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LIVER CIRRHOSIS.

Cirrhosis is a consequence of chronic liver disease characterized by replacement of liver tissue by fibrous scar tissue as well as regenerative nodules , leading to progressive loss of liver function. Cirrhosis is most commonly caused by alcoholism and hepatitis C, but has many other possible causes.

Causes
Alcoholic liver disease (ALD). This develops in 15% of individuals who drink heavily for more than a decade. Alcohol seems to injure the liver by blocking the normal metabolism of protein, fats, and carbohydrates. Patients may also have concurrent alcoholic hepatitis with fever, hepatomegaly, jaundice, and anorexia.

Chronic hepatitis C. Infection with this virus causes inflammation, and low grade damage to the liver that over several decades can lead to cirrhosis.

Chronic hepatitis B. The hepatitis B virus is probably the most common cause of cirrhosis worldwide. Hepatitis B causes liver inflammation and injury that over several decades can lead to cirrhosis. Hepatitis D is dependent on the presence of hepatitis B, but accelerates cirrhosis in co-infection.

Non-alcoholic steatohepatitis (NASH). In NASH, fat builds up in the liver and eventually causes scar tissue.

Primary biliary cirrhosis. May be asymptomatic or pt may complain of fatigue, pruritus, and non-jaundice skin hyperpigmentation with hepatomegaly. There is prominent alkaline phosphatase elevation as well as elevations in cholesterol and bilirubin.

Primary sclerosing cholangitis. PSC is a progressive cholestatic disorder presenting with pruritus, steatorrhea, fat soluble vitamin deficiencies, and metabolic bone disease. There is a strong association with inflammatory bowel disease (IBD), especially ulcerative colitis.

Autoimmune hepatitis. This disease is caused by the immunologic damage to the liver causing inflammation and eventually scarring and cirrhosis.

Hereditary hemochromatosis. Usually presents with family history of cirrhosis, skin hyperpigmentation, diabetes mellitus, pseudogout, and/or cardiomyopathy, all due to signs of iron overload

Wilson's disease. Autosomal recessive disorder characterized by increased hepatic copper content on liver biopsy.

Alpha 1-antitrypsin deficiency (AAT). Autosomal recessive disorder. Patients may also have COPD, especially if they have a history of tobacco smoking. Serum AAT levels are low.

Cardiac cirrhosis. Due to chronic right sided heart failure which leads to liver congestion.

Cystic fibrosis Drugs or toxins Certain parasitic infections (such as schistosomiasis)

Symptoms
Many people with cirrhosis have no symptoms in the early stages of the disease. However, as scar tissue replaces healthy cells, liver function starts to fail and a person may experience the following symptoms:

Exhaustion, fatigue, loss of appetite, nausea, weakness,

weight loss, abdominal pain As the disease progresses, complications may develop. In some people, these may be the first signs of the disease.

Complications of Cirrhosis
Edema and ascites. This develops when the liver loses its ability to make the albumin. Bruising and bleeding. Jaundice. Due to decreased absorption of bilirubin.

Pruritus. Bile products deposited in the skin may cause intense itching. Gallstones. If cirrhosis prevents bile from reaching the gallbladder, gallstones may develop.

Hepatic encephalopathy - the liver does not clear ammonia and related nitrogenous substances from the blood, which are carried to the brain, These toxins can dull mental functioning and cause personality changes, coma, and even death. Signs of the buildup of toxins in the brain include neglect of personal appearance, unresponsiveness, forgetfulness, trouble concentrating, or changes in sleep habits.

Sensitivity to medication. Cirrhosis slows the liver's ability to filter medications from the blood. This causes a person to be more sensitive to medications and their side effects.

Portal hypertension. Normally, blood from the intestines and spleen is carried to the liver through the portal vein. But cirrhosis slows the normal flow of blood through the portal vein, which increases the pressure inside it. this leads to the following complications:

Esophageal Varices. When blood flow through the portal vein slows, blood from the intestines and spleen backs up into blood vessels in the stomach and esophagus.

