Case 180615-1

11-year-old, male, castrated, mixed-breed dog.

The patient’s owners noticed few drops of fresh blood on the patient’s bed, pale mucous membranes, black stools, and lethargy for approximately three days duration. The referring veterinarian noted that the patient was anemic. Ultrasound at that time revealed a suspected gastric ulcer, hepatomegaly with an irregular contour, abdominal lymphadenomegaly, splenic nodules, and gallbladder thickening. The patient was later submitted to an emergency service, at which point it was bradycardic and had marked subcutaneous edema. Blood work showed anemia, hypoproteinemia, hypoalbuminemia, lowered BUN, hypocholesterolemia, hypoglycemia, and prolonged clotting times (indicative of hepatic failure). Due to concern for hepatic neoplasia and poor prognosis, humane euthanasia was elected.

The subcutaneous tissue along the ventral aspect of the neck, the ventral aspect of the abdomen, and the distal aspects of the limbs was expanded up to 1 cm thick by yellow-tinged, clear, gelatinous material (edema). The liver was 1.1 kg (2.8% of body weight). More than 100, irregularly shaped, 0.5- to 2-cm-diamter, well-demarcated, slightly depressed, soft, dark-red foci were scattered on the capsular surface of all liver lobes and extended into the subjacent parenchyma. The remaining hepatic parenchyma was firm and yellow-tinged. The adipose tissue within the omentum and retroperitoneum was also yellow-tinged.

One section of liver is examined. Areas of viable hepatic parenchyma abut large regions of massive hepatocellular atrophy and loss. Atrophied hepatocytes form discontinuous, irregularly oriented hepatic cords that are isolated from each other by small to large amounts of loosely packed collagen fibers. Rare hepatocytes are swollen with pale eosinophilic cytoplasm and karyorrhectic nuclei. Small numbers of lymphocytes and macrophages that often contain intracytoplasmic, finely granular, gold-brown pigment (hemosiderin) are present within the collagen. Sinusoids are moderately to markedly dilated and congested. Areas of hepatocellular loss are replaced by large lakes of hemorrhage and fibrin. In unaffected areas, centrilobular hepatocytes have pale eosinophilic cytoplasm with intracytoplasmic, clear, variably sized vacuoles.

Liver tissue was submitted for amanitin quantification and results were within normal limits. A trichrome stain showed marked fibrosis within the sinusoids. A reticulin stain highlighted severe loss of normal lobular architecture in the regions of sinusoidal dilation and hemorrhage. Immunohistochemistry for CD31 and Factor VIII showed immunoreactive cells lining the sinusoids in areas within and adjacent to dilated sinusoids.

N/A.

Liver: hemangiosarcoma

The acute onset of clinical signs in conjunction with hepatocellular and renal proximal tubular necrosis initially raised the concern for hepatotoxicity, especially amanitin intoxication. However, amanitin was not detected in the liver tissue submitted for toxicology and additional toxicologic testing was not pursued. The multifocal pattern of the lesions was considered to be inconsistent with a toxic insult, which typically produces a more zonal pattern of hepatocellular destruction. The fibrosis present in the sinusoids would also be unusual for an acute actinghepatocellular toxin.

Immunohistochemistry with CD31 and Factor VIII revealed immunoreactive cells lining the sinusoids. It is challenging to determine whether these represent reactive endothelial cells or hemangiosarcoma. Given the clinical presentation, the presence of a hemangiosarcoma in the right auricle, and atypia seen in the immunoreactive endothelial cells, an intrasinusoidal hemangiosarcoma is the most likely diagnosis. The amount of liver parenchyma affected was enough to result in hepatic failure.

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