Focus on Cirrhosis of the Liver (Relates to Chapter 44, “Nursing Management: Liver, Pancreas, and Biliary Tract Problems” in the textbook) Copyright ©

Focus on Cirrhosis of the Liver

(Relates to Chapter 44, (Relates to Chapter 44, “Nursing Management: “Nursing Management:

Liver, Pancreas, and Biliary Tract Liver, Pancreas, and Biliary Tract Problems” Problems”

in the textbook)in the textbook)

Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.

2

Description

•A chronic progressive A chronic progressive disease of the liverdisease of the liver Extensive parenchymal cell Extensive parenchymal cell

degenerationdegeneration Destruction of parenchymal Destruction of parenchymal

cells cells


3

Cirrhosis


Fig. 44-4. Cirrhosis that developed secondary to alcoholism. The characteristic diffuse nodularity of the surface is due to the combination of regeneration and scarring of the liver.

4

Description

• Liver cells attempt to regenerate.Liver cells attempt to regenerate. Regenerative process is Regenerative process is

disorganized.disorganized.• Abnormal blood vessel and bile duct Abnormal blood vessel and bile duct formationformation

•New fibrous connective tissue distorts New fibrous connective tissue distorts liver’s normal structure, impedes blood liver’s normal structure, impedes blood flow.flow.

•Poor cellular nutrition and hypoxia Poor cellular nutrition and hypoxia result.result.


5

Description

• Insidious, prolonged course•Ninth leading cause of

death in United States•Fourth leading cause of

death in persons ages 35 to 54

•Twice as common in men


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Etiology and Pathophysiology

• Factors that can lead to cirrhosisFactors that can lead to cirrhosis Chronic alcohol abuseChronic alcohol abuse

•Excessive alcohol ingestion is the Excessive alcohol ingestion is the single most common cause of single most common cause of cirrhosis.cirrhosis.

•Alcohol has a direct hepatotoxic effect. Alcohol has a direct hepatotoxic effect. •First change from excessive alcohol First change from excessive alcohol intake is fat accumulation in liver intake is fat accumulation in liver cells.cells.

•With continued abuse, scar formation With continued abuse, scar formation occurs.occurs.


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Etiology and Pathophysiology Nonalcohol fatty liver disease Nonalcohol fatty liver disease

(NAFLD) (NAFLD) Malnutrition that occurs Malnutrition that occurs

concurrently with excessive concurrently with excessive alcohol intake, extreme dieting, alcohol intake, extreme dieting, malabsorption, and obesitymalabsorption, and obesity

Environmental factors, as well as a Environmental factors, as well as a genetic predisposition genetic predisposition

Postnecrotic cirrhosisPostnecrotic cirrhosis•Complication of viral, toxic, or Complication of viral, toxic, or idiopathic hepatitisidiopathic hepatitis


8

Etiology and Pathophysiology Biliary cirrhosisBiliary cirrhosis

•Associated with chronic biliary Associated with chronic biliary obstructionobstruction

•Diffuse fibrosis of liver with Diffuse fibrosis of liver with jaundicejaundice

Cardiac cirrhosisCardiac cirrhosis•From long-standing severe From long-standing severe right-sided heart failureright-sided heart failure


9

Clinical Manifestations

Early manifestationsEarly manifestations•Onset usually insidiousOnset usually insidious•GI disturbances:GI disturbances:

AnorexiaAnorexia DyspepsiaDyspepsia FlatulenceFlatulence Nausea/vomiting Nausea/vomiting Change in bowel habits Change in bowel habits


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Early manifestations (cont’d)Early manifestations (cont’d)•Abdominal painAbdominal pain• FeverFever• LassitudeLassitude•Weight lossWeight loss• Enlarged liver or spleen Enlarged liver or spleen


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Late manifestationsLate manifestations• Two causative mechanismsTwo causative mechanisms

Hepatocellular failureHepatocellular failure Portal hypertension Portal hypertension


12

Pathophysiology of Cirrhosis


Fig. 44-5. Continuum of liver dysfunction in cirrhosis and resulting manifestations. ADH, Antidiuretic hormone;ALT, alanine aminotransferase; AST, aspartate transaminase.

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Fig. 44-6. Systemic clinical manifestations of liver cirrhosis.

