacement
o Undisplaced fracture with intact periosteum heals 2x faster than displaced fracture
 Blood supply to the fracture fragments
o Less blood supply, slower healing

Assessment of fracture

 Clinical examination
o Bending, twisting, compression force to fracture site
 (+)ve movement – Not yet united
 (-)ve movement – Clinical union
o Pain assessment
 Radiological examination
o Bony callus with fracture line apparent – Clinical union. Protect from undue stress until
radiographic union

Abnormal healing of fracture

 Malunion
o Heal in unsatisfactory position with residual bony deformity
 Delayed union
o Longer time to heal
 Non-union
o Fail to heal with resultant formation of fibrous union or false joint (Pseudoarthrosis)
General principles of fracture treatment
1. Do no harm
 Prevent further damage to important soft tissue by careless first air or transport
 Prevent damage to soft tissue by incorrect plaster cast or excessive traction
 Prevent opening the path to infection by careless and injudicious application of open
reduction with internal fixation
2. Base treatment on accurate diagnosis and prognosis
 When external callus or combination of external and internal callus can be expected, perfect
reduction and rigid fixation are not essential
 When internal callus alone can be expected, perfect reduction and rigid fixation is required
3. Select treatment with specific aim
 To relieve pain
 To obtain and maintain satisfactory position of fracture fragments
 To allow and if necessary to encourage bony union
 To restore optimum function
4. Cooperate with the law of nature
 Avoid preventing or delaying normal healing
5. Make treatment realistic and practical
 What is the aim of treatment?
 Is it likely to accomplish this aim with this treatment?
 Will the end result justify the means/method?

Emergency life support

 Preliminary care
o Immediate care outside hospital
 Airway, Breathing, Circulation
o Fracture and Dislocation
 Splint before the patient is moved to minimize pain and soft tissue injury
 Traction to straighten gross deformity and to hold limb while being splinted
 Upper limb – splint to trunk
 Lower limb – splint to opposite limb
o Hospital
 History
 A llergies
 M edication
 P ast history
 L ast meal
 E vents related to accident
 Treatment based on ABCs in basic life support
Fracture and Dislocation
Vascular injury and nerve impairment must be assessed.
Examine for other fracture as well as soft tissue injury and visceral lesion.
Fractured extremity must be splinted before radiological examination.

Treatment of closed fracture

1. Protection alone (Without reduction or immobilization)
 Upper-limb with simple sling
 Lower limb with crutches

Indication:

 Undisplaced fracture of the ribs, phalanges, metacarpal

 Clavicle fracture on children
 Mild compression fracture on the spine
 Impacted fracture of the upper end of humerus
 After clinical union has been obtained

Risks:

 Fracture may become displaced for a very young child or uncooperative adult
 Need radiographic exam at regular interval

2. Immobilisation by external splinting (Without reduction)

 External splint is relative immobilization (movement can still occur inside the limb or trunk).
 Use plaster of paris cast, metallic or plastic splint

Indication:

 Relatively undisplaced but unstable fracture.

 e.g. Long bone fracture with sideway shift of the fragment but good contact and no significant
angulation or rotation and doesn’t require reduction.

Risks:

 Muscle pull and gravitational forces may cause further displacement. Such as angulation, rotation,
or overriding that is unacceptable.
 Repeated radiographic examination is required
 Improper application of cast or splint may cause local pressure sores overlying bony prominence
that result impairment venous and arterial circulation.
 3. Closed reduction by manipulation + immobilization

Indication:

 Displaced fracture that require reduction and can be accurately reduced and maintained by closed
means.

Risks:

 May cause further damage to soft tissue (Vessels, Nerve, Periosteum)

 Excessive traction may cause arterial spasm, particularly at the elbow and kneem with resultant
compartment syndrome.
 Pressure sores over bony prominences.

4. Closed reduction by continuous traction + immobilization

 Young children with skin traction
 Older children and adult with skeletal traction

Indication:

 Unstable oblique, spiral, comminuted fracture of major long bone.

 Unstable spinal fracture
 Skeletal traction for fracture with vascular injury, excessive swelling, and skin loss.

Risks:

 Arterial spasm with resultant compartment syndrome.

 Superficial skin loss in skin traction.
 Pin track infection in skeletal traction.
 Excessive traction may distract fracture fragments causing delayed or even non-union.

5. Closed reduction + functional fracture bracing

 Closed reduction
 Continuous traction for a few days
 Immobilization in plaster cast for 3 weeks
 Hinged cast braced or plastic brace is applied

Indication:

 Fracture of the shaft of tibia

 Distal 3rd femur
 Ulnar fracture in adult
Contraindication:

 Interthrocanter fracture, Subthrocanter fracture, Midshaft femur fracture, Radius shaft fracture,
Intra-articular fracture

Risks:

 Failure to maintain acceptable position of fracture fragment

6. Closed reduction by manipulation followed by external skeletal fixation

Indication:

 Severely comminuted (Unstable) fracture of the shaft of tibia or femur

 Type 3 open fracture with excessive soft tissue injury including artery and nerve
 Unstable fracture of pelvis, humerus, radius, metacarpal

Risks:

 Pin track infection with / without osteomyelitis

 Ring sequestrum

7. Closed reduction followed by internal skeletal fixation

Indication:

 Fracture that can be reduced by closed means but can’t be maintained by external immobilization.
 e.g. unstable femur neck fracture

Risks:

 Failure to obtain satisfactory position of fracture fragment

 8. Open reduction followed by internal skeletal fixation
 Fracture site is exposed surgically so that the fracture fragments may be reduced perfectly
under direct vision
 Reduction is maintained by metallic device

Indication:

 When closed reduction by manipulation is not possible

 When there is coexistent vascular injury that requires operation and repair
 To facilitate nursing care and prevent serious complication

Contraindication:

 Tibia shaft fracture and Humerus shaft fracture (Managed by closed nailing / functional fracture
bracing)

9. Excision of fracture fragment and replacement by endoprosthesis

Indication:

 Femoral head fracture (High incidence of avascular necrosis – nonunion)

 Comminuted radial head fracture
 If elbow joint is grossly unstable, because of coexistent ligament injury
 Severely comminuted + grossly unstable supracondylar fracture of humerus
 Severely comminuted fracture of patella
 Comminuted fracture of humerus head

Contraindication:

 Fractures in children

Risks:

 Infection
 In elderly, endoprosthesis can migrate through osteoporotic bone of pelvis or femur
Treatment of open fracture

