Vol. 10, Issue 12, Part C (2025)

Hepatic Encephalopathy (HE) is a significant neuropsychiatric complication arising from impaired hepatic function or the diversion of portal blood away from the liver. In veterinary medicine, HE is most frequently associated with congenital or acquired portosystemic shunts (CPSS, APSS), acute hepatic failure, and chronic liver disease in dogs, while in cats it is additionally linked to hepatic lipidosis and dietary arginine deficiency. Although well documented in human medicine, HE in companion animals remains comparatively underreported, contributing to ongoing gaps in understanding pathophysiology and optimal diagnostics. The primary objective of this review is to summarize current knowledge on the classification, mechanisms, and clinical aspects of HE in dogs and cats, and to highlight parallels with human HE research.
HE is classified into three types: Type A (acute liver failure), Type B (portosystemic bypass without intrinsic liver disease), and Type C (cirrhosis or chronic hepatopathy), with severity ranging from minimal cognitive deficits to seizures and coma. The pathogenesis is multifactorial and centers on the accumulation of neurotoxins particularly ammonia resulting from impaired hepatic detoxification or shunting of portal blood. Additional contributors include altered neurotransmission, inflammatory cytokine activity, oxidative stress, electrolyte imbalances, and the accumulation of other gut-derived toxins. Ammonia-induced astrocyte swelling represents a major mechanism underlying neurologic dysfunction.
Diagnostic evaluation incorporates clinical history, neurological assessment, laboratory analyses, imaging, and, when indicated, cytology or histopathology. Treatment depends on the underlying etiology but often includes medical stabilization, ammonia-reducing strategies, nutritional modification, hepatoprotective agents, antimicrobial therapy, or surgical correction of portosystemic shunts. Early recognition and targeted therapy are critical for improving outcomes. Continued investigation is needed to refine diagnostic criteria and optimize management strategies for HE in veterinary species.