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Late manifestations (cont’d)Late manifestations (cont’d)• JaundiceJaundice

Decreased ability of liver cells to Decreased ability of liver cells to conjugate and excrete bilirubinconjugate and excrete bilirubin

Functional derangement of liver Functional derangement of liver cellscells

Compression of bile ducts by Compression of bile ducts by overgrowth of connective tissueovergrowth of connective tissue


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Jaundice (cont’d)Jaundice (cont’d) Minimal or severe, depending Minimal or severe, depending

on liver damageon liver damage Late stages of cirrhosisLate stages of cirrhosis

• Patient usually will be Patient usually will be jaundiced.jaundiced.

If biliary tract obstructed, If biliary tract obstructed, pruritus can occur.pruritus can occur.


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•Skin lesionsSkin lesions Due to increase in circulating Due to increase in circulating

estrogen caused by inability estrogen caused by inability of liver to metabolize steroid of liver to metabolize steroid hormoneshormones


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•Skin lesions (cont’d)Skin lesions (cont’d) Spider angiomas Spider angiomas

•Small dilated blood vessels with Small dilated blood vessels with bright red center and spiderlike bright red center and spiderlike branchesbranches

•Nose, cheeks, upper trunk, neck, Nose, cheeks, upper trunk, neck, shoulders shoulders

Palmar erythemaPalmar erythema•Red area on palms of bands that Red area on palms of bands that blanches with pressureblanches with pressure


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• Endocrine disordersEndocrine disorders Steroid hormones of the Steroid hormones of the

adrenal cortex, testes, and adrenal cortex, testes, and ovaries are metabolized and ovaries are metabolized and inactivated by the normal liver.inactivated by the normal liver.

Damaged liver is unable to Damaged liver is unable to metabolize these hormones, metabolize these hormones, and various manifestations and various manifestations occur. occur.


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•Hematologic disordersHematologic disorders SplenomegalySplenomegaly

•From backup of blood from From backup of blood from portal veinportal vein

Bleeding tendencies Bleeding tendencies • Decreased production of Decreased production of hepatic clotting factorshepatic clotting factors


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•Peripheral neuropathyPeripheral neuropathy Dietary deficiencies of Dietary deficiencies of

thiamine, folic acid, and thiamine, folic acid, and cobalamin (vitamin Bcobalamin (vitamin B1212))


21

Complications

•Portal hypertension Portal hypertension • Esophageal and gastric Esophageal and gastric

varicesvarices•Peripheral edema and Peripheral edema and

ascitesascites•Hepatic encephalopathyHepatic encephalopathy•Hepatorenal syndromeHepatorenal syndrome


22

Complications

Portal hypertensionPortal hypertension• Characterized byCharacterized by

Increased venous pressure in Increased venous pressure in portal circulationportal circulation

SplenomegalySplenomegaly AscitesAscites Large collateral veinsLarge collateral veins Esophageal varicesEsophageal varices Systemic hypertensionSystemic hypertension


23

Complications

Portal hypertension (cont’d)Portal hypertension (cont’d)•Primary mechanism is Primary mechanism is

increased resistance to increased resistance to blood flow through the blood flow through the liver.liver.


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Complications

Portal hypertension (cont’d) Portal hypertension (cont’d) • Esophageal varices Esophageal varices

Complex of tortuous veins at Complex of tortuous veins at lower end of esophaguslower end of esophagus

Develop in areas where Develop in areas where collateral and systemic collateral and systemic circulations communicatecirculations communicate


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Complications

• Esophageal varices (cont’d)Esophageal varices (cont’d) Contain little elastic tissue Contain little elastic tissue

and are fragileand are fragile Bleeding esophageal varices Bleeding esophageal varices

•Most life-threatening Most life-threatening complication of cirrhosiscomplication of cirrhosis

80% of variceal hemorrhages80% of variceal hemorrhages


26

Complications

Portal hypertension (cont’d)Portal hypertension (cont’d)•Gastric varicesGastric varices

Located in upper portion of Located in upper portion of stomachstomach

20% of variceal hemorrhages20% of variceal hemorrhages


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Complications

Portal hypertension (cont’d)Portal hypertension (cont’d)• Internal hemorrhoids Internal hemorrhoids

Occur because of the dilation Occur because of the dilation of the mesenteric veins and of the mesenteric veins and rectal veins rectal veins

•Caput medusaeCaput medusae Ring of varices around the Ring of varices around the

umbilicus umbilicus Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.

Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 28

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Complications

Peripheral edema and ascitesPeripheral edema and ascites• EdemaEdema

↓ ↓ Colloidal oncotic pressure Colloidal oncotic pressure from impaired liver synthesis of from impaired liver synthesis of albuminalbumin

↑ ↑ Portacaval pressure from Portacaval pressure from portal hypertensionportal hypertension

Occurs as ankle/presacral Occurs as ankle/presacral edemaedema


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Complications

Peripheral edema and ascites Peripheral edema and ascites (cont’d)(cont’d)

•AscitesAscites Accumulation of serous fluid in Accumulation of serous fluid in

peritoneal or abdominal cavityperitoneal or abdominal cavity Abdominal distention with Abdominal distention with

weight gainweight gain Common manifestation of Common manifestation of

cirrhosiscirrhosis


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Ascites


Fig. 44-7. Mechanisms for development of ascites.

Gross Ascites


Fig. 44-8. Gross ascites.

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Complications

•Ascites (cont’d)Ascites (cont’d) Factors involved in the Factors involved in the

pathogenesis pathogenesis •↓ ↓ Serum colloidal oncotic Serum colloidal oncotic pressurepressure

•↑ ↑ Levels of aldosteroneLevels of aldosterone•Portal hypertensionPortal hypertension•↑ ↑ Flow hepatic lymphFlow hepatic lymph•Impaired water excretion Impaired water excretion


34

Complications

Hepatic encephalopathyHepatic encephalopathy•Neuropsychiatric Neuropsychiatric

manifestationmanifestation• Terminal complication in Terminal complication in

liver diseaseliver disease


35

Complications

Hepatic encephalopathy (cont’d)Hepatic encephalopathy (cont’d)• Etiologic factorsEtiologic factors

Disorder of protein metabolism and Disorder of protein metabolism and excretionexcretion•Liver unable to convert ammonia to Liver unable to convert ammonia to urea, or blood shunted past liver urea, or blood shunted past liver through, so ammonia stays in systemic through, so ammonia stays in systemic circulationcirculation

•Ammonia crosses blood-brain barrier Ammonia crosses blood-brain barrier and causes neurologic toxic and causes neurologic toxic manifestations.manifestations.


36

Complications

Hepatic encephalopathy Hepatic encephalopathy (cont’d)(cont’d)

• Etiologic factors (cont’d)Etiologic factors (cont’d) Altered astrocyte functionAltered astrocyte function

•Regulate blood-brain barrier Regulate blood-brain barrier and detoxification of ammoniaand detoxification of ammonia


37

Complications


•Clinical manifestationsClinical manifestations Changes in neurologic and Changes in neurologic and

mental responsiveness mental responsiveness •Ranging from sleep disturbance Ranging from sleep disturbance to lethargy to deep coma to lethargy to deep coma


38

Complications

Hepatic encephalopathy (cont’d)Hepatic encephalopathy (cont’d)• Grading system used to Grading system used to

classify stagesclassify stages Stages 0 through 4Stages 0 through 4 4 is most advanced.4 is most advanced.

• AsterixisAsterixis Characteristic symptomCharacteristic symptom Flapping tremors involving arms Flapping tremors involving arms

and hands and hands


39

Complications


• Fetor hepaticusFetor hepaticus Musty, sweet odor on Musty, sweet odor on

patient’s breathpatient’s breath Accumulation of digestive by-Accumulation of digestive by-

products that liver is unable products that liver is unable to degradeto degrade


40

Complications

Hepatorenal syndromeHepatorenal syndrome•Serious complication of Serious complication of

cirrhosiscirrhosis• Functional renal failure with Functional renal failure with

AzotemiaAzotemia OliguriaOliguria Intractable ascitesIntractable ascites


41

Complications

Hepatorenal syndrome (cont’d)Hepatorenal syndrome (cont’d)•No structural abnormality of No structural abnormality of

kidneykidney•Splanchnic and systemic Splanchnic and systemic

vasodilation and ↓ arterial vasodilation and ↓ arterial blood volumeblood volume Renal vasoconstriction occurs Renal vasoconstriction occurs

with renal failure.with renal failure.


