Review spotlights hepatic encephalopathy in horses
Bottom line
Hepatic encephalopathy remains a high-stakes differential in horses with acute or progressive neurologic signs, and a new review in Veterinary Clinics of North America: Equine Practice pulls together the latest thinking on how the syndrome develops and how clinicians can manage it. The article, by Sarah F. Colmer, Kathryn J. Timko, and Amanda N. Samuels, describes hepatic encephalopathy as a consequence of hepatic insufficiency or portosystemic shunting that allows ammonia and other neurotoxins to accumulate, with signs ranging from subtle behavior change to seizures and recumbency. The review also emphasizes an important clinical caveat: hyperammonemia can occur in horses without primary hepatic dysfunction, which broadens the differential list when a horse presents with encephalopathy. (aaep.org)
Why it matters: For equine veterinarians, the message is practical as much as academic. Hepatic encephalopathy can look like other neurologic emergencies, but timely recognition changes case management, safety precautions, and prognosis. Background guidance from Merck and AAEP materials supports the review’s focus on combining neurologic findings with liver-associated clinicopathologic changes, imaging, and, when needed, biopsy, while also remembering that blood ammonia can help identify gastrointestinal or nonhepatic hyperammonemia in the right case. Standard management still centers on stabilizing the horse, protecting handlers, correcting fluid, electrolyte, and glucose abnormalities, reducing intestinal ammonia production and absorption, and treating the underlying liver or shunting disorder. (merckvetmanual.com)
What to watch: Expect this review to reinforce more routine ammonia testing in neurologic horses and to sharpen discussion around how clinicians distinguish hepatic encephalopathy from nonhepatic hyperammonemic syndromes. (aaep.org)
Key facts
- Topic
- Hepatic encephalopathy in horses
- Publication
- Veterinary Clinics of North America: Equine Practice
- Authors
- Sarah F. Colmer, Kathryn J. Timko, and Amanda N. Samuels
- Cause
- Hepatic insufficiency or portosystemic shunting
- Key toxins
- Ammonia and other neurotoxins
- Clinical signs
- Subtle behavior change, ataxia, seizures, and recumbency
- Important caveat
- Hyperammonemia can occur without primary hepatic dysfunction
- Clinical takeaway
- Blood ammonia testing may help distinguish hepatic from nonhepatic encephalopathy
A newly published review in Veterinary Clinics of North America: Equine Practice is putting hepatic encephalopathy back in focus for equine clinicians, summarizing what is known about the syndrome’s pathophysiology, diagnosis, and treatment. In the review, Sarah F. Colmer, Kathryn J. Timko, and Amanda N. Samuels describe hepatic encephalopathy as a neurologic syndrome linked to hepatic insufficiency or portosystemic shunting, with ammonia and other neurotoxins central to disease expression. Clinical signs can be subtle early on, then progress to marked behavior change, ataxia, seizures, and recumbency. (merckvetmanual.com)
That focus comes amid broader renewed attention to equine liver disease. Elsevier’s listing for the upcoming Equine Practice issue frames “the equine liver” as a timely topic, citing advances in equine hepatitis and liver-related conditions in recent years. Older equine literature has long treated hepatic encephalopathy as one of the most important complications of liver failure, but newer clinical resources continue to stress that it remains both diagnostically challenging and potentially reversible if recognized early. (hatchards.co.uk)
The review’s most useful point for clinicians may be its reminder that hyperammonemia is not synonymous with primary liver failure. Published equine case reports and retrospective work describe intestinal or idiopathic hyperammonemia causing severe neurologic disease in horses without clear evidence of hepatic dysfunction. AAEP neurologic field guidelines likewise recommend adding blood ammonia to the standard workup, when feasible, to help rule out hepatic or gastrointestinal encephalopathy. That means a horse with altered mentation, head pressing, aimless wandering, or sudden aggression may warrant ammonia testing even when chemistry findings do not neatly support hepatopathy. (pubmed.ncbi.nlm.nih.gov)
On treatment, the review aligns with established equine guidance: address the underlying cause, reduce production and absorption of ammonia, and provide supportive care while protecting both the horse and staff. Merck’s large-animal guidance notes that horses with hepatic encephalopathy can be aggressive and unpredictable, so sedation may be necessary, though doses should be conservative because many sedatives depend on hepatic metabolism. Nutritional management also remains central, with small, frequent feedings and diets designed to provide energy without excessive protein burden. (merckvetmanual.com)
Direct expert commentary on this specific review was limited in public sources, but the wider veterinary literature is consistent on the main mechanisms. Companion-animal and human reviews continue to place ammonia at the center of hepatic encephalopathy pathogenesis, while also highlighting inflammation and other metabolic contributors as reasons clinical severity does not always track perfectly with a single ammonia value. A 2024 meta-analysis in human medicine again found a significant association between circulating ammonia and hepatic encephalopathy, while noting roles for creatinine, albumin, sodium, and inflammatory cytokines. That broader literature supports the equine review’s framing of hepatic encephalopathy as a multifactorial syndrome, not just an isolated lab abnormality. (pubmed.ncbi.nlm.nih.gov)
Why it matters: For veterinary professionals, especially ambulatory equine practitioners and hospital teams triaging neurologic horses, this review is a reminder to keep hepatic encephalopathy high on the list even when the presentation is messy. The syndrome sits at the intersection of internal medicine, neurology, nutrition, and emergency care. Missing it can delay appropriate diet changes, ammonia-lowering therapy, liver-directed diagnostics, and basic handler-safety measures. Just as important, recognizing that nonhepatic hyperammonemia exists can prevent clinicians from anchoring too narrowly on liver disease and overlooking gastrointestinal or other causes. (aaep.org)
For referral centers, the review also reinforces the value of a layered diagnostic approach: neurologic examination, clinicopathology, ammonia measurement, ultrasound, and biopsy when the horse is stable enough and the result will change management. Prognosis still depends heavily on the underlying disease process and the extent of fibrosis or regenerative capacity, not just the presence of encephalopathy itself. Horses that can be stabilized early may recover, while those with severe chronic fibrosis face a much narrower path. (merckvetmanual.com)
What to watch: The next step is whether this review changes everyday workups in the field and hospital, particularly by prompting more routine ammonia testing in neurologic horses and more explicit differentiation between hepatic encephalopathy and nonhepatic hyperammonemic syndromes. (aaep.org)