Gustillo-Anderson classification of open fractures

1. A clean wound less than 1cm in length
2. Laceration >1cm in length but without extensive soft tissue damage, skin flaps, avulsions
3A. Extensive soft tissue damage but adequate bone coverage (Segmental fracture & Gunshot wound)
3B. Extensive soft tissue damage with extensive periosteal stripping and devascularised bone that
require skin flaps or free grafts. Usually with gross contamination
3C. Vascular injury requiring repair

Type 1 & 2 – primary closure

Type 3 – delayed closure (Left open for first 4-7 days)
Open fracture is a surgical emergency

Treatment
1. Cleansing the wound
Cleanse all the dirt with sterile water / isotonic saline solution (Golden period 6-7 hours)
2. Excision of devitalized tissue (Debridement)
3. Treatment of fracture
Small wound -> closed reduction
Extensive wound -> skeletal traction or seketal fixation (External or Internal)
4. Closure of wound
Leave open fractures open
After 4-7 days, if there’s no infection -> delayed primary suture
Loss of skin -> split thickness skin graft
Suction drainage -> to prevent accumulation of blood and serum in the wound
5. Antibacterial drug
6. Prevention of tetanus
Anesthesia: General, 6 hours fasting.
Fracture complication
1. Skin
a. Tattoo effect from abrasions
b. Sores (Pressure, Bed, Cast)
2. Vascular
a. Traction and pressure lesion
b. Compartment syndrome
c. Gangrene
d. Venous thrombosis & pulmonary embolism
3. Neurological
a. Traction and pressure lesions
4. Joint complication
a. Septic arthritis (Post-op)
5. Bone
a. Osteomyelitis (Post-op)

Compartment syndrome / Volkmann’s ischemia

Increased pressure of progressive edema within rigid osteofocal compartment of either forearm or the leg
(between the knee and ankle) threatens the circulation to the enclosed (intracompartment) muscle and
nerve.
Most frequently: Flexor compartment of forearm; Anterior tibial compartment of the leg.
Compartments:
Forearm: Leg:

 Anterior  Anterior
o Superficial flexor o Tibialis anterior
o Deep flexor  Lateral
 Posterior o Peroneus muscle (Longus, Brevis)
o Superficial extensor  Posterior
o Deep extensor o Superficial
o Deep

Nerve can withstand 2-4 hours, but can regenerate.

Muscle can withstand 6 hours, but can’t regenerate.
Necrotic muscle tissue is replaced by fibrous scar tissue that gradually shorten to produce compartmental
contracture.

Etiology
1. Proximal (Extracompartmental) occlusion of the main artery supplying the compartment
2. Intracompartmental injury to either bone, soft tissue, or both with resultant hemorrhage
Most common injury that cause compartment syndrome:
1. Displaced supracondylar fracture of the humerus with damage to the brachial artery in children
2. Excessive longitudinal traction in treatment of fracture of the femoral shaft in children with
resultant arterial spasm
3. Fracture (as well as surgical osteotomies) of the proximal third of the tibia
4. Drug induced coma with resultant pressure on major arteries from lying on a hard surface in an
awkward position for a prolonged period

Clinical picture (5P): Pain, Pulseless, Pallor, Paresthesia, Paralysis

If it is intracompartment, pulse maybe palpable
If extracompartment + damaged nerve, pain may not present

Slit catheter (Rorabeck) to measure intracompartment pressure

Normal: 0-8 mmHg | >30-40 – fasciotomy cito
Fascia must be left wide open at least 7 days – delayed primary suture.
Surgical stabilization of associated fracture
Deep Vein Thrombosis & Pulmonary Embolism

 Common cause of morbidity and mortality in adult orthopaedic patient.

 Veins in lower limb and pelvis are more susceptible.
 Adult > Children. Higher risk in smoker and women on contraceptive pill.
 Cause: Venous stasis

Risk factor:

 Prolonged bed rest

 Tight cast / bandage
 Increased coagulability
 Vessel wall damage
 Inactivity of muscle

After fracture -> Phlebothrombosis -> Loose and pass to the lung -> Pulmonary embolism

Diagnosis
DVT in calf: Local pain, tenderness in posterior midline, distal swelling.
Homan’s sign -> Passive dorsiflexion of the ankle aggravates pain.
DVT in thigh: entire lower limb is swollen.
<50% can be diagnosed clinically.
Diagnostic methods: Venogram, Doppler USG, Phletysmography.

Pulmonary Embolism
Sudden chest pain, dyspnea, hemoptysis

Prevention:

 Avoid constant local pressure on vein -> actively contracts injured limb
 Elastic compressive stocking
 CPM (Continuous Passive Movement)
 High risk of DVT -> LMWH

Treatment

 Anticoagulant: Heparin / Warfarin

 In femoral vein -> thrombectomy
DVT above the knee is more likely to embolise the lung
Difference in fracture in children and adult

No Children
1 Fractures more common
Relatively slender bones and carefree capers
2 Stronger and more active periosteum
Less readily torn, intact periosteal hinge can be
used in closed reduction
3 More rapid fracture healing
Because periosteum is more osteogenic
4 Special problems of diagnosis
Varying radiographic appearance of epiphyseal
plate (Before/After development of secondary
centre of ossification)
5 Spontaneous correction of residual deformities
6 Differences in complication
Compartment syndrome more common
Growth disturbance
7 Different emphasis on method of treatment
Virtually all fractures of long bones – closed
reduction (Manipulation/Continuous traction)
Result must be optimal because they have to
last a long lifetime
8 Torn ligament and dislocation less common
Stronger and more resilient ligament and
fibrous capsule
9 Less tolerance of major blood loss
Adult
Fractures less common but more serious
More force is required to break bones
Weaker and less active periosteum
Less rapid fracture healing
Fewer problems of diagnosis
Epiphyseal plate has closed
No spontaneous correction of residual deformities
Differences in complication
Open fracture more common
Major artery injury, DVT, PE
Different emphasis on method of treatment
Undisplaced and impact fracture – protection only
More frequently requires open reduction
Torn ligament and dislocation more common
Better tolerance of major blood loss

Salter Harris Classification

 I. Complete separation of entire epiphysis without any fracture through bone.
Etiology: Shearing force
More common in newborn and young children
Treatment: Closed reduction
Prognosis: Excellent

II. Fracture-separation extends along the epiphyseal plate to a variable distance, then out through a
portion of the metaphysis producing a triangular metaphyseal fragment.
Etiology: Shearing & bending force
More common in older children
Treatment: Closed reduction
Prognosis: Excellent

III. Intra-articular fracture, extends from the joint surface to the deep zone of epiphyseal plate, then
along the plate to its periphery.
Etiology: Intra-articular shearing force
More common in teenager
Treatment: Open reduction and Internal fixation (ORIF)
Prognosis: Good

IV. Intra-articular fracture, extends from the joint surface through the epiphysis, across the entire
thickness of epiphyseal plate, and through a portion of the metaphysis.
Most common: Lateral condyle of humerus
Treatment: Open reduction and Internal fixation (ORIF)
Prognosis: Bad

V. Crushing of one part of the epiphyseal plate

Most common: Knee and ankle
No weight bearing for 3 weeks
Prognosis: Poor
Fractures in children
Hand fractures
Mallet finger (Baseball finger)
 Avulsion of fragment of bone from the base of distal phalanx into which the tendon is inserted, or
extensor tendon rupture proximal to its insertion.

