Synopsis
Recognise necrotising soft-tissue infection before late skin signs, resuscitate toxin-mediated shock and secure immediate operative exploration, debridement and organism-directed therapy.
- Necrotising soft-tissue infection spreads along fascia, thromboses small vessels and destroys tissue faster than antibiotics can achieve source control.
- Early skin may look modest; severe escalating pain, oedema beyond erythema and systemic toxicity carry more weight than colour.
- Do not use a low LRINEC score, normal radiograph or absent gas to rule out disease.
Key red flags
Pain out of proportion to visible skin change is an early necrotising-infection warning.
Deep severe pain beyond the visible erythematous margin, particularly when rapidly worsening, is an important early feature before skin necrosis develops.
Investigation priorities
Determine whether clinical suspicion warrants operative exploration without diagnostic delay.
Management branches
Disproportionate pain, rapid progression, fascial signs or systemic toxicity creates meaningful suspicion.
- Use ABCDE, obtain large-bore access, measure lactate and glucose, send blood cultures and organ-function tests and begin physiology-guided crystalloid resuscitation.
- Contact senior surgery, anaesthesia, critical care and microbiology simultaneously and communicate why operative exploration cannot wait for diagnostic certainty.
Key medicines
Empirical piperacillin–tazobactam, clindamycin and vancomycinWhere the local severe soft-tissue pathway selects it, give piperacillin–tazobactam 4.5 g intravenously every six hours plus clindamycin 1.2 g every six hours and weight- and level-guided intravenous vancomycin.
Benzylpenicillin plus clindamycin for confirmed GASGive benzylpenicillin 2.4 g intravenously every four hours plus clindamycin 1.2 g intravenously every six hours after microbiology confirms susceptible group A Streptococcus.