Hepatic Encephalopathy
Also known as: HE
CatDogUrgency: Emergency
Also known as: HE
In short
Hepatic encephalopathy is a serious, potentially life-threatening neurological syndrome caused by liver dysfunction or abnormal blood vessels (shunts) that allow toxins like ammonia to accumulate in the brain. Recognizing early signs like lethargy, pacing, and head pressing is crucial for timely veterinary intervention and management.
TL;DR. Hepatic encephalopathy is a serious neurological condition where a damaged or abnormal liver fails to filter toxins from the bloodstream, leading to brain dysfunction, disorientation, and behavioral changes.
Lethargy and depression are among the most common early signs of hepatic encephalopathy in dogs.
Hepatic encephalopathy (HE) is a complex metabolic syndrome that directly impacts the central nervous system. Under normal conditions, your pet's liver acts as a highly efficient filtration system. When your dog or cat digests food, bacteria in the intestines break down proteins, producing various byproducts. The most prominent of these byproducts is ammonia, a highly toxic compound. In a healthy animal, blood carrying these toxins travels from the intestines directly to the liver via the portal vein. The liver then extracts these toxins, detoxifies them, and converts them into harmless substances like urea, which are safely excreted in the urine.
When an animal develops hepatic encephalopathy, this vital filtration process breaks down. This failure typically occurs due to moderate to severe liver disease, liver insufficiency, or abnormal blood vessels known as portosystemic shunts. Because the liver cannot perform its detoxifying duties, gut-derived neurotoxins—primarily ammonia—bypass hepatic clearance entirely. These toxins enter the systemic bloodstream, circulate throughout the body, and cross the blood-brain barrier. Once inside the brain, they disrupt normal neurotransmitter function, cause swelling of brain cells, and lead to progressive central nervous system dysfunction.
Understanding this condition is critical for pet owners because the symptoms can be incredibly distressing and, if left untreated, life-threatening. Because the brain is highly sensitive to these circulating toxins, even minor fluctuations in liver function or diet can trigger sudden, severe neurological crises.
The underlying causes of hepatic encephalopathy in dogs and cats generally fall into two categories: structural vascular abnormalities and primary liver failure. By far, the most common cause identified in young veterinary patients is a congenital portosystemic shunt (PSS).
"In dogs and cats, congenital extrahepatic or intrahepatic portal-tosystemic venous communications are the most frequent cause of HE; up to 95% of affected animals demonstrate neurologic clinical signs."
— Small Animal Critical Care Medicine, p. 511
These portosystemic shunts are abnormal blood vessels that act as a "bypass lane," routing blood from the digestive tract directly into the main circulatory system before the liver has a chance to filter it. These shunts are typically a single congenital vessel, although multiple extrahepatic or intrahepatic shunts can occasionally occur. Another vascular cause includes hepatic arteriovenous malformations, which also disrupt normal blood flow through the liver.
In older pets, hepatic encephalopathy is more commonly associated with acquired, chronic liver diseases that lead to liver failure or cirrhosis. When liver tissue becomes severely scarred or diseased, it loses the functional capacity to process toxins.
Furthermore, several secondary factors can lower your pet's threshold for developing hepatic encephalopathy or trigger an acute crisis. For instance, concurrent inflammatory diseases can release inflammatory proteins called cytokines into the bloodstream, which worsens brain swelling and makes the brain more sensitive to ammonia. This explains why two pets with the exact same blood ammonia levels might show vastly different levels of neurological impairment. Other common triggers include high-protein meals, constipation (which increases toxin production in the gut), gastrointestinal bleeding, and certain medications.
The clinical signs of hepatic encephalopathy can be highly variable, fluctuating in severity throughout the day. They often worsen shortly after a meal when protein digestion produces a surge of ammonia.
Head pressing is a critical neurological warning sign that requires immediate veterinary attention.
Diagnosing hepatic encephalopathy requires a systematic approach. Because the neurological signs of this condition are not specific to the liver, your vet must rule out other potential causes, such as primary brain diseases, toxins, or other metabolic disorders.
