Chronic liver insufficiency

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)... 

Depending on the time period involved in the course of the disease, acute liver failure without pre-existing liver disease can initially be differentiated by massive liver cell disintegration due to a variety of causes. In contrast, chronic liver insufficiency with pre-existing liver disease is mostly found in advanced liver cirrhosis with a progressive loss of function. A sudden necrotising episode is also able to precipitate the change from chronic and still compensated liver insufficiency into acute liver failure ( acute on chronic ) in the same way that acute liver failure which has been overcome can develop into chronic liver insufficiency. 

Chronic liver insufficiency is due to the progression of an already existing chronic liver disease. This generally tends to be advanced cirrhosis of varied aetiology. Basically, however, any liver disease can be a potential cause of chronic liver insufficiency. Alcohol and infections as well as certain medicaments are also deemed to be common causes. A great number of substances and events can trigger liver insufficiency. 

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)... 

General manifestations of the disease The clinical picture of chronic liver insufficiency is characterized by general symptoms such as fatigue, apathy, lack of appetite, lack of concentration, infirmity, sensation of repletion and meteorism. 

Decompensation in chronic liver insufficiency is characterized by the development of severe, life-threatening complications ... 

Tab. 20.4 So-called minor signs of chronic liver insufficiency...

Ascites and oedema are also found in severe hepatic diseases, pointing to serious disorders in the water and electrolyte metabolism. These complications are signs of decompensation in fiver cirrhosis or chronic liver insufficiency. At the same time, pleural effusion may also be evident. Cirrhosis-related pleural effusion without concomitant ascites has been described as a rarity. (see chapter 16)... 

Intensive care Patients with ALE or with decompensated chronic liver insufficiency (such as coma stages II-IV, refractory ascites, hepatorenal syndrome, disseminated intravascular coagulation, gastrointestinal bleeding) require monitoring and treatment in an intensive care unit, preferably in a transplantation centre. (7,13,60, 66, 77)... 

The subacute course is rare. It is found more frequently in women than in men. The onset is acute, the symptoms are more severe and the disease progresses for months. The prognosis is serious, since chronic liver insufficiency often develops. Mortality is high. 

Complications The following complications have been reported (i.) cholangitis, (2.) obstructive jaundice, (i.) intrahepatic cholelithiasis, (4.) sepsis, (J.) portal hypertension (oesophageal varices, portal vein thrombosis, chronic Budd-Chiari syndrome, etc.), (6.) thrombosis of the inferior vena cava, (7.) amyloidosis, (8.) immune complex-associated glomerulonephritis, (9.) metastases, (10.) acute on chronic liver insufficiency or acute liver failure, and (11.) bronchobiliary fistula. 

Unlike the liver, skeletal muscle and brain are devoid of an effective urea cycle and consequently must rely on glutamine synthesis for ammonia removal. In Uver failure, muscle becomes the major route for ammonia detoxification. Evidence consistent with this notion includes reports of increased glutamine production by skeletal muscle in chronic liver insufficiency (Ganda and Ruderman, 1976). More recently it has been shown that chronic hyperammonemia resulting from portacaval... 

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