42

Diagnostic Studies

•History/physical History/physical examinationexamination

• Laboratory testsLaboratory tests Liver function testsLiver function tests Serum electrolytesSerum electrolytes CBCCBC


43

Diagnostic Studies

• Laboratory tests (cont’d)Laboratory tests (cont’d) Prothrombin timeProthrombin time Serum albuminSerum albumin Stool for occult bloodStool for occult blood Analysis of ascitic fluidAnalysis of ascitic fluid

• Liver biopsy Liver biopsy


44

Collaborative Care

•RestRest•Administration of B-Administration of B-

complex vitaminscomplex vitamins•Avoidance of alcohol, Avoidance of alcohol,

aspirin, acetaminophen, aspirin, acetaminophen, and NSAIDsand NSAIDs

•Management of ascites Management of ascites


45

Collaborative Care

•Prevention and Prevention and management of esophageal management of esophageal variceal bleedingvariceal bleeding

•Management of Management of encephalopathyencephalopathy


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Collaborative Care

•AscitesAscites High-carbohydrate, low-NaHigh-carbohydrate, low-Na++

diet diet (2 g/day)(2 g/day)

DiureticsDiuretics Paracentesis Paracentesis

•Removes fluid from abdominal Removes fluid from abdominal cavitycavity

•Temporary measureTemporary measure


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Collaborative Care

•Ascites (cont’d)Ascites (cont’d) Peritoneovenous shuntPeritoneovenous shunt

•Continuous reinfusion of ascitic Continuous reinfusion of ascitic fluid from the abdomen to the fluid from the abdomen to the vena cavavena cava

•Not first-line therapyNot first-line therapy•Complications : Thrombosis, Complications : Thrombosis, infection, fluid overload, DIC infection, fluid overload, DIC


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Collaborative Care

• Esophageal and gastric Esophageal and gastric varicesvarices Goal: Avoid Goal: Avoid

bleeding/hemorrhagebleeding/hemorrhage Avoid alcohol, aspirin, and Avoid alcohol, aspirin, and

irritating foods. irritating foods. Respiratory infection Respiratory infection

promptly treatedpromptly treated


49

Collaborative Care

If bleeding occurs, stabilize If bleeding occurs, stabilize patient, manage airway, patient, manage airway, provide IV therapy.provide IV therapy.

Drug therapy may include Drug therapy may include •Octreotide (Sandostatin)Octreotide (Sandostatin)•Vasopressin (VP, Terlipressin)Vasopressin (VP, Terlipressin)•Nitroglycerin (NTG)Nitroglycerin (NTG)•ββ-adrenergic blockers-adrenergic blockers


50

Collaborative Care

• Endoscopic sclerotherapyEndoscopic sclerotherapy Treatment for acute/chronic Treatment for acute/chronic

bleeding varicesbleeding varices Agent (morrhuate Agent (morrhuate

[Scleromate])[Scleromate])•Thromboses and obliterates Thromboses and obliterates distended veinsdistended veins


51

Collaborative Care

• Endoscopic ligationEndoscopic ligation Banding of varicesBanding of varices Fewer complications than Fewer complications than

sclerotherapysclerotherapy•Balloon tamponadeBalloon tamponade

Controls hemorrhage by Controls hemorrhage by compression of varicescompression of varices

Uses Sengstaken-Blakemore Uses Sengstaken-Blakemore tubetube


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Sengstaken-Blakemore Tube


Fig. 44-9. A, Sengstaken-Blakemore tube. B, Tube inserted into esophagus and stomach.

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Collaborative Care

•Supportive measures for Supportive measures for acute bleedacute bleed Fresh frozen plasmaFresh frozen plasma Packed RBCsPacked RBCs Vitamin KVitamin K Histamine receptor blockersHistamine receptor blockers Proton pump inhibitorsProton pump inhibitors Lactulose (Cephulac) Lactulose (Cephulac) Neomycin Neomycin


54

Collaborative Care

• Long-term managementLong-term management β-adrenergic blockersβ-adrenergic blockers Repeated sclerotherapy/band Repeated sclerotherapy/band

ligationligation Portosystemic shuntsPortosystemic shunts Propranolol (Inderal)Propranolol (Inderal)


