Episode 204: Necrotizing Fasciitis


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Jan 01 2025 9 mins   78




We discuss the recognition and treatment of necrotizing fasciitis.


Hosts:

Aurnee Rahman, MD

Brian Gilberti, MD






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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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