Cirrhosis of Liver

Introduction
The term cirrhosis was first used by Rene Laennec (1781-1826) to describe the abnormal liver color of individuals with alcohol induced liver disease. Derived from Greek word Kirrhos means Yellowish brown color.

Definition: Cirrhosis is a chronic progressive disease of the liver characterized by extensive degeneration and destruction of the liver parenchymal cells.

The liver cells attempt to regenerate, but the regenerative process is disorganized, resulting in abnormal blood vessels and bile duct architecture.

Contd.
The liver slowly deteriorates and malfunctions due to chronic injury. Scar tissue replaces healthy liver tissue, partially blocking the flow of blood through the liver.

Contd.
Scarring also impairs the liver's ability to:
control infections remove bacteria and toxins from the blood process nutrients, hormones, and drugs make proteins that regulate blood clotting produce bile to help absorb fatsincluding cholesteroland fat-soluble vitamins

Incidence :
The overall incidence of cirrhosis in the US is approximately 360 per 100,000 population It is the 10th leading cause of death in the US, with mortality rate of 9.2 deaths per 100,000 populations. Of those deaths, 45% were alcohol related. Men are more likely than women to have alcoholic cirrhosis. Worldwide, post necrotic cirrhosis is the most common in women. Mortality is higher from all types of cirrhosis in men and non whites.

Etiology:
1. Not clearly defined 2. Alcohol. Heavy alcohol for several years can cause chronic injury to the liver and damages. For women, consuming two to three drinks including beer and wine per day and for men, three to four drinks per day, can lead to liver damage and cirrhosis. A common problem in alcoholic is protein malnutrition.

Cont..
3. Obesity: WHO ,2008, estimated that more than 200 million men and close to 300 million women were obese, obesity is a common cause of chronic liver disease , 17% of liver cirrhosis is attributable to excess body weight. 4. Chronic hepatitis C. Chronic hepatitis C causes inflammation and damage to the liver over time that can lead to cirrhosis and approximately 20% patient will develop cirrhosis.

Cont..
Chronic hepatitis B and D. Hepatitis B and D is virus that infects the liver and can lead to cirrhosis, but it occurs only in people who already have hepatitis B. approximate 10%- 20% will develop cirrhosis.

Nonalcoholic fatty liver disease (NAFLD). This is associated with obesity, diabetes, protein malnutrition, coronary artery disease, and corticosteroid medications.

Cont..
Autoimmune hepatitis. It is caused by the body's immune system attacking liver cells and causing inflammation, damage, and eventually cirrhosis. genetic factors -About 70 percent of those with autoimmune hepatitis are female. Diseases that damage or destroy bile ducts. Several different diseases( cholangitis) can damage or destroy the ducts that carry bile from the liver, causing bile to back up in the liver and leading to cirrhosis.

 Inherited diseases. Cystic fibrosis, alpha-1 antitrypsin deficiency, hemochromatosis, Wilson disease, galactosemia, and glycogen storage diseases are inherited diseases that interfere the liver function properly, cirrhosis can result.
Drugs, toxins, and infections. drug reactions( Acetaminophen, isonazide, methotrexate) prolonged exposure to toxic chemicals, parasitic infections, and repeated bouts of heart failure with liver congestion.

Cont.

Types of cirrhosis :
Alcoholic (historically called Laennecs cirrhosis) cirrhosis: also called micro nodular or portal cirrhosis and usually associated with alcohol abuse. The first change in the liver from excessive intake is an accumulation of fat in the liver cells; uncomplicated fatty changes in the liver are potentially reversible if the person stops drinking alcohol. If the alcohol abuse continues, widespread scar formation occurs throughout the liver.

Cont..
Post necrotic cirrhosis( macro nodular):most common world wide, massive loss of liver cells with irregular patterns of regenerating cells due to complication of viral, toxic or idiopathic (autoimmune) hepatitis. Billiary cirrhosis: is associated with chronic billiary obstruction and infection. There is diffuse fibrosis of the liver with jaundice. Cardiac cirrhosis: chronic liver disease results from long-standing, severe right side heart failure with corpulmonale, constrictive pericarditis, and tricuspid insufficiency.

