What causes HPN in dogs? - briefly
The exact cause of hepatocellular necrosis (HPN) in dogs remains largely unknown, though it is often associated with exposure to toxic substances or certain medications that can damage liver cells. Additionally, some underlying health conditions such as viral infections and immune-mediated diseases may contribute to the development of HPN in dogs.
What causes HPN in dogs? - in detail
Hepatic portosystemic encephalopathy (HPN) in dogs is a complex condition that arises due to various factors, primarily related to liver dysfunction and abnormal shunting of blood. The liver plays a critical role in detoxifying substances such as ammonia, which is produced by the intestines during protein metabolism. When the liver is compromised or when there are anomalies that bypass the liver's filtration system, ammonia and other toxins can accumulate in the bloodstream, leading to neurological symptoms characteristic of HPN.
One of the primary causes of HPN in dogs is congenital portosystemic shunts (CPSS). These are abnormal connections between the portal vein, which carries blood from the intestines and spleen to the liver for detoxification, and the systemic circulation, typically through the caudal vena cava. In CPSS, a portion of the blood bypasses the liver, allowing toxins such as ammonia to enter the general circulation without being filtered out. This congenital defect can occur in various forms, including single extrahepatic shunts (the most common type), multiple extrahepatic shunts, and intrahepatic shunts.
Another significant cause of HPN is liver disease, which can be either acute or chronic. Acute liver failure may result from toxin exposure, such as ingestion of certain drugs (e.g., acetaminophen), plants (e.g., blue-green algae), or mushrooms (e.g., Amanita species). Chronic liver disease can be due to various factors, including infectious agents like leptospirosis, copper storage diseases in breeds predisposed to copper accumulation (e.g., Bedlington Terriers and Dalmatians), and chronic inflammatory conditions such as autoimmune hepatitis. These conditions lead to progressive liver damage and impairment of its detoxification capabilities.
Furthermore, certain acquired portosystemic shunts can develop in dogs due to various pathological processes. For instance, portal hypertension, which is an increase in pressure within the portal venous system, can result from conditions such as cirrhosis or thrombosis of the portal vein. This elevated pressure can lead to the formation of acquired shunts that bypass the liver and contribute to the development of HPN.
In summary, HPN in dogs is caused by a combination of congenital and acquired factors that compromise the liver's ability to filter toxins from the bloodstream. Congenital portosystemic shunts are a common cause, along with liver disease and acquired shunts resulting from portal hypertension. Understanding these underlying mechanisms is crucial for effective diagnosis and treatment of HPN in canine patients.