01OverviewDefinition, clinical context and the essential points that orientate the chapter.
Diagnosis begins with tempo. Ask when pain started, how quickly the boundary changed, recent trauma, injection, operation, bite, water or soil exposure, ulcers and previous antibiotics. Establish diabetes, immunosuppression, renal or liver disease, vascular disease and anticoagulation, but do not require a risk factor. Examine beyond the coloured area, comparing temperature, induration, tenderness and sensation. Mark and time the skin boundary only if doing so does not create false reassurance or delay theatre.
Early skin may show only erythema or swelling. Disproportionate deep pain, tenderness beyond visible change and a wooden fascial feel are more concerning than crepitus, bullae, dusky necrosis and anaesthesia, which often appear later. Examine perfusion, compartments, joints and the entire limb and girdle because infection can cross regions. Fournier disease needs perineal and abdominal source assessment; cervical disease needs airway planning. A painless area can mean nerve and tissue death rather than recovery.
Treat physiology and source in parallel. Apply the current adult sepsis pathway, obtain blood cultures when this does not delay antibiotics and give oxygen for a clinical indication. Use balanced isotonic crystalloid in measured two-hundred-and-fifty-millilitre boluses over ten to fifteen minutes with reassessment, generally not exceeding one litre before senior critical-care review. Start broad-spectrum intravenous therapy under the local necrotising-infection protocol and immediate microbiology advice, accounting for allergy, renal function, water or soil exposure and prior colonisation.
Imaging is subordinate to surgery. Plain films or CT may show gas, fascial fluid or an underlying foreign body, and ultrasound can locate an abscess, but absence of gas is common and no scan excludes early necrosis. Use cross-sectional imaging only when diagnosis is genuinely uncertain, the patient is stable and it will not defer exploration. The same principle applies to transfer: bring the required surgeons to the patient or operate for source control when transfer would create unsafe delay.
Index debridement confirms, maps and excises disease. Incise generously along the affected plane and inspect skin, fat, fascia, named vessels and nerves and all muscle groups. Non-adherent fascia, thrombosed vessels, fixed staining, haemorrhagic bullae, thin fluid and non-contractile muscle support the diagnosis, but absence of one classic sign does not clear tissue. BOASt describes zone 1 as obvious necrosis, zone 2 as likely infection and zone 3 as normal; remove zones 1 and 2 with a three-centimetre zone-3 cuff.
Sampling must preserve microbiological value. Take about five deep specimens across different zones with a new sterile instrument and no-touch technique for each. Label the anatomical site and mark the normal-zone sample separately, alert the laboratory and request microscopy and culture. Blood cultures supplement rather than replace tissue. Histology can assist at a viable margin but should never delay sufficient excision. Avoid relying on a superficial swab, which samples colonisation and not the advancing fascia.
Leave the wound open and document with diagrams or governance-compliant photographs. The treating team reviews the patient within six hours of diagnosis or surgery. Worsening shock, pain, skin change or laboratory trajectory means incomplete source control until proven otherwise and demands repeat exploration. Planned re-look often finds evolving viability even when physiology improves. Plastic and reconstructive surgeons plan negative-pressure therapy, grafts or flaps only after all infected tissue is removed.
Amputation can be life-saving but is not a single-operator decision. At least two consultants from relevant specialties document why excision cannot control disease while preserving a viable limb. Continue analgesia, organ support, nutrition, glucose control and thrombosis prevention around repeat operations. Later care addresses scar and contracture, prosthetics if needed, neuropathic and phantom pain, psychological trauma, return to function and public-health advice when invasive group A streptococcal disease affects close contacts.
Key points
- Necrotising infection is a clinical and operative diagnosis. Pain beyond erythema, rapid change, systemic toxicity and high-risk host features outweigh a low score or reassuring early skin.
- Do not use LRINEC to rule disease out; normal sodium, white count or CRP early in the course cannot make a dangerous examination safe.
- Start sepsis resuscitation and broad-spectrum intravenous antibiotics without delay, but never let ICU stabilisation, CT or inter-hospital transfer postpone immediate surgical exploration.