Pathophsiology :
Liver insult due to alcohol ingestion, viral hepatitis, exposure to toxin Hepatocyte damage Liver inflammation - WBCs, nausea, vomiting, pain, fever, anorexia, fatigue Alteration in blood and lymph flow

Cont..
Liver necrosis liver fibrosis and scarring portal hypertension - Ascities, edema, - Spleenomegaly ( thrombocytopenia, leucopenia) - Varices (esophageal varices, hemorrhoids, anemia) billirubin metabolism hyperbilirubinemia, jaundice

Cont..
bile in gastrointestinal tract light colored stool urobilinogen Dark Urine vit K absorption- bleeding tendency metabolism of protein, carbohydrate, fats hypoglycemia, plasma protein- ascites and edema androgen and estrogen detoxification( hormone metabolism)- estrogen and androgens hormone Gynecomastia, loss of body hair, menstrual dysfunction, spider angioma, palmer erythema, testicular atrophy

Cont..
Aldesterone metabolism so levels sodium and water retention-- edema Biochemical alteration - AST, ALT levels, bilirubin, low serum albumin, prolong prothombin time, elevated alkaline phosphatase. Liver failure Hepatic encephalopathy Hepatic coma Death

Clinical manifestations
Early manifestations No symptoms GI disturbances: anorexia, dyspepsia, flatulence, weakness, fatigue, nausea, vomiting, weight loss, abdominal pain, bloating, diarrhea, constipation Abdominal pain, dull and heavy feeling Fever, lassitude, weight loss, enlargement of liver and spleen.

Cont
Later manifestations: Results from liver failure and portal hypertension Jaundice Peripheral edema Ascites Others: Skin lesion, hematological disorders, endocrine disturbances, and peripheral neuropathy Advanced stage: small and nodular liver

Jaundice
It results from the functional derangement of liver cells and compression of bile duct by connective tissue overgrowth Jaundice occurs as a result of decreased ability to conjugate and excrete bilirubin If obstruction of the biliary tract occurs, obstructive jaundice may also occur and usually accompanied by pruritus

Skin lesion
Spider angioma ( telangiectasia or spidernavi) are small dilated blood vessels with a bright red center point and spider like branches occurs in nose, cheeks, upper trunk, neck and shoulders. Palmer erythema, a red area that blanches with pressure, is located on the palm of the hand. Both lesions are due to increase estrogen in blood as a result of the damaged livers inability to metabolized steroid hormone.

Hematologic problem
Thrombocytopenia, leucopenia, anemia, due to spleenomegaly (back flow of blood from portal vein into the spleen.) Anemia due to inadequate RBC production and survival, and due to poor diet, poor absorption and bleeding from varices. Coagulation problems result from the livers inability to produce prothrombin and blood clotting and manifested by hemorrhagic phenomena or bleeding tendencies e.g. epistaxis, purpura, gingival bleeding, heavy menstrual flow.

Endocrine problem
In men: Gynecomastia, loss of axillary and pubic hair, testicular atrophy and impotence with loss of libido due to increased estrogen level. In younger female, amenorrhea may occur and in older, bleeding may occur. aldosterone hormone may cause sodium water retention and potassium loss. Peripheral neuropathy: probably due to dietary deficiency of thiamine, folic acid and cobalamin.

Clinical Manifestations

Complication
Portal hypertension

The nodules and scar tissue can compress hepatic veins within the liver. This causes the blood pressure within the liver to be high, a condition known as portal hypertension. Portal venous pressure is more than 15mmHg or 20 cm of water (normal 5-10mm Hg)

Cont
Is characterized by venous pressure in the portal circulation, spleenomegaly, large collateral vein, ascites, systemic hypertension, and esophageal varices. The common area to form collateral channels are in the lower esophagus( the anastomosis of the left gastric vein and azygos vein), the parietal peritoneum, rectum. High pressures within blood vessels of the liver occur in 60% of people who have cirrhosis.

Cont..
Esophageal Varices:

Esophageal Varices are a complex of tortuous veins at the lower end of the esophageal enlarged and swollen as a result of portal hypertension. 10-30% of UGI bleeding due to rupture of varices. 80% bleeding due to esophageal Varices. 20% due to gastric varices.

Cont..
Peripheral edema and Ascites: Edema results from decreased colloidal oncotic pressure from impaired liver synthesis of albumin (hypoalbuminia) Ascites is the accumulation of serous fluid in the peritoneal cavity. Protein move from the blood vessels via the larger pore of sinusoids into the lymph space. When the lymphatic system is unable to carry off the excess protein and water, they leak through the liver capsule into the peritoneal cavity.

Cont.. Hepatic encephalopathy/Coma:

Hepatic encephalopathy is a neuropsychiatric manifestation of liver damage. It can occur in any condition in which liver damage causes ammonia to enter the systemic circulation without liver detoxification. Liver is unable to convert ammonia to urea. The ammonia crosses the blood brain barrier and produces neurologic toxic manifestations.

Stages of Hepatic Encephalopathy

Stages 1 Clinical Symptoms Normal level of consciousness with periods of lethargy and euphoria; reversal of daynight sleep patterns Increased drowsiness; disorientation; inappropriate behavior; mood swings; agitation Clinical Signs Asterixis; impaired writing and ability to draw line figures.

Asterixis; fetor hepaticus.

Stages Contd.
Stages 3 Clinical Symptoms Stuporous; difficult to rouse; sleeps most of time; marked confusion; incoherent speech Clinical Signs Asterixis; increased deep tendon reflexes; rigidity of extremities.

