Necrotizing Fasciitis The Flesh Eating Bacteria

Vic V Vernenkar, D.O. General Vascular Surgery St. Barnabas Hospital Bronx, N.Y.

Background
An insidiously advancing soft tissue infection. Widespread fascial necrosis. Polymicrobial Most closely linked group A betahemolytic. Most cases caused by other bacteria.

Syndromes
Type I is polymicrobial Type II is group A strep Type III is gas gangrene or clostridial necrosis. A variant of type I is salt water NF caused by vibrio species.

Pathophysiology
Organisms spread from sub Q tissues along superficial and deep planes, facilitated by bacterial enzymes and toxins. Infection causes vascular occlusion, ischemia, necrosis. Superficial nerves damaged, producing anesthesia. Septicemia ensues

Pathophysiology
M1 and M3 surface proteins increase adherence of the bacteria to the tissues, protect from phagocytosis. Streptococcal pyrogenic exotoxins release cytokines and produce hypotension.

Morbidity and Mortality

Mortality rate as high as 25%. Cases with sepsis and renal failure have a mortality rate as high as 70%.

Age and History

Approximately 50% of cases of streptococcal NF occur in young and previously healthy patients. Begins with fevers and chills. 2-3 days later erythema, vesicles, bullae. Serosanguinous fluid drains from area. Can occur at surgical sites, IV sites, ulcers, bites, many times no previous wound.

Types
Type I usually occurs after trauma or surgery. May be mistaken for simple wound cellulitis, but severe pain and systemic toxicity is a clue to underlying necrosis. Also observed in urogenital or anogenital infections.

Types
Type II is the so-called flesh eating bacterial infection caused by group A strep. Type III, or clostridial necrosis is gas gangrene. This skeletal muscle infection may be associated with trauma or recent surgery.

Physical
General findings include: Rapidly advancing erythema, painless ulcers along fascial planes, black necrotic eschar. Septicemia is typical and leads to severe systemic toxicity, rapid death. Crepitus may be evident in diabetics.

Physical
In type II the widespread underlying tissue necrosis can be demonstrated by passing a probe through the tissue. Gas not usual In type I, bacteria work synergistically to cause what appears to be a simple cellulitis Gas may be evident Observed in perineum.

Features Suggesting It
Rapid progression Poor therapeutic response Blistering necrosis Cyanosis Extreme tenderness High temperatures, tachycardia, hypotension, altered mental status.

Causes
Group A beta-hemolytic strep not only cause. Haemophilus, and Staph also associated. Diabetes predisposes a patient to NF. Immunosupression predisposes a patient to NF. Still, 50% occur in young healthy people.

Causes
Type III NF caused by clostridium perfringes. Can occur in association with colon cancer and leukemia. In type II, varicella infection and the use of NSAIDs may be predisposing.

Laboratory
Cannot be relied upon. May facilitate diagnosis, but clinical is more important. WBC>14000, BUN> 15, Na < 135.

Radiology
Standard x-rays of little use. CT more sensitive. MRI and CT can delineate and determine extent of surgical resection.

Medical Therapy
Treat without delay Team approach ICU admission Monitor hemodynamics Antibiotics- combination or single Hyperbaric oxygen

Antibiotics
Combination: cover G- and G+ and anaerobes. Ampicillin, gentamycin, flagyl. Single coverage: Imipenem covers aerobes, pseudomonas. Vancomycin for methicillin resistant staph.

Surgical Care
Immediate debridement Do it over and over. Amputation may be required if limb affected. Incisions should be deep and extend to healthy tissue. Excise necrotic areas, irrigate. Dressing changes in OR

Complications
Sepsis and renal failure Metastatic cutaneous plaques Systemic toxicity and death Loss of limb, deformities, psychosocial issues Medical/legal issues.

Examples