Hepar
The equine liver weighs approximately 5 kg (about 1% of body weight) and lies primarily on the right side of the abdomen, tucked against the diaphragm. Unlike many species, the horse has no gallbladder; bile is produced continuously and drains directly into the duodenum. The liver performs over 500 metabolic functions including bile production, protein synthesis, glycogen storage, detoxification, and bilirubin metabolism. It receives dual blood supply from the hepatic artery (oxygenated) and the portal vein (nutrient-rich blood from the GI tract).
The equine liver lacks a gallbladder; bile drains continuously into the duodenum via the hepatic and common bile ducts. Liver enzymes (GGT, SDH, AST, ALP) and bile acids are key diagnostic markers. The liver has remarkable regenerative capacity; clinical signs may not appear until >70% of hepatic function is lost. Ultrasound is valuable for assessing liver size and echogenicity.
Fatty infiltration of the liver, often secondary to negative energy balance.
Chronic liver damage caused by ingestion of plants containing pyrrolizidine alkaloids (e.g., Senecio spp., Crotalaria, Echium). Megalocytosis and biliary fibrosis are characteristic histopathological
Acute hepatic necrosis associated with administration of equine-origin biological products.
Inflammation of the bile ducts and liver parenchyma.
Focal bacterial infection within the liver parenchyma.
Formation of biliary calculi (gallstones) in the bile ducts. Uncommon but clinically significant when present.
Acute fatal hepatitis in foals (1-6 weeks old) caused by Clostridium piliforme. Characterized by focal hepatic necrosis with intracellular filamentous bacteria.
Fatty infiltration of the liver, often secondary to negative energy balance. Signs include: Inappetence; weight loss; jaundice; depression; elevated liver enzymes
Chronic liver damage caused by ingestion of plants containing pyrrolizidine alkaloids (e.g., Senecio spp., Crotalaria, Echium). Megalocytosis and biliary fibrosis are characteristic histopathological findings. Signs include: Weight loss; jaundice; photosensitization; neurological signs (hepatic encephalopathy); often fatal; photosensitization (unpigmented skin); icterus; hepatic encephalopathy (head pressing, aimless wandering, yawning); diarrhea
Acute hepatic necrosis associated with administration of equine-origin biological products. Signs include: Acute onset depression; jaundice; hepatic encephalopathy; head pressing; high mortality
Inflammation of the bile ducts and liver parenchyma. Signs include: Fever; jaundice; colic; weight loss; elevated GGT and bilirubin
Focal bacterial infection within the liver parenchyma. Signs include: Intermittent fever; weight loss; colic; elevated fibrinogen; detected on ultrasound
Formation of biliary calculi (gallstones) in the bile ducts. Uncommon but clinically significant when present. Signs include: Recurrent colic; weight loss; intermittent fever; icterus; elevated liver enzymes (GGT, ALP)
Acute fatal hepatitis in foals (1-6 weeks old) caused by Clostridium piliforme. Characterized by focal hepatic necrosis with intracellular filamentous bacteria. Signs include: Peracute death in foals; profound depression; fever; icterus; diarrhea; convulsions
The equine liver lacks a gallbladder; bile drains continuously into the duodenum via the hepatic and common bile ducts. Liver enzymes (GGT, SDH, AST, ALP) and bile acids are key diagnostic markers. The liver has remarkable regenerative capacity; clinical signs may not appear until >70% of hepatic function is lost. Ultrasound is valuable for assessing liver size and echogenicity.
See the Liver on our interactive 3D horse model. Open 3D Model