Gas Gangrene

A rapidly progressive, life threatening necrotising soft tissue infection classically caused by Clostridium perfringens and related clostridial species, characterised by extensive myonecrosis, gas production within tissue, and profound systemic toxicity.

It is one of the most surgically urgent infections encountered in clinical practice. Survival is directly dependent on the speed of recognition and, critically, prompt radical surgical debridement.

Antibiotic therapy alone is entirely inadequate to control this infection given the devitalised, poorly perfused nature of the affected tissue.

Pathophysiology

• Clostridium perfringens is an anaerobic, spore forming, Gram positive bacillus. It proliferates within devitalised, hypoxic tissue, following traumatic wound contamination, surgical site infection or, less commonly, haematogenous spread in the context of underlying malignancy.
• It produces potent exotoxins, principally alpha toxin (a lecithinase causing direct cell membrane destruction).
• These drive extensive, rapidly spreading myonecrosis and profound systemic toxicity disproportionate to the apparent extent of the wound itself.
• Gas production, reflecting bacterial fermentation within the necrotic tissue, produces the characteristic crepitus on examination and gas visible on imaging.
• Gas is a late and inconsistent sign rather than an early or universally present feature. Its absence must never be used to exclude the diagnosis in a clinically compatible presentation.
• The broader category of necrotising soft tissue infection additionally includes:
  • polymicrobial necrotising fasciitis, frequently a mixed aerobic and anaerobic infection, sometimes termed type one
  • monomicrobial necrotising fasciitis, classically caused by Streptococcus pyogenes, sometimes termed type two
• Both share the same fundamental surgical emergency status and management approach as clostridial myonecrosis, even where the specific causative organism differs.

• Severe pain at the site of infection, characteristically disproportionate to the visible examination findings, is among the most important and earliest clinical clues.
• It frequently precedes overt skin changes by hours.
• It is a critical warning sign that should never be dismissed or attributed to the underlying wound or injury alone.
• Rapid progression over hours, with spreading erythema or dusky discolouration and oedema.
• As the infection advances, skin changes include bullae (which may become haemorrhagic) and, eventually, the characteristic bronze or purplish discolouration with a thin, watery, foul smelling ("dishwater") discharge.
• Crepitus on palpation reflects gas within the tissue, though this last sign is often a late finding.
• Profound systemic toxicity, frequently out of proportion to the apparent local findings early in the disease course, includes tachycardia, hypotension and, characteristically, a disproportionately alert mental status relative to the severity of physiological derangement.
• In more advanced disease there is evidence of haemolysis (from the direct haemolytic action of clostridial toxins) and disseminated intravascular coagulation.
• Seek a relevant history of recent trauma (particularly with significant tissue devitalisation or contamination) or surgery.
• Less commonly, there is an identifiable underlying source for haematogenous spread, including colonic malignancy. This is particularly relevant in cases without an obvious traumatic or surgical portal of entry.
• The diagnosis must remain a clinical priority based on the presenting features, regardless of whether a clear precipitating history is immediately apparent.

• The diagnosis is fundamentally clinical, and surgical exploration should never be delayed for confirmatory imaging or laboratory testing where the clinical suspicion is significant, given the extremely time critical nature of this condition and the direct relationship between delay to surgical debridement and mortality.
• Plain radiography or computed tomography may demonstrate soft tissue gas, supporting the diagnosis where present.
• The absence of visible gas on imaging does not exclude the diagnosis.
• Imaging should never be pursued at the expense of delaying definitive surgical management in a patient with a strongly compatible clinical presentation.
• Laboratory findings include marked leucocytosis, elevated creatine kinase (reflecting extensive muscle necrosis), evidence of haemolysis, coagulopathy and acute kidney injury.
• They support assessment of severity but do not themselves establish or exclude the diagnosis.
• The diagnosis remains fundamentally a clinical and, surgical determination, made through direct visual inspection of the affected tissue at operation.
• Gram stain and culture of tissue obtained at surgical debridement provides definitive microbiological confirmation and identification of the causative organism, though this should occur as part of, rather than as a prerequisite for, urgent surgical intervention.
• A number of validated clinical scoring systems exist to help stratify risk of necrotising soft tissue infection based on laboratory parameters.
• These tools are intended to support and heighten clinical suspicion rather than to replace urgent surgical assessment and exploration where the clinical picture is genuinely concerning.
• A low or reassuring score must never be used to defer surgical evaluation in a patient with a convincing clinical presentation.

• Emergency, extensive surgical debridement of all necrotic and infected tissue is the single most important intervention. It must not be delayed for any reason once the diagnosis is suspected clinically.
• The surgical principle is radical excision back to healthy, bleeding, viable tissue.
• Return to theatre for repeated debridement over subsequent days is frequently required, as the extent of tissue viability becomes clearer.
• Amputation is considered where limb threatening or life threatening extensive involvement cannot otherwise be adequately controlled.
• Broad spectrum, high dose intravenous antibiotic therapy is initiated immediately and empirically alongside surgical preparation, given the frequently polymicrobial nature of necrotising soft tissue infection beyond classical clostridial myonecrosis alone.
• A typical regimen combines a broad spectrum beta lactam, such as piperacillin with tazobactam 4.5 g intravenously four times daily, or a carbapenem, with clindamycin 900 mg intravenously every eight hours.
• Clindamycin is given specifically for its toxin production suppressing effect (as detailed under toxic shock syndrome).
• Benzylpenicillin 2.4 g intravenously every four to six hours is added specifically where clostridial infection is confirmed or strongly suspected, given reliable activity against Clostridium species, generally continued alongside the broader spectrum regimen and clindamycin pending definitive culture results and clinical response.
• Aggressive haemodynamic resuscitation and intensive supportive care address the profound systemic toxicity, shock physiology, coagulopathy and organ dysfunction characteristic of this condition.
• Care is provided within an intensive care setting, with close monitoring, given the potential for rapid deterioration even following apparently adequate initial surgical source control.
• Hyperbaric oxygen therapy is used as an adjunct in some centres, based on the theoretical rationale of directly inhibiting clostridial alpha toxin production and improving tissue oxygenation.
• It must never be used as an alternative to, or cause delay of, urgent surgical debridement, and its use should not compromise timely access to definitive surgical care.
• Intravenous immunoglobulin is considered as an adjunctive therapy, particularly for streptococcal necrotising fasciitis, following the same rationale and evidence base as detailed under toxic shock syndrome, given the overlapping toxin mediated pathophysiology in streptococcal disease specifically.
• Ongoing surgical management comprises repeated surgical reassessment and debridement, together with staged reconstruction once infection is controlled and the wound bed is adequately prepared.
• Overall prognosis and functional outcome depend heavily on the speed and adequacy of the initial and subsequent debridement.
• This reinforces the central importance of prompt recognition and surgical referral as the determining factor in survival and outcome from this condition.