This enlarged blood vessels,have thin walls and carry high pressure, and thus are more likely to burst. If they do burst, the result is a serious bleeding problem in the upper stomach or esophagus that requires immediate medical attention

Liver cancer. Hepatocellular carcinoma, a type of liver cancer commonly caused by cirrhosis. Problems in other organs e.g.

Cirrhosis can cause immune system dysfunction, leading to infection.) Fluid in the abdomen (ascites) may become infected with bacteria normally present in the intestines (spontaneous bacterial peritonitis). Hepatorenal syndrome - insufficient blood supply to the kidneys, causing acute renal failure. This complication has a very high mortality (over 50%).

Diagnosis
The gold standard for diagnosis of cirrhosis is a liver biopsy, through a percutaneous transjugular laparoscopy, or fine-needle approach. However, a biopsy is not necessary if the clinical, laboratory, and radiologic data suggests cirrhosis.

Lab findings
The following findings are typical in cirrhosis: Aminotransferases - AST and ALT are moderately elevated, Alkaline phosphatase - usually slightly elevated. Bilirubin - may elevate as cirrhosis progresses. Albumin - levels fall as the synthetic function of the liver declines with worsening cirrhosis since albumin is exclusively synthesized in the liver

Prothrombin time - increases since the liver synthesizes clotting factors. Globulins - increased due to shunting of bacterial antigens away from the liver to lymphoid tissue. Serum sodium - hyponatremia due to inability to excrete free water resulting from high levels of ADH and aldosterone.

Thrombocytopenia - due to both congestive splenomegaly as well as decreased thrombopoietin from the liver. Coagulation defects - the liver produces most of the coagulation factors and thus coagulopathy correlates with worsening liver disease.

Pathophysiology
The liver plays a vital role in synthesis of proteins (e.g. albumin, clotting factors and complement), detoxification and storage of vitamin. In addition, it participates in the metabolism of lipids and carbohydrates. Cirrhosis is often preceded by hepatitis and fatty liver (steatosis), independent of the cause. If the cause is removed at this stage, the changes are still fully reversible.

The pathological hallmark of cirrhosis is the development of scar tissue that replaces normal parenchyma, blocking the portal flow of blood through the organ and disturbing normal function.

Research shows the pivotal role of stellate cell, a cell type that normally stores vitamin A, in the development of cirrhosis. Damage to the hepatic parenchyma leads to activation of the stellate cell, which becomes contractile and obstructs blood flow in the circulation.

The fibrous tissue bands separate hepatocyte nodules, which eventually replace the entire liver architecture, leading to decreased blood flow throughout. The spleen becomes congested, which leads to hypersplenism and increased sequestration of platelets.

Treatment
liver damage from cirrhosis cannot be reversed, but treatment could stop or delay further progression and reduce complications. A healthy diet is encouraged, as cirrhosis may be an energyconsuming process. Close follow-up is often necessary..

Antibiotics will be prescribed for infections, and various medications can help with itching. laxatives, such as lactulose, decrease risk of constipation; their role in preventing encephalopathy is limited

Treating underlying causes


Alcoholic cirrhosis caused by alcohol abuse is treated by abstaining from alcohol. Treatment for hepatitis-related cirrhosis involves medications used to treat the different types of hepatitis, such as interferon for viral hepatitis and corticosteroids for autoimmune hepatitis.

Cirrhosis caused by Wilson's disease, in which copper builds up in organs, is treated with chelation therapy (e.g. penicillamine) to remove the copper.

Preventing further liver damage Regardless of underlying cause of cirrhosis, alcohol and acetaminophen, as well as other potentially damaging substances, are discouraged. Vaccination of susceptible patients should be considered for Hepatitis A and Hepatitis B.

Prevention of complications
Ascites Salt restriction is often necessary, as cirrhosis leads to accumulation of salt (sodium retention). Diuretics may be necessary to suppress ascites.

Esophageal variceal bleeding For portal hypertension, propranolol is a commonly used agent to lower blood pressure over the portal system. In severe complications from portal hypertension, transjugular intrahepatic portosystemic shunting is occasionally indicated to relieve pressure on the portal vein. As this can worsen encephalopathy, it is reserved for those at low risk of encephalopathy, and is generally regarded only as a bridge to liver transplantation or as a palliative measure.