Etiology:

 Unexpected passive flexion of the distal interphalang joint with extensor tendon under tension.

Clinical feature:

 Interphalang joint remained flexed and cannot be actively extended.

Treatment:

 Splinting the finger in a molded plaster cast with distal interphalang extended and proximal
interphalang flexed, for 3 weeks
 ORIF with K-wire if the bone fragment is displaced to restore perfect joint surface

Boxer’s fracture

 Fracture of the neck of the 5th metacarpal

 Depression in metacarpal head and posterior angulation

Treatment:

 Flexing the metacarpophalangeal joint and proximal interphalang at a right angle, then push the
metacarpal head back to position.
 Immobilisation with padded plaster cast, no longer than 2 weeks
 If unstable -> Transfix the distal fragment with K-wire
Bennett fracture

 Fracture dislocation of 1st carpometacarpal joint

 A small triangular shaped fragment of base of the metacarpal still in proper relation with trapezium,
but the rest of the metacarpal is dislocated and in flexed position

Etiology:

 Longitudinal force of 1st metacarpal with thumb flexed

Clinical feature:
Local Swelling, tenderness, and reluctance to use the thumb

Treatment:
Closed reduction with cast
1st metacarpal is extended, then press the metacarpal base inward and the head outward
Continuous tape traction
ORIF with K-wire / AO Screw

Rolando fracture
Intra-articular fracture of the 1st carpometacarpal joint with Y-shaped configuration
Wrist & Forearm
Colles fracture

 Distal end radius fracture with displacement to dorsal (posterior)

 Mechanism of injury: Break fall with open hand while forearm is pronated

Clinical feature:

 Dinner fork deformity

Radiographic examination

 Stable: Little comminution

 Unstable: Gross comminution

Treatment:

 Undisplaced: Below elbow cast for 4 weeks

 Displaced: Closed reduction
 Unstable: <60% OREF

Aftercare

 Elevating forearm to minimize swelling

 Thumb, finger, elbow, and shoulder exercised

Complication

 Finger stiffness
 Shoulder stiffness
 Malunion
 Residual subluxation of distal radio-ulnar joint

Smith fracture (Reverse Colles)

Fracture of distal end radius displacement of distal fragment to volar
Mechanism of injury: Fall or blow on the back of the flexed wrist

Treatment:
Reduction with supination of the wrist
ORIF
Above elbow cast for 6 weeks in supination
Galeazzi fracture dislocation

 Displaced fracture of distal 3rd radius shaft and dislocation of distal radioulnar joint

Treatment: ORIF

Monteggia fracture dislocation

 Fracture of the proximal half of ulna and dislocation of proxiumal radioulnar joint

Mechanism of injury:

 Hyperextention and pronation injury

 Direct blow over the ulnar border of the forearm

Treatment: ORIF
Humerus
Intercondyle fracture

 Mechanism of injury: Severe fall on the point of flexed elbow

Treatment:

 ORIF (For single & double fracture)

 Prosthetic elbow replacement for severely comminuted fracture

Supra-condyle fracture

 Mechanism of injury: hyperextension injury or fall on the hand with elbow flexed
 Most common & most serious humerus fracture

Risks:

 Malunion
 Compartment syndrome of nerve and muscle in the forearm

Diagnosis

 Deformity in the elbow region, swollen and tense

 Assess peripheral circulation and function
 If impairment of circulation -> Urgent reduction

Treatment

 Undisplaced: Immobilisation with elbow flexed for 3 weeks

 Displaced: Closed reduction using periosteal hinge + percutaneous pinning. Cast for 3 weeks

Complication:

 Volkmann’s ischemia
o Brachial artery maybe caught / kinked in the fracture site
 Peripheral nerve injury
o Median nerve injury
o Radial and ulnar nerve less common
 Malunion
Shaft humerus fracture

 Mechanism of injury: Direct blow to humerus

Clinical feature:

 Flail arm
 Patient tries to support with opposite arm
 Check radial nerve lesion

Treatment:

 Closed reduction
 Open reduction indication:
 Brachial artery injury requiring repair
 Progressive loss of radial nerve function

Transverse fracture:

 Closed reduction
 U-shaped slab
 Clinical union in 6 weeks

Spiral and comminuted fracture:

 No reduction required
 Patient sit upright + U-shaped slab
 Functional brace after 2 weeks of cast

Complication:

 Radial nerve injury

 Delayed union / non-union
Neck humerus fracture

 More common in elderly

 Impact fracture of humerus neck
 Mechanism of injury: minor fall on the hand with extended arm

Treatment:

 Arm sling for 6 weeks

 After 1 week -> pendulum exercise
 In young patient, unstable fracture -> ORIF

Complication:

 Persistent shoulder stiffness

Shoulder
Anterior dislocation of shoulder
Humeral head is driven forward and avulses the cartilaginous glenoid labrum and capsule from the outer
margin of glenoid cavity (Bankart lesion)

Mechanism of injury:

 External rotation and extension of shoulder

 Fall on the hand or posterolateral aspect of the shoulder

Clinical feature:

 Something has given way / gone out of place and unable to use arm
 Shoulder look square due to anterior and medial displacement of humeral head into subcoracoid
 Always examine circumflex (Axillary) nerve function

Radiographic examination:
Humeral head lying in subcoracoid

Treatment:
Reduction should be done as soon as possible
General anaesthetic might be required
Stimson technique

 Patient is left prone with arm hanging over the side of bed
 After 10-20 minutes, the shoulder may reduce

Hippocratic method

 Gently increased traction is applied to the arm with shoulder in slight abduction, while assistant
applied firm contra-traction to the body

Kocher method (Not recommended, risk of nerve, vessel, and bone injury)

 Elbow is bend in 90⁰ angle and held close to the body

 Slowly rotate the arm 75⁰ laterally
 Lift part of the elbow forward
 Finally rotate arm medially

