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2013/06/29
Infections of the upper limbs :
MMHs experience
Necrotizing fasciitis
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Introduction
A relatively infrequent infection of the subcutaneous tissue that destroys
fascia; it may lead to loss of limb or life
It progresses rapidly and can cause death within 24 hours.
NF was first described in 1848. In 1920, Meleney identified 20 patients in
China in whom hemolytic streptococcus was the sole organism. Wilson
coined the term necrotizing fasciitis in 1952 and found no specific
pathologic bacteria related to the disease.
Terms for NF have included flesh-eating bacteria syndrome, flesh eating
disease, suppurative fasciitis, hospital gangrene, and necrotizing erysipelas.
spread at a rate of up to 2.54 cm per hour (Engel 1994).
Necrotizing Fasciitis
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Introduction
At the time, pathogenesis was described due to the beta-
haemolytic streptococci (BHS) group A (Streptococcus
pyogenes), as a community-acquired infection and a
synergistic infection of aerobes and anaerobes mostly
acquired with gun shot injury or neoplasms of the
gastrointestinal tract.
A new organism, Vibrio vulnificus, is now recognized as
causing a distinctive clinical syndrome of rapidly
progressive necrotizing fasciitis, septicaemia and death
while several other vibrios have also been incriminated.
Classification of skin and skin-structure infections
Uncomplicated infections
superficial: impetigo, ecthyma,
deeper: erysipelas, cellulitis
hair follicle associated: folliculitis, furunculosis
abscess: carbuncle, other cutaneous abscesses
Complicated infections
secondary infections of diseased skin
acute wound infections
traumatic
bite-related
post-operative
chronic wound infections
diabetic foot infections
venous stasis ulcers
pressure sores
perianal cellulitis abscess
Necrotizing fasciitis
polymicrobial fasciitis (type I)
Fourniers gangrene
synergic necrotizing cellulitis with fasciitis and myonecrosis
streptococcal gangrene (type II)
fasciitis due to V. vulnificus and other Vibrio species
Myonecrosis
crepitant myonecrosis
clostridial myonecrosis
traumatic gas gangrene
atraumatic gas gangrene
synergic necrotizing cellulitis with fasciitis and myonecrosis
non-crepitant myonecrosis
streptococcal gangrene with myonecrosis
A. hydrophila myonecrosis
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Streptococcus pyogenes
Gram positive cocci
Occurs in pairs or chains
facultative anaerobic Group A
streptococci (GAS)
hemolytic on blood agar
fermentative metabolism (does not
require air), but is aerotolerant.
grows optimally in anoxic conditions
(e.g. deep tissues)
very common pathogen of humans (5-
15% asymptomatic carriage)
Necrotizing fasciitis may present as a sequelae of pharyngitis or
varicella or as a complication of surgical or endoscopic procedures,
including caesarian section, vaginal delivery with episiotomy,
percutaneous endoscopic gastrostomy, laparoscopy, dental extraction,
or liposuction.
In a series of 39 pediatric cases, the most common initiating factor in 13
of them was varicella (chicken pox).
More commonly, the onset of necrotizing fasciitis can be related to
trauma such as insect bites.
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WHO IS AT RISK?
more frequently in patients who are suffering from debilitating
conditions
Immunocompromised patients, including those with human
immunodeficiency virus (HIV), or organ transplant.
those with intravenous drug or alcohol problems, and those with
systemic illnesses such as diabetes mellitus, peripheral vascular disease,
malignancy, obesity or atherosclerosis
Postoperative patients and patients with burns or traumatic wounds also
have an elevated risk.
In children, its a rare complication of varicella (chickenpox).
However, previously healthy persons can also develop the disease.
Symptoms and Signs
affected skin is painful, red, hot and swollen
progresses to violet discoloration, blisters may form
necrosis of subcutaneous tissues (flesh eating)
fever and systemic toxicity
low blood pressure
rapid heart beat
progression is rapid (hours) and often fatal
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Pathophysiology
Organisms spread from the subcutaneous tissue along the
superficial and deep fascial planes, presumably facilitated by
bacterial enzymes and toxins. This deep infection causes
vascular occlusion, ischemia, and tissue necrosis. Superficial
nerves are damaged, producing the characteristic localized
anesthesia. Septicemia ensues with systemic toxicity.
Important bacterial factors include surface protein expression
and toxin production. M-1 and M-3 surface proteins, which
increase the adherence of the streptococci to the tissues, also
protect the bacteria against phagocytosis by neutrophils.
Streptococcal pyrogenic exotoxins (SPEs) A, B, and C are
directly toxic and tend to be produced by strains causing NF.