Hepatic encephalopathy High-protein food increases the nitrogen balance, and would theoretically increase encephalopathy; in the past, this was therefore eliminated as much as possible from the diet. Recent studies show that this assumption was incorrect, and high-protein foods are even encouraged to maintain adequate nutrition.

Hepatorenal syndrome The hepatorenal syndrome is defined as a urine sodium less than 10 mmol/L and a serum creatinine > 1.5 mg/dl (or 24 hour creatinine clearance less than 40 ml/min) after a trial of volume expansion without diuretics.

Spontaneous bacterial peritonitis Cirrhotic patients with ascites are at risk of spontaneous bacterial peritonitis. (norfloxacin 400 mg PO bid for 7 d; ciprofloxacin and other broad-spectrum antibiotics can be used.

Transplantation If complications cannot be controlled or when the liver ceases functioning, liver transplantation is necessary. Survival from liver transplantation has been improving over the 1990s, and the five-year survival rate is now around 80%, depending largely on the severity of disease and other medical problems in the recipient.

mgt
There is no cure for this condition and mangement aims at attempts to control the aetiologic factors such as alcoholism and preventing further damage to the liver and giving symptomatic supportive care.

Use of colchine which is an inhibitor of collagen synthesis may be benenficial in the treatment of cirrhosis and has been effective in significantly prolonging the lives of patients with cirrhosis. Pt is put on bed rest if he or she is restless he/she can be sedated by use of largactil or valium, the head of the bed is raised in order to improve gaseous exchange.

Nutritional measures ensure complete abstinence of alcohol , give a diet high in carbohydrates, proteins and fat free,salt is restricted in order to control edema and ascites. Administer vitamins supplements as prescribed.

Incase of massive melena or hematemesis resulting from raptured varices, quantative replacement of blood loss is essentual to prevent shock and further deterioration of liver function. Vasoconstrictors (vasopressin) can also be administered to control haemorrhage.

To control fluid retention the patients are put on bed rest and strict fluid and sodium restriction should be instituted. a diet low in sodium and fluid intake of not more than 1500ml/day. The goal of therapy is aimed at a loss of not more than 1kg /day of body weight in the presence of ascites and peripheral edema and not more than 0.5 /day in the presence of ascites only. Daily weight checks, monitors the amount of fluid lost.

If no weight change following 1 week of bed rest , sodium and fluid restriction the patient is put on antidiuretics e.g spironolactone. aggressive diuretic therapy should be avoided because it may be complicated by depletion of plasma volume and reduction of renal function so it is necessary to monitor the pt electrolytes and fluid status frequently .

Short term control of intractable ascites may also be done through the surgical implantation of a plastic shunt between the peritoneal cavity and superior venacava (laveen or denver shunt) as a result of this procedure ascitic fluid is continously re infused in to the venous system. This procedure may be accompanied by complications such as infection, disemninated intravascular coagulopathy and it is contraindicated in in pts with coma, varices infection, coagulopathy or CCF.

Therapeutic paracentesis is performed when the cirrhotic pt with ascitis is experiencing acute respiratory distress or is in danger of rupturing an umbilical hernia . upto 3L of fluid may be removed over a period of 4 hours. ascitis tend to reaccumulate within several days.

If paracentesis is done repeatedly in a pt with cirrhosis it may lead to protein and volume depletion , hemorrhage , infection of ascitic fluid and chronic ascitic leak

For pt with hepatic encephalopathytreatment of this condition centers around decreasiing amonia production in the colon and eliminating or treating factors that precipitate the encephalopathy such as GIT bleeding. When an acute GIT bleeding ocurs in the lumen , blood is promptly removed from the bowel lumen by means of enema and laxative so that nitrates load is reduced. Oral administration of neomycin is given to reduce amonia production.

Nurse should assess the level of activity intorealance and degree of fatigue, lethargy and malaise when performing activity of daily living and assist with activities and hygiene when fatigued and encourage rest, and assist with selection and pacing of desired activities and exercises.

Assess the degree of discomfort related to pruritus and edema, keep the pt fingernails short and smooth , provide skin care by massaging with emmollints, turning every 2 hours or initiate use of pressure mattress.