- The index operation systematically examines skin, subcutaneous fat, fascia, neurovascular structures and every relevant muscle group and documents the anatomical extent.
- Excise obvious and likely infected zones plus a three-centimetre cuff of normal zone-3 skin and fascia under the current BOASt advisory technique; absence of dishwater fluid does not exclude infection.
- Take ideally five deep microbiology samples from all zones using separate instruments and no-touch technique, label healthy-zone samples separately and alert the laboratory that necrotising infection is suspected.
- Do not primarily close the wound at the first operation. Review the patient and operative result within six hours and return sooner whenever physiology or local findings fail to improve.
- A decision to amputate requires at least two consultants from different relevant specialties; reconstructive, rehabilitation and psychological planning begins while serial source control continues.
02AetiologyUnderlying causes, associations and risk factors, with why each one matters.
Polymicrobial infection
Mixed aerobic and anaerobic organisms exploit devitalised tissue, diabetes, vascular disease or abdominal and perineal sources and commonly produce gas and extensive fascial spread.
Monomicrobial streptococcal disease
Group A streptococcus can enter through trivial or unseen trauma and cause rapidly progressive fasciitis, toxic shock and severe pain in a previously healthy person.
Clostridial myonecrosis
Traumatic contamination or spontaneous clostridial infection destroys muscle, generates gas and causes profound haemolysis, shock and systemic toxicity.
Water and unusual exposure
Marine, freshwater, animal, injection and healthcare-associated exposures alter likely organisms and empiric coverage and should be relayed to microbiology immediately.
03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.
- 1Fascial plane spread
Organisms and enzymes track rapidly along poorly vascularised fascia beyond visible erythema, making surface appearance underestimate the operative field.
- 2Microvascular thrombosis
Inflammation and toxins occlude small vessels, causing ischaemia, anaesthesia and antibiotic-inaccessible necrosis that can only be controlled by excision.
- 3Toxin-mediated shock
Streptococcal or staphylococcal superantigens trigger vasodilation, capillary leak, myocardial dysfunction and coagulopathy disproportionate to the visible wound.
- 4Muscle destruction
Myositis and myonecrosis release potassium, myoglobin and lactate, adding hyperkalaemia, renal injury and metabolic acidosis to septic physiology.
- 5Incomplete-source persistence
Any retained zone of infected fascia or muscle continues microbial and toxin production, explaining rapid deterioration after inadequate first surgery.
04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.
Exquisite pain beyond mild erythema, rapid boundary change and deep induration before bullae or necrosis should trigger the emergency surgical pathway.
Dusky staining, haemorrhagic bullae, cutaneous anaesthesia, crepitus and spontaneous thin fluid indicate advanced tissue and microvascular destruction.
Profound muscle pain, swelling, weakness, rapidly rising CK, hyperkalaemia and shock suggests muscle involvement and greater systemic toxin burden.
Hypotension with multiorgan dysfunction and severe soft-tissue pain can precede obvious local necrosis in invasive group A streptococcal disease.
Diabetes, vascular disease, ulceration or perineal and postoperative sources favour mixed infection but do not predict the full operative extent.
Persistent vasopressor need, acidosis, pain progression or new skin change after debridement indicates residual disease and requires immediate re-exploration.
05InvestigationsWhat to request, why it matters and how to interpret it.
Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.
- 01
First-line operative explorationFirst stepFirst line - Why
- Confirm fascial or muscle necrosis and remove its source immediately.
- Interpretation and limitations
- Direct assessment is decisive and therapeutic; proceed on strong clinical suspicion without requiring diagnostic imaging or laboratory-score permission.
- 02
Blood cultures - Why
- Identify bacteraemia and support later narrowing of therapy.
- Interpretation and limitations
- Obtain before antibiotics only when this causes no meaningful delay; negative cultures do not exclude local necrotising infection.
- 03
Five deep tissue specimens - Why
- Define causative organisms from multiple anatomical zones.
- Interpretation and limitations
- Use separate sterile instruments and no-touch technique, label each site and the healthy-zone sample and alert microbiology for urgent processing.