Patient sit on a reduction chair; with gentle traction of the arm over the back of the padded chair. The
dislocation is reduced
X-ray to confirm reduction and exclude fracture
Arm sling for 3 weeks

Complication:
Early: Late:

 Rotator cuff tear  Shoulder stiffness

 Nerve injury  Unreduced dislocation
 Vascular injury  Recurrent dislocation
 Fracture dislocation

Recurrent anterior dislocation of shoulder

 Hill-sachs lesion – Dent in the posterior aspect of humeral head

 The lesion is detected in special 60⁰ projection with humerus internally rotated

Treatment:

 Surgical repair of soft tissue:

 Bankart operation
 Putti-Platt operation
 Arm sling bandaged to trunk with shoulder internally rotated for 6 weeks
Posterior dislocation of shoulder

 Mechanism of injury:
o Fall on the front of the shoulder
o Fall on the hand with shoulder adducted and internally rotated
 Can occur in epilepsies, electrical shock, alcoholics

Clinical feature:

 Patient’s arm seems locked in adduction and internal rotation

Radiographic examination:

 AP cannot detect
 Superoinferior (Axillary) projection with shoulder abducted to confirm humeral head in posterior
position

Treatment:

 External rotation of the shoulder while applying forward pressure on the dislocated humeral head
 Arm sling for 3 weeks
 Confirm with X-ray – AP and Superoinferior / Axillary projections

Fracture and dislocation of shoulder

Avulsion of greater tuberosity in anterior dislocation

Treatment:
Closed reduction
If completely displaced + complete dislocation -> ORIF
Elderly: Prosthetic shoulder replacement

Acromio-clavicular (AC) joint subluxation and dislocation

 Shoulder separation
 Acromion driven downward and clavicle pulled upward by the action of trapezius muscle
 AC joint capsule torn

Mechanism of injury:

 Severe fall on the top of shoulder

Frequently in athletes, body contact sport
Coracoclavicular ligament

 Not torn – subluxated

 Torn – Luxated / dislocated

Clinical feature:

 Pain on shoulder
 Tenderness on AC joint

Radiographic:

 Patient steadily while holding weight

 Subluxation: slight depression of acromion
 Dislocation: lost contact completely

Treatment:

 Subluxation: arm sling for a few weeks with / without strapping

 Dislocation: Open reduction, capsular repair
 Insertion of threaded wire through acromion across the AC joint into the clavicle for 6 weeks
 Screw fixation of clavicle into coracoid process

Sterno-clavicular joint dislocation

Mechanism of injury: Severe blow / fall on the front of shoulder

Clinical feature:
Local tenderness
Prominence of medial end of clavicle

Treatment:
Reduced by local pressure over the dislocated medial end of the clavicle
Local pressure pad, strapping, and arm sling for 3 weeks
Knee

 Hinge joint which occurs flexion, extension, rotation

 Medial & lateral stability: medial & lateral collateral ligament
 Anterior & posterior: Anterior and posterior cruciate ligament

Medial collateral ligament tear

Mechanism of injury:

 Force from the lateral side, knee become valgus and open knee joint in the medial side
Unhappy triad:
1. Medial ligament tear
2. Medial meniscus tear
3. ACL tear

Clinical feature:

 Patient feel something giving way in knee at the moment of injury

 Joint fills with blood
 Pain and tenderness
 Knee abduction aggravates pain

Radiographic examination: Stress radiograph

Treatment:

 Partial tear:
o aspiration of hemarthrosis
o Immobilization of extended knee in cast for 6 weeks
 Complete tear:
o Elderly: Immobilisation
o Young person: Surgical repair

Tear of lateral ligament

 Less common
 Traction injury of peroneal nerve is a frequent complication
Tear of cruciate ligament
ACL
Mechanism of injury:

 Tibia driven forward on the femur

 Hyperextension of knee

Examination:

 Anterior drawer sign – Flexed knee is unstable when tibia is pulled forward
 Lateral pivot shift – Apply valgus strain when tibia is internally rotated. (+)ve – subluxation of tibia
plateau

PCL
Rerverse mechanism of ACL

Examination:

 Posterior drawer sign – Flexed knee is unstable when tibia is pushed backwards

Treatment:

 Isolated cruciate ligament tear – medial & lateral ligament intact

 Quadriceps and hamstring are strong enough to stabilize the knee+
 Immobilise with cast for 6 weeks
 For athlete: surgical repair

Complication:

 Residual knee instability

 Knee stiffness
 Calcification
Traumatic dislocation of the knee

 Complete dislocation – tear of all 4 major ligaments

Mechanism of injury:

 Extremely severe injury to the knee. (e.g. automobile accidents)

Most serious complication:

 Injury to popliteal artery -> Risk of distal gangrene

 Medial / lateral popliteal nerve injury

Treatment:

 Urgent Reduction
 Repair of popliteal artery (If damaged)
 Surgical repair of major ligaments
Femur
Femoral shaft fracture
Mechanism of injury:

 Violent direct injury (e.g. automobile accidents)

Unstable fracture - Extensive tear of periosteum and comminution
Massive internal hemorrhage -> Shock
Union requires ≥ 20 weeks

Clinical feature:

 Swollen thigh
 Deformed & unstable

Treatment:
Splint to relieve pain and prevent soft tissue injury
Shock must be treated immediately

 Non-operative:
o Fewer risk
o Suitable for majority of femoral shaft fracture
o Longer hospital stay
o Longer non-weight bearing period
o Continuous traction for 12 weeks (Until clinical union – No tenderness at fracture site)
o No weight bearing until radiographic union
o 1/3 distal femur fracture -> Functional fracture bracing
 Operative:
o ORIF – Intramedullary nail

Indication for ORIF:

 Failure with closed means

 Multiple injury
 Femoral artery injury requiring repair
 Elderly patient
 Pathological fracture

Complication:

 Shock
 Fat embolism
 Persistent stiffness
Femoral neck fracture

 Subcapital, transcervical, and basilar may be

considered together
 Women > Men
 More in elderly people >60 Y.O.

