Cirrose hepática associada à ingestão de Cycas revoluta em canino

Abstract

Background: Cycas revoluta (“sago palm”) is a toxic ornamental plant which, when ingested, can cause hepatotoxic effects, gastrointestinal signs, and neurological alterations. Albeit rarely, C. revoluta ingestion can culminate with chronic severe hepatitis associated with hepatic fibrosis. The objective of this work is to report a case of hepatic cirrhosis consequent to ingestion of C. revoluta in a dog and describe the clinical and pathological aspects that accompany the development of chronic hepatopathy, as a way to provide information that may help diagnosis of this condition. Case: A 9-month-old male mongrel dog was presented for examination with a history of increased abdominal volume and anorexia 20 days after ingesting the seeds of Cycas revoluta. Laboratory exams revealed hypochromic microcytic anemia, neutrophilic leukocytosis, monocytosis, thrombocytopenia, decreased albumin, and elevation of the enzymes alanine aminotransferase and alkaline phosphatase. Ultrasound scanning showed presence of hepatomegaly, a heterogeneous hepatic parenchyma, and free fluid in the peritoneum. The animal was treated and was discharged from the hospital. Twenty days later, the patient returned to the hospital exhibiting prostration, vomiting, ascites, and pale mucous membranes. The alterations observed in the previous laboratory exams persisted except for thrombocytopenia, which was absent. A new treatment was administered, and the animal was discharged three days later. However, the patient returned once again exhibiting hyporexia, hemorrhagic diarrhea, and slight prostration that progressed to severe prostration, lateral decubitus and death approximately two months after ingesting the plant. Necropsy revealed a markedly poor body condition, slight icterus, limb edema, ascites and hydrothorax, and an atrophied liver with a yellowish color and an irregular, but firm, capsule surface. Additional alterations included portosystemic shunts in mesenteric blood vessels, a dark red content in the lumen of the intestine along with reddened mesenteric lymph nodes, and edema and emphysema in the lungs. Histologically, there was proliferation of fibrous connective tissue in the hepatic parenchyma with the formation of fibrous bridges, regenerative nodules, slight biliary duct proliferation, and moderate, diffuse intracytoplasmic vacuolization in hepatocytes. Discussion: The diagnosis of poisoning by ingestion of Cycas revoluta was based on the observation of the ingestion of the plant in addition to the clinical signs, complementary exams, and pathological findings. The clinical signs were characteristic of involvement of the digestive tract and acute hepatic lesion caused by C. revoluta. The biochemical alterations and the clinicopathological findings observed indicated occurrence of hepatic failure after ingestion of the plant. Anemia, neutrophilia, thrombocytopenia, elevation of hepatic enzymes and hypoalbuminemia as seen in this case are commonly described in cases of poisoning by C. revoluta. Edema, icterus and hemorrhage are consequent to hepatic failure caused by necrosis of hepatocytes and their replacement by proliferation of fibrous connective tissue, which characterizes a chronic histologic pattern. The observation of cirrhosis at the pathological examination indicated occurrence of a chronic hepatopathy that resulted from loss of hepatocytes consequent to acute lesion caused by ingestion of the plant.