fc28cirrhosis of liver ppt

8/12/2019 Fc28cirrhosis of Liver Ppt

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Cirrhosis of Liver


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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.


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Definition:

Cirrhosis is a chronic progressive disease of theliver 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 ductarchitecture.


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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 bloodprocess nutrients, hormones, and drugs

make proteins that regulate blood clotting

produce bile to help absorb fatsincludingcholesteroland 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 10thleading 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 defined

2. Alcohol. Heavy alcohol for several years can cause chronic

injury to the liver and damages.

For women, consuming two to three drinksincluding 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 womenwere 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 timethat 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 itoccurs 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, andcorticosteroid medications.


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Cont.. Autoimmune hepatitis.Itis caused by the body's

immune system attacking liver cells and causinginflammation, 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) candamage 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 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 isan 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 cellswith irregular patterns of regenerating cells due tocomplication of viral, toxic or idiopathic(autoimmune) hepatitis.

Billiary cirrhosis:is associated with chronic billiaryobstruction and infection. There is diffuse fibrosisof the liver with jaundice.

Cardiac cirrhosis:chronic liver disease results fromlong-standing, severe right side heart failure withcorpulmonale, constrictive pericarditis, andtricuspid 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 metabolismhyperbilirubinemia,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

hormoneGynecomastia, 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 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.


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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.


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Endocrine problem

In men: Gynecomastia, loss of axillary and pubichair, testicular atrophy and impotence with loss of

libido due to increased estrogen level.

In younger female, amenorrhea may occur and inolder, bleeding may occur.

aldosteronehormone 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


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Complication

Portal hypertension

The nodules and scar tissue can compress

hepatic veins within the liver.

This causes the blood pressure within the liver tobe high, a condition known as portal

hypertension.

Portal venous pressure is more than 15mmHg or20 cm of water (normal 5-10mm Hg)


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Cont

Is characterized by venous pressure in the

portal circulation, spleenomegaly, large collateralvein, ascites, systemic hypertension, and

esophageal varices.

The common area to form collateral channels arein 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 portalhypertension.

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 oncoticpressure from impaired liver synthesis of albumin(hypoalbuminia)

Ascites is the accumulation of serous fluid in theperitoneal cavity.

Protein move from the blood vessels via the largerpore of sinusoids into the lymph space.

When the lymphatic system is unable to carry offthe excess protein and water, they leak throughthe 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 EncephalopathyStages Clinical Symptoms Clinical Signs

1 Normal level of

consciousness with

periods

of lethargy and euphoria;reversal of

daynight sleep patterns

Asterixis; impaired

writing and ability

to draw

line figures.

2 Increased drowsiness;disorientation;

inappropriate behavior;

mood swings; agitation

Asterixis; fetorhepaticus.


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Stages Contd.Stages Clinical Symptoms Clinical Signs

3 Stuporous; difficult to

rouse; sleeps most

of time; marked

confusion; incoherent

speech

Asterixis; increased

deep tendon reflexes;

rigidity

of extremities.

4 Comatose; may not

respond to painfulstimuli.

Absence of asterixis;

absence of deeptendon

reflexes; flaccidity of

extremities.


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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 tominimize 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 arerecorded 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

C


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Cont..

Hepatorenal syndrome:

Hepatorenal syndrome is a serious complication

of cirrhosis characterized by functional renal

failure with advancing azotemia, oliguria, andascites.


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Diagnosis

Liver function test : alkaline phosphate, ALT,ASTand yglutamyl transpeptidase ( GGT)

Blood test: total protein, albumin, serumbilirubin and globulin, serumammonia

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


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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 caseprotein is limited.

Restrict fluid


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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 positionactivation 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 (upto5-6l 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 monitorurine 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 IsengstakenBlakemore 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 to200 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 totreat acute GI hemorrhage


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Sclerotherapy


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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 bandis slipped over the tissue, causing necrosis,

ulceration, and eventual sloughing of the

varix.


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Esophageal Banding


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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 portalcirculation and the hepatic vein reducing

portal hypertension.


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Stenting

t


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cont,..

Surgical management

Liver transplantation

Removing the liver and replacing it with a

healthy donor organ is another way totreat 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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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.

Cont


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Cont.. 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 preventhemorrhage

Avoid unnecessary injection and apply gentle pressure afterinjection

Instruct the client to avoid vigorous nose blowing, strainingwith bowel movement.

Provide stool softener to prevent straining with rupture ofvarices

Advice to use soft tooth brush to prevent gum bleeding

(2) Activity intolerance related to bed rest, fatigue, lack of


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( ) y , f g , fenergy, and altered respiratory function secondary toascites.

Goal: The patient will maintain a balance between rest andactivity 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 fromjaundice and edema


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jaundice and edema

Goal: Decrease potential for pressure ulcerdevelopment; breaks in skin integrity

Interventions:

Assess degree of discomfort related to pruritusand edema.

Note and record degree of jaundice and extent ofedema.

Keep patientsfingernails short and smooth. Provide frequent skin care; avoid use of soaps and

alcohol-based lotions.

Cont


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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 48 hours. Instructpatient and family in this activity.

Restrict sodium as prescribed.

Perform range of motion exercises every 4 hours;elevate edematous extremities wheneverpossible.

(4) High risk for injury related to altered clotting


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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, removeobstacles in room, prevent falls).

Provide frequent surveillance to orient patient and

avoid use of restraints. Replace sharp objects (razors) with safer terms.

Cont


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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 bleedinggums.

Record vital signs at frequent intervals, dependingon patient acuity (every 14 hours).

Keep patient quiet and limit activity.

(5) Disturbed body image related to changes in


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(5) stu bed body age e ated to c a ges

appearance, and role function.

Goal: Patient verbalizes feelings consistent with

improvement of body image and self-esteem

Intervention:

Assess changes in appearance and the meaningthese changes have for patient and family.

Encourage patient to verbalize reactions and

feelings about these changes.

Assess patients and familys 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).

Nsg diagnosis cont


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Nsg diagnosis cont.

(6) Fluid volume excess related to portalhypertension 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


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References

Brunner And Siddhartha's (2004).Medical-

Surgical Nursing (12thEd)

Chintamani .Lewiss Medical Surgical Nursing,Mosby .2011

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

M. Joycee Black, Hokanson Jane Hawks.MedicalSurgical Nursing. Clinicalmanagement for positive outcomes. 7thed.2005.


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fc28cirrhosis of liver ppt

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