55

Collaborative Care

•Shunting proceduresShunting procedures Used more after second Used more after second

major bleeding episodemajor bleeding episode Surgical vs. nonsurgicalSurgical vs. nonsurgical


56

Collaborative Care

•Nonsurgical procedureNonsurgical procedure Transjugular intrahepatic Transjugular intrahepatic

portosystemic shunt (TIPS) portosystemic shunt (TIPS) •Tract (shunt) between systemic Tract (shunt) between systemic and portal venous systemand portal venous system

•Used to redirect portal blood flowUsed to redirect portal blood flow•Decreases portal venous pressure Decreases portal venous pressure and decompresses varices and decompresses varices


57

Total Portal Division After TIPS


Fig. 44-10. Total portal diversion after transjugular intrahepatic portosystemic shunt (TIPS). A, Portal venogrambefore TIPS shows filling of large esophageal varices (arrows). B, After insertion of a TIPS, flow to varices iseliminated. Intrahepatic portal vein flow is now reversed, with the direction of intrahepatic flow toward the TIPS.

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Collaborative Care

•Surgical proceduresSurgical procedures Portacaval shuntPortacaval shunt

•Decreases bleeding episodesDecreases bleeding episodes•Does not prolong life; patient Does not prolong life; patient dies of hepatic encephalopathy dies of hepatic encephalopathy


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Portosystemic Shunts


Fig. 44-11. Portosystemic shunts. A, Portacaval shunt. The portal vein is anastomosed to the inferior vena cava,diverting blood from the portal vein to the systemic circulation. B, Distal splenorenal shunt. The splenic vein isanastomosed to the renal vein. The portal venous flow remains intact while esophageal varices are selectivelydecompressed. (The short gastric veins are decompressed.) The spleen conducts blood from the high pressureof the esophageal and gastric varices to the low-pressure renal vein.

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Collaborative Care

•Surgical procedures Surgical procedures (cont’d)(cont’d) Distal splenorenal shunt Distal splenorenal shunt

(Warren shunt)(Warren shunt)•Leaves portal venous flow Leaves portal venous flow intactintact•↓ ↓ Incidence of hepatic Incidence of hepatic

encephalopathyencephalopathy•With time, blood flow to liver ↓With time, blood flow to liver ↓


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Collaborative Care

•Hepatic encephalopathyHepatic encephalopathy Goal: Decrease ammonia Goal: Decrease ammonia

formationformation•Sterilization of GI tract with Sterilization of GI tract with antibiotics (e.g., neomycin)antibiotics (e.g., neomycin)

•Lactulose (Cephulac) traps NH3 in Lactulose (Cephulac) traps NH3 in gut.gut.

•Cathartics/enemasCathartics/enemas Treatment of precipitating causeTreatment of precipitating cause


62

Collaborative Care

•Drug therapyDrug therapy No specific drug therapyNo specific drug therapy Drugs are used to treat Drugs are used to treat

symptoms and complications symptoms and complications of advanced liver disease. of advanced liver disease.


63

Nutritional Therapy

•Diet for patient without Diet for patient without complicationscomplications High in calories (3000 High in calories (3000

kcal/day)kcal/day) ↑ ↑ carbohydratecarbohydrate Moderate to low fatModerate to low fat Protein restriction rarely Protein restriction rarely

justifiedjustified


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Nutritional Therapy

•Protein supplements if Protein supplements if protein-calorie malnutritionprotein-calorie malnutrition

• Low-sodium diet for patient Low-sodium diet for patient with ascites and edema with ascites and edema


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Nursing ManagementNursing Assessment

• Past health historyPast health history Chronic alcoholismChronic alcoholism Viral hepatitisViral hepatitis Chronic biliary diseaseChronic biliary disease

• Physical examinationPhysical examination• MedicationsMedications• Weight loss Weight loss • JaundiceJaundice


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Nursing ManagementNursing Assessment

•Abdominal distentionAbdominal distention•Nausea/vomitingNausea/vomiting•Altered mentationAltered mentation•RUQ painRUQ pain•Abnormal laboratory valuesAbnormal laboratory values


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Nursing ManagementNursing Diagnoses

• Imbalanced nutrition: Less Imbalanced nutrition: Less than body requirementsthan body requirements

