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Hepatic Encephalopathy in Dogs

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Introduction

Hepatic encephalopathy is a neurological condition that can arise due to a portosystemic shunt (PSS) or liver dysfunction. Dogs suffering from this condition will have impaired mental status, which is classified in stages depending on the severity of the disease. Hepatic encephalopathy affects dogs of all ages.

Causes of Hepatic Encephalopathy in Dogs

Hepatic encephalopathy is often associated with the presence of a portosystemic shunt. In a normal system, the portal vein collects blood from the systemic circulation and channels it to the liver where toxins are filtered and removed from the blood. In animals with a portosystemic shunt, this normal process is disrupted since there’s an abnormal connection between the portal vein or one of its branches to another vein, effectively causing the blood to bypass filtration by the liver.

Aside from a PSS, a dysfunctional liver could also lead to this condition. Due to an impaired liver function, the concentration of toxins in the blood increases, which subsequently leads to neurological abnormalities.

Other underlying conditions and risk factors could precipitate the development of this condition. Pet owners should be mindful of:

  • Hypokalemia (decreased potassium levels in the blood)
  • Alkalosis (a condition wherein the body’s pH is too high)
  • Dehydration
  • Gastrointestinal bleeding
  • Medications like tetracyclines, antihistamine, and methionine
  • Transfusion—transfused blood may be incompatible or have a high concentration of ammonia or other toxins.
  • Infection
  • Some sedatives and anesthetics
  • Low blood sugar level

 Pathophysiology of Hepatic Encephalopathy in Dogs

Since blood is not filtered due to a portosystemic shunt or a dysfunctional liver, digestive waste products accumulate. Following the increased concentration of these toxic metabolites, amino acid imbalance occurs, causing abnormality in the serum. With increasing levels of toxins in the blood, brain cells are damaged and neurological functions are affected. Toxic metabolites that are often associated with neurological impairment include:

Ammonia: This compound is a by-product of the digestion of protein. In a normal process, the liver metabolizes ammonia and converts it into the non-toxic urea, which the blood carries to the kidney before excreting it in the urine. In animals with impaired liver or those with PSS, ammonia is not removed from the blood.

Mercaptans: This compound is a by-product when bacteria degrade the amino acid methionine in the digestive tract. This is another waste product that must be removed from the portal blood as well.

Aromatic amino acids: When the ratio of aromatic to branched-chain amino acid is high, amino acid imbalance occurs, leading to the progression of hepatic encephalopathy.

Clinical Signs

Clinical signs of hepatic encephalopathy in dogs are categorized into four different stages, depending on the severity of the condition.

Stage I: Pet owners will notice a slight change of demeanor in their dogs. The animal could also exhibit mild signs like lack of appetite, confusion, and irritability.

Stage II: At this point, the dog will exhibit more pronounced signs of neurological impairment like uncoordinated gait, lethargy, disorientation, blindness, and personality changes.

Stage III: If the dog’s condition progresses to this stage, pet owners will notice severe signs like incoordination, seizures, excessive production of saliva, confusion, and occasional aggression.

Stage IV: At this stage, the condition would cause complete unresponsiveness, coma, or death.

Other non-neurological signs like vomiting, diarrhea, frequent drinking and urination, as well as weight loss may also be present in all stages of the illness. Sedated animals will also experience slow recovery due to reduced metabolic function of the liver.

Diagnosis

Signs and symptoms of hepatic encephalopathy in dogs are consistent with other neurologic disorders. Thus, the veterinarian will use various diagnostic techniques to arrive at a definite diagnosis.

Blood Test

Blood tests are used to determine liver function. Most likely, the veterinarian would request tests like total protein, blood urea nitrogen, total bilirubin, total cholesterol, total ammonia, glucose, and total bile acids. Amino acid balance can also be assessed using a blood amino acid analysis. If the result reflects a high concentration of tyrosine and low branched-chain amino acid concentration, this is indicative of reduced liver function.

Imaging

While blood tests determine liver function, results from those tests alone can’t determine the definitive cause of encephalopathy. The veterinarian may require some imaging tests as well.

Ultrasound and X-ray. These imaging techniques provide the veterinarian with a visual of the liver or portal vein. However, there are instances when ultrasound results are not sharp enough and the vet may request further imaging tests. X-ray helps determine if there is enlargement or abnormality in the liver.

CT Angiography Portography Exam. If a congenital portosystemic shunt is suspected, this imaging technique may be required so that the veterinarian can have a visual of the blood vessel. However, this diagnostic test is only helpful if there is only one PSS vessel. For multiple PSS, a laparoscopic exam or liver biopsy may be needed. To perform this diagnostic test, the dog will have to be under general anesthesia.

MRI

For a more detailed visual of the brain and its processes, the veterinarian may request for an MRI (magnetic resonance imaging). This imaging test will help determine if the neurologic symptoms that the dog exhibit is related to liver disorder or some other brain diseases.

Treatment

Treatment for hepatic encephalopathy in dogs is focused on lowering ammonia levels and resolving amino acid imbalance. Underlying conditions must also be addressed. To meet these treatment goals, the veterinarian may follow one or a combination of these treatment approaches.

Medical Intervention

  • IV fluid therapy can help correct metabolic alkalosis or hypokalemia.
  • Antibiotics may also be prescribed to reduce the number of gastrointestinal bacteria.
  • A low-protein and a BCAA-rich diet may be necessary to lower ammonia levels.
  • Medications like mannitol may be used to reduce fluid build-up in the brain. Anticonvulsants can also be used for patients suffering from seizures.
  • Non-absorbable fermented carbohydrates like lactulose may be administered to decrease the absorption of ammonia.

Surgery

If a congenital portosystemic shunt is the main precipitating factor, the veterinarian may consider surgery as the best option to treat the condition. The procedure will involve the ligation of the shunt to stop it from channeling blood to the wrong part of the body.

Complications

Possible complications that can arise from this condition are nervous system damage in severe cases, post-surgical issues like wound infection or hemorrhage, and in extreme cases, this could end in death.

Prognosis and Long-term Management

Prognosis is largely dependent on the underlying condition that led to hepatic encephalopathy. At its early stages, this condition is very treatable. For dogs that undergo surgical ligation of the portosystemic shunt, the prognosis is very good and most clinical signs are resolved following the procedure.

To facilitate faster recovery and prevent recurrence of the disorder, pet owners must be proactive in following these guidelines:

  • Medications must be administered as prescribed.
  • The dog needs to be fed a specially-formulated diet designed to reduce toxins and take some of the burden off the liver.
  • Monitoring is necessary and the veterinarian may request for subsequent blood tests to check the patient’s progress. Thus, a follow-up appointment with the veterinarian may be scheduled after discharge.

Dogs with hepatic encephalopathy can relapse especially if the underlying condition is not completely cured. In this case, long-term nutritional and medical management may be needed to resolve the clinical signs of this disorder.

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