Compartment, Downer, and Muscle Crush Syndromes of Cattle
David R. Hodgson • Stephanie J. Valberg
Muscle damage commonly accompanies the downer syndrome in large animals. The downer syndrome is discussed in greater detail in Chapter 35.
Animals weakened by disorders such as hypocalcemia are more prone to tearing adductor or semitendinosus and membranosus muscles in attempts to rise.25,160 Initial traumatic laceration of muscle leads to edema and inflammation, both of which may exacerbate local tissue degenerative changes. In addition, the weight of a recumbent animal on dependent muscle groups creates significant increases in intramuscular pressure, resulting in decreased perfusion and ischemia of muscle and nerve. Signs of weakness and peroneal or tibial nerve paralysis most commonly accompany this type of injury. Mild elevations in serum CK can be expected in cows that are recumbent, but elevations greater than 5000 U/L usually indicate traumatic muscle damage. Treatment requires correcting the underlying cause of recumbency, fluid therapy if renal damage is evident, NSAIDs, good nursing care, adequate footing and bedding, and lifting or rolling the animal several times a day. Aquatherapy using float tanks for cattle also appears to be beneficial in relieving the pressure on muscle groups.
FIG. 42.16 Postanesthetic myoneuropathy showing paralysis of the right femoral and peroneal nerves.
Postanesthetic Myoneuropathy
Postanesthetic myoneuropathy is a condition that has become much more prevalent since the advent of inhalation general anesthesia. The disorder can be categorized as occurring in two forms: (1) localized myopathy-neuropathy and (2) generalized myopathy somewhat similar to malignant hyperthermia.
Localized Myoneuropathy
CLINICAL SIGNS. Localized myopathy-neuropathy occurs in about 6% of horses undergoing general anesthesia.148 It is most prevalent in muscles that are in contact with a hard surface during anesthesia or those in which arterial blood supply is compromised through positional occlusion.
Commonly affected muscles include triceps, deltoid, masseter, hindlimb extensors, or if the horse has been in dorsal recumbency, the hindlimb adductor and gluteal muscles.160-162 Injury can also occur to nerves in these areas, resulting in temporary radial, peroneal, or femoral nerve paralysis (Fig. 42.16). Clinical signs may be apparent on recovery or may be delayed for periods of up to 30 to 60 minutes after the horse has recovered from anesthesia. Affected muscles may be swollen, hot, and painful on deep palpation, and the horse is often reluctant to bear weight on the affected limb. Myasthenia (weakness) of affected muscles is common, particularly with peripheral nerve involvement. In some horses this condition may limit the animal's ability to stand for some time following anesthesia. The loss of muscle strength, particularly when involving adductor muscles, can contribute to orthopedic injury during repeated attempts to rise. Many horses with mild to moderate muscle injury recover over a period of hours to days even if untreated.162■ Etiology A variety of factors acting alone or in combination has been suggested to contribute to this disorder. The most important factors include duration of anesthesia, ischemia, and hypoperfusion as a result of prolonged immobility, muscle compression, systemic hypotension, and hypoxia.162-166 There is increased lactate efflux from dependent muscles during anesthesia in horses that develop a myopathy, supporting the contention that these muscles experience compromised perfusion.165,167,168 Halothane anesthesia has a greater propensity than isoflurane to compromise tissue oxygen delivery even in nondependent muscles.164 If mean arterial pressure is allowed to fall below 70 mm Hg for several hours during inhalation anesthesia, particularly if mechanical ventilation is used, the incidence of postanesthetic myopathy increases substantially.166,167
■ Diagnosis Diagnosis is based on a history of anesthesia or prolonged recumbency, clinical signs, and possibly clinical pathology examinations.
Laboratory findings include elevations in serum CK and subsequently serum AST and serum LDH activities. Elevations in CK activities of thousands to tens of thousands of IU/L are commonly demonstrated in horses with moderate forms of the myopathy.■ Treatment Horses demonstrating only minor localized manifestations of the myopathy usually have an uncomplicated recovery with little or no treatment.162 Supportive care, including the use of anti-inflammatory drugs, dimethyl sulfoxide, and dantrolene sodium 2 to 4 mg/kg PO q8h to q24h for up to 48 hours, is often sufficient in mild to moderate cases.168 Significant muscle atrophy may develop over the ensuing 3 to 4 weeks but will usually resolve within 2 to 3 months. Treatment of more severe cases is outlined under generalized reactions.
■ Control Correct positioning and judicious use of padding and water- or air-filled mattresses can reduce dependent muscle pressure by up to 50%, thereby aiding in the reduction of this disorder. In addition, by elevating the upper limb during anesthesia, the pressure on the lower limbs is significantly reduced. Pulling the lower forelimb forward also markedly reduces pressure in the dependent triceps muscle. When the horse is in dorsal recumbency, padding under the shoulders and hips is absolutely imperative.
Maintaining anesthesia at the lightest plane possible for a specific surgical procedure is beneficial in prophylaxis. Similarly, if possible, maintaining systemic mean arterial blood pressure above 80 to 85 mm Hg during anesthesia is advisable. The use of ionotropic agents such as dobutamine during anesthesia has been useful in reducing the occurrence of anesthetic myopathies. Administration of dantrolene sodium (2 to 4 mg/ kg PO) 1 hour before induction of anesthesia may result in a reduction in the incidence of this myopathy; however, it should be noted that decreased cardiac output can occur in conjunction with higher dantrolene doses.