• Impaired skin integrityImpaired skin integrity• Ineffective breathing patternIneffective breathing pattern• Excess fluid volumeExcess fluid volume•Dysfunctional family Dysfunctional family

processes: Alcoholismprocesses: Alcoholism


68

Nursing ManagementPlanning

•Overall goalsOverall goals Relief of discomfortRelief of discomfort Minimal to no complicationsMinimal to no complications Return to as normal a Return to as normal a

lifestyle as possible lifestyle as possible


69

Nursing ManagementNursing Implementation

•Health promotionHealth promotion Treat alcoholism.Treat alcoholism. Identify hepatitis early and Identify hepatitis early and

treat.treat. Stress importance of Stress importance of

adequate nutrition.adequate nutrition. Identify biliary disease early Identify biliary disease early

and treat.and treat.


70


•Acute interventionAcute intervention RestRest Oral hygieneOral hygiene Between-meal nourishmentBetween-meal nourishment Explanation of dietary Explanation of dietary

restrictionsrestrictions


71


•Acute intervention (cont’d)Acute intervention (cont’d) Accurate I/OAccurate I/O Daily weightsDaily weights Abdominal girthAbdominal girth

•Kneeling position, if possibleKneeling position, if possible Extremities measurementExtremities measurement


72


•Acute intervention (cont’d)Acute intervention (cont’d) ParacentesisParacentesis

•Patient void immediately Patient void immediately beforebefore

•High Fowler’s or side of bedHigh Fowler’s or side of bed•Monitor for electrolyte Monitor for electrolyte imbalances.imbalances.

•Monitor dressing for Monitor dressing for bleeding/leakage.bleeding/leakage.


73


•Acute intervention (cont’d)Acute intervention (cont’d) Check respiratory status Check respiratory status

frequently.frequently.•Semi- or high Fowler’sSemi- or high Fowler’s

Skin careSkin care•Turning schedule, at least every 2 Turning schedule, at least every 2 hourshours

ROM exercisesROM exercises Coughing/deep breathing Coughing/deep breathing

exercisesexercisesCopyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.

74


•Acute intervention (cont’d)Acute intervention (cont’d) Monitor for electrolyte Monitor for electrolyte

disturbances.disturbances.•Diuretic therapy alters Diuretic therapy alters electrolytes.electrolytes.

•HypokalemiaHypokalemia•Cardiac dysrhythmias, hypotension, Cardiac dysrhythmias, hypotension,

tachycardia, muscle weaknesstachycardia, muscle weakness Observe for bleeding disorders.Observe for bleeding disorders. Always be a supportive listener.Always be a supportive listener.


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•Acute intervention (cont’d)Acute intervention (cont’d) Bleeding varicesBleeding varices

•Close observation for signs of Close observation for signs of bleedingbleeding

•Balloon tamponade careBalloon tamponade care• Explanation of procedureExplanation of procedure•Check for patency.Check for patency.•Position of balloon verified by x-Position of balloon verified by x-

ray ray


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•Acute intervention (cont’d)Acute intervention (cont’d)•Balloon tamponade (cont’d)Balloon tamponade (cont’d)

•Saline lavage/NG suction to Saline lavage/NG suction to remove bloodremove blood

•Monitor for complications (i.e., Monitor for complications (i.e., aspiration pneumonia).aspiration pneumonia).

•Scissors at bedsideScissors at bedside•Semi-Fowler’s positionSemi-Fowler’s position•Oral/nasal careOral/nasal care


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•Acute intervention (cont’d)Acute intervention (cont’d) Hepatic encephalopathyHepatic encephalopathy

•Maintain safe environment.Maintain safe environment.•Assess carefully.Assess carefully.

• Level of responsivenessLevel of responsiveness•Sensory and motor abnormalitiesSensory and motor abnormalities• Fluid/electrolyte imbalancesFluid/electrolyte imbalances•Acid-base balanceAcid-base balance• Effects of treatment measuresEffects of treatment measures


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•Acute intervention (cont’d)Acute intervention (cont’d) Hepatic encephalopathy Hepatic encephalopathy

(cont’d)(cont’d)•Neurologic assessment every 2 Neurologic assessment every 2 hourshours

•Prevention of constipationPrevention of constipation•Limited physical activityLimited physical activity•Control of hypokalemiaControl of hypokalemia•Ensuring proper nutritionEnsuring proper nutrition


