A challenging case: A collie with acute neurologic signs - Veterinary Medicine
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A challenging case: A collie with acute neurologic signs
This collie's condition has been historically identified in small-breed dogs. So after these clinicians narrowed down the potential causes of their patient's signs, the definitive diagnosis was surprising.


In a telephone interview about four weeks later, the owner reported that the dog seemed normal and that the lactulose dose had been reduced to 0.15 ml/kg given orally three times a day. About two months later, the dog experienced a recurrence of its neurologic signs. The dog was still receiving Prescription Diet Canine l/d and lactulose at the dosage mentioned above. An exploratory celiotomy with portal scintigraphy to confirm the absence of a shunt was offered to the owner but was declined. The patient was euthanized after failing to improve after 48 hours of aggressive supportive care provided by a local veterinary hospital.

Necropsy and definitive diagnosis

A necropsy examination was performed. The only gross abnormalities consisted of several punctate gastric ulcers and mucosal hemorrhages. No evidence of anomalous portosystemic vasculature was present, and the liver appeared normal. The findings of a gross examination of the central nervous system were unremarkable. Histologic examination of serial sections of the brain and cervical spinal cord revealed bilaterally symmetric areas of polymicrocavitation of the white matter of the cerebral cortices, pons, caudal cerebellar peduncle, medulla oblongata, and cervical spinal cord. Alzheimer type II astrocytes were observed in the basal nuclei and hippocampal areas. A focal area of neuronal necrosis accompanied by gliosis was also noted in the hippocampus. Histologic changes noted in the liver were similar to those described previously, although several foci of regenerative nodular change were also noted. The only other clinically relevant finding was multifocal lymphocytic-plasmacytic erosive gastritis. The histologic diagnoses were primary hepatic microvascular dysplasia with changes in the brain consistent with hepatic encephalopathy.5


Hepatic microvascular dysplasia has been described only recently in veterinary medicine. Atypical liver morphology associated with macroscopic portosystemic shunting has been well-reported in the veterinary literature.1,3-6 However, the diagnosis of hepatic microvascular dysplasia without any macroscopic anomalies did not surface until 1996 when it was described as a congenital disorder of hepatic vasculature in a kindred of Cairn terriers.7 Hepatic microvascular dysplasia is defined as an abnormal liver with apposed hepatic venous and portal vessels that communicate through random small-caliber or juvenile-like interconnecting microvascular channels, thus bypassing the sinusoids.7,8 Hepatic microvascular dysplasia can develop as an isolated disease or in conjunction with portosystemic shunting.9 Although uncommon, dogs with hepatic microvascular dysplasia may manifest with any of the constellation of clinical abnormalities associated with hepatic encephalopathy. However, the disease remains clinically occult in many cases.7

It has been hypothesized that the natural remodeling of embryogenic vitelline veins is disrupted, resulting in the persistence of functional vitelline veins, and that this is the most likely cause of hepatic microvascular dysplasia.8 Vitelline veins normally break down and form sinusoids during the terminal stages of embryogenesis. As a result, blood is shunted from the portal system to the central vein and, subsequently, to the systemic venous circulation.10 Another proposed theory describes ultrastructural changes in the sinusoidal capillaries that result in reduced endothelial permeability and limited access to hepatocellular surfaces.7,10

The incidence of hepatic microvascular dysplasia is still unknown because of the difficulty and controversy of the diagnosis. Classic congenital and acquired vascular anomalies can often be presumptively diagnosed based on the clinical history, signalment, and the results of routine serum chemistry profile testing, liver function testing (e.g. bile acids assay), hepatic ultrasonography, and nuclear scintigraphic scanning.7 However, dogs with hepatic microvascular dysplasia may have no clinical signs or marked serum chemistry abnormalities. Even when hepatic microvascular dysplasia has clinical manifestations, the extreme variability of clinical presentations can make the diagnosis difficult. Also, as demonstrated in the patient described here, the results of routine clinicopathologic tests can be normal or nonspecific. The variation in the severity of disease is theorized to be a direct reflection of the number of persistent vitelline veins.8


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