Hepatic encephalopathy in dogs: causes, diagnosis and treatment
This post looks at hepatic encephalopathy in dogs, which is a multifactorial disorder of the central nervous system with factors of varying relevance depending on the clinical situation.
Hepatic encephalopathy in dogs: causes
Hepatic encephalopathy (HE) in dogs is a complex metabolic alteration of the central nervous system, the causes of which can include hepatocellular damage, urea cycle enzyme deficiencies and vascular abnormalities:1
- Vascular abnormalities: The most common cause of HE in animals is an abnormal connection between the portal vein and the systemic circulation (a portosystemic shunt or PSS).
- Urea cycle enzyme deficiencies: Argininosuccinate synthetase deficiency can cause hyperammonaemia or hepatocellular destruction due to the liver’s inability to break down ammonia into urea.
- Hepatocellular damage: Fulminant hepatic failure can cause acute HE. It is usually associated with viral or drug-related causes. It may also be the result of acute decompensation of an otherwise stable chronic hepatobiliary disease, which triggers HE due to associated complications.
Pathophysiology
When the liver’s detoxification functions are disrupted and/or bypassed, portal blood constituents pass unaltered directly into the systemic circulation.1 Ammonia entering into the circulatory system and, ultimately, the central nervous system leads to neurological abnormalities.2
Clinical signs
The signs of hepatic encephalopathy can vary in intensity from moderate, which are difficult to identify as a significant alteration (e.g., lethargy), to severe (ataxia, weakness, stupor, pressing the head against a wall or floor, circling, amaurosis, pacing, seizures and coma).3
Affected animals may also show systemic signs associated with their liver disease, including vomiting (often the first predominant clinical presentation), diarrhoea, weight loss, polydipsia, polyuria and anorexia. Dogs with advanced liver failure may have ascites.1
Diagnosis
The diagnosis of HE should primarily be based on the anamnesis, clinical signs and additional findings.1
Laboratory tests play a role in the diagnosis of portosystemic shunts. Haematological findings include mild-to-moderate nonregenerative anaemia; blood chemistry tests generally reveal hypoalbuminaemia, decreased serum urea levels and mildly elevated ALT, AST and alkaline phosphatase. Serum bilirubin concentration is usually normal, as are functional coagulation tests. However, some animals with fulminant hepatic failure show marked increases in liver enzymes and bilirubin. Some patients may have hypercholesterolaemia and fasting hypoglycaemia. The urinalysis may return dilute urine or the presence of ammonium biurate crystals. Dogs with urate stones may also have haematuria, pyuria and proteinuria.1
More specific tests include the measurement of fasting and postprandial serum levels of ammonia and bile acids. The bile acid test is the simplest and most reliable. If there is a PSS, there will be a high postprandial concentration of bile acids in the systemic circulation. Although changes in serum bile acids are also observed in other diseases, postprandial elevation (≥ 100 µmol/L) in a young dog together coupled with microhepatia is a strong indication of a PSS.1
Testing serum ammonia gives an indication of liver function and high levels in the systemic circulation is always indicative of liver dysfunction. The chances of detecting hyperammonaemia are greater when blood is drawn a few hours after eating.1
With respect to diagnostic imaging, note that plain X-rays only provide secondary data. Arteriography has been the method of choice for years, despite being invasive. Ultrasound is useful for intrahepatic PSSs, when the abnormal vessels in the liver are dilated or they communicate with the inferior vena cava. Doppler ultrasound can identify the location of the suspect vessel and direction of blood flow.1
HE produces significant changes in the electroencephalogram. Triphasic waves focused in the temporal areas have been reported in dogs.1
Magnetic resonance imaging reveals characteristic changes of HE. Hyperintense lesions in the basal ganglia (particularly the lentiform nucleus – the putamen and the globus pallidus), seen in the T1-weighted sequence, have been widely reported in humans. The hyperintense regions are thought to be due to manganese deposition.1
The use of scintigraphy is well documented in the diagnosis of hepatocellular disease in domestic animals. These images are based on the detection of the radiation emitted by the radiopharmaceutical.1 Another application of scintigraphy in veterinary medicine is the diagnosis of PSSs. The technique used is called transcolonic portal scintigraphy. It is the method of choice as it is bloodless and can be used to quantify the scope of the PSS anomaly. This means a prognosis can be developed and the patient can be reassessed after its surgical resolution.1
Treatment
The therapeutic goal in HE patients is to restore normal neurological function. This involves identifying and correcting triggers, reducing the absorption of toxins produced by enteric organisms (primarily ammonia) and reducing the interaction between enteric bacteria and nitrogenous substances.1
The basic approach to HE management combines a low-protein diet, agents that act locally to reduce the formation of absorbable ammonia and speed up intestinal evacuation, and antibiotics to eliminate ammonia-producing bacteria and other enteric toxins. Treatment should be implemented for the indefinite control of clinical signs, as in chronic liver failure or acquired PSS, or for symptomatic control prior to corrective surgery.1
References:
1. Pellegrino, F. C. (2009). Encefalopatía hepática en perros y gatos. Anales De Veterinaria De Murcia 25; 21–45. Accessed at https://revistas.um.es/analesvet/article/view/100161
2. Gow G.A. (2017). Hepatic Encephalopathy. Veterinary Clinics of North America: Small Animal Practice 47; (3): 585–599.
3. Fossum T.W. et al. Cirugía en pequeños animales (3rd ed., 2009). Chap. 20, 543. Elsevier España.
