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Jan 2025
9m 12s

Episode 204: Necrotizing Fasciitis

CORE EM
About this episode

We discuss the recognition and treatment of necrotizing fasciitis.

Hosts:
Aurnee Rahman, MD
Brian Gilberti, MD

Download Leave a Comment Tags: Critical Care, General Surgery

Show Notes

Table of Contents

0:00 – Introduction

0:41 – Overview

1:10 – Types of Necrotizing Fasciitis

2:21 – Pathophysiology & Risk Factors

3:16 – Clinical Presentation

4:06 – Diagnosis

5:37 – Treatment

7:09 – Prognosis and Recovery

7:37 – Take Home points


Introduction

  • Necrotizing soft tissue infections can be easily missed in routine cases of soft tissue infection.
  • High mortality and morbidity underscore the need for vigilance.

Definition

  • A rapidly progressive, life-threatening infection of the deep soft tissues.
  • Involves fascia and subcutaneous fat, causing fulminant tissue destruction.
  • High mortality often due to delayed recognition and treatment.

Types of Necrotizing Fasciitis

  • Type I (Polymicrobial)
    • Involves aerobic and anaerobic organisms (e.g., Bacteroides, Clostridium, Peptostreptococcus).
    • Common in immunocompromised patients or those with comorbidities (e.g., diabetes, peripheral vascular disease).
  • Type II (Monomicrobial)
    • Often caused by Group A Streptococcus (Strep pyogenes) or Staphylococcus aureus.
    • Can occur in otherwise healthy individuals.
    • Vibrio vulnificus (associated with water exposure) is another example.
  • Fournier’s Gangrene (Subset)
    • Specific to perineal, genital, and perianal regions.
    • Common in diabetic patients.
    • Higher mortality, especially in females.

Pathophysiology

  • Spread Along Fascia
    • Poor blood supply in fascial planes allows infection to advance rapidly.
    • Tissue ischemia worsened by vascular thrombosis → rapid necrosis.
  • High-Risk Patients
    • Diabetes with vascular compromise.
    • Recent surgeries or trauma (introducing bacteria into deep tissue).
    • Immunosuppression (e.g., cirrhosis, malignancy, or immunosuppressive meds).
    • NSAID use may mask symptoms, delaying diagnosis.

Clinical Presentation

Early Signs & Symptoms

  • Severe Pain out of proportion to exam findings.
  • Erythema (often with indistinct borders).
  • Fever, Malaise (systemic signs of infection).
  • Rapid progression with possible color changes (red → purple).
  • Bullae Formation (fluid-filled blisters) and skin necrosis/gangrene.
  • Crepitus in polymicrobial cases (gas production in tissue).

Late-Stage Signs

  • Systemic toxicity: hypotension, multi-organ failure if untreated.

Diagnosis

  • Clinical Suspicion Is Key
    • Pain out of proportion, rapid progression, systemic signs.
    • The “finger test” (small incision to explore fascial planes).
  • Surgical Consultation
    • Early surgical exploration is often the definitive diagnostic step.
  • Lab Tests
    • LRINEC Score (CRP, WBC, Hemoglobin, Sodium, Creatinine, Glucose) to stratify risk.
    • Not definitive but can guide suspicion.
  • Imaging
    • CT scan may reveal gas in tissues, fascial edema, or muscle involvement.
    • Must not delay surgical intervention if clinical suspicion is high.

Treatment Principles

  • Immediate & Aggressive Surgical Debridement
    • Often multiple surgical procedures are required as necrosis progresses.
    • Debridement back to healthy tissue margins.
  • Empiric Broad-Spectrum Antibiotics
    • Cover gram-positive (including MRSA), gram-negative, and anaerobes.
    • Examples include:
      • Vancomycin or Linezolid (for MRSA).
      • Piperacillin-tazobactam or Carbapenems (for gram-negative & anaerobes).
      • Clindamycin (to inhibit bacterial toxin production).
    • Adjust based on culture results later.
  • Adjunct Therapies
    • Hyperbaric Oxygen Therapy (if available) for resistant cases.
    • Evidence is mixed; not universally accessible.
  • Supportive Care
    • Intensive monitoring, often in an ICU setting.
    • Fluid resuscitation & vasopressors for septic shock.

Prognosis & Disposition

  • High Mortality Rate
    • Influenced by infection site, patient’s baseline health, and speed of intervention.
  • Importance of Rapid Intervention
    • Early recognition, aggressive surgery, and antibiotics improve survival.
  • Long-Term Considerations
    • Patients may require extensive rehabilitation.
    • Reconstructive surgery often needed for tissue deficits.
  • Disposition
    • Operative management is mandatory; patients do not go home.
    • Critical care admission is typical for hemodynamic monitoring and support.

Five Key Take-Home Points

  • High Suspicion Saves Lives: Recognize severe pain out of proportion as a critical red flag.
  • Know Your NF Types & Risk Factors: Type I polymicrobial vs. Type II monomicrobial, plus subsets (Fournier’s).
  • Clinical Diagnosis Above All: LRINEC and imaging help, but timely surgical exploration is paramount.
  • Combined Surgical & Medical Therapy: Early debridement + broad-spectrum antibiotics (including toxin inhibition) is lifesaving.
  • Extended Recovery & Mortality Risks: High mortality if missed or delayed. Expect prolonged rehab and possible multiple surgeries.

Resources & Further Reading


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