Postanesthetic Myelopathy and Encephalopathy
Robert J. MacKay
A sudden-onset progressive myelopathy that is recognized during recovery from anesthesia has been described in horses and in a single calf.1-6 Most of the horses initially described were large, young, and in dorsal recumbency under halothane anesthesia.
There is a tendency for affected animals to be hypotensive during anesthesia. Paraparesis, ataxia, recumbency, or paraplegia is usually apparent during recovery from anesthesia but may be delayed as long as several days. Other reported signs include cutaneous hypalgesia and areflexia of the hindquarters and occasionally the thoracic limbs. Treatment is ineffective, and in all reported cases, the animals were been euthanized after a brief period during signs progressed rapidly. Lesions occur mainly in the lumbosacral spinal cord, although cervicothoracic segments also may be involved. There is malacia predominantly within gray matter (poliomyelomalacia), with associated mild to severe hemorrhage (hematomyelia) in most cases. Postanesthetic myelopathy is rare. CNS disease/ myelomalacia contributed to 5% and 4% of anesthesia-related deaths in noncolic cases in the Confidential Enquiry of Perioperative Equine Fatalities (CEPEF), phases 2 and 3.7Rare cases of postanesthetic encephalopathy have been described in horses.5,8 Clinical signs include dementia, pacing and circling, cortical (“central”) blindness, ataxia, hypermetria, and recumbency. In mild cases, blindness may be the only clinical sign. The onset of signs ranged from a few hours after recovery from anesthesia to several weeks later. The major pathologic finding in affected horses that did not survive was cerebrocortical necrosis, particularly in regions of the cortex supplied by terminal arterial branches (“watershed zones”).
Although the pathogenesis of postanesthetic myelopathy is incompletely understood, it is proposed that compromise to the blood supply to the spinal cord is caused by hypotension or pressure from the abdominal viscera on the great veins (caudal vena cava, azygos vein).
Systemic hypoxia, hypovolemia, and hypercapnia may underlie postanesthetic encephalopathy.8 Factors suspected to increase the risk of postanesthetic encephalopathy include positioning in dorsal recumbency during anesthesia, use of multiple anesthetics, use of halothane for anesthesia, endotoxemia, and shock. Differential diagnoses for myelopathy include orthopedic conditions such as limb fractures, spinal fracture, myopathy, and peripheral neuropathy secondary to recumbency. The differential diagnosis for encephalopathy includes numerous metabolic, infectious, and toxic disorders. Prognosis for recovery in cases of myelopathy is poor or hopeless. In contrast, most horses with encephalopathy recover completely. The risk of these complications probably can be reduced by supporting adequate blood pressure and ventilation in patients under anesthesia, minimizing anesthesia duration, and preventing dorsal recumbency whenever possible.