An 11-year-old 54.9-lb (27-kg) neutered male mixed-breed dog was presented to Long Island Veterinary Specialists for evaluation
of lethargy and depression of several days' duration. Three days before presentation, the owner had observed a generalized
seizure that lasted several minutes. The dog had a previous history of epilepsy, which was being treated with phenobarbital
(2.5 mg/kg orally b.i.d.), and of urinary incontinence, which was being treated with phenylpropanolamine (1 mg/kg orally b.i.d.).
Two and a half years before this presentation, the dog had been presented to Long Island Veterinary Specialists for evaluation
of a large palpable abdominal mass that had been confirmed on abdominal ultrasonographic examination. An exploratory laparotomy
had revealed a pale liver and a 30-x-20-cm splenic mass. A splenectomy had been performed. Histologic examination of a liver
biopsy sample had revealed no marked lesions. Histologic examination of the splenic tissue had revealed hyperplastic nodules
in the parenchyma. These lesions consisted of multiple coalescing nodules of lymphoid tissue with hyperplastic reticuloendothelial
stroma interspersed throughout and focally extensive hemorrhagic and coagulation necrosis consistent with nodular splenic
hyperplasia with an acute splenic hematoma. The dog had recovered from surgery without incident, and no abnormalities had
been found at a recheck examination two weeks after surgery.
Two months later, the dog had been presented for evaluation of unproductive vomiting soon after a meal. Radiographic evaluation
of the abdomen had been consistent with gastric dilatation-volvulus. Emergency gastric decompression had been performed with
an orogastric tube. An exploratory laparotomy had confirmed gastric dilatation-volvulus; the stomach had been repositioned,
and a belt-loop gastropexy had been performed. The liver had appeared mottled. Histologic examination of a liver biopsy sample
had revealed vacuolar degeneration of the hepatocytes and several small discrete, nonstaining, confluent vacuoles within the
cytoplasm of the hepatocytes; these changes were consistent with mild, diffuse hepatic lipidosis. The dog had recovered without
incident, and no abnormalities had been found at a recheck examination three weeks after surgery.
Physical examination and diagnostic procedures
At presentation, the dog had pale mucous membranes and a distended abdomen. A complete blood count, serum chemistry profile,
and urinalysis had been performed four days before presentation. Abnormal complete blood count findings (Table 1) had been a leukocytosis, a neutrophilia with a left shift, and a moderate regenerative anemia. The differential diagnoses
for these abnormalities were trauma, a coagulopathy, hemorrhage, neoplasia, and immune-mediated, infectious, and inflammatory
diseases. The serum chemistry profile had revealed only an elevated alkaline phosphatase activity (234 U/L, reference range
= 5 to 131 U/L), which we thought could be due to drug-induced or hepatobiliary disease or an endocrinopathy. The urine had
been cloudy with 1+ protein and a specific gravity of 1.040.
Table 1. Abnormal Complete Blood Count Results
We performed abdominocentesis and obtained serosanguineous fluid. Cytologic examination of the fluid revealed blood, scattered
erythrophagocytic macrophages, and a few mesothelial cells, which were consistent with chronic hemoperitoneum. Our differential
diagnoses for the hemoperitoneum were trauma, ruptured neoplasms, and coagulopathies. We also performed an abdominal ultrasonographic
examination, which revealed two large (about 5-x-7-cm), complex masses within the right and left liver lobes. Our differential
diagnoses for the masses included neoplasia and nodular hyperplasia. No abnormalities were seen on a three-view radiographic
metastatic screening of the thorax.