Necrotising fasciitis Flashcards
What is necrotising fasciitis?
Necrotic infection of the deep fascia and subcutaneous fat. Toxin and enzyme release causes muscle necrosis by interrupting microcirculation with vascular thrombosis.
Early recognition and debridement along with appropriate antimicrobial therapy are essential as delayed care carries a high morbidity and mortality (20-40%).
What different types of necrotising fasciitis are you aware of?
Classification based on microbial aetiology.
Type 1: Polymicrobial
- often anaerobic sp. inc Clostridium
- 75% of cases
- risk factors include DM, HIV, IVDU, alcohol abuse, immnocompromise
Type 2: Group A Strep +/- Staph aureus
- 20-30% cases
- associated with toxic shock syndrome
- immunocompetent individuals
- mortality >32%
Type 3: Gram-negative monomicrobial (e.g. Vibrio)
- uncommon
- high mortality 30-40%
Type 4: Fungal (usually Candida)
- trauma and burns patients
- mortality highest >50%
How does necrotising fasciitis present?
- Pain out of proportion to the extent of external injury
- May have been a notable bite or skin/soft tissue injury.
- Skin changes include: erythema, bullae, ecchymoses, skin necrosis, crepitus
- In late or severe cases may present with: Toxic shock, sepsis, multiorgan failure.
How should necrotising fasciitis be investigated?
- History and examination - it is a clinical diagnosis and investigations should not delay emergency debridement.
- Blood tests: FBC, U&E, glucose, CRP, CK, calcium, coagulation
- Microbiology: blood cultures, tissue swabs/samples
- Histology
- Radiology: CT usually most practical, MRI most sensitive and specific
LRINEC - Laboratory risk indicator for NEC has a high PPV and NPV Parameters include: - glucose - WCC - CRP - Creatinine - Hb - Na
A score of 8 is strongly predictive.
How would you manage necrotising fasciitis?
- Resuscitation A-E approach
Specific features include - Surgical
i) not delaying early debridement
ii) return to theatre in 24 hrs for relook - Antimicrobials (with Med Micro input):
i) Empirical includes extended spectrum Beta lactam and clindamycin (Linezolid and clindamycin have synergistic effect - clindamycin has toxin suppression).
ii) Benzylpenicillin + clindamycin if gram positive
iii) Ceftriaxone or ciprofloxacin if mixed gram + and gram - - IVIG
- Hyperbaric oxygen therapy in clostridia infection
- Supportive care
How does IVIG work in streptococcal or staphylococcal necrotising soft tissue infection?
4 main ways:
- Induces antibodies against toxin
- Neutralises superantigens
- Inhibits membrane attack complex and complement activation
- Facilitates opsonisation of group A strep organisms.
What is toxic shock syndrome?
Toxic shock syndrome is caused by exotoxin release following staphylococcal or streptococcal infection.
It presents as the rapid onset of fever, diffuse macular rash, hypotension and multi organ dysfunction.
Shedding of skin/desquamation is seen 1-2 weeks after onset.
Staph TSS is caused by TSS toxin-1. Those who develop TSS from staph lack the Ab against TSS toxin-1.
Strep TSS is from invasive infection which releases super antigens (pyrogenic exotoxins) causing widespread inflammatory response. Was historically associated with retained tampons or RPOC.
Treatment is with broad spectrum Abx including clindamycin (inhibits exotoxin synthesis by inhibiting 50s subunit of the bacterial ribosome).
Staph infection should include vancomycin therapy.
What is PVL?
PVL is Panton-Valentin Leukocidin.
Cytotoxin which kills leucocytes.
Associated with S.aureus infection (MRSA and MSSA).
Most commonly presents with soft-tissue infections
Can cause necrotising pneumonia and cavitation and oral mucosal involvement.
What are the causes of cavitating lung lesions?
Infective causes:
- TB
- S.aureus (PVL producing)
- Klebsiella
- mycobacterium
- aspergillus
Non-infective causes:
- malignancy
- vasculitis
- Rheumatoid disease
- sarcoidosis