- 04
Sepsis and organ panel - Why
- Measure systemic severity and guide resuscitation and drug adjustment.
- Interpretation and limitations
- Trend blood gas and lactate, FBC, renal and liver profiles, coagulation, fibrinogen, glucose, CK, potassium and group and screen without delaying source control.
- 05
CT or MRI only when non-delaying - Why
- Clarify deep distribution or an alternative diagnosis in a stable equivocal case.
- Interpretation and limitations
- Gas and fascial fluid increase suspicion, but a normal study cannot exclude early disease and scanning must stop if it postpones theatre.
- 06
Histopathology - Why
- Support diagnosis and margin assessment from excised tissue.
- Interpretation and limitations
- Send appropriately labelled viable-edge and affected tissue when available, but frozen section or final histology must not dictate whether obviously infected tissue is removed.
- 07
Limb perfusion and compartment assessment - Why
- Detect concurrent arterial occlusion or pressure-related ischaemia.
- Interpretation and limitations
- Record pulses, Doppler, named nerves and compartment findings and activate vascular or fasciotomy care alongside infection surgery when abnormal.
06Differential diagnosisRealistic alternatives and the features that help distinguish them.
Severe cellulitis
Erythema and tenderness remain primarily cutaneous and improve with antibiotics, without fascial non-adherence, disproportionate pain or rapidly evolving systemic toxicity.
Acute compartment syndrome
Post-traumatic passive-stretch pain and tense compartments can occur without infection, although infected oedema can produce both conditions simultaneously.
Deep abscess
A localised fluid collection can cause fever and pain but usually lacks long-segment fascial spread and extensive tissue non-viability.
Pyomyositis
Intramuscular infection may form a focal abscess and bacteraemia, while necrotising myositis produces faster diffuse muscle death and shock.
Venous or arterial catastrophe
Phlegmasia and acute limb ischaemia cause swelling, colour change and severe pain and require parallel vascular examination and imaging only when it does not delay surgery.
07ManagementImmediate care, first-line treatment, alternatives and escalation.
01RecognitionMobilise theatre while resuscitatingFirst stepRapid deep pain, spreading tissue change or toxicity makes necrotising infection clinically plausible.+
- 1Call the responsible surgical consultant, anaesthesia, intensive care and microbiology and book immediate NCEPOD-1 exploration.
- 2Apply the sepsis pathway, draw cultures if non-delaying and start local broad-spectrum intravenous therapy immediately.
- 3Use small reassessed crystalloid boluses and blood products or vasopressors through critical care according to physiology.
- 4Do not await LRINEC, CT, transfer or complete physiological normalisation before source-control surgery.
02DebridementExcise every infected zoneThe patient reaches theatre with suspected fascial or muscle necrosis.+
- 1Expose all involved planes and systematically document skin, fat, fascia, neurovascular structures and muscle groups.
- 2Remove zones of obvious and likely infection with a three-centimetre normal-tissue cuff while protecting useful viable structures.
- 3Take about five separately instrumented deep samples across zones, label them precisely and notify the laboratory.
- 4Leave the wound open and record the residual anatomy, uncertain tissue, reconstruction options and planned time for re-look.
03Re-lookProve source control before reconstructionInitial debridement is complete or physiology and local findings remain abnormal.+
- 1Review within six hours and return immediately for any failure to improve, treating deterioration as retained infection.
- 2Excise newly demarcated non-viable tissue and repeat cultures when clinically useful until the wound is clean and physiology responds.
- 3Make any amputation decision with at least two appropriate consultants and documented patient-centred reasoning where possible.
- 4Reconstruct only after source control, then deliver nutrition, mobility, scar, pain, psychological and prosthetic rehabilitation.
Key medicines and prescribing safety2 treatments · regimens, roles and cautions+
Immediate broad-spectrum parenteral antibiotics
Give the current trust necrotising-infection regimen at full protocol adult doses immediately after cultures when cultures cause no delay; include Gram-positive, Gram-negative and anaerobic cover and add toxin-suppressing therapy when microbiology recommends it.Agent and dose depend on immediate allergy, renal and hepatic function, prior resistant organisms and water, farm, injection or healthcare exposure; never narrow on a superficial swab or allow antibiotics to postpone debridement.