"The diagnosis of HE is made when an animal has clinical signs compatible with the condition, and alterations on a biochemical panel and liver function tests confirming moderate to severe liver disease... At the same time, none of the clinical signs described are specific for HE and other potential diagnoses, including other metabolic disorders, toxin o"
— Small Animal Critical Care Medicine, p. 512
Your vet will begin with a comprehensive physical and neurological exam, followed by a suite of diagnostic tests:
Diagnostic imaging, such as ultrasound or scintigraphy, helps veterinarians identify abnormal blood vessels bypassing the liver.
The treatment of hepatic encephalopathy is divided into two phases: stabilizing an acute, life-threatening neurological crisis, and long-term medical or surgical maintenance.
An acute encephalopathic crisis is a medical emergency that requires immediate, intensive veterinary hospitalization.
For pets that cannot undergo surgery, or those being stabilized prior to surgery, long-term medical therapy focuses on reducing toxin production in the gut.
For pets diagnosed with a congenital portosystemic shunt, surgery is the treatment of choice. A surgeon will place a device (such as an ameroid constrictor) around the abnormal vessel. This device slowly closes the shunt over several weeks, allowing the liver to gradually adapt to increased blood flow without causing sudden, dangerous high blood pressure in the portal system (portal hypertension).
The long-term outlook for pets with hepatic encephalopathy depends heavily on the underlying cause and whether surgical correction is possible.
For dogs with congenital portosystemic shunts, surgical correction often permanently resolves clinical signs, allowing them to live normal, healthy lives.
For pets managed medically, the prognosis is highly variable. Some animals can achieve complete recovery and successful long-term control, especially if their acute crises are triggered by a definable, manageable event.
"The treatment of acute encephalopathic crises... is worthwhile because some animals can go on to complete recovery and successful long-term medical management, particularly if the acute crisis was triggered by a definable event (e. g. , acute GI bleeding in a dog with chronic liver disease and portal hypertension)."
— Internal Medicine, p. 625
However, if the underlying cause is progressive, end-stage liver failure (cirrhosis), medical management is palliative, aimed at maintaining quality of life for as long as possible.
Because congenital portosystemic shunts are genetic developmental defects, they cannot be prevented. However, responsible breeding practices—including screening parent dogs of predisposed breeds—can help reduce the incidence of these vascular anomalies.
For pets with known liver disease, preventing acute encephalopathic crises involves strict adherence to prescribed diets, avoiding high-protein treats, and monitoring closely for signs of gastrointestinal bleeding or infection, which can trigger a sudden neurological decline.
Hepatic encephalopathy can progress rapidly from mild lethargy to life-threatening seizures or coma. You must seek emergency veterinary care immediately if your pet exhibits any of the following signs:
If your pet has been diagnosed with liver disease and you notice subtle changes, such as a sudden loss of appetite, mild drooling, or increased lethargy, contact your veterinarian promptly to adjust their medical management before a crisis develops.
Several breeds of dogs and cats have a documented predisposition to congenital portosystemic shunts or underlying liver conditions that can lead to hepatic encephalopathy.
If you own one of these breeds, pay close attention to any subtle behavioral changes, slow growth, or prolonged recovery from anesthesia, as these can be early indicators of an underlying liver shunt.
Treatment must be prescribed by a licensed veterinarian based on your pet. Specific drug doses are intentionally not shown here.
Hepatic encephalopathy is a serious, potentially life-threatening neurological syndrome caused by liver dysfunction or abnormal blood vessels (shunts) that allow toxins like ammonia to accumulate in the brain. Recognizing early signs like lethargy, pacing, and head pressing is crucial for timely veterinary intervention and management.
Central blindness、Depression、Disorientation、Lethargy、Personality change、Polydipsia、Polyuria、Ptyalism
Ammonia tolerance test、Biochemical panel、Blood ammonia levels、Liver histopathology、Pre- and postprandial bile acids、Rectal portal scintigraphy
Treatment must be prescribed by a licensed veterinarian based on your pet. Specific drug doses are intentionally not shown here.
This article is for general education and is not a substitute for professional veterinary advice. If your pet is unwell, please consult a veterinarian.
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