Pathophysiology of Necrotizing Fasciitis
Necrotizing fasciitis begins when bacteria invade the subcutaneous tissues through a breach in the skin, triggering an inflammatory cascade that causes obliterative endarteritis with thrombosis of surrounding vessels, leading to critical reduction in blood flow and subsequent tissue necrosis that spreads rapidly along fascial planes. 1
Initial Bacterial Invasion and Entry Points
The pathophysiologic process starts with localized infection allowing entrance of normally commensal bacteria into the subcutaneous tissues. 1 In 80% of cases, the infection extends from a skin lesion—often trivial injuries such as minor abrasions, insect bites, injection sites, or boils. 2 The remaining 20% of patients have no visible skin lesion, suggesting hematogenous spread from distant infection sites. 3
The infection specifically targets the superficial fascia, which comprises all tissue between the skin and underlying muscles (the subcutaneous tissue), not the muscular fascia or aponeurosis as the name might suggest. 2
Microbial Patterns and Tissue Destruction Mechanisms
Two distinct pathophysiologic patterns exist based on bacterial etiology:
Type I (Polymicrobial)
- Involves mixed aerobic and anaerobic organisms, with an average of 5 pathogens per wound and up to 15 different organisms cultured. 2, 1
- Most organisms originate from bowel flora (coliforms and anaerobic bacteria). 2
- Associated with four clinical settings: bowel surgery/penetrating abdominal trauma, decubitus or perianal abscess, injection drug use sites, and spread from Bartholin or vulvovaginal infections. 2
Type II (Monomicrobial)
- Predominantly caused by Streptococcus pyogenes (Group A Streptococcus), which produces potent exotoxins. 1
- Other causative organisms include S. aureus, V. vulnificus, A. hydrophila, and anaerobic streptococci. 2
- Cases arising after varicella or trivial injuries are almost always due to S. pyogenes, with mortality approaching 50-70% when accompanied by hypotension and organ failure. 2, 1
Vascular Compromise and Tissue Necrosis
The critical pathophysiologic mechanism is obliterative endarteritis with thrombosis of surrounding vessels, resulting in critical reduction in blood flow to affected tissues. 1 This vascular compromise explains several key features:
- The infection spreads along fascial planes well beyond superficial signs like erythema. 2
- Tissue damage occurs from release of endogenous cytokines and bacterial toxins. 3
- The characteristic "wooden-hard" feel of subcutaneous tissues results from edema and necrosis extending beyond visible skin involvement. 2
- Skin anesthesia develops frequently due to thrombosis of cutaneous nerves and vessels. 2
Systemic Toxicity Mechanisms
Tissue damage and systemic toxicity result from the release of endogenous cytokines and bacterial toxins. 3 This produces:
- High fever and systemic toxicity 2
- Altered mental status and lethargy 2
- Progression to hypotension and multi-organ failure in severe cases, with mortality rates of 50-70% 1, 4
- Overwhelming sepsis syndrome and multiple organ system failure as the ultimate cause of death 3
Anatomic Spread Pattern
The infection tracks along fascial planes, creating a broad erythematous tract in the skin along the route of infection as it advances. 2 Approximately two-thirds of cases involve the lower extremities. 2, 4 The fascial planes can be readily dissected with a blunt instrument well beyond wound margins, demonstrating the extent of tissue destruction. 2
Host Factors Amplifying Pathophysiology
Diabetes mellitus is present in 70.8% of cases and represents the single most important risk factor, likely due to impaired wound healing and microvascular disease. 1 Other conditions that impair cellular immunity and amplify the pathophysiologic process include alcoholism, HIV/AIDS, leukemia, other malignancies, arteriosclerotic vascular disease, and venous insufficiency with edema. 2, 1