Cirrhosis; Causes, Effects, Implications, and Management
Cirrhosis is the final stage of injury to the liver. It is characterized by fibrosis of the connective tissue and degeneration of the liver cells, impairing the function of the liver. The pathophysiological causes of cirrhosis are unknown, but it is commonly seen in people suffering from biliary obstructions, chronic hepatitis and other infections of the liver, malnutrition, and alcoholism.
The most common form of the disease in the USA is Laennec's cirrhosis. It is generally associated with alcoholism, although not all alcoholics will develop it. and it may also be seen in non-alcoholics. Pathologic changes include:
- Fatty infiltration
- A proliferation of fibrous tissue
The onset of cirrhosis may be gradual, with gastrointestinal disturbances such as anorexia, nausea, vomiting, abdominal pain, and distension. Portal hypertension commonly develops with shunting of portal blood into the systemic circulation.
What are Ascites?
Ascites are the accumulation of abnormal amounts of fluid in a person's abdomen. It may develop as a result of portal vein hypertension, an obstruction of the hepatic vein, a fall in plasma colloid osmotic pressure due to impaired albumin synthesis, the increased retention of sodium, or the impaired excretion of water.
Clinical Sign and Symptoms
Clinical signs of cirrhosis include encephalopathy, ascites, bleeding, and muscle wasting. The biochemical features of cirrhosis are low serum albumin, raised alkaline phosphatase, raised aspartate transaminase (AST), and prolonged prothrombin time. Episodes of bleeding may occur and precipitate encephalopathy or ascites in susceptible patients. This bleeding is more likely in those with esophageal varices.
Varices in the esophagus and the upper part of the stomach may develop as a complication of portal hypertension.
The high blood pressure forces out pockets in the walls of the esophagus. In this condition, the level of SGOT is elevated and the BSP (bromosulphthalein) excretion time is reduced.
Vitamin deficiencies (i.e. the fat-soluble A, D, E, and K) and lower levels of hematocrit and hemoglobin are commonly seen and may be due to malnutrition, gastrointestinal bleeding, or both.
The Objectives of Management and the Role of Diet
Clinical, biochemical, and dietary data (from patient's notes and diet history) provide information for the development of a nutritional care plan for sufferers of cirrhosis. Providing a diet that will deal with the malnutrition associated with liver diseases is the goal of nutritional therapy for these patients. A diet that is high in energy is recommended-approximately 45-50 kcal per kg ideal body. weight per day.
The principles of Dietary Modification and Planning Menus
The protein of high nutritional value must be provided to enable damaged liver cells to be repaired. An intake of 1 g protein per kg body weight is the ultimate goal. However, individual requirements for protein must be considered and a patient's intake must be adjusted as the disease gets worse or improves. Most clinicians recommend an initial protein intake high enough to maintain nitrogen equilibrium but low enough to prevent hepatic coma (about 35-50 g per day). In the late stages of cirrhosis, it is usually necessary to keep the patient indefinitely on this sort of restricted protein intake. Protein intake should be restricted to less than 35 g daily if signs of coma develop.
A diet high in carbohydrates (200-300 g daily) should be provided in order to achieve the desired energy levels without using the body's own protein.
In many cirrhotic patients, fats are not well absorbed because of biliary obstructions, or a decrease in the production of bile salt, or a fatty infiltration of the liver For some patients the substitution of medium-chain triglycerides for part of the dietary fat is effective in reducing steatorrhoea; however, in advanced cirrhosis, the substitution is not recommended.
Vitamins and minerals
Malabsorption of fat-soluble and B-complex vitamins occurs in alcoholic and biliary cirrhosis. Serum calcium, magnesium, and zinc are all decreased. Potassium supplements are sometimes needed to correct a deficiency resulting from nausea, vomiting, diarrhea, antibiotic therapy, or a reduced intake of protein. Vitamin supplements may be advisable to replenish liver stores and to repair damage to tissues, especially if the patient is suffering from anorexia.
Sodium should be restricted if edema and ascites are present. A severe restriction of sodium for many months is often necessary in order to remove excess fluid. If ascites are present, sodium should be restricted to 1,500-2,000 mg per day. On such very low sodium diets, all food used must be both naturally low in sodium and prepared without compounds containing sodium. The diet needs. care in order to provide an adequate protein intake without exceeding the sodium allowance.
Reduction in the fiber content of a diet is necessary for patients with advanced cirrhosis, for whom there is a danger of hemorrhage from esophageal varices Small meals of liquid or soft food are recommended.
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