Cirrhosis of Liver. Introduction The term cirrhosis was first used by Rene Laennec (1781-1826) to...

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Cirrhosis of Liver

Transcript of Cirrhosis of Liver. Introduction The term cirrhosis was first used by Rene Laennec (1781-1826) to...

Page 1: Cirrhosis of Liver. Introduction The term cirrhosis was first used by Rene Laennec (1781-1826) to describe the abnormal liver color of individuals with.

Cirrhosis of Liver

Page 2: Cirrhosis of Liver. Introduction The term cirrhosis was first used by Rene Laennec (1781-1826) to describe the abnormal liver color of individuals with.

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.

Page 3: Cirrhosis of Liver. Introduction The term cirrhosis was first used by Rene Laennec (1781-1826) to describe the abnormal liver color of individuals with.

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.

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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.

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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 fats—including

cholesterol—and fat-soluble vitamins

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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.

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Etiology: 1.Not clearly defined2.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.

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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.

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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.

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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.

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Cont….• 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.

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Types of cirrhosis : • Alcoholic (historically called Laennec’s 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.

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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.

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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

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Cont.. Liver necrosis →liver fibrosis and scarring → portal

hypertension

- Ascities, edema,- Spleenomegaly ( thrombocytopenia, leucopenia)- Varices (esophageal varices, hemorrhoids, anemia)

↓ billirubin metabolism – hyperbilirubinemia, jaundice

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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

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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

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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.

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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

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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

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Skin lesionSpider 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 liver’s inability to metabolized steroid hormone.

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Hematologic problemThrombocytopenia, 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 liver’s inability to produce prothrombin and blood clotting and manifested by hemorrhagic phenomena or bleeding tendencies e.g. epistaxis, purpura, gingival bleeding, heavy menstrual flow.

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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.

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Clinical Manifestations

Page 28: Cirrhosis of Liver. Introduction The term cirrhosis was first used by Rene Laennec (1781-1826) to describe the abnormal liver color of individuals with.

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)

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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.

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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.

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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.

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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.

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Stages of Hepatic Encephalopathy Stages Clinical Symptoms Clinical Signs

1 Normal level of consciousness with periodsof lethargy and euphoria; reversal ofday–night sleep patterns

Asterixis; impaired writing and ability to drawline figures.

2 Increased drowsiness; disorientation;inappropriate behavior; mood swings; agitation

Asterixis; fetor hepaticus.

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Stages Contd. Stages Clinical Symptoms Clinical Signs

3 Stuporous; difficult to rouse; sleeps mostof time; marked confusion; incoherentspeech

Asterixis; increased deep tendon reflexes; rigidityof extremities.

4 Comatose; may not respond to painful stimuli.

Absence of asterixis; absence of deep tendonreflexes; flaccidity of extremities.

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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)

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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

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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

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Contd.

• Electrolyte status is monitored and corrected if abnormal.

• Sedatives, tranquilizers, and analgesic medications are discontinued

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Cont.. Hepatorenal syndrome:

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

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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

Page 43: Cirrhosis of Liver. Introduction The term cirrhosis was first used by Rene Laennec (1781-1826) to describe the abnormal liver color of individuals with.

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

Page 44: Cirrhosis of Liver. Introduction The term cirrhosis was first used by Rene Laennec (1781-1826) to describe the abnormal liver color of individuals with.

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.

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Management contd.

• Bed Rest: useful therapy–upright position activation of the renin-

angiotensin-aldosterone system and sympathetic nervous systemresults in reduced renal glomerular filtration and sodium excretion and a decreased response to loop diureticsavoid

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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

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Parencentesis

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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

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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)

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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

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Sengstaken Blakemore Tube

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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

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Sclerotherapy

Page 54: Cirrhosis of Liver. Introduction The term cirrhosis was first used by Rene Laennec (1781-1826) to describe the abnormal liver color of individuals with.

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.

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Esophageal Banding

Page 56: Cirrhosis of Liver. Introduction The term cirrhosis was first used by Rene Laennec (1781-1826) to describe the abnormal liver color of individuals with.

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.

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Stenting

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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.

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Contd.

• Direct surgical ligation of varices– splenorenal, mesocaval, and portacaval

venous shunts

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Shunt

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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.

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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

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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.’

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Cont..• Interventions : • Assess patient’s 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

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(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).

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(3) Impaired skin integrity related to pruritus from jaundice and edema

Goal: ‘Decrease potential for pressure ulcer

development; breaks in skin integrity’

Interventions:• Assess degree of discomfort related to pruritus

and edema.• Note and record degree of jaundice and extent of

edema.• Keep patient’s fingernails short and smooth.• Provide frequent skin care; avoid use of soaps and

alcohol-based lotions.