Balanced isotonic crystalloid for sepsis hypoperfusion
Give 250 mL intravenously over 10–15 minutes, reassess circulation and pulmonary tolerance after each bolus and repeat as required up to 1,000 mL before mandatory senior review of further fluid, vasopressor and critical-care needs.Use smaller or slower boluses and earlier critical-care input in heart failure, renal failure, frailty or pregnancy; stop for pulmonary oedema and do not delay blood products, vasopressors or operative source control.
08ComplicationsImportant consequences, why they occur and why they matter clinically.
Septic shock and multiorgan failure
Persistent toxin and inflammatory burden causes vasoplegia, respiratory failure, coagulopathy, kidney injury and death without immediate source control.
Major tissue loss
Radical excision leaves exposed vessels, nerves, tendon and bone requiring serial debridement, negative-pressure therapy, grafts or complex flap reconstruction.
Amputation
Extensive myonecrosis, unsalvageable perfusion or uncontrolled systemic disease can require life-saving amputation decided by at least two consultants.
Recurrent infection
Missed skip areas, premature closure or insufficient re-look allows residual disease to advance beneath apparently improved skin.
Long-term disability
Muscle loss, contracture, neuropathic pain, scars and psychological trauma impair mobility, self-care, work and body image after survival.
09Monitoring and follow-upTreatment response, safety checks and longer-term review.
- Track mental state, temperature, heart rate, pressure, respiratory status, capillary refill, lactate and urine output during resuscitation and around every operation.
- Re-examine the full marked and unmarked tissue field for pain, induration, sensation, colour, bullae, crepitus and spread, without using an unchanged surface boundary as proof of control.
- Trend renal and liver function, blood count, coagulation, fibrinogen, CK, potassium, calcium, glucose and acid-base state and treat organ complications promptly.
- Review antimicrobial cultures, susceptibilities, doses, renal adjustment and source control with microbiology every day and after each new specimen result.
- Inspect the open wound and every anatomical zone at planned and emergency re-look, documenting viable tissue and readiness for reconstruction.
- Follow nutrition, wound closure, joint range, strength, sensation, scar, pain, mobility, prosthetic needs, mood and return-to-life goals after survival.
10Special situationsVariants, exceptions and circumstances that change the usual approach.
Pain can disappear late
Cutaneous anaesthesia from nerve and microvascular destruction may replace severe pain and represents progression rather than improvement.
LRINEC is not a gatekeeper
Laboratory abnormalities support severity but insufficient sensitivity makes a low score unsafe for excluding early surgically treatable disease.
No dishwater fluid is not negative
Classic operative fluid and an easy fascial sweep are inconsistent findings, so the entire tissue assessment determines excision.
Normal-looking skin can overlie infection
Non-adherent fascia and zone-2 disease can extend beneath apparently healthy surface, explaining the specified normal-zone cuff.
Five samples answer different anatomy
Separately instrumented specimens reveal spatial microbiology and reduce confusion from contamination compared with one pooled sample.
Failure after surgery means source first
Escalating antibiotics cannot sterilise retained avascular fascia, so prompt repeat exploration precedes diagnostic complacency.
11Common pitfallsFrequent interpretation and management errors.
- 01
Using a low LRINEC score, absence of gas or early mild erythema to exclude a rapidly evolving clinical syndrome.
- 02
Waiting for CT, transfer, ICU normalisation or microbiology results before immediate surgical exploration.
- 03
Making a short diagnostic incision that neither exposes the full plane nor permits complete excision.
- 04
Sending one superficial swab or pooled specimen instead of multiple separately instrumented deep anatomical samples.
- 05
Primarily closing the index wound or reconstructing before serial assessment confirms source control.
- 06
Responding to postoperative deterioration only by broadening antibiotics rather than returning to theatre for residual disease.