These pyrogenic exotoxins, together with streptococcal
superantigen (SSA), lead to the release of cytokines and
produce clinical signs such as hypotension. The poor
prognosis in NF has been linked to infection with certain
streptococcal strains.
Diagnostic tests
early diagnosis and recognition of what one is dealing with
(Sawin et al. 1994, Jayatunga et al. 1993, Ward &Walsh 1991)
NF is a limb- and life-threatening soft tissue infection that may
at first appear to be benign, low grade cellulitis (Wang & Shih
1992).
Other potential flags which could alert a clinician are pain
disproportionate to the signs (Ward & Walsh 1991 p. 488), as
well as erythema, oedema (Wang & Shih 1992), a purple blue
spot progressing to grayish green slough and a deep blue and
purple, almost black areola which spreads rapidly (Hamelink
radiotherapy, obesity, hypertension with atheroscleroses, 1983
p. 656).
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Computerised tomography and MRI have been used to assist
in clinical diagnoses.
In a study of 20 patients with necrotizing fasciitis to
investigate the use of computerised tomography, asymmetric
fascial thickening and fat stranding were seen in 16 cases, gas
tracking along fascial planes in 11 cases and abscesses were
found in seven. Computerised tomography appeared to be
useful as an adjunctive diagnostic tool. MRI has been used to
define the extent of the fasciitis. It has identified soft tissue
edema infiltrating the fascial planes of the entire chest wall
prior to local gangrenous cutaneous signs of infection by many
hours, allowing rapid surgical incisional drainage with success.
Confusion can occur with MRI, however, between cellulitis
and necrotizing fasciitis [9]. Because the sensitivity of MRI
exceeds its specificity, MRI can over-estimate the extent of
deep fascial involvement. A negative result with no deep
fascial involvement is useful to exclude necrotizing fasciitis or
to determine the depth of soft-tissue involvement.
Microbiologic diagnosis
Blister fluid, discharge from open lesions, frank pus and any
skin sepsis should be sampled for microscopy with Gram stain
and cultured for BHS, aerobic and anaerobic bacteria.
Blood cultures should also be collected.
Samples of tissue removed at debridement should be ground
up with antibiotic inhibitors and incubated in a fluid
enrichment medium.
New techniques include rapid streptococcal diagnostic kits and
a polymerase chain reaction (PCR) involving SPE genes (eg,
SPE-B)
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Type I
Synergistic gangrene or polymicrobial infection
most common form of NF
Type I occurs most often in older patients with
preexisting medical conditions such as diabetes.
caused by mixed flora, typically anaerobes and facultative
aerobic, such as group A streptococcus, Bacteroides
fragilis, Staphylococcus aureus, species of Clostridium,
Pseudomonas aeruginosa, Enterobacteriaceae, and others.
Its seen in postoperative patients and patients with
diabetes or other immunosuppressive conditions.
Type II
occur in any age group, and, as in the case of our patient, those
individuals may not have any pre-existing medical conditions
Pure group A Streptococcus infection or group A Strep and
Staph aureus
caused by group A streptococcus or, rarely, by group B
streptococcus.
Its seen in any age group, commonly after minor trauma,
include blunt trauma, postoperative complications, animal or
insect bites, and subcutaneous insulin injections, although it
may develop even in the absence of any underlying medical
condition.
Some cases suggest that hematogenous spread from a distant
site of infection, such as a sore throat, may occur.
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IDENTIFYING NECROTIZING
FASCIITIS
The presenting symptomatology is characterized by three
stages: early, advanced, and critical.
Early stage
Francis et al. (1993) stated that the necrosis of the fascia
with the subsequent interference and thrombosis of
dermal vasculature is the natural course of events.
manual exploration of the surrounding tissue to see if the
fascia could be separated from surrounding tissue.
This loosening of tissue is indicative that necrosis has
spread beyond what had been debrided so that further
debridement would be indicated at that point.
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Advanced stage
As the disease progresses to the advanced stage over two
to four days, the skin becomes tense, swollen, shiny, and
purplish, and develops hemorrhagic fluid-filled blisters.
The skin takes on a tissue paperlike appearance with
overlying skin anesthesia (a clue that this is not simple
cellulitis), because of the destruction of cutaneous nerves.
Subcutaneous emphysema or crepitation can be palpated,
if gas-forming bacteria are involved.
HEMORRHAGIC BLISTER
ASSOCIATED WITH BULLOUS
HEMORRHAGIC CELLULITIS
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Clear or hemorrhagic bullae may
develop, but the serous or hemorrhagic
fluid turns into gray foul-smelling fluid
termed
dishwater pus
Critical stage
With progression to the critical stage, at four to five days,
the purple and blue areas become gangrenous. Necrosis
with skin sloughing is plainly visible. If left untreated,
death may ensue within hours.