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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 4–8 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.

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(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.

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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 1–4 hours).

• Keep patient quiet and limit activity.

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(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 patient’s and family’s previous coping

strategies.

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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).

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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.

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References

• Brunner And Siddhartha's (2004).Medical- Surgical Nursing (12th Ed)

• Chintamani .Lewis’s Medical Surgical Nursing, Mosby .2011

• Cirrhosis of Liver, emedicine, Available from: www.emedicinehealth.com/cirrhosis/page8_em.htm

• M. Joycee Black, Hokanson Jane Hawks. Medical –Surgical Nursing. Clinical management for positive outcomes. 7th ed. 2005.

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Thank You

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Liver cirrhosis case

• Mrs MW, 59 years old, is divorced and unemployed. She was admitted to an acute medical ward at the hospital presenting with general malaise, a grosslydistended abdomen, swollen ankles and jaundice. It was also noted that she smelt of alcohol and was showing signs of alcohol withdrawal

Page 76: Cirrhosis of Liver. Introduction The term cirrhosis was first used by Rene Laennec (1781-1826) to describe the abnormal liver color of individuals with.

• 1 What is cirrhosis of the liver?• 2 List possible causes of cirrhosis.• 3 What other clinical signs and

symptoms may Mrs MW present with?• 4 What drug treatment, including dose,

would you recommend for Mrs MW’s• alcohol withdrawal? What

recommendations would you make if the patient was

• unable to take the medication orally?

Page 77: Cirrhosis of Liver. Introduction The term cirrhosis was first used by Rene Laennec (1781-1826) to describe the abnormal liver color of individuals with.

What is cirrhosis of the liver?• Cirrhosis is defined as the histological

development of regenerative nodules surrounded by fibrous bands in response to chronic liver injury.

• It is an advanced stage of liver fibrosis that is accompanied by distortion of the hepatic vasculature.

Page 78: Cirrhosis of Liver. Introduction The term cirrhosis was first used by Rene Laennec (1781-1826) to describe the abnormal liver color of individuals with.

List possible causes of cirrhosis• Causes of cirrhosis can usually be identified by the patient’s history combined• with serological and histological investigation.• . Alcoholic liver disease and hepatitis C and B are the most common causes of

cirrhosis• The association of excessive alcohol consumption with liver disease has been

recognised for centuries.• After the identification of the hepatitis C virus and of non-alcoholic steatohepatitis

in obese patients with diabetes, the diagnosis of cirrhosis without an apparent cause (cryptogenic cirrhosis) is rarely made.

• Genetic causes of cirrhosis include haemochromatosis and Wilson’s disease.• Epidemiological studies have identified a number of factors that contribute to the

risk of developing cirrhosis. • Regular (moderate) alcohol consumption, age older than 50 years, and male

gender are examples that increase cirrhosis risk in chronic hepatitis C infection, and older age, obesity, insulin resistance or type 2 diabetes, hypertension and hyperlipidaemia in non-alcoholic steatohepatitis.

Page 79: Cirrhosis of Liver. Introduction The term cirrhosis was first used by Rene Laennec (1781-1826) to describe the abnormal liver color of individuals with.

What other clinical signs and symptoms may Mrs MW present with?

• Cirrhosis is often asymptomatic until complications of liver disease are present.

• Mrs MW may present with itching, jaundice, dark urine, pale fatty stools,

• abdominal pain, nausea, fatigue, bleeding – such as nose bleeds, hepatic encephalopathy, hepatomegaly, ascites, distended abdominal veins, spider angiomata, palmar erythema and asterixis. She may also present with the signs and symptoms of alcohol withdrawal, which include irritability, anxiety, tachycardia, tremor, sweating, confusion and hallucinations.

Page 80: Cirrhosis of Liver. Introduction The term cirrhosis was first used by Rene Laennec (1781-1826) to describe the abnormal liver color of individuals with.

What drug treatment, including dose, would you recommend for Mrs MW’s alcohol withdrawal? What recommendations would you make if the patient was unable to take the medication orally?

• Long-acting benzodiazepines (e.g. diazepam and chlordiazepoxide) are used to attenuate alcohol withdrawal symptoms but they also have a dependence potential.

• To minimise the risk of dependence, administration should be for a limited period only (e.g. chlordiazepoxide 20 mg 4 times daily, gradually reducing to zero over 7–14 days).

• Mild alcohol withdrawal symptoms may be treated with a lower starting dose, such as 15 mg four times a day.

