Cirrhosis

54 Cirrhosis




Overview/pathophysiology


Cirrhosis is a chronic, serious disease in which normal configuration of the liver is changed, resulting in cell death. When new cells are formed, the resulting scarring causes disruption of blood and lymph flow. Although pathologic changes do not occur for many years, structural changes can lead to liver failure (end-stage liver disease). Complications may include inability to metabolize bilirubin and resultant jaundice; difficulty producing serum proteins, including albumin and certain clotting factors, hyperdynamic circulation and decreased vasomotor tone, pulmonary changes (ventilation-perfusion mismatch) and sometimes cyanosis, changes in nitrogen (N) metabolism (e.g., inability to convert ammonia to urea), and difficulty metabolizing some hormones (especially the sex hormones). Complications related to portal hypertension include development of ascites, bleeding esophageal and gastric varices, portal-systemic collaterals, encephalopathy, and splenomegaly.




Alcoholic (Laënnec’s) cirrhosis:


Associated with long-term alcohol abuse; accounts for 50% of all cirrhosis cases. Changes in liver structure caused by cirrhosis are irreversible, but compensation of liver function can be achieved if the liver is protected from further damage by cessation of alcohol consumption and proper nutrition.


Cirrhosis also can be caused by any chronic liver disease: chronic hepatitis B, chronic hepatitis C, hereditary hemochromatosis, non-alcoholic fatty liver disease (NAFLD), autoimmune hepatitis, Wilson’s disease, and alpha-1-antitrypsin deficiency.


The presence of cirrhosis places the patient at risk for development of hepatocellular carcinoma (primary liver cancer) as well as decompensated liver disease (liver failure).



Biliary cirrhosis:


Associated with chronic retention of bile and inflammation of bile ducts; accounts for 15% of all cirrhosis cases. It may be further classified as follows.



Primary biliary cirrhosis (PBC):

An inflammatory disease of intrahepatic bile ducts. This slowly progressive disease has other findings, including steatorrhea, xanthomatous (yellow tumors) neuropathy, osteoporosis, and portal hypertension. Hypercholesterolemia, hyperlipidemia, and hepatomegaly are found in approximately 85% of patients with PBC.



Secondary biliary cirrhosis:

Results from chronic obstruction to bile flow, usually from an obstruction outside the liver, such as calculi, neoplasms, or biliary atresia.



Health care setting


Primary care with possible hospitalization for complications



Assessment




Signs and symptoms:


Up to 40% of patients with cirrhosis have no symptoms. Others exhibit symptoms in varying degrees, depending on the degree of impaired hepatocellular function. Symptoms may include weakness, fatigability, weight loss, pruritus, fever, anorexia, nausea, occasional vomiting, abdominal pain, diarrhea, menstrual abnormalities, sterility, impotence, loss of libido, and hematemesis. Urine may be dark (brownish) because of the presence of urobilinogen, and stools may be pale and clay colored because of the absence of bilirubin.



Physical assessment:


Jaundice, hepatomegaly, ascites, peripheral edema, pleural effusion, and fetor hepaticus (a musty, sweetish odor on the breath). There may be slight changes in personality and behavior, which can progress to coma (a result of hepatic encephalopathy); spider angiomas, testicular atrophy, gynecomastia, pectoral and axillary alopecia (a result of hormonal changes); splenomegaly; hemorrhoids (a result of portal hypertension complications); spider nevi; purpuric lesions; and palmar erythema. Asterixis (i.e., jerking movements of the hands and wrists when the wrists are dorsiflexed with the fingers extended) may be present in advanced cirrhosis.



History of:


Excessive alcohol ingestion, chronic hepatitis B or C infection, exposure to hepatotoxic drugs or chemicals, biliary or metabolic disease.



Diagnostic tests




Hematologic:


Red blood cells may be decreased in hypersplenism and decreased with hemorrhage. White blood cells and platelet counts may be decreased with hypersplenism and increased with infection.



Serum biochemical tests:



Bilirubin levels:

Elevated because of failure in hepatocyte metabolism and obstruction in some instances. Very high or persistently elevated levels are considered a poor prognostic sign.



Alkaline phosphatase levels:

Normal to mildly elevated in most cases; in PBC it is elevated 2-3 times normal.



Aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels:

Usually elevated to more than 300 U with acute liver failure and normal or mildly elevated with chronic liver failure. ALT is more specific than AST for hepatocellular damage.



Albumin levels:

Reduced, especially with ascites. Persistently low levels suggest a poor prognosis. This test is not a perfect indicator of liver function because it is affected by poor nutrition and fluid status.



Na+ levels:

Normal to low. Na+ is retained but is associated with water retention, which results in normal serum Na+ levels or even a dilutional hyponatremia. Often severe hyponatremia is present in the terminal stage and is associated with tense ascites and hepatorenal syndrome.



K+ levels:

Slightly reduced unless patient has renal insufficiency, which would result in hyperkalemia. Chronic hypokalemic acidosis is common in patients with chronic alcoholic liver disease.



Glucose levels:

Hypoglycemia possible because of impaired gluconeogenesis and glycogen depletion in patients with severe or terminal liver disease.



Blood urea nitrogen levels:

May be slightly decreased because of failure of Krebs cycle enzymes in the liver or elevated because of bleeding or renal insufficiency.



Ammonia levels:

May be elevated because of inability of the failing liver to convert ammonia to urea and shunting of intestinal blood via collateral vessels. Gastrointestinal (GI) hemorrhage, infection, or an increase in intestinal protein from dietary intake increases ammonia levels. Note: Serum ammonia sample must be transported to the lab immediately for processing.



Coagulation:

Prothrombin time (PT)/international normalized ratio (INR) is elevated and, in severe liver disease, unresponsive to vitamin K therapy. The failing liver is unable to synthesize clotting factors. Coagulation abnormalities usually include factor V, but also factors II, VII, IX, and X.



Urine tests:


Urine bilirubin is increased; urobilinogen is normal or increased; and proteinuria may be present.



Liver biopsy:


Provides a definitive diagnosis of cirrhosis; however, clinically it is not always advisable because of the high risk of bleeding. When it is performed, a specimen of liver is obtained for microscopic analysis and diagnosis of cirrhosis, hepatitis, or other liver disease. After local anesthetic is administered and patient’s skin is prepared, a large needle is inserted into the eighth or ninth intercostal space in the midaxillary line. It is critical that patient hold his or her breath at the end of expiration to elevate the liver maximally. Patient movement or failure to sustain expiration can result in puncture through the lung rather than the liver. Type and crossmatching may be performed before the procedure in anticipation of hemorrhagic complications. Percutaneous liver biopsy is contraindicated in patients with markedly prolonged PT or very low platelet counts because of the risk of hemorrhage. In these patients, a transvenous biopsy via the jugular and hepatic vein may be attempted instead. Liver biopsy also may be done laparoscopically.



Radiologic studies:


Ultrasound may be used to assess size of liver and spleen, screen for liver tumors (particularly hepatocellular carcinoma), and assess for signs of biliary obstruction. Computed tomography (CT) scan of the abdomen is performed to evaluate size and location of tumors and nodules and to rule out gallbladder disease. Percutaneous transhepatic cholangiography (PTC) reveals extent of obstruction via contrast dye. Endoscopic retrograde cholangiopancreatography (ERCP) is a fiberoptic technique used to show obstructions of the common bile and pancreatic ducts as potential causes of jaundice. Liver scans enable visualization of the spleen and liver via injection of radioisotopes. Note: After injection of the dye, patient may experience nausea, vomiting, and transient elevated temperature.



Angiographic studies:


Establish portal vein patency and visualize portosystemic collateral vessels to determine cause of and effective treatment for variceal bleeding. Portal venous anatomy must be established before such operations as portal systemic shunt or hepatic transplantation. In patients with previously constructed surgical shunts, loss of patency may be confirmed as a factor leading to the present bleeding episode. The most common procedure is portal venography by indirect angiography. The femoral artery is catheterized, and contrast material is injected into the splenic artery. Contrast material flows through the spleen into the splenic and portal veins.


• Hepatic vein wedge pressure is measured by introducing a balloon catheter into the femoral vein and threading it into a hepatic vein branch.
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Jul 18, 2016 | Posted by in NURSING | Comments Off on Cirrhosis

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