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Definition

Clostridial myonecrosis is a rapidly progressing, necrotizing infection of muscle that is characterized by severe local and systemic clinical signs [4–6]. It may also be referred to as clostridial myositis, malignant edema, or clostridial cellulitis [4].

Risk factors

Clostridial myonecrosis can develop after any intramuscular injection, and has been reported after flunixin meglumine (most commonly), dipyrone, Vitamin B with or without iron, tripellennamine, dexamethasone, furosemide, vaccines, among others [4–6].

Pathogenesis

All of these syndromes are referencing necrotizing soft tissue infections with Clostridium perfringens, Clostridium septicum, Clostridium chauvoei, and Clostridial sporogenes that develop after intramuscular injections or muscular trauma [5]. It is not known if these infections result from inoculation of clostridial spores at the time of injection or injury, or if these spores are quiescent within the tissue and they germinate after a muscle injury creates a suitable anaerobic environment [5, 6]. Proliferation of clostridial organisms results in the production of extracellular enzymes and exotoxins, which propagate the local tissue injury and progress to signs of systemic toxemia.

Prevention

Due to the variety of medications associated with clostridial myonecrosis, it is difficult to eliminate the risk; however, flunixin meglumine, B vitamins, and tripellennamine appear higher risk and should be avoided. It would seem advisable to maximize aseptic techniques for intramuscular injection and use alternate routes of administration for medication, if available.

Diagnosis

Clinical signs of clostridial myonecrosis (colic, lethargy, inappetence, pyrexia, progressive localized painful, emphysematous swelling) develop within 48–72 hours of intramuscular injection [4–6]. Palpable subcutaneous emphysema in the affected muscle was present in 34 out of 37 cases [4]. The emphysema is often rapidly progressive along muscle planes and is associated with systemic signs of fever, obtundation, and shock [4–6]. A presumptive diagnosis can be based on a history of recent intramuscular injection and local swelling, pain, and emphysema. Ultrasound is helpful in identifying emphysema within the deeper tissues. Treatment should not be delayed until there is a confirmed diagnosis, but presence of Gram‐positive rods on Gram stain provides further support and anaerobic culture of Clostridia is confirmatory [5, 6].

Treatment

Aggressive treatment is necessary once clostridial myonecrosis is suspected or confirmed. Aggressive antimicrobial therapy should be instituted promptly and continued for 10–14 days [5]. High‐dose intravenous penicillin should be started to treat the clostridial infection [5, 6]. Other antimicrobial agents have been suggested but lack the same spectrum against Clostridia (ampicillin, cephalosporins, tetracyclines) or will not attain high tissue concentrations (metronidazole) [6]. Intravenous fluid therapy is started to support the cardiovascular system. Non‐steroidal anti‐inflammatory medication and other analgesic agents are administered, and other treatments (fresh frozen plasma, platelet transfusion, etc.) may be given as needed [5]. Another mainstay of treatment is surgical fenestration of the area to allow drainage of the accumulated fluid and gas, debridement of necrotic tissue, and oxygenation of the affected area [4–6]. Fenestration and debridement may need to be extended into previously unaffected areas on subsequent days. If clostridial myonecrosis involves the cervical muscles, it may be necessary to place a tracheostomy tube to secure the airway or a feeding tube for enteral nutrition, because edema may progress cranially to cause dyspnea and dysphagia.

Expected outcome

Prognosis for clostridial myonecrosis is guarded to poor [4–6]. Horses may not survive despite aggressive medical and surgical treatment. Owners should be warned that the recovery period may be protracted and there will be extensive tissue loss in the affected area.