• In all cases, the patient should be counselled about the proposed length of the treatment course.

• Benzodiazepines should not be prescribed if the patient is likely to continue drinking alcohol. In patients unable to take medication by the oral route, diazepam may be administered by intramuscular or slow intravenous injection (into a large vein, at a rate of not more than 5 mg/min), at a dose of 10 mg, repeated if necessar after not less than 4 hours. Alternatively, diazepam may be administered via the rectal route as a rectal solution or suppository. The intramuscular route should only be used when both the oral and intravenous routes are not possible.

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• Mrs MW weighs 61 kg (with the ascites) and her laboratory data are as follows:

• Total protein 49 g/L (63–80 g/L)• Albumin 20 g/L (32–50 g/L)• Total bilirubin 114 micromol/L (<17 micromol/L)• ALP 382 IU/L (100–300 IU/L)• ALT 88 IU/L (5–42 IU/L)• INR 1.6• GGT 306 IU/L (<50 IU/L)• Diagnosis of alcoholic cirrhosis of the liver was made based on Mrs MW’s

clinical• features, liver function tests, abdominal ultrasound, CT scan and liver

biopsy.

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• Describe how Mrs MW’s laboratory results relate to her diagnosis.

• 2 What treatment would you recommend to reduce her risk of bleeding?

• 3 What medications would you advise Mrs MW to avoid in view of her bleeding risk?

• 4 What treatment options are available to help Mrs MW abstain from alcohol in the future?

Page 83: Cirrhosis of Liver. Introduction The term cirrhosis was first used by Rene Laennec (1781-1826) to describe the abnormal liver color of individuals with.

Describe how Mrs MW’s laboratory results relate to her diagnosis.

• Albumin is synthesised in the liver and has a long half-life of around 20 days.

• Mrs MW’s low serum albumin is indicative of chronic liver disease.

• Albumin synthesis is also depressed in states of poor nutrition.

• Bilirubin is carried within the plasma by albumin to the liver, where it is conjugated by glucuronidation.

• Subsequently, low circulating albumin levels and/or damage to the liver cells result in reduced conjugation of the bilirubin.

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• Blockage of the biliary tract (e.g. cholestasis) will result in increased levels of conjugated bilirubin.

• Bilirubin levels of more than 35 micromol/L can result in visual signs of jaundice.

• The concentration of both the unconjugated and conjugated bilirubin are likely to be raised in Mrs MW. However, only total bilirubin was measured in this case.

• Alkaline phosphatase (ALP) is present in high concentrations in the cells lining the biliary tract and an ALP level exceeding 300 IU/L, together with a raised bilirubin as in the case of Mrs MW, is indicative of cholestasis. Jaundicebecomes progressively more severe in unrelieved cholestasis.

• Alanine aminotransferase (ALT) is present in high concentrations in the liver and the enzyme is released during hepatocellular damage and a modestly raised level like Mrs MW’s is indicative of chronic liver disease.

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• The increased susceptibility to bleeding observed in patients with liver failure (raised INR) results from depressed fibrinogen levels and the reduced synthesis of clotting factors by the cirrhotic liver.

• In addition, the absorption of fat-soluble vitamin K is impaired in cholestasis and subsequently the synthesis of vitamin K-dependent clotting factors is reduced.

• Gamma-glutamyl transferase (GGT) is found in the liver, but this test is relatively non-specific. It is released following tissue damage and is raised in cholestasis in parallel with ALP. GGT release is stimulated by alcohol and some drugs (such as phenytoin and carbamazepine), and therefore the GGT level can be used to assess abstinence in alcoholics, like Mrs MW.

Page 86: Cirrhosis of Liver. Introduction The term cirrhosis was first used by Rene Laennec (1781-1826) to describe the abnormal liver color of individuals with.

What treatment would you recommend to reduce her risk of bleeding?

• Mrs MW has a raised INR value of 1.6 and is therefore at increased risk of bleeding.

• Vitamin K can be given to correct the vitamin deficiency, either as an intravenous injection or orally. Konakion MM is phytomenadione (10 mg/mL) in amixed micelles vehicle.

• Konakion MM may be administered by slow intravenous injection or by infusion in glucose 5%.

• For oral administration, the water-soluble preparation menadiol sodium phosphate, is used in patients with hepatic disease, especially biliary obstruction.

• The usual dose is 10 mg daily. Alternatively, phytomenadione tablets may be used in those patients who do not have impaired fat absorption.

• If vitamin K is ineffective in controlling the clotting times (monitored via the INR result) then fresh frozen plasma may be required.

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What medications would you advise Mrs MW to avoid in view of her bleeding risk?

