Felipedia

Ischaemic neuromyopathy

This is a disorder that occurs not infrequently in cats caused by thromboemboli usually associated with cardiomyopathy. While hypertrophic cardiomyopathy has now become the most important cardiac disorder in cats following the discovery of the role of taurine deficiency in dilated cardiomyopathy, in one review aortic thromboembolism reportedly occurred in approximately 50% of cats with hypertrophic cardiomyopathy, 25% of cats with dilated cardiomyopathy, and 25% of cats with restrictive cardiomyopathy. It has also been seen in a small percentage of cats with cardiomyopathy associated with excessive moderator bands. In one report on 100 cats with distal aortic thromboembolism, the average age was 7.7 years, with the neutered male being overrepresented. Evidence of preexisting cardiac disease was found in 11% of the cases, with murmur or arrhythmia noted in > 50 % of the cases on presentation, and the most frequent underlying disease was hypertrophic feline cardiomyopathy. Cardiovascular disease (cardiomyopathy and thromboembolism) associated with taurine depletion was an unexpected finding in 3 of 6 healthy adult cats during a potassium - depletion study.

The cause of the disease and emboli formation in the heart are uncertain, although recent studies suggest a possible role for vitamin B12 and arginine in cardiomyopathy and arterial thromboembolism. Predisposing factors to thrombus formation may include exposed vascular subendothelial tissue, abnormal circulation patterns and heightened platelet activity, and increased blood coagulability. The origin of the embolus is a thrombus, an aggregate of fibrin and platelets attached to an endocardial surface, usually within the left atrium. An embolus breaks loose from the cardiac thrombus and occludes one or more branches of the aorta. The emboli may be carried to any site within the arterial circulation. The most common site of occlusion is the aortic trifurcation. Embolic occlusion at this site obstructs internal and external iliac arteries and the median sacral artery. Emboli which extend into the iliac arteries have been termed "saddle thrombi". A less common embolic site is the brachial artery. Vasoactive substances released from embolic platelet products, such as serotonin, thromboxane A2, prostaglandins and 5-hydroxytryptamine may impair collateral circulation. Cats of the Persian breed may be at risk for ischemic neuromyopathy, although this has been disputed.

Clinical signs are acute in onset and usually include pelvic limb pain during the first 24 hours, plantigrade stance, and paraparesis or paralysis. Signs may be unilateral or bilateral. Femoral pulse may be weak or absent, the cranial tibial and gastrocnemius muscles are firm and often painful, and the limb(s) are cool. Distal limb muscles below the stifle are particularly affected. Flexion and extension of both hip and stifle joints and the patellar reflex are usually present, although initially, limb(s) may be held rigidly extended because of ischemic muscle contracture. Pain sensation to noxious stimuli is typically absent in the distal limbs. The nail bed of pelvic limbs is cyanotic. Left forelimb paralysis is seen with brachial artery embolization.

Electrodiagnostic studies reveal an absence of or markedly reduced evoked potentials from interosseous and cranial tibial muscles. Nerve conduction velocities are frequently reduced. Chest radiography may indicate cardiopulmonary disease (pulmonary edema, biventricular failure), and electrocardiographic/echocardiographic abnormalities are common (e.g., increased septal and/or left ventricular free wall thickness). Diagnosis of occlusive vascular disease can be confirmed from an aortogram. Pathologically, changes occur in skeletal muscle and peripheral nerve. Lesions in peripheral nerves begin in the mid-thigh region, with the central fibers in a fascicle being more susceptible than peripheral fibers. The majority of fibers show changes of axonal degeneration, while others have evidence of paranodal/segmental demyelination. In skeletal muscle, ischemic myopathy characterized by focal necrosis, myophagia, internalized nuclei, and occasional mononuclear cell infiltrates, contributes to the clinical signs.