Septic shock, manifested by hypotension, delirium,
hepatic dysfunction, and acute renal failure, may develop
as early as 24 hours after the onset of the process from the
release of bacterial toxins.
Even with aggressive management, septic shock,
neurologic deterioration, and eventual death occur at an
alarmingly high rate.
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Conventional Treatment of
Necrotizing Fasciitis
Prompt presumptive diagnosis based on clinical findings
Early initiation of broad-spectrum antibiotics directed at polymicrobial
flora
Early surgical exploration and aggressive debridement, usually
followed by serial debridements
Critical Care Support: hemodynamic and ventilatory support, adequate
analgesia and sedation, adequate nutrition, peptic ulcer and deep
venous thrombosis prophylaxis
Intravenous immune globulin
Hyperbaricoxygen therapy
Clinical indicators for surgical intervention in necrotizing
fasciitis
Indicator
Failure of improvement
Profound toxic effects occurring at the
onset of infection
Extensive necrosis
Compartment syndrome suspected
Remarks
After 24~48 hours of parenteral
antibiotics for presumed cellulitis, no
decrease in signs and symptoms is
detected
Profound toxic effects include significant
malaise, weakness, generalized
aching, loss of appetite, and loss of
concentration.
Necrosis or gas is noted in the wound
or is evident on radiographs
Compartment syndrome may occur
when edema within the muscle
group surrounded by fascia
compressed blood vessels and can
result in an ischemic injury.
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Brief History
This is a 56-year-old female patient.
Past history: DM, HTN, mental retardation.
Chief complain:
Left hand swelling, tenderness about one week ago.
No trauma history was told.
Clinical Course
4/16 Stay in other hospital for antibiotics
treatment.
4/18 Transfer to our ER, lab data: WBC
20k. Left hand sever swelling,
tenderness and ulceration with
gangrene change on left thumb
were noted. Emergent operation
for fasciotomy and debridement
were performed.
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Operation finding:
Incision of left thumb and palm with much of abscess.
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4/18 Post-op: antibiotics use (Fortum
+ Minocin), wound care and pain
control. WBC 19k, CRP 24.4.
4/20 Because of persisted fever,
Prostaphyllin was
prescribed.
4/21 Wound culture: B-hemolysis
streptococcus group B,
sensitive to Vancomycin and
Cleocin.
4/23 Debridement, amputation left
thumb and drain insertion were
performed.
4/26 WBC 13.8k, CRP 3.88.
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4/27 Debridement was performed. Tendon
exposure was noted.
5/03 WBC 9.4k, CRP 0.73.
5/04 Reverse radial forearm flap and STSG
were performed.
5/07 Change to oral form antibiotics (Keflex).
5/13 MBD and OPD follow up.
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2012/12/30
2013/1/1 Visit our ER, lab data:
WBC 11000, admission
antibiotics : cepharosporin, I
and D at bedside
2013/1/2 Left hand severe
swelling, tenderness and pus
noted. Emergent operation
for fasciotomy and debridement
2013/1/6 Wound culture:
B-hemolytic streptococcus
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2013/1/2 Left hand severe
swelling, tenderness and
pus noted.
Emergent operation
for fasciotomy and
debridement
2013/1/9
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Necrotizing fasciitis due to Vibrio
species
Vibrionaceae() comprise three genera() :
Vibrio (), Aeromonas ()and
Plesiomonas().
These comma-shaped Gram negative rods are all
aquatic organisms associated with shell fish.
All Vibrio species., except V. vulnificus, usually
cause intense diarrhea.

(Vibrio parahemolyticus)(
)
(Vibrio vulnificus)
Vibriovulnificus
1976
primary septicemia

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Necrotizing fasciitis due to Vibrio
vulnificus
Antibiotics should be commenced in high dosage
but are additional to surgical intervention. A
combination of ceftazidime (or cefotaxime) with
ciprofloxacin (or another quinolone) or
tetracycline (or doxycycline) should be given in
maximum dosage.
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Case 1 Case 1
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Typical findings in necrotizing fasciitis include gray
discoloration of the fascia and lack of resistance to
dissection with a blunt instrument along fascial planes.
1st day
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17th day
20th day
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2003/1/13 2003/3/20
Case 2
2004/6/2
Case 4
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2004/6/3
2004/6/4
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2004/6/5
2004/6/7
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2004/6/10
2004/6/13
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2004/6/19
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2004/7/31
Case 5
2005/1/5
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Conclusion
Necrotizing fasciitis remains an important cause of
morbidity and mortality.
In colder temperate climates, community-acquired
infection is usually due to the beta-hemolytic
streptococci, especially S. pyogenes, while in summer
months of hot climates there is an increasing
recognition of this infection due to Vibrio spp.