Garden classification:
I. Incomplete
II. Complete but undisplaced
III. Complete, partially displaced
IV. Completely displaced

Clinical features of displaced fracture

Mechanism of injury:

 Trying to catch oneself after falling

 Sudden torsional force on hip that fractures the femur neck

Clinical feature:

 Pain and instability at fracture site

 Entire lower limb in external rotation
 Shortening of the limb
 No obvious swelling – hemorrhage into the joint, not soft tissues

Radiographic examination (AP & Cross table lateral):

 Distal fragment externally rotated and shifted proximally

 Femoral neck appears short

Treatment:

 Closed reduction + Internal fixation

 Reduction by flexing, adducting, internally rotating, and extending the leg
 ORIF by DHS (Dynamic Hip Screw) or 3 parallel cannulated screw
 Hemiarthroplasty
Complication

 Avascular necrosis of femoral head

 Non-union
 Degenerative joint disease of the hip

Hip joint dislocation

Posterior hip joint dislocation
Mechanism of injury:

 Force on hip in flexed and adducted position

 e.g. Dashboard injury; fall on flexed knee

Clinical feature

 Hip in flexion, adduction, internal rotation, shortening

 Painful muscle spasm in the hip

Radiographic examination:

 Femoral head lies above the acetabulum

Treatment:

 Closed reduction within 8 hours (reduce risk of avascular necrosis)

o Apply upward traction on the flexed thigh in external rotation
o Forward pressure to the femoral head from behind can also be applied
 Traction for 3 weeks / Immobilisation with hip spica cast in extension, adduction, and external
rotation for 3 weeks

Posterior fracture dislocation

50% posterior hip dislocation, a portion of the posterior lip (labrum) of the acetabulum is pushed off

Treatment: Open reduction

Complication:

 Avascular necrosis of the femoral head

 Sciatic nerve lesion
 Post traumatic degenerative joint disease
Anterior dislocation of the hip

 Violent injury that forces the hip into extension, abduction, and external rotation

Radiographic examination:

 Femoral head below the acetabulum in the region of the obturator foramen
 Oblique projection reveals that it is anterior

Treatment:

 Closed reduction
o Apply traction on flexed thigh, internal rotation, and adducting the hip
o Immobilization with spica cast (flexion, adduction, internal rotation) for 3 weeks

Complication:

 Avascular necrosis
 Degenerative joint disease

Pelvis fracture
Pelvis, consist of:

 Sacrum
 2 innominate bone (Ilium, Ischium, Pubicum)

Mechanism of injury:

 Violent injury (e.g. automobile accidents, fall from heights)

Complication:

 Extensive internal hemorrhage from torn vessels

 Extravasation from ruptured bladder / urethra

Clinical feature

 Shock from internal hemorrhage

 Local swelling / tenderness
 Unstable fracture:
 Deformity of the hip
 Instability of pelvic ring
Radiological projections:

 AP
 Tangential projection
 Inlet projection
 Right & left oblique projections
Complex pelvis fracture requires CT-scan

Emergency treatment:

 Treat the shock

 Urine catheter to check bladder / urethra injury
 Cystogram

Treatment:

 Pelvis bone is cancellous type with abundant blood supply, so it unites rapidly
 Aim – To prevent malunion and resultant disturbance of function

Stable fractures of the pelvis

Isolated fracture that do not transgress the pelvic ring
Treatment: Do not require reduction

 Isolated ilium fracture

o Mechanism of injury: direct injury
o Treatment: relief from weight bearing until pain subsides
 Isolated pubic rami fracture
o Mechanism of injury: fall / straddle injury
o If both pubic rami is fractured -> urethral / bladder rupture

Unstable fractures of the pelvis

Fracture that transgress the pelvic ring

 Antero-posterior compression fracture

o Mechanism of injury: Severe crushing injury from front to back
o The 2 innominate bones are forced apart anteriorly at symphysis pubis, sacro-iliac joint
spread open
o Treatment: Internal rotation of both lower limbs + Side to side molding compression over
padded iliac crests
  Lateral compression fracture
o Mechanism of injury: Severe blow on one side / crushing injury from side to side
o The pubic rami are fractured and displaced on the side of impact and the second site of
disruption is either the sacrum or sacroiliac joint on the same side
o Treatment:
 Avoid pelvic binder / pelvic sling – will increase displacement
 May reduce spontaneously when lying on a firm surface
 Combined lateral compression and rotation fracture
o Pubic rami fracture on the opposite side of impact
o Sacrum or Illiac wing fractured on the same side of impact
o Treatment:
 apply traction on the lower limb of displaced segment, and externally rotating it
 Then full hip spica cast in external rotation
 Vertical shear fracture
o Mechanism: Fall from great heights
o Pubic rami and either sacrum or illium are fractured on the same side
o Treatment:
 Skeletal traction
 If there’s bladder injury -> OREF
 If complex & unstable fracture -> ORIF
 Aftercare for unstable pelvic fracture
o No weight bearing until clinical union usually 2 months
o No weight bearing for 3 months for vertical shear

Complication of pelvic fracture:

 Shock from internal hemorrhage

 Bladder / Urethra rupture
 Injury to sacral plexus of nerves
Stress Fracture / Fatigue Fracture
Weight bearing bones fatigue as a result of repeated stress and develop a small crack
The crack doesn’t proceed to a displaced fracture

Common example:

 2, 3, 4 metatarsals fracture in military recruits (March fracture)

 Lower end of fibula fracture in runners
 Upper 3rd tibia fracture in Jumpers and ballet dancers

Clinical feature

 Local pain, aggravated by activity, relieved by rest

 Local deep tenderness

Radiographic examination

 Tiny crack may not be apparent radiologically

 Subperiosteal & endosteal new bone appear during healing process

Treatment

 Cease responsible activity until crack heals

Congenital
Club foot / Congenital Talipes Equino Varus (CTEV)
A combination of deformities, including:

 Forefoot adduction & supination through the mid tarsal joint

 Heel varus through the sub-talar joint
 Equinus through the ankle joint
 Medial deviation of the whole foot in relation to the knee

Incidence

 2 in 1000 live birth

 50% bilateral
 Boys 2x more than girls

Etiology:

 Unknown
 Ultrastructural and histochemical studies suggest a neuromuscular cause

Diagnosis

 Mild
o Must be distinguished from positional equinovarus, which result from intra-uterine position
and can be readily corrected
 Severe
o Must be differentiated from teratologic type of severe club foot associated with spina bifida /
arthrogryposis

Treatment

 Plaster cast applied weekly for 6 weeks

 Cast treatment may be continued or the feet strapped to a denis browne type clubfoot splint by
adhesive tape. Adhesives changed weekly for 8 weeks
 Either a denis browne type of boot splint or an articulated ankle-foot orthosis (AFO) is worn day
and night for 3 months
 Straight last or outflare boots are used for day wear until 3 Y.O.
Developmental Dysplasia of the Hip (DDH)

 Congenital abnormality resulting in dysplasia and possible subluxation / dislocation of hip joint
secondary to laxity and mechanical factor

