Portal hypertension, defined as portal vein intravascular pressure > 10 mmHg, is the result of increased vascular resistance in the portal circulation, increased portal venous blood flow, or both.
In veterinary medicine, where portal pressure is seldom measured directly, the diagnosis of portal hypertension often is inferred from identification of associated complications including multiple acquired portosystemic shunts, ascites and hepatic encephalopathy.
The portal vein, which receives blood from the intestines, spleen and stomach, can be compromised vascularly by a number of conditions such as:
- Congenital or acquired portosystemic shunts
- Congenital hepatic fibrosis
- Arterioportal fistula
- Chronic hepatitis
- Encapsulating peritoneal sclerosis
Portal hypertension in dogs can lead to arteriovenous shunts either prehepatic, intraheptic or posthepatic (vena caval). Additional complications such as hepatic fibrosis and cirrhosis, ascites and hypersplenism can also develop. Alterations in pancreatic perfusion, usually marked pancreatic vein distension, may result predispose to development of pancreatitis.
Clinical symptoms are often absent, but mental depression, lethargy, ascites and abdominal distension may be evident. The ascites, which is formed due to accumulation of a pure transudate abdominal effusion in the absence of significant hypoalbuminaemia is uncommon in dogs and characteristic of pre-sinusoidal portal hypertension.
Sublingual vein distension may be apparent on close inspection of the tongue.
Blood tests often reveal elevated levels of ammonia and other encephalotoxins related to hepatic encephalopathy.
Diagnosis usually requires ultrasonographic imaging or radiographic dye imaging (computed tomography angiography) to confirm the suspicion.
Treatment of portal hypertension primarily is aimed at controlling the complications of portal hypertension, especially ascites and hepatic encephalopathy and addressing the initiating cause.
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