• Medications known to increase the risk of bleeding in cirrhotic patients include

• aspirin, clopidogrel, dipyridamole, corticosteroids, NSAIDs, heparin and warfarin.

• Mrs MW would need to be counselled about the risks associated with these medications and advised to always check with the pharmacist before buyingany medications over the counter

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What treatment options are available to help Mrs MW abstain from alcohol in the future?

• Disulfiram is an aversive therapy that works by inhibiting acetaldehyde dehydrogenase.

• Interactions between disulfiram and alcohol can result in potentially severe reactions, such as myocardial infarction, congestive heart failure, respiratorydepression and death.

• Patients taking disulfiram should be warned of the possible presence of alcohol in liquid medicines, tonics, foods and even in toiletries and mouthwashes.

• Patient adherence to disulfiram is poor and there is a lack of strong evidence for its effectiveness, thus it is not routinely recommended.

• Acamprosate is indicated for the maintenance of abstinence in alcohol dependent adults. • It appears to decrease brain hyper excitability during alcohol withdrawal, which may reduce

alcohol consumption.• Treatment should be initiated as soon as possible after the alcohol-withdrawal period is

complete.• The recommended period of treatment with acamprosate is one year and treatment should

be combined with counselling. • The GGT level can be monitored as a marker of abstinence from alcohol.

Page 89: Cirrhosis of Liver. Introduction The term cirrhosis was first used by Rene Laennec (1781-1826) to describe the abnormal liver color of individuals with.

• Mrs MW, 59 years old, is divorced and unemployed. She was admitted to an acute medical ward at the hospital presenting with general malaise, a grossly

• distended abdomen, swollen ankles and jaundice. It was also noted that she smelt of alcohol and was showing signs of alcohol withdrawal.

• On examination, Mrs MW was found to be encephalopathic. The doctors decided to treat her encephalopathy and ascites.

Page 90: Cirrhosis of Liver. Introduction The term cirrhosis was first used by Rene Laennec (1781-1826) to describe the abnormal liver color of individuals with.

• What is hepatic encephalopathy? What are the clinical signs and symptoms?

• 2 What factors may precipitate hepatic encephalopathy?

• 3 List two treatment options for the management of Mrs MW’s hepatic encephalopathy. Describe the mechanism of action for one of these.

• 4 What factors are likely to have contributed to the development of ascites in Mrs MW?

• 5 Name two treatment options for the management of Mrs MW’s ascites. Describe the pharmacology of these therapies, including any potential side-effects. What would you monitor in order to determine whether the therapy was effective?

Page 91: Cirrhosis of Liver. Introduction The term cirrhosis was first used by Rene Laennec (1781-1826) to describe the abnormal liver color of individuals with.

What is hepatic encephalopathy? What are the clinical signs and symptoms?

• Hepatic encephalopathy is a neuropsychiatric syndrome which may complicate almost all types of liver disease.

• It may occur intermittently and be reversible or may occur acutely, with rapid progression to coma and death.

• Mrs MW presented with signs of hepatic encephalopathy including flapping tremor of the hands, intellectual deterioration, slurred speech, confusion, drowsiness and irritability.

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2 What factors may precipitate hepatic encephalopathy?

• Factors that may precipitate hepatic encephalopathy include:

• hypokalaemia and/or profound diuresis caused by a brisk response to a potent diuretic,

• diarrhoea and vomiting, because of the resulting fluid and electrolyte imbalance, constipation,

• a large protein meal or gastrointestinal haemorrhage, infection, especially peritonitis,

• and CNS depressant drugs, such as opioids or benzodiazepines.

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List two treatment options for the management of Mrs MW’s hepatic encephalopathy. Describe the mechanism of action for one of these.

• Treatment goals for hepatic encephalopathy include provision of supportive care, identification and removal of precipitating factors, reduction in the nitrogenous load from the gut and optimisation of long-term therapy.

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• Therapy should be directed toward improving mental status via bowel cleansing with lactulose or with enemas. The dose of lactulose should be titrated to give two soft stools per day without diarrhoea.

• Lactulose is metabolised in the colon to lactic, acetic and formic acids, causing the pH of the colon to drop from 7 to 5.

• Colonic acidification with lactulose alters the bacterial population and favours the growth of weak ammonia-producing bacteria rather than proteolytic ammonia producers such as E. coli.

• In addition, the drop in colon pH leads to ionisation of nitrogenous products with a subsequent reduction in their absorption from the gastrointestinal tract into the blood.