Improvement in nerve conduction velocities and evoked potentials correlates well with return of limb function. Femoral pulses frequently return within 1 to 2 weeks. At present there are no results that show that any treatment of the aortic thromboembolism produces a significantly better recovery than no therapy. Surgical embolectomy does not appear to be warranted; besides, cats with unstabilized cardiomyopathy are definite surgical risks. Use of thrombolytic agents to dissolve the emboli awaits clinical trials. For animals that are in pain, movement should be restricted. Morphine sulfate, at 0.1 mg/kg, subcutaneously, will produce analgesia (without excitement) for 4 hours. This can be repeated every 4 to 6 hours for 2 days. In an attempt to prevent future episodes, affected cats should receive aspirin, at 25 mg/kg PO, every third day, for life. Aspirin inhibits platelet aggregation and preserves collateral circulation. While aspirin might prevent recurrences, it will have little effect on the underlying cardiomyopathy. It has been reported that there is no difference in survival time or rate of recurrence with warfarin vs. aspirin, and that low-dose aspirin (5 mg PO q3d) is an inexpensive option for thromboprophylaxis that seems to be as effective as high-dose aspirin (40 - 162 mg PO q 2 - 4 d) and warfarin. Supportive care for initial cardiac decompensation includes administration of oxygen, diuretics, fluid therapy, glucocorticoids, and external heat.

Although the collateral circulation does return in the majority of cases with return of function to varying degrees (some cats with extensive limb necrosis do not recover; others retain dropped hocks) within 6 weeks to 6 months (an increase in nerve conduction studies and evoked potentials may correlate with return of limb function [164]), the long-term prognosis is guarded to poor because of the potential of further thromboembolism. Other potential complications are associated with reperfusion of ischemic tissues and include release of toxic factors such as lactic acid, potassium, and myocardial depressant factor. Thus, the severity of the cardiac disease usually determines prognosis. Limb complications may include necrosis requiring amputation or wound management, and limb contracture. In one retrospective study of idiopathic feline hypertrophic cardiomyopathy, analysis of survival revealed that all cats with thromboembolism were dead 6 months after diagnosis. In another study involving cats with distal aortic thromboembolism, the average, long-term survival in the 37% of cases that survived the initial thromboembolic episode was approximately 12 months, while the remaining cases either died (28%) or were euthanized (35%). Long-term survival time is reportedly significantly shorter in cats with congestive heart failure during the initial episode. Hypothermia has been associated with poor outcome.

Ischemic neuromyopathy secondary to aortic foreign body obstruction have occasionally been reported in cats. In one case, in addition to muscle and nerve damage similar to that described above in thromboembolic disease, spinal cord infarction was present in lumbosacral spinal cord gray matter resulting in clinical signs of a lumbosacral syndrome (absent anal tone, bladder incontinence, megacolon, pelvic limb paresis, and flaccid analgesic tail). Removal of the foreign body by aortotomy was successful in another cat that recovered almost completely within one year after the surgery (external coaptation splints facilitated return of function of the pelvic limbs). Post-surgical therapy included heparin (100 U/kg IV q4h for 3 days), aspirin (25 mg/kg PO every 3 days for a total of 4 treatments), cefazolin (20 mg/kg IV q6h for 4 days), and methylprednisolone sodium succinate (20 mg/kg IV immediately after surgery and again 6 hours later).

Thromboembolic disease is not common in dogs but may be seen associated with hypercoagulable states, bacterial endocarditis, dirofilariasis, hyperadrenocorticism, neoplasia, cardiac disease (although thromboembolism secondary to cardiomyopathy has not been reported in dogs). Yet curiously, aortic thromboembolism in dogs has been reported infrequently. In one report of 36 dogs with aortic thromboembolism, 4 had severe atherosclerosis associated with thyroid disease. Thrombotic occlusion of the distal aorta and/or the iliac arteries in dogs results in signs of pelvic limb weakness, pain and collapse. Diagnosis is based on clinical signs, angiography and ultrasonography. In one report, dogs that survived the acute episode received aspirin in an attempt to prevent recurrence of thrombosis and all regained pelvic limb function. For dogs that survived longer than one month after the acute episode, repeat thrombosis was uncommon. Aortic thromboembolism in dogs carries a more favorable prognosis than feline aortic thromboembolism.

A possible genetic predisposition to femoral artery occlusion occurs in Cavalier King Charles Spaniels. The condition is usually subclinical due to sufficient collateral circulation (femoral pulse may be undetectable unilaterally or bilaterally).