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•Ambulatory and home careAmbulatory and home care Symptoms of complicationsSymptoms of complications Written instructions with Written instructions with

adequate explanations for adequate explanations for patient/familypatient/family

When to seek medical attentionWhen to seek medical attention Remission maintenanceRemission maintenance Abstinence from alcohol Abstinence from alcohol Caring attitude alwaysCaring attitude always


80

Nursing ManagementEvaluation

• Maintenance of food/fluid Maintenance of food/fluid intake to meet needsintake to meet needs

• Maintenance of muscle tone Maintenance of muscle tone and energy and energy

• Maintenance of skin Maintenance of skin integrityintegrity

• Normalization of fluid Normalization of fluid balancebalance


81

Nursing ManagementEvaluation

• Maintenance of blood Maintenance of blood pressure and urinary outputpressure and urinary output

• Reports increased ease of Reports increased ease of breathingbreathing

• Experiences normal Experiences normal respiratory rate/rhythmrespiratory rate/rhythm


82

A patient with advanced cirrhosis with ascites A patient with advanced cirrhosis with ascites is short of breath and has an increased is short of breath and has an increased respiratory rate. The nurse should:respiratory rate. The nurse should:

1. Initiate oxygen therapy at 2 L/min to 1. Initiate oxygen therapy at 2 L/min to increase gas exchange. increase gas exchange. 2. Notify the health care provider so a 2. Notify the health care provider so a paracentesis can be performed.paracentesis can be performed.3. Ask patient to cough and deep breathe to 3. Ask patient to cough and deep breathe to clear respiratory secretions.clear respiratory secretions.4. Place the patient in Fowler’s position to 4. Place the patient in Fowler’s position to relieve pressure on the diaphragm. relieve pressure on the diaphragm.

Audience Response Question


Case Study


84

Case Study

• 35-year-old woman was 35-year-old woman was admitted with hepatic coma.admitted with hepatic coma.

•History of numerous History of numerous hospitalizations since age 19hospitalizations since age 19 Usually for psychosomatic and Usually for psychosomatic and

nervous disordersnervous disorders


85

Case Study

•Denies alcoholism and Denies alcoholism and having more than 3 oz of having more than 3 oz of alcohol per dayalcohol per day States “the girls and I have States “the girls and I have

social drinks”social drinks”


86

Case Study

•Review of old medical Review of old medical records shows progressive records shows progressive weakness, weight loss, weakness, weight loss, anorexia, jaundice, edema, anorexia, jaundice, edema, ascites, and mental ascites, and mental disorientation.disorientation.


87

Case Study

•Accepts treatment only Accepts treatment only during crisesduring crises

•Upon admission, she is Upon admission, she is stuporous and hypotensive, stuporous and hypotensive, and has twitching and and has twitching and asterixis.asterixis.


88

Case Study

•She is thin and She is thin and malnourished with marked malnourished with marked edema on lower extremities edema on lower extremities and ascites.and ascites.

• Liver and spleen are both Liver and spleen are both palpable.palpable.


89

Case Study

• Jaundice and spider Jaundice and spider angiomas are present. angiomas are present.

• Evidence of bruising Evidence of bruising throughout bodythroughout body


90

Case Study

•Previous liver biopsies Previous liver biopsies indicatedindicated At age 29, fatty liverAt age 29, fatty liver At age 31, cirrhosis with At age 31, cirrhosis with

hyaline necrosishyaline necrosis


91

Case Study

• Laboratory valuesLaboratory values Total bilirubin 11 mg/dLTotal bilirubin 11 mg/dL AST 80 U/mLAST 80 U/mL ALT 70 U/mLALT 70 U/mL LDH 700 U/mLLDH 700 U/mL Serum ammonia 220 mg/dLSerum ammonia 220 mg/dL WBC 21,450/uLWBC 21,450/uL Hematocrit 24%Hematocrit 24%


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Discussion Questions

1.1.What clinical What clinical manifestations of cirrhosis manifestations of cirrhosis does she have?does she have?

2.2.Explain the results of her Explain the results of her diagnostic findings.diagnostic findings.


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Discussion Questions

3.3. What is the priority of What is the priority of care for her?care for her?

4.4. What patient and family What patient and family teaching is essential?teaching is essential?


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