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• Third, the osmotic laxative effect speeds the intestinal transit, thereby decreasing the time available for the absorption of potentially toxic nitrogen compounds. It is imperative to monitor

• Mrs MW’s bowel frequency while treating with lactulose since fluid and electrolyte

• imbalances secondary to diarrhoea may precipitate hepatic encephalopathy.

• Mrs MW’s mental test score should also be repeated to assess benefit.

• Neomycin (4 g daily in divided doses) is a non-absorbable antibiotic which may be used to reduce the number of bacteria in the bowel that normally break down protein.

• Neomycin therapy is usually limited to one week’s therapy because some absorption may occur with a risk of nephrotoxicity and ototoxicity.

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What factors are likely to have contributed to the development of ascites in Mrs MW?

• Mrs MW presented with a swollen abdomen, swollen ankles, pitting oedema and breathlessness. There are two key factors involved in the pathogenesis of ascites formation, namely, sodium and wate retention and portal hypertension.

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• The development of renal vasoconstriction in cirrhosis is partly a homeostatic response involving increased renal sympathetic activity and activation of the renin–angiotensin system to maintain blood pressure during systemic vasodilatation.

• Decreased renal blood flow decreases glomerular filtration rate and thus the delivery and fractional excretion of sodium.

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• Cirrhosis is associated with enhanced reabsorption of sodium both at the proximal tubule and at the distal tubule. Increased reabsorption of sodium in the distal tubule is due to the increased circulating concentrations of aldosterone, occurring secondary to the reduced hepatic metabolism of aldosterone.

• However, some patients with ascites have normal plasma concentrations of aldosterone, leading to the suggestion that sodium reabsorption in the distal tubule may be related to enhanced renal sensitivity to aldosterone.

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• In compensated cirrhosis, sodium retention can occur in the absence of vasodilatation and effective hypovolaemia. Sinusoidal portal hypertension can reduce renal blood flow even in the absence of haemodynamic changes in the systemic circulation, suggesting the existence of a hepatorenal reflex.

• Portal hypertension increases the hydrostatic pressure within the hepatic sinusoids and favours transudation of fluid into the peritoneal cavity. Systemic vasodilatation, the severity of liver disease and portal pressure contribute to the abnormalities of sodium handling in cirrhosis.

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Name two treatment options for the management of Mrs MW’s ascites. Describe the pharmacology of these therapies, including any potential side-effects. What would you monitor in order to determine whether the therapy was effective?

• Management of ascites aims to mobilise ascitic fluid, relieve abdominal discomfort

• and breathlessness and to exclude infection. Diuretics have been the mainstay

• of treatment of ascites since the 1940s when they first became available.

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• Spironolactone, an aldosterone antagonist, is the drug of choice since

• secondary hyperaldosteronism often coexists in patients with hepatic ascites.

• Aldosterone is usually metabolised by the liver and is highly protein bound, therefore the free aldosterone levels are raised in cirrhosis. Spironolactone competes with aldosterone for receptor sites in the distal tubule, resulting in potassium retention and sodium and water loss.

• The initial dose of spironolactone is 100–200 mg and can be slowly increased according to response. There is a lag of 3–5 days between the beginning of spironolactone treatment and the onset of the natriuretic effect.

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• The aim is to remove the fluid gradually with a maximum weight loss of

• 0.5 kg/day in the absence of peripheral oedema, or 1.0 kg/day if peripheral

• oedema is present. Too rapid a diuresis will result in intravascular fluid loss rather than the peripheral oedema.

• The diuretic should be stopped if the serum sodium falls below 120 mmol/L or if there is a rising serum creatinine. Urinary electrolytes should be monitored to ensure that the spironolactone therapy is effective.

• The aim is to reverse the sodium/potassium ratio in the urine so that• more sodium than potassium is excreted. Most frequent side-effects

of spironolactone are those related to its anti-androgenic activity, such as decreased libido, impotence and gynaecomastia in men and menstrual irregularities in women.

• Other side-effects include hyperkalaemia, uraemia, hyponatraemia and nausea.

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• In addition to spironolactone, ascites can be managed by paracentesis.

• That is the removal (‘tapping’) of ascitic fluid from the peritoneal cavity under aseptic conditions.

• A colloid (human albumin solution (20%)) is infused (40 Ml (8 g of albumin) per litre of ascites drained) intravenously during paracentesis, in order to prevent intravascular volume depletion and the onset of renal failure.

• Following paracentesis, ascites recurs in the majority (93%) if diuretic therapy is not reinstituted, but recurs in only 18% of patients treated with spironolactone.

• Cirrhotic ascites can become infected and if peritonitis occurs• survival depends on early, vigorous antibiotic therapy. The

patient should be monitored for signs of infection