Carry out range of motion 4hourly , elevate edemotous extremities whenever possible. Observe for hemorrhage manifestations e.g ecchymosis,epistaxis,petechie and bleeding gums and record vital signs at frequent intervals depending on pts condition every 1-4 hrs. administer vit K as prescribed.

For pt with infective breathing due to ascitis you should elevate the head of the bed to at least 30 degrees , conserve the pt energy by providing periods of rest .

For those pt with varices the nurse should avoid activities that increase intra-abdominal pressure e.g constipation,chronic cough,straining to minimise the risk of bleeding of the esophageal or gastric varices. Observe the pt closely for early detection of hemorrhage and prompt treatment.

Assess the pt cognitive status every 4-8 hrs, monitor medications to prevent administration of those that precipitate hepatic encephalopathy. monitor labaratory data esp serum amonia level. Notify physician incase of any changes in neurological status and cognitive function.

Portal hypertension:
Portal hypertension is defined as a portal pressure gradient of 12 mm Hg or greater and is often associated with varices and ascites. Many conditions are associated with portal hypertension, of which cirrhosis is the most common cause.

Two factors that increase blood pressure in the portal blood vessels are: Increased volume of blood flowing through the vessels Increased resistance to the blood flow through the liver

The most common cause of portal hypertension is increased resistance to blood flow caused by extensive scarring of the liver in cirrhosis, which is most often due to chronic excessive alcohol intake.

Portal hypertension leads to the development of new veins (called collateral vessels) that directly connect the portal blood vessels to the general circulation, bypassing the liver. Because of this bypass, substances (such as toxins) that are normally removed from the blood by the liver can pass into the general circulation.

Collateral vessels develop at specific places. The most important are located at the lower end of the esophagus and at the upper part of the stomach. These vessels become engorged and full of twists and turn (esophageal Varices) or stomach (gastric Varices).

These engorged vessels are fragile and prone to bleeding, sometimes seriously and occasionally with fatal results. Other collateral vessels may develop on the abdominal wall and at the rectum.

Portal hypertension often causes the spleen to enlarge because the pressure interferes with blood flow from the spleen into the portal blood vessels. Pressure in the portal blood vessels may cause proteincontaining (ascitic) fluid from the surface of the liver and intestine to leak into the abdominal cavity.

Symptoms and Diagnosis


Portal hypertension itself does not cause symptoms, but some of its consequences do. If a large amount of ascitic fluid accumulates, the person's abdomen (distends). This distention is painless. An enlarged spleen may cause a vague sense of discomfort in the upper left part of the abdomen. Esophageal and gastric Varices bleed easily and sometimes massively. Much less commonly, varicose veins in the rectum bleed.

When substances that are normally removed from the liver pass into the general circulation and reach the brain, they may cause confusion or drowsiness (hepatic encephalopathy).

Collateral vessels may be visible on the skin over the abdominal wall or around the rectum. Because most people with portal hypertension also have severe liver dysfunction, they may have symptoms of liver failure, such as a tendency to bleed and bruising.

Treatment
Treatment with a non-selective beta blocker is often commenced once portal hypertension has been diagnosed, and almost always if there has already been bleeding from esophageal varices.

Typically, this is done with either propranolol or nadolol. The addition of a nitrate, such as isosorbide mononitrate, to the beta blocker is more effective than using beta blockers alone and may be the preferred regimen in those people with portal hypertension who have already experienced variceal bleeding.

In acute or severe complications of the hypertension, such as bleeding varices, intravenous octreotide (a somatostatin analogue) or intravenous terlipressin (an antidiuretic hormone analogue) is commenced to decrease the portal pressure.

Bleeding from esophageal varices is a medical emergency. Drugs such as vasopressin may be given intravenously to constrict the bleeding veins, and blood transfusions are given to replace lost blood. An endoscopic examination is usually done to confirm that the bleeding is from varices.

If the bleeding continues or recurs repeatedly, a surgical procedure may be done to create a bypass ( a shunt) between the portal venous system and the general venous system. This bypass lowers pressure in the portal vein because pressure is much lower in the general venous system.