Comatose; may not respond to painful stimuli.

Absence of asterixis; absence of deep tendon reflexes; flaccidity of extremities.

Contd.
Serum ammonia is decreased: by less protein diet and by antibiotic agents e.g. neomycin sulfate, it reduces the number of intestinal bacteria capable of converting urea to ammonia Susceptible patients: excessive diuresis, dehydration, infections, surgery, fever, and some medications (sedative agents, tranquilizers, analgesic agents, and diuretic medications that cause potassium loss)

Cont..
Lactulose: to reduce serum ammonia level Low-protein diet: 1.0 and 1.5 g/kg or up to 0.5g/kg Intravenous administration of glucose to minimize protein breakdown Administration of vitamins to correct deficiencies Correction of electrolyte imbalances (especially potassium with potclor) Neurologic status is assessed frequently

Contd.
Fluid intake and output and body weight are recorded each day. Vital signs are measured and recorded every 4 hours. Serum ammonia level is monitored daily. Protein intake is restricted in patients who are comatose or refractory encephalopathy

Contd.
Electrolyte status is monitored and corrected if abnormal. Sedatives, tranquilizers, and analgesic medications are discontinued

Cont..
Hepatorenal syndrome:

Hepatorenal syndrome is a serious complication of cirrhosis characterized by functional renal failure with advancing azotemia, oliguria, and ascites.

Diagnosis
Liver function test : alkaline phosphate, ALT,AST and y glutamyl transpeptidase ( GGT) Blood test: total protein, albumin, serum bilirubin and globulin, serum ammonia Prothombin time is prolonged (normal: 10-14sec) Liver cell biopsy to identify liver cell changes Ascites fluid test Liver ultrasound CT Scan: enlarged or atrophied, characteristics Stool for occult blood Endoscopy

Management
Medical management Dietary modification: table salt, salted butter, margarine, ordinary can and frozen foods should be avoided. The diet should be adequate calories and protein (75- 100 gm/day) unless hepatic encephalopathy is present, in which case protein is limited. Restrict fluid

Contd.
Diuretics: spironolactone, aldosterone blocking agents. Vitamins B and fat soluble vitamins (A, D, E, K). Corticosteroids drugs to improve liver function in post necrotic cirrhosis. Daily weight loss should not exceed 1 to 2 kg (2.2 to 4.4 lb) in patients with ascites and peripheral edema or 0.5 to 0.75 kg (1.1 to 1.65 lb) in patients without edema.

Management contd.
Bed Rest: useful therapy
upright position activation of the reninangiotensin-aldosterone system and sympathetic nervous systemresults in reduced renal glomerular filtration and sodium excretion and a decreased response to loop diureticsavoid

Contd.
Paracentesis: removal of fluid (ascites) from the peritoneal cavity through a small surgical incision or puncture made through the abdominal wall under sterile conditions (upto 5-6l removal is safe) Insertion of a peritoneovenous shunt to redirect ascitic fluid

Parencentesis

Management Contd.
Replace Fluid and Electrolytes: intravenous fluids with electrolytes and volume expanders are provided to restore fluid volume and replace electrolytes Transfusion of blood components also may be required An indwelling urinary catheter to monitor urine output

Contd.
Pharcological therapy:
Vasopressin (portal pressure) Vasopressin +Nitroglycerine ( portal pressure) Somatostatin and octreotide ( bleeding)

Balloon Temponade: used for controlling hemorrhage

Use of double ballon teamponade Isengstaken Blakemore tube)

Contd.
Used to to exert pressure on the cardia (upper orifice of the stomach) and against the bleeding varices The balloon in the stomach is inflated with 100 to 200 mL of air. An x-ray is done to confirm proper positioning of the gastric balloon

Sengstaken Blakemore Tube

Management Contd.
Sclerotherapy: In endoscopic sclerotherapy , a sclerosing agent is injected through a fiberoptic endoscope into the bleeding esophageal varices to promote thrombosis and eventual sclerosis. The procedure has been used successfully to treat acute GI hemorrhage

Sclerotherapy

Contd.
Esophageal banding therapy (variceal band ligation) a modified endoscope loaded with an elastic rubber band is passed through an overtube directly onto the varix (or varices) to be banded. After suctioning the bleeding, the rubber band is slipped over the tissue, causing necrosis, ulceration, and eventual sloughing of the varix.

Esophageal Banding

Contd.
Transjugular intrahepatic portosystemic shunting (TIPS) Method of treating esophageal varices in which a cannula is threaded into the portal vein by the transjugular route. An expandable stent is inserted and serves as an intrahepatic shunt between the portal circulation and the hepatic vein reducing portal hypertension.