Incidence

 1,5 in 1000 live birth

 >50% bilateral
 Girls 8x more likely than boys

Etiology & Pathology

 Joint laxity
 Flexed hips are passively extended

Diagnosis & Treatment

0-3 months
Barlow test

 Flexed hips are alternatively adducted while pressing femur downward & abducted while pressing
femur upward
 (+)ve if hip is dislocatable but not dislocated
Ortolani sign

 Dislocated hip can be reduced by abducting while lifting the femur forward

Treatment

 Gentle reduction of the hip and maintained with frejka pillow splint / pavlik harness

3-18 months

 Limitation on passive abduction

 Apparent shortening on the involved limb
 Prominence of the hip

Galeazi sign

 Apparent limb length discrepancy after hips are flexed & knee level compared

Telescoping thigh

 The femur move to & fro within the thigh

Treatment:

 Lengthening the tight adductor and hamstring muscle with continuous tape traction for a few
weeks
 Subcutaneous adductor tenotomy
 Closed reduction of the hip
 Maintain with hip spica cast in stable position of flexion and abduction

18 months – 5 Years
Trendelenburg’s sign

 When standing on one foot, pelvis level drops on the opposite side
 Unilateral dislocation – When walking, body shifts to the involved side to maintain balance
 Bilateral dislocation – When walking, trunk shifts from one side to the other (waddling like a duck)

Treatment:

 Open reduction
 Innominate osteotomy

>5 years
Treatment: Innominate osteotomy
Klipple-Feil Syndrome

 Congenital fusion (synostosis) between varying numbers of cervical spine due to failure in vertebral
segmentation

Clinical feature:

 Neck is short and stiff

 Posterior hairline is low and transverse
 Head sometimes tilts to one side
 Congenital high scapula may co-existS
 Bilateral soft tissue web (From mastoid process to shoulder) in some children

Treatment:

 Surgical treatment to improve appearance

o Partial excision of high scapula
o Z-plasty of soft tissue webbing

Muscular Torticollis / Wry Neck

 Head tilted / laterally flexed and rotated toward the affected side.
 Etiology unknown, 40% had difficult deliveries
 Within the first few weeks, a large swelling develop in one sternocleidomastoid (SCM) muscle
 The swelling is called “SCM tumor” (Hypertrophy of fibrous tissue within muscle)
 Muscle gradually shortens (Contracture)

Radiological examination:

 To differentiate from Klipple-Feil syndrome

 20% muscular torticollis also have DDH

Treatment:

 The first few months of life -> Daily stretching for at least a year
 Resistant & recurrent muscular torticollis -> Operative incision of SCM muscle contracture
 Miscellaneous
Degenerative disorders
Osteoarthritis

 Local deterioration of articular cartilage. Characterised by progressive degeneration of the cartilage,

hypertrophy and remodeling of the subchondral bone & secondary inflammation of synovial
membrane

Incidence

 >60 Y.O. – 25% women | 15% men

 >80 Y.O. – 80% men & women

Etiology

 Primary idiopathic degenerative joint disease

o Normal aging process in cartilage
 Secondary degenerative joint disease
o Congenital abnormalities (e.g. DDH)
o Infection of joint
o Non-specific inflammatory disorder (Rheumatoid Arthritis)
o Metabolic arthritis (Gout)
o Hemarthrosis
o Injury

Pathogenesis
Articular cartilage

 Loss of proteoglycans -> Cartilage softens (Chondromalacia)

 In central area
o The softened, fibrillated cartilage is abraded down to subchondral bone (Eburnation)
 In peripheral area
o Hypertrophy and hyperplasia to form thickened rim of cartilage around the joint margin
(Chondrophyte)
o Chondrophyte undergoes endochondral ossification forming Osteophyte

Subchondral bone

 In central area
o Subchondral bone becomes eburnated, hypertrophy and becomes radiographically dense
 In peripheral area
o Subchondral bones become atrophic and radiographically less dense
 The redistribution of biomechanical stress in joint lead to remodeling of subchondral bone
 The joint becomes incongruent
Synovial membrane & fibrous cartilage

 The fibrous capsule becomes thickened and fibrotic, limiting joint motion

Muscle

 Muscle spasm because of pain, eventually becomes contracture

Clinical feature & Diagnosis

 Pain
 Joint crepitus
 Articular gelling (Stiff joint after resting)
 Swelling on the joint

Radiographic examination:

 Narrowing articular cartilage

 Subchondral sclerosis & cyst
 Osteophyte
 Joint remodeling and incongruity

Prognosis

 In lower limb, prognosis is bad, particularly the hip

Treatment:
Aim:  Encourage patient to be active
 Correct existing deformity
 Help patient understand
 Improve function
 Psychological support
 Strengthen muscle
 Alleviate pain
 Rehability
 Suppress inflammation

Drugs

 NSAID

Orthopaedic appliances

 Local rest of joint with removable splint, cane, crutches

Orthopaedic operations

 Prophylactic
 Arthroscopic debridement and irrigation of large joint

Therapeutic procedure

 Osteotomy near the joint -> Improve joint biomechanic

 Arthroplasty (Joint reconstruction)
 Arthrodesis (Joint fusion)
 Permanent relief of pain, but loss of motion
 Soft tissue operation
 Release tight muscle and extension of contracted capsule
 Transplantation of partial joint
Frozen shoulder
Diffuse capsulitis of the glenohumeral joint, particularly in older person

Etiology
Intrinsic (Inside shoulder) Extrinsic (Outside shoulder)

 Calcific supraspinalis tendinitis  Anything that causes pain in shoulder

 Partial tear of musculotendinous cuff  Cervical spondylosis
 Bicipital tendinitis  Cervical disc herniation
 Prolonged immobilization  Myocardia infarction
 Basal pleuritis

Pathogenesis

 The inflamed capsule becomes adherent to the humeral head, rather like adhesive tape (adhesive
capsulitis) and undergoes contracture
 The shrunken capsule prevents motion on the glenohumeral joint which becomes frozen

Clinical feature

 Inflammatory phase
o Shoulder pain, muscle spasm in muscles about the shoulder
 Sub-acute
o Joint stiffness

Treatment

 Local rest with armsling

 Local heat and analgesic
 If motion is not returning -> surgical manipulation

Prognosis

 Good, self-limiting process

 Shoulder thaws slowly within 1-2 years
Rheumatoid Arthritis
One type of inflammatory polyarthritis, characterized by a variable but prolonged clinical course with
exacerbation and remission of joint pain and swelling that may lead to deformities