Generalized Anesthetic Reactions
CLINICAL SIGNS. Postanesthetic reactions involving multiple muscle groups can result in clinical signs of anxiety, hyperthermia, tachycardia, tachypnea, profuse sweating, and myoglobinuria.163,164 Horses may not be able to rise and may struggle violently, resulting in prolonged, traumatic recoveries. In some cases a progressive increase in body temperature and muscular contractures may develop under anesthesia, and a fulminant metabolic and respiratory acidosis may be noted.20,169,170 These animals can die within a matter of hours. In some cases, shock and pigmenturia may lead to renal failure.
■ Pathogenesis The generalized form of myopathy cannot be explained by the compartmental syndrome alone. Halothane and succinylcholine have been the most frequently implicated inciting agents for generalized anesthetic-induced myonecrosis in all susceptible species, including the horse.19,169,170 There appear to be several possible explanations for generalized anesthetic reactions. In some cases, systemic hypotension and hypoxemia may create local ischemic lesions, with the pathologic changes becoming more generalized as a result of the stress of anesthesia and the sensitivity of muscle cells to anesthetic agents or muscle relaxants.162,166 In other cases, malignant hyperthermia19,169-171 may be responsible for clinical signs of muscle contracture, heat production, and systemic acidosis resulting from excessive calcium release by the sarcoplasmic reticulum. In swine, malignant hyperthermia is caused by a genetic mutation in the ryanodine receptor 1 (RYRl) gene.172 A mutation in the same gene has been identified in Quarter Horses. Horses with this mutation may develop fatal malignant hyperthermia following halothane anesthesia.173,174 A further possible cause of generalized anesthetic myopathies is the triggering of severe myonecrosis in horses with an underlying exertional myopathy.
Horses with recurrent exertional rhabdomyolysis may be at risk for excessive release of calcium from the sarcoplasmic reticulum during halothane anesthesia, and horses with polysaccharide storage myopathy may develop rhabdomyolysis due to metabolic changes with anesthesia.19,20,175,176■ Diagnosis Diagnosis is based on clinical signs, particularly in horses undergoing inhalation anesthesia. Routine monitoring of body temperature during anesthesia may aid in the early detection of MH. Some animals may also demonstrate metabolic and respiratory acidosis and hyperkalemia.173 Genetic screening for MH in Quarter Horses and American Paint Horses may be warranted before elective procedures.
■ Treatment Severely affected cases provide a significant therapeutic challenge. Aims of therapy should include (1) relief of pain, (2) correction of fluid and electrolyte abnormalities, (3) attempts to prevent ongoing necrosis, and (4) high-quality nursing care. Many of the same principles described for treatment of exertional rhabdomyolysis can be used for treatment of postanesthetic myoneuropathy. In severely affected recumbent horses, pain relief and sedation may help prevent struggling and progression of the myopathy.162,163 Detomidine combined with butorphanol is effective in reducing struggling. Violent struggling only exhausts the horse and increases the potential for further injury and muscle damage. Constant rate infusions of butorphanol, opioids, or detomidine may aid in pain control where practical. Similarly, administration of NSAIDs may help to reduce ongoing degenerative changes in muscle. Dantrolene sodium 2 to 4 mg/kg PO q8h to q24h decreases release of calcium from the sarcoplasmic reticulum, helping to break the cycle of muscle damage. Volume expansion and diuresis may prevent renal toxicity.162
The most common metabolic derangement with anesthetic- related myopathies is a metabolic and/or respiratory acidosis.
If specific therapy for metabolic acidosis is necessary, intravenous administration of sodium bicarbonate can be used. For optimum results, doses are calculated on the basis of the results of acidbase analysis. If facilities for acid-base analysis are not available and the horse appears severely compromised, IV administration of sodium bicarbonate at a dosage of 0.5 to 1.0 mEq/kg slowly is recommended. If hyperthermia and contracture develop during anesthesia, discontinuation of anesthesia is advisable. Additional attempts to cool the animal with alcohol or coldwater baths may also be indicated. Administration of a large amount of soluble, lyophilized dantrolene sodium for intravenous administration may alleviate clinical signs in these horses. However, availability and expense of the agent in this form restrict its use. A dosage rate of 1 mg/kg IV may be appropriate, although more controlled studies are required.162Good nursing care is important in severely affected horses. This involves providing well-padded areas on which horses can lie. Prevention or minimization of trauma around the eyes and appropriate care of decubital sores are important. Recumbent animals may require frequent turning to allow reperfusion of compressed muscle masses. Continued fluid therapy with polyionic fluids and possibly caloric supplementation may be indicated. The use of slings and pools to assist recumbent animals to rise has also been tried.162 Recovery from the myopathy may occur with no apparent residual lesions. In contrast, recovery from some severe forms of the disorder may be accompanied by muscle atrophy, fibrosis, and scarring.162
■ Prevention The principles described for localized myoneuropathies apply to the prevention of generalized anesthetic- related myopathies. In addition, dantrolene sodium has been shown to reduce the incidence of MH in susceptible humans and pigs. Similar effects might be anticipated in horses. Because of limited controlled studies, the dosage rate for prevention of MH in the horse is not clearly defined. Administration at a rate of 4 mg/kg PO 1 to 2 hours before anesthesia may be beneficial in reducing the incidence of MH; however, 6 mg/ kg may cause decreased cardiac output and hypotension.168,177