Diagnosis
Inflammation and/or soreness can be appreciated as raised, hardened and/or painful areas during normal clinical examination of the area. Abscess formation should be considered if the local muscle swelling appears severe or if the horse develops a fever.
Treatment
Avoid use of that location for further injections and apply warm compresses for analgesia. Warm compresses can also be used to help mature the abscess prior to establishing external drainage. In severe cases of muscle soreness, systemic non‐steroidal anti‐inflammatory treatment may be necessary. Drain abscess at a dependent location. The gluteal muscles are particularly difficult to drain if abscessation develops.
Expected outcome
Although most localized muscle soreness or abscessation resolves without long‐term consequence, fibrotic myopathy may develop after intramuscular injection [3]. This may be an additional consideration when administering intramuscular medications to performance horses.
Clostridial Myonecrosis
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.
Intra‐Synovial Administration
Intra‐synovial medication may be used for diagnostic purposes (local anesthetic agents) or for therapeutic purposes (anti‐inflammatory medications, chrondroprotective agents, or antimicrobial therapy).
Post‐Injection Synovitis and Lameness
Definition
A post‐injection flare is an acute, non‐septic inflammatory response to the medication [7, 8]. Aside from the discomfort of the patient and the anxiety of the owner, the biggest concern related to a post‐injection flare is differentiating it from septic synovitis. Septic synovitis is an inflammatory response of the synovial cavity associated with infection.
Risk factors
Substandard aseptic technique
Post‐injection flares:Injected substance: corticosteroids, local anesthetics, hyaluronate, and polysulfated glycosaminoglycans
Post‐injection synovial sepsis:In humans: failure of aseptic technique, experience of practitioner, use of multi‐dose vials, injection through infected tissue, concurrent systemic infection, and use of immunosuppressive drugs [9, 10]In horses:Corticosteroids [11–13]Polysulfated glycosaminoglycan or hyaluronic acid [11]Combination of corticosteroid‐polysulfated glycosaminoglycan [13]Dexamethasone had higher risk than betamethasone [12]Treating veterinarian [12, 13], >20 years in practice by the treating veterinarian [14]Technical factors: <7‐minute preparation time, clipping the site, not using gloves, using the same needle to draw up medication and do the injection, and having someone other than the veterinarian performing the procedure preparing the site [14].
Pathogenesis
Post‐injection flare is a chemical synovitis, presumably due to an inflammatory reaction to the medication or substance within the medication. Developing an infection after intra‐synovial injection is related to the amount and type of bacterial contamination and the type of medication being administered. Some intra‐synovial medications potentiate infection to a greater degree than other medications. For example,