Incidence

 1,5% of adult population

 Women 3x more likely than men
 Peak onset 20-40 Y.O.
 Most frequest site: hand

Etiology

 Exageration of normal immune mechanism

 Hypersensitivity – a continuous immunological response of an immunogenetically susceptible
person

Pathogenesis

 Inflammatory granulation tissue infiltrate the sub-synovial connective tissue causing it to become
swollen and boggy
 The inflammation and granulation tissue eventually replaced by reparative fibrosis / scar formation
and become joint contracture and deformity

Clinical feature & Diagnosis

 Pain and stiffness in joint every morning (Morning stiffness)

 Inflammation in involved joint (swelling, heat, pain, loss of function)
 Subcutaneous rheumatoid nodules in 30% patients
 Deformities

Radiological examination:

 Soft tissue swelling and joint effusion

 Regional osteoporosis & osteolytic erosions in subchondral bone
 Narrowing of cartilage
 Subluxation and dislocation of joint

Laboratory:

 Elevated WBC
 Elevated ESR
 Rheumatoid Factor
Treatment
Drugs

 NSAID
 SAARDs (Methotrexate, Gold salt, Chloroquin)
 Corticosteroid

Orthopaedic appliances

 Removable splint to relieve pain and prevent deformity

Operation

 Synovectomy or the involved joint

 Arthroplasty
 Arthrodesis

Prognosis:

 30% so mild that physician is not consulted

 50% able to return to work
 Only 10% severely disabled
Neuromuscular disorder
Principle of Orthopaedic treatment in neuromuscular disorder:
1. Prevention of muscular deformity
2. Correcting of existing musculoskeletal deformity
3. Improvement of muscle balance
4. Improvement of function
5. Improvement of gait or appearance
6. Rehabilitation

Cerebral Palsy
Non progressive brain disorder that develop before, during, or relatively after birth
Incidence 6 in 10.000 population alive
7 in 100.000 die at childbirth

Etiology

 Anorexia, Cerebral birth injury 10%

 Pre-natal: Genetic, Congenital cerebral malformation, Prenatal intracranial hemorrhage
 Post-natal: Erythroblastosis

Pathogenesis
Loss of function in one neuron system -> release of normal control over independent system that tend to
overact (Release phenomenon)

3 types of cerebral palsy:

 Spastic – Corticospinal system lesion in cerebral motor cortex (65%)

 Athetoid – Extrapyramidal system lesion in basal ganglia (20%)
 Ataxic type – Cerebellar and brain stem lesion (5%)

Clinical feature
Fail to achieve motor development milestones and intellectual disability

 Spastic type
o Spastic paralysis of voluntary movement and increased muscle tone
 Athetoid type
o Involuntary movement in muscle group of face and all four limbs
 Ataxic type
o Disturbed coordination of muscle group and lack of equilibrium
Prognosis

 Hemiplegic
o 70% normal IQ – All will walk
 Spastic diplegic
o 60% with IQ > 80 – 75% will walk
 Quadriplegic
o 90% Intelectual disability – 25% will walk
Athetoid & Ataxic -> problems with motor skills and verbal even with normal IQ
1/3 of all CP – So severe that treatment is ineffective -> Institutional care
1/6 so mild that treatment is unnecessary
1/2 can be treated realistically

Treatment
Drug

 Injection of Botulinum Toxin -> Relieve muscle spasm

Physical & Occupational therapy

 Passive stretching of spastic muscle to prevent deformity

Orthopaedic appliances

 Removable splint to prevent deformity

 Brace & crutch to help walking

Surgery (For spastic type)

 Tendon lengthening
 Tendon transfer
 Arthrodesis
Poliomyelitis
A viral infection that affects the motor cell (anterior horn) of spinal cord and is capable of producing
permanent paralysis

Clinical feature

 Prodromal (2 days)
o Headache, malaise, muscular ache
 Acute phase (2 months)
o Fever, severe headache, neck rigidity, painful sprain, tenderness in affected muscle, and
flaccid paralysis
 Recovery phase (Up to 2 years)
o Gradual recovery of any transient paralysis
 Residual paralysis phase (Lifetime)

Treatment
Acute phase Residual paralysis phase

 Bed rest  Tendon lengthening

 Symptomatic treatment  Tendon transfer
 Removable splint to prevent deformity  Tenodesis
 Osteotomy near a joint
Recovery phase
 Arthrodesis
 Exercise  Leg length equalization
 Brace

Post-Polio syndrome
Increasing muscle weakness, fatigue, and discomfort in involved extremities after suffering acute paralytic
poliomyelitis

Etiology

 Gradual degeneration of involved terminal axon

 Gradual decrease in muscle strength when getting older

Treatment

 Reassuring polio doesn’t recur

 Exercise to increase strength
 Light braces when necessary
Carpal Tunnel Syndrome

 Entrapment of median nerve in carpal tunnel

Carpal tunnel consists of:

 4 Flexor digitorum superficialis

 4 Flexor digitorum profundus
 Flexor pollicis longus
 Flexor carpi radialis
 Median nerve

Etiology:

 Edema of acute & chronic trauma

 Inflammatory edema associated with rheumatoid tenosynovitis
 Osteophytes in the carpal joints
 Ganglion
 Lipoma

Incidence

 Most common in middle aged women

Clinical feature

 Pain and paresthesia in the sensory distribution of median nerve in the hand
 Clumsiness of finger function
 Weakness and atrophy of thenar muscle (Abductor policis brevis)
 Nerve conduction studies for diagnosis confirmation

Treatment
Early stage
Immobilisation of wrist
Avoidance of strenuous work for a few weeks
If inflammatory -> Local injection of hydrocortisone
Surgical decompression – longitudinal division of transverse carpal ligament
Rickets
A generalized disease of growing bone, characterized by a failure of calcium salt to be deposited promptly
in organic bone matrix (osteoid) as well as in the preosseus cartilage of the epiphyseal plate at the zone of
calcifying cartilage

Etiology

 Vit D deficiency
 Chronic renal insufficiency
 Renal tubular insufficiency

Pathology

 Decrease in calcified matrix (bone)

 Increase in uncalcified matrix (osteoid)
 Uncalcified area are soft

Diagnosis
Suggested by “Rachitic Rosary”

 Clinical enlargement at the sites of epiphyseal plates, particularly at the distal end of each radius
and at the costochondral junctions
Established by

 Radiographic change in growing end of long bones:

o Widened radiolucent zone in epiphyseal plate and generalized coarse appearance of all area
of bone

Infant

 Convulsion
 Tetany
 Irritability
 Delayed physical development
 Weakness
 Failure to thrive
Children

