Decompensation portal

Hepatobiliary disease occurs due to bile duct obstruction from abnormal bile composition and flow. Hepatomegaly, splenomegaly, and cholecystitis may be present. Hepatic steatosis may also be present due to effects of malnutrition. The progression from cholestasis (impaired bile flow) to portal fibrosis and to focal and multilobar cirrhosis, esophageal varices, and portal hypertension takes several years. Many patients are compensated and asymptomatic but maybe susceptible to acute decompensation in the event of extrinsic hepatic insult from viruses, medications, or other factors.7... 

Approximately 20% of patients with chronic HBV infection develop complications of decompensated cirrhosis, including hepatic insufficiency and portal hypertension. HBV is a risk factor for development of hepatocellular carcinoma. 

Azizov KhA (1998) Surgical treatment of the patients with a liver cirrhosis in conditions portal hypertension decompensation with ascite syndrome. MD Thesis (in Russian) Tashkent, Uzbekistan, p 45... 

Drugs that affect coagulation (e.g. niacin, fibrates) should be avoided or used with caution in coagulopathy or in patients who have previously decompensated or who have varices/portal hypertension. They may also... 

Both drugs are gastric irritants and should probably be avoided in patients with varices or a history of variceal bleeding or coagulopathy, or a risk thereof. Niacin can also cause thrombocytopenia. This patient has a varix and would be at risk of a variceal bleed if decompensation occurred. Niacin and acipimox also commonly cause pruritus. They are also vasodilators and may potentiate the effect of drugs that lower blood pressure (spironolactone, propranolol, furosemide), which are used to treat ascites and portal hypertension. 

Despite cirrhosis, this patient is maintaining good hepatocyte function (normal albumin and bilirubin, mildly raised INR) and the metabolic and excretory capacity of the liver should not be significantly reduced. The patient has portal hypertension, so blood flow to the liver will be impaired, which will reduce the first-pass metabolism of highly extracted drugs (extraction ratio >0.7). This will result in greater bioavailability of oral doses of these drugs. It is important to note that the patient could rapidly deteriorate into a state of decompensation where liver function would be markedly affected. 

Transmission of HBV occurs sexually, parenteraUy, and perinataHy. In the United States, transmission occurs predominantly through sexual contact or injection-drug use. International travel is also an important risk factor. Approximately 20% of patients with chronic HBV infection develop complications of decompensated cirrhosis, including hepatic insufficiency and portal hypertension. HBV is a risk factor for development of hepatocellular carcinoma. 

The decompensated stage, i.e. manifest liver insufficiency, can present as cellular decompensation (e. g. in the case of acute liver failure due to toxic or inflammatory mass necrosis) or be expressed only in the form of portal decompensation (e.g. in cases of postsinusoidal intra-hepatic portal hypertension). As a rule, chronic liver insufficiency is accompanied by a combined decompensation with a loss in function of the liver cells and, at the same time, the sequelae of portal decompensation (collateral varicosis, encephalopathy, ascites, hepatorenal syndrome, variceal bleeding), (see chapters 15 19 and 35)... 

The clinical picture of chronic liver insufficiency comprises both a compensated and decompensated form. These two stages of manifest chronic liver insufficiency affect the hepatocellular area or the portal system either exclusively or predominantly (= cellular or portal compensation or decompensation) mostly they occur as a combined form of disease. The resulting spectrum of clinical and laboratory findings will reflect either a global or partial insufficiency of the liver, (s. p. 376)... 

Portal decompensation The various forms manifest as (i.) hypersplenism, (2.) increasing collateral varicosis with a simultaneous rise in the splanchnic flow due to hyperdynamic circulation and vasodilatation in the area of the splanchnic vessels, (3.) hepatic encephalopathy, and (4.) oedema and ascites. (see chapters 14,15 and 16)... 

Amiodarone has been associated with steatohepadtis with advanced fibrosis, presenting with hepatic decompensation and portal hypertension, with ascites and recurrent hemorrhage from esophageal varices [42 ]. There was marked histological similarity between amiodarone-induced liver disease and alcoholic and non-alcoholic steatohepatitis. 

Resection is currently indicated among patients with single asymptomatic HCC and extremely well-preserved liver function, who have neither clinically significant portal hypertension nor abnormal bilirubin (Bruix and Llovet 2002 Llovet et al. 2003). However, less than 5% of cirrhotic patients with HCC fit these criteria (Llovet et al. 1999). Liver transplantation benefits patients who have decompensated cirrhosis and one tumor smaller than 5 cm or up to three nodules smaller than 3 cm, but donor shortage greatly limits its applicability (Bruix and... 

---