Transcript Necrotizing Fasciitis

Necrotizing Fasciitis
Dolan Wenner, D.O.
Internal Medicine Lecture Series
1/31/07
Necrotizing Fasciitis
Definition – commonly referred to as
“flesh-eating bacteria,” it is a rare infection
of the deeper layers of the skin and
subcutaneous tissue (fascia)
Organisms
Most common associated organism is group A
beta-hemolytic streptococci
Other isolated organisms: Staph. aureus,
Clostridium perfringens, Staph. Epidermidis,
enterococci, Enterobacteriaceae species, E. coli,
Proteus mirabilis, Klebsiella pneumonia,
Pseudomonas aeruginosa,
Bacteroides/Prevotella species, anaerobic grampositive cocci
Pathophysiology
Organisms spread from the subcutaneous tissue
along the superficial and deep fascial planes 
facilitated by bacterial enzymes and toxins
M1 and M3 surface proteins – increase
adherence of streptococci to the tissues, also
protects bacteria against neutrophilic
phagocytosis
Streptococcal pyrogenic exotoxins (SPEs) A, B,
C and streptococcal superantigens (SSA) – lead
to the release of cytokines and produce clinical
signs such as hypotension
Pathophysiology
Deep infection can cause
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Vascular occlusion
Ischemia
Tissue necrosis
Nerve damage
Septicemia (systemic toxicity)
Necrotizing Fasciitis syndromes
Type I (polymicrobial)
Type II group A beta-steoptococcal
Type III gas gangrene (clostridial
myonecrosis)
NF – Type I
Polymicrobial
Typically occurs after surgery or trauma
Can be mistaken for simple wound cellulitis
May also be observed with urogenital or
anogenital infections
Aerobic and anearobic bacteria usually found in
combination  work synergistically
Variant of NF – saltwater NF, usually minor skin
would contaminated with saltwater that contains
Vibrio species
NF – Type II
So-called “flesh-eating bacterial infection”
Monomicrobial
Caused by group A beta-streptococcus
Varicella infection and use of non-steroidal
anti-inflammatory drugs may be
predisposing factors
NF – Type III
Gas gangrene (clostridial myonecrosis)
Usually caused by Clostridium perfringens
When this type occurs spontaneously,
Clostridium septicum most likely etiologic
agent  usually occur in association with
colon CA or leukemia
Skeletal muscle infection may be
associated with recent surgery or trauma
NF – History and Physical Exam
History
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Fever and chills
Erythema noted
Supralesional vesiculation or bullae formation
Serosanguinous fluid drainage
Recent history of skin biopsy, illicit drug use,
frostbite, chronic venous stasis ulcers, open
bone fractures, insect bites, surgical wounds,
and skin abcesses
History of Diabetes
NF – History and Physical Exam
Physical Exam
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Rapidly advancing erythema
Painless ulcers
Black necrotic eschar may be evident at the
borders of the affected areas
Vesiculation or bullae formation may be noted
Sepsis/shock
Gas may be evident (crepitus)
Pain out of proportion to exam
Cellulitis vs. NF
The following may suggest NF
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Rapid progression
Poor therapeutic response
Blistering necrosis
Cyanosis
Extreme local tenderness
High temperature
Tachycardia
Hypotension
Altered level of consciousness
Lab Studies
Elevated WBCs
Hyponatremia
Elevated BUN
Anemia
Hypocalcemia
Acidosis
Thrombocytopenia
Prolonged PT associated with higher mortality
rate
Imaging Studies
Standard radiographs – little value unless
free air is depicted, as with gas-forming
infections
CT – can show subcutaneous air
T2-weighted MRIs may show well-defined
regions of high signal intensity in the deep
tissues  sensitivity exceeds specificity
CT and MRI may be useful in directing
rapid surgical debridement
Other Tests
Excisional deep tissue biopsy is gold
standard
Gram staining (can help delineate
between Type I and Type II)
Cultures
Treatment
Transfer pt to ICU or Surgical ICU
Maintain hemodynamic parameters
Surgical Debridement
Combination antibiotic therapy
Single antibiotic therapy
Vancomycin
Hyperbaric oxygen (HBO)  may reduce
mortality rate, but no literature to support
IVIG  anecdotal evidence
Treatment
Surgical Debridement
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Incisions should be deep and extend beyond
the areas of necrosis until viable tissue is
reached
Wound should be well irrigated
Hemostasis should be maintained
Wound should be kept open
Debridement and evaluations should be
repeated on a daily basis
Treatment
Antimicrobial therapy
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Ampicillin (Principen, Omnipen)
Gentamicin (Garamycin, Jenamicin)
Clindamycin (Cleocin)
Metronidazole (Flagyl)
Imipenem and cilastatin (Primaxin)
Ampicillin and sulbactam (Unasyn)
Piperacillin-tazobactam (Zosyn)
Vancomycin
Amphotericin B
NF – Complications
Sepsis and renal failure
Metastatic plaques may occur
Septicemia leads to severe system toxicity
and rapid death unless treated quickly and
appropriately
NF - Prognosis
Poor prognosis linked to certain
streptococcal strains
Mortality rate can be as high as 25%
Cases of NF with renal failure and sepsis
have mortality rate as high as 70%
Early recognition and appropriate
treatment can help ensure better
prognosis
Thank you!
Question 1
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What is the most common organism
associated with necrotizing fasciitis
(“flesh-eating disease”)?
E. coli
Group A beta-hemolytic streptococci
Pseudomonas aeruginosa
Proteus mirabilis
Question 1
A.
B.
C.
D.
What is the most common organism
associated with necrotizing fasciitis
(“flesh-eating disease”)?
E. coli
Group A beta-hemolytic streptococci
Pseudomonas aeruginosa
Proteus mirabilis
Question 2
A.
B.
C.
D.
What test is considered the “gold
standard” for diagnosis of necrotizing
fasciitis?
MRI
CT scan
Excisional deep tissue biopsy
Cultures
Question 2
A.
B.
C.
D.
What test is considered the “gold
standard” for diagnosis of necrotizing
fasciitis?
MRI
CT scan
Excisional deep tissue biopsy
Cultures
Question 3
A.
B.
C.
D.
What is the organism that is most
commonly associated with Type III
necrotizing fasciitis?
Group A beta-hemolytic streptococci
Proteus mirabilis
Clostridium perfringens
Staphylococcus aureus
Question 3
A.
B.
C.
D.
What is the organism that is most
commonly associated with Type III
necrotizing fasciitis?
Group A beta-hemolytic streptococci
Proteus mirabilis
Clostridium perfringens
Staphylococcus aureus
The End