 Deformity in the lower limb

 Severe genu varum, valgum, torsional deformity
 Small stature

Treatment
Vit D
Orthopaedic management
Night splint for deformity
Osteotomy if severe rachitic deformities persist
Stop Vit D 1 month pre-op to avoid hypercalcemia

Osteomalacia
Rickets in adult

Pathology
Decrease in calcified matrix
Increase in uncalcified matrix
“Looser’s zones” – pseudofractures from healing of multiple microstress fractures
Osteoporosis
A generalized disease of the bone, characterized by combination of decreased osteoblastic formation of
matrix and increased osteoclastic resorbtion, with a resultant decrease in total amount of bone in skeleton

Etiology

 Hormonal osteoporosis
 Disuse osteoporosis
 Post-menopausal & Senile osteoporosis

Pathology

 Bone becomes thin and sparse -> Fragile / brittle and more susceptible to fracture
 Pathological fracture predominantly in cancellous area of bone
 Neck of femur, Neck of humerus, Distal end of radius, Vertebral bodies

Clinical diagnosis

 Chronic & intermitten back pain (Micro fractures)

 Loss of standing & sitting height
 Reduced physical performance
 Dorsal kyphosis (Dowager’s hump)

Radiographic diagnosis

 Bone densitometry (DEXA)

Treatment

 Estrogen for post-menopausal osteoporosis

 Calcium
 Calcitonin
 Biphosphonate (Most effective: Alendronate)
 Vitamin D
 Exercise
 Back pain from microfractures -> Light, close fitting brace
Paget’s Disease (Osteitis Deformans)
Disseminated bone disorder characterized by slowly progressive enlargement & deformity of multiple bone
associated with acceleration of bone deposition and resorption

Incidence

 4% of >55 Y.O. people

Etiology

 Unknown
 Virus affecting osteoclast

Pathology

 Accelerated bone turnover with excessive osteoclast resorption & osteoblast deposition
 2 Phase: Osteolytic (Large but weak bones), followed by Osteosclerotic (Large, thick, and dense
bones)
 Most common sites: Tibia, Femur, Pelvis, Vertebral bodies, & Skull
 Progressive deformity results from enlargement and bending of bone

Diagnosis

 Mild form -> No symptom

 Severe -> Bone pain that is severe
 Lower limb become progressively bowed, Heads become larger, and shorter stature

Radiographic examination

 Enlargement, deformity and porosity of involved bones during osteolytic phase

 Increased irregular density of bone in osteosclerotic phase

Treatment

 Anti-resorptive agent:
 Biphosphonate & calcitonin -> Inactivate osteoclasts
Tendon Injury
Closed tendon injury

 Normal tendon rupture with stress activity

o e.g. mallet finger
 Treatment: Repair / replace the abnormal part of tendon

Open tendon injury

 Open division of tendon -> immediate surgical repair

 Adhesion between injured tendons can significantly interfere with hand function
 Profundus & superficialis tendon must be repaired even if in critical area (No man’s land)
o No man’s land: between distal palmar crease & proximal interphalang joint
 If not, proximal end should be advanced and secured to the distal phalanx with a “pull-out” wire
 Post-op management: Early controlled & supervised finger motion to prevent adhesions
Bone

 Long bones
 Short bones
 Flat bones
Compact / Cortical bone:

 Solid mass of bone, commonly seen as a superficial layer of bone, that provides strength
Spongiosa / Cancellous bone:

 A less dense trabeculated network of bone, spicules making up the substance of most bone and
surrounding inner marrow cavity

Bone cell:

 Osteoblast
o The type of differentiated messenchymal cell, that are essential for osteogenesis or
ossification. Since they alone can produce intercellular substance in which calcification can
later occur.
 Osteoclast
o Large, multinucleated cells that lie on uncovered bone surface and are capable of resorbing
or removing bone

Bone remodelling
Wolff’s Law
Bone in a healthy person will adapat to the loads under which it is placed
e.g. Marked cortical thickening on concave side of curved bone

Bone function

 Anatomical structure
o Rigid framework to withstand force
o Lever for locomotor function of skeletal muscle
o Protection for vulnerable viscera
 Physiological organ
o Contain hemopoetic tissue
o Reservoir of Ca, Phospor, Mg, Na

Orthopaedi

 In 1741, Nicolas Andry coined the word Orthopaedi

 The book is called “Orthopaedia – The Art of Preventing and Correcting Deformities in Children”
 Orthos – Correct / Straight
 Pais – Child
Bone Development
Bone comes from mesoderm
5th week – limb bud appears, in central axis mesenchymal cells condense into a short cylinder
6th week – Mesenchymal model differentiate into cartilage model
7th week – Osteoblast secrete collagen & proteoglycan into matrix, forming primary center of ossification
7th week – 6 months – Endochondral & Intramembranous ossification
Endochondral ossification -> Replacement of cartilage by bone
Intramembranous ossification -> Osteoblast lay down bone directly, no intermediate cartilaginous phase
6 months – Tubulation (Formation of medullary cavity)

Indication for Amputation (3D)

 Dead / Dying
o 90% caused by peripheral vascular disease
o Other cause of limb death: severe trauma, burns, frostbite
 Dangerous
o Malignant tumor, potentially lethal sepsis, crush injury
o In crush injury, releasing the compression may result in renal failure (Crush syndrome)
 Damned nuisance
o Retaining the limb may be worse than having no limb
o Reasons: Pain, Gross malformation, Recurrent sepsis, Severe loss of function
Damage Control Orthopaedics
An approach that contain & stabilize orthopaedic injuries so that the patient overall physiology can
improve

Purpose:

 To avoid worsening of the patient’s condition by the second hit of a major orthopaedic procedure
 To delay definitive fracture repair until a time when overall condition is optimized
Minimal invasive technique such as external fixation are used initially
Focus on:

 Hemorrhage control
 Management of soft tissue injury
 Achievement of provisional fracture stability
 While avoiding additional insults

Pathophysiology
First Hit MODS / ARDS

Reaction Second Hit

Resolution MODS / ARDS

First hit: Traumatic injuries leads to systemic inflammation

Second hit: Secondary inflammation insults that can reactivate the systemic inflammation & precipitate
late MODS
e.g. Sepsis & surgical procedures

Patient selection

 Stable patient -> Local preferred method for managing the orthopaedic injury
 Unstable & extreme – Damage control orthopaedics (DCO)
 Borderline -> probably best with DCO
o e.g. polytrauma + ISS >20 (Injury severity score) + Additional thoracic trauma

When to operate again:

 Day 2, 3, & 4 -> not safe because marked immune response and increased generalized edema
 Day 6-8 -> Less inflammatory response