When presented with a patient affected by sago palm toxicosis, routine diagnostics (eg, CBC, chemistry panel, urinalysis) should be performed. While the patient is hospitalized, daily blood work should include packed cell volume/total solids, blood glucose, and hepatic panel (including liver enzymes and albumin). For patients that develop evidence of hepatic injury, additional clinicopathologic and diagnostic testing should include coagulation parameters (eg, prothrombin time [PT], activated partial thromboplastin time [aPTT], platelet count,) serum bile acids (or ammonia), and abdominal ultrasound.
In dogs with AHN secondary to sago palm toxicosis, clinicopathologic findings may include elevations in liver enzymes (eg, aspartate transaminase, alanine aminotransferase, alkaline phosphatase) and/or abnormal bile acids; however, elevations may not occur for 24 to 48 hours and may last from 2 to 9 days.1 Other findings may include anemia (secondary to melena) or hemoconcentration (secondary to dehydration), evidence of liver failure (eg, hyperbilirubinemia, hypoalbuminemia, hypocholesterolemia, hyper- or hypoglycemia, hyperlactatemia), leukocytosis, thrombocytopenia, and coagulopathy (eg, prolonged PT, aPTT). Increased blood urea nitrogen (BUN) caused by prerenal azotemia or GI bleeding2 or decreased BUN secondary to liver failure may also be seen.
Ideally, abdominal ultrasound should be performed to rule out other underlying disease (see Differential Diagnoses for Acute Hepatic Injury or Hepatopathy). However, ultrasound may not reveal any obvious gross ultrasonographic findings with AHN. To better assess this, liver biopsies should ideally be performed, provided the patient is not coagulopathic. Histopathologic lesions seen with sago palm toxicosis include marked focal centrilobular and midzonal coagulation necrosis, along with cirrhosis.2
Related Article: Diagnosing Liver Disease