Stenting

cont,..
Surgical management Liver transplantation Removing the liver and replacing it with a healthy donor organ is another way to treat liver cancer or liver cirrhosis About 80-90 percent of people who undergo liver transplantation, survive.

Contd.
Direct surgical ligation of varices
splenorenal, mesocaval, and portacaval venous shunts

Shunt

Cont..
Treat underlying cause: if cirrhosis is from heavy alcohol use, the treatment is to completely stop drinking alcohol. If cirrhosis is caused by hepatitis C, then treatment of hepatitis C Avoidance of hepatotoxic substances.

Nursing Management
Assessment History taking: past and present health history (alcohol intake, medication, infection etc) chief complain sign and symptoms of disease Physical examination Psychosocial assessment

Nursing Diagnosis
(1) Ineffective tissue perfusion related to bleeding tendencies and varices that may hemorrhage Goal Hemorrhage will be prevented as evidenced by absence of bleeding, normal vital sign and urine output of at least 0.5 ml/kg.

 Interventions : Assess patients condition Monitor for bleeding from gums, melena, hematuria, hematemasis Assess vital sign for sign of shock Monitor urine output Protect patient from physical trauma to prevent hemorrhage Avoid unnecessary injection and apply gentle pressure after injection Instruct the client to avoid vigorous nose blowing, straining with bowel movement. Provide stool softener to prevent straining with rupture of varices Advice to use soft tooth brush to prevent gum bleeding

Cont..

(2) Activity intolerance related to bed rest, fatigue, lack of energy, and altered respiratory function secondary to ascites. Goal: The patient will maintain a balance between rest and activity as evidenced by the absence of fatigue Interventions: Assess level of activity tolerance and degree of fatigue, lethargy, and malaise when performing routine ADLs. Assist with activities and hygiene when fatigued. Encourage rest when fatigued or when abdominal pain or discomfort occurs. Assist with selection and pacing of desired activities and exercise. Provide diet high in carbohydrates with protein intake consistent with liver function. Administer supplemental vitamins (A, B complex, C, and K).

(3) Impaired skin integrity related to pruritus from jaundice and edema Goal: Decrease potential for pressure development; breaks in skin integrity ulcer

Interventions: Assess degree of discomfort related to pruritus and edema. Note and record degree of jaundice and extent of edema. Keep patients fingernails short and smooth. Provide frequent skin care; avoid use of soaps and alcohol-based lotions.

Cont
Massage every 2 hours with emollients; turn every 2 hours Initiate use of alternating-pressure mattress or low air loss bed. Recommend avoiding use of harsh detergents. Assess skin integrity every 48 hours. Instruct patient and family in this activity. Restrict sodium as prescribed. Perform range of motion exercises every 4 hours; elevate edematous extremities whenever possible.

(4) High risk for injury related to altered clotting mechanisms and altered level of consciousness Goal: Patient is conscious, no hemetemesis, melena. Intervention Assess level of consciousness and cognitive level. Provide safe environment (pad side rails, remove obstacles in room, prevent falls). Provide frequent surveillance to orient patient and avoid use of restraints. Replace sharp objects (razors) with safer terms.

Cont..
Observe each stool for color, consistency, and amount. Be alert for symptoms of anxiety, epigastric fullness, weakness, and restlessness. Test each stool and emesis for occult blood. Observe for hemorrhagic manifestations: ecchymosis, epistaxis petechiae, and bleeding gums. Record vital signs at frequent intervals, depending on patient acuity (every 14 hours). Keep patient quiet and limit activity.

(5) Disturbed body image related to changes in appearance, and role function. Goal: Patient verbalizes feelings consistent with improvement of body image and self-esteem Intervention: Assess changes in appearance and the meaning these changes have for patient and family. Encourage patient to verbalize reactions and feelings about these changes. Assess patients and familys previous coping strategies.

Cont
Assist patient in identifying short-term goals. Encourage and assist patient in decision making about care. Identify with patient resources to provide additional support (counselor, spiritual advisor). Assist patient in identifying previous practices that may have been harmful to self (alcohol and drug abuse).

Nsg diagnosis cont.

(6) Fluid volume excess related to portal hypertension and hyperaldesteronism as evidenced by weight gain, depended edema, ascites (7) Dysfunctional family processes, alcoholism related to abuse of alcohol and inadequate coping ability as evidenced by deteoriation in family relationship, family denial, neglected obligation.

References
Brunner And Siddhartha's (2004).MedicalSurgical Nursing (12th Ed) Chintamani .Lewiss Medical Surgical Nursing, Mosby .2011 Cirrhosis of Liver, emedicine, Available from: www.emedicinehealth.com/cirrhosis/page8_e m.htm M. Joycee Black, Hokanson Jane Hawks. Medical Surgical Nursing. Clinical management for positive outcomes. 7th ed. 2005.

Thank You