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.


Initial therapy included intravenous administration of lactated Ringer's solution supplemented with 40 mEq/L of potassium chloride (90 ml/kg/day) to maintain the dog's hydration, provide for ongoing losses, and correct the hypokalemia. Atropine sulfate administration (0.02 mg/kg intravenously and 0.02 mg/kg subcutaneously) resolved the sinus bradycardia, which suggested that the cardiac arrhythmia was caused by excess vagal tone. We also administered doxycycline (5.5 mg/kg intravenously b.i.d.) and metoclopramide hydrochloride (0.2 mg/kg subcutaneously q.i.d.) and withheld food and water for 24 hours.

Follow-up tests

Table 2 : Results of Initial Laboratory Tests
Twelve hours after admission, the patient showed marked clinical improvement. The vomiting and nystagmus resolved, the ptyalism improved, and the animal was able to ambulate, although it remained mildly tetraparetic and ataxic. We performed further diagnostic tests, consisting of a fasting plasma ammonia concentration, sulfobromophthalein clearance test, and an ACTH stimulation test, to rule out biochemically occult hepatic disease and atypical hypoadrenocorticism. The plasma ammonia and pre-ACTH and one-hour post-ACTH stimulation cortisol concentrations were within the reference ranges, but the sulfobromophthalein retention was abnormal (Table 2).1,2 Results of the tick-borne disease panel were normal except for elevated Lyme IgM and IgG antibody concentrations (Table 2). It was later confirmed that the dog had been vaccinated annually for Lyme disease, which could potentially explain the elevated titers, but a Western blot analysis was not performed. The blood cholinesterase activity and lead and ivermectin concentrations were also within reference ranges (Table 2).

Based on these results, hepatic encephalopathy became the primary differential diagnosis, although not all of the dog's clinical signs were consistent with classic manifestations of a metabolic encephalopathy.3 We planned a laparoscopic exploratory examination and hepatic biopsy. The results of prothrombin time and activated partial thromboplastin time tests performed before surgery were normal (Table 2). The patient was premedicated with hydromorphone, and anesthesia was induced with propofol. Isoflurane and oxygen were given to sustain anesthesia. We performed a second abdominal ultrasonographic examination while the dog was anesthetized to look for anomalous portosystemic vasculature, but none were found. Gross laparoscopic findings were largely unremarkable, although the liver subjectively appeared slightly small. No evidence of anomalous vasculature was present. We submitted five hepatic biopsy samples obtained from the right lateral, right medial, and caudate liver lobes for histologic examination, quantitative copper analysis (Table 2), and aerobic and anaerobic bacterial culture and antimicrobial sensitivity testing.

Figure 1 : A photomicrograph of a hepatic biopsy sample of the dog in this case. Note the absence of normal portal and central areas of the hepatic lobule and random placement of small vessels and bile ductules, which are consistent with hepatic microvascular dysplasia (hematoxylin-eosin stain; bar = 15 μm).
We began administering lactulose (0.5 ml/kg orally t.i.d.) after recovery from anesthesia to reduce ammonia production and facilitate ammonia elimination from the gastrointestinal system. Lactulose accomplishes this by acidifying intestinal contents, which allows colonic trapping of ammonium ions and decreased systemic absorption of ammonia. It also provides a nonprotein substrate for colonic bacteria and causes osmotic diarrhea.4 The hepatic culture results were negative for both aerobic and anaerobic bacterial growth, but the doxycycline administration makes interpretation of the culture results difficult. Histologic examination of the hepatic biopsy samples revealed some portal areas with a normal complement of artery, vein, and bile duct, but most fields had no discernible portal or central areas. Instead, small vessels and bile ductules were randomly positioned throughout the sections. The histopathologic diagnosis was hepatic microvascular dysplasia (Figure 1). The sections were reviewed by three board-certified anatomic pathologists, all of whom concurred with the diagnosis.


Over the next three days, the patient's clinical signs and hypokalemia resolved, and parenteral fluid therapy was tapered off gradually. By the fourth day of hospitalization, the dog was clinically normal and eating and drinking. Outpatient therapy consisted of a diet specifically formulated for dogs with hepatic dysfunction (Prescription Diet Canine l/d—Hill's Pet Nutrition), oral doxycycline (6.1 mg/kg b.i.d. for 10 days), and lactulose (0.5 ml/kg orally t.i.d.).


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