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.


A definitive diagnosis of hepatic microvascular dysplasia is based on histologic examination of hepatic tissue. Histologic lesions can vary among liver lobes, with some appearing normal and others being completely abnormal. For this reason, it is best to obtain biopsy samples from more than one liver lobe.7 Although not performed in this case, additional diagnostic tests to rule out macroscopic portosystemic vascular anomalies could have included mesenteric angiography, splenic portography, or transcolonic scintigraphy.10 Each of these imaging techniques has limitations because a shunt distal to the point of contrast injection (as with mesenteric portography) or a shunt located close to the liver (as with transcolonic scintigraphy) could be overlooked.8 A nuclear scan would have been helpful in this case but was not performed after the biopsy samples were obtained because we thought that the isolation required at our institution after radioisotope administration was not in the patient's best interest. Although unlikely given the work-up performed, this patient may have had hepatic microvascular dysplasia and a macroscopic shunt.

Dogs that present with clinical signs of hepatic microvascular dysplasia are often older (2 or 3 years old), can have relatively unremarkable blood test results, and have lower preprandial and postprandial serum bile acid concentrations when compared with dogs having macroscopic anomalies.8,9 Like most hepatic vascular diseases, hepatic microvascular dysplasia has been historically identified in toy and small-breed dogs.7-11 According to a literature review, this case is only the second reported in a large-breed dog (> 30 kg).8 Females have been overrepresented in reported studies, making up 70% of the documented cases.10 As with portosystemic shunting, neurologic and gastrointestinal signs are the most common presenting clinical signs. This dog's vomiting may have resulted from gastric ulceration and inflammation. The mechanisms by which hepatic disease causes gastrointestinal inflammation and hemorrhage are complex and poorly understood but may result from reduced mucosal microcirculation and reduced mucosal renewal.12 Gastrointestinal hemorrhage and hypokalemia, which were both present in the case, are known to exacerbate hepatic encephalopathy13 and may have contributed to this dog's acute decompensation. However, the dog's neurologic signs were atypical because the disease presented primarily with focal signs referable to the central vestibular system as opposed to the global and diffuse cerebral cortical signs typically seen with hepatic encephalopathy.

Common neurologic abnormalities in dogs with hepatic encephalopathy are usually suggestive of a diffuse cerebral disease process and include central blindness, alterations in mentation or behavior, head-pressing, and, less commonly, seizures. Ptyalism can be a feature of hepatic encephalopathy, but it occurs more frequently in cats.3 Hepatic encephalopathy is typically seen as a result of decreased functional liver mass in combination with portosystemic shunting of blood.3 So hepatic encephalopathy is often seen in dogs with either congenital or acquired portosystemic shunts. Acquired shunts can often result from chronic hepatitis, cirrhosis, and portal vein hypoplasia.

Although not proven, it is possible that a concurrent disease such as an unidentified toxicosis (e.g. from possible carrion consumption) or infection could have caused this patient's clinical signs. Plasma ivermectin concentrations do not reliably correlate with brain ivermectin concentrations. Brain ivermectin concentrations may be more related to defective blood-brain barrier protective mechanisms than to plasma concentrations of the drug.14 Even though serum, not central nervous system samples, was tested for ivermectin concentrations, ivermectin toxicosis from the type of heartworm preventive administered would be extremely rare.14,15 Both antemortem and postmortem diagnostic findings were most consistent with hepatic microvascular dysplasia and hepatic encephalopathy.

An antibiotic-responsive encephalitic syndrome, although poorly documented in the literature, is anecdotally incriminated by clinicians of many disciplines as a common cause of acute intracranial disease. In many cases, rickettsial organisms are often speculated as the etiologic agent. The neurologic manifestations of Rocky Mountain spotted fever, ehrlichiosis, and borreliosis have been well-described in animals and people and are consistent with this dog's neurologic signs.16,17 After considering that this dog had elevated serum antibodies to Borrelia burgdorferi, that new infectious diseases are constantly emerging with the advent of sophisticated diagnostic testing methods, and that intoxications can be extremely difficult to definitively diagnose, we cannot totally discount the possibility that this dog had a doxycycline-responsive infectious disease or a toxicosis and that the hepatic microvascular dysplasia was an incidental but important finding.16,17 Although rare, tetracycline has been associated with adverse reactions and can be hepatotoxic.15


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