Both types are characterized by previous minor
trauma but a salt water source is also involved with
infection by Vibrio spp.
The infection is more common in
immunocompromised, diabetics or patients over 40
years old, especially those with some type of
underlying disease such as cirrhosis.
Management is similar for both types of infection,
requiring acute surgical debridement, intravenous
antibiotics, fluid replacement and intensive care.
Mortality can vary from 5% to 50% depending on the
length of incubation of the infection prior to
presentation, its recognition by the clinical team and
appropriate aggressive therapy
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Paronychia
Paronychia is an infection beneath the eponychial
fold.
Risk factors for development include:
Manicures
Fingernail biting
Hangnails
J Hand Surg 2011;36A:14031412.
Acute Paronychia
Rapid onset of erythema, edema, and discomfort or
tenderness of the proximal and lateral nail folds
Accumulation of purulent material under the lateral
nail fold.
Am Fam Physician. 2008;77(3):339-346
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Surgical Treatment
Surgical intervention for paronychia is generally
recommended when an abscess is present.
Simple technique to drain a paronychial abscess
involves lifting the nail fold with the tip of a 21- or
23-gauge needle.
Techniques in Hand and Upper Extremity Surgery 9(2):120121, 2005
Chronic Paronychia
SCC
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Chronic Paronychia
Treatment of chronic paronychia includes avoiding
exposure to contact irritants and appropriate
management of underlying inflammation or
infection.
Treatment: Topical antifungal agent or Topical
steroids
Patient profile
Name: x
Chart number: 19270226
Gender: male
Age: 61 years old
Admission date: 2011/11/30
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Past History
Coronary artery disease, TVD s/p CABG
Mitral valve s/p mitral valvuloplasty
Complete AV block with symptomatic
bradycardia s/p permanent pacemaker
Type 2 diabetes mellitus
End stage renal disease under CAPD
Hypertension
PAOD of lower extremities
Present illness
Paronychia visited other clinics, partial nail removal
was done
An unhealing wound on his right middle finger since
1.5 months ago.
Pain (+) and tenderness (+)
Gangrenous change with pus formation of the nail
fold skin
Wound debridement on 2011/10/5
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Present illness
After discharge, ischemia change and pain on right
middle finger persisted
CTA revealed severe PAOD over right radial artery
CTA (11/20)
Multifocal stenosis of
radial arteries. Severe
atherosclerosis.
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CXR (11/30)
Operation (12/01)
ProcedureBypass surgery of right hand
Operative Findings:
Radial artery distal part still pulsated bleeding after
incision
Large size cephalic vein was harvested
Bypass from brachial artery to distal radial artery
Post-OP pulsation(+), doppler checking (+)
Cephalic vein graft
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Operation figure
Cephalic vein
(18cm in length),
graft reversed for
antegrade blood
flow.
End to side
anastomosis,
diameter: 8 mm.
Post-op 1 week
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Local debridement (12/11)
Post-op 2 weeks
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Follow-up
3 months later
Patent of vein graft,
but native radial
artery obliteration.
Wound healing, rest
pain decrease
11/20/2011 2/18/2012
Introduction
Peripheral arterial occlusion disease (PAOD) of
upper extremity requiring surgical revascularization
is an uncommon condition.
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Introduction
Symptomatic upper extremity arterial occlusive
disease is uncommon because of the abundant
collateral network and the infrequency of
atherosclerosis in the upper extremity. Patients who
present with upper extremity ischemia range from
young adults with nonatherosclerotic causes to
elderly patients with atherosclerosis.
Etiology of hand PAOD
Acute ischemia
Thromboembolism (cardiac origin 72.2%)
Traumatic & iatrogenic vascular injury
Chronic ischemia
Atherosclerotic vascular disease
Previously untreated trauma
Thoracic outlet obstruction
Subclavian steal syndrome
Connective tissue disorders
Vasculitis
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Symptoms of PAOD
Exercise intolerance
Rest pain
Tissue loss (Gangrene)
Revascularization
Upper extremity arterial reconstruction
First reported by Garrett et al in 1965
Thromboembolectomy
Bypass surgery
As a result of the relative rarity of these procedures, however, no
single large series exists.
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Feb-8-2012
2012/11/1 2012/11/3
64y/o, F
Type 2 diabetes mellitus
End stage renal disease under
H/D for 6 years
Hypertension
A-V shunt op , bil upper limbs
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2012/11/5 2012/11/8
2012/11/27 2012/12/8
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2012/12/10 2012/12/19
2013/6/27
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Conclusion
Hand infections are diverse, and vary in etiology
Hand infections have potential for serious morbidity
Early identigfication and aggressive operative and
medical therapy should be combined
Thanks for your attention!