Cirrhosis

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cirrhosiscirrhosis
nscobienscobie

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DescriptionDescription
Regenerative process is Regenerative process is
disorganized, resulting in abnormal disorganized, resulting in abnormal
blood vessel and bile duct blood vessel and bile duct
relationships from fibrosisrelationships from fibrosis

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DescriptionDescription
Normal lobular structure distorted by Normal lobular structure distorted by
fibrotic connective tissuefibrotic connective tissue
Lobules are irregular in size and Lobules are irregular in size and
shape with impaired vascular flowshape with impaired vascular flow
Insidious, prolonged courseInsidious, prolonged course

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StatisticsStatistics
> 50% of liver disease is directly > 50% of liver disease is directly
related to alcohol consumptionrelated to alcohol consumption
Of the estimated 15 million alcoholics Of the estimated 15 million alcoholics
in the USA 10-20% have or will in the USA 10-20% have or will
develop cirrhosisdevelop cirrhosis

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StatisticsStatistics
Direct correlation between alcohol Direct correlation between alcohol
consumption in any geographic area consumption in any geographic area
and the death rate from cirrhosis in and the death rate from cirrhosis in
that area that area

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Etiology and PathophysiologyEtiology and Pathophysiology
Cell necrosis occursCell necrosis occurs
Destroyed liver cells are replaced Destroyed liver cells are replaced
by scar tissueby scar tissue
Normal architecture becomes Normal architecture becomes
nodularnodular

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Etiology and PathophysiologyEtiology and Pathophysiology
Four types of cirrhosis:Four types of cirrhosis:
–Alcoholic (Laennec’s) cirrhosisAlcoholic (Laennec’s) cirrhosis
–Postnecrotic cirrhosisPostnecrotic cirrhosis
–Biliary cirrhosisBiliary cirrhosis
–Cardiac cirrhosisCardiac cirrhosis

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Etiology and PathophysiologyEtiology and Pathophysiology
Alcoholic (Laennec’s) CirrhosisAlcoholic (Laennec’s) Cirrhosis
–Associated with alcohol abuseAssociated with alcohol abuse
–Preceded by a theoretically reversible Preceded by a theoretically reversible
fatty infiltration of the liver cellsfatty infiltration of the liver cells
–Widespread scar formation Widespread scar formation

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Etiology and PathophysiologyEtiology and Pathophysiology
Postnecrotic CirrhosisPostnecrotic Cirrhosis
–Complication of toxic or viral hepatitisComplication of toxic or viral hepatitis
–Accounts for 20% of the cases of Accounts for 20% of the cases of
cirrhosiscirrhosis
–Broad bands of scar tissue form Broad bands of scar tissue form
within the liverwithin the liver

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Etiology and PathophysiologyEtiology and Pathophysiology

Biliary CirrhosisBiliary Cirrhosis
–Associated with chronic biliary Associated with chronic biliary
obstruction and infectionobstruction and infection
–Accounts for 15% of all cases of Accounts for 15% of all cases of
cirrhosiscirrhosis

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Etiology and PathophysiologyEtiology and Pathophysiology

Cardiac CirrhosisCardiac Cirrhosis
–Results from longstanding severe Results from longstanding severe
right-sided heart failureright-sided heart failure

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Manifestations of Liver CirrhosisManifestations of Liver Cirrhosis
Fig. 42-5

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Clinical ManifestationsClinical Manifestations
Early ManifestationsEarly Manifestations
Onset usually insidiousOnset usually insidious
GI disturbances: GI disturbances:
–Anorexia Anorexia
–Dyspepsia Dyspepsia
–Flatulence Flatulence
–N-V, change in bowel habitsN-V, change in bowel habits

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Clinical ManifestationsClinical Manifestations
Early ManifestationsEarly Manifestations
Abdominal painAbdominal pain
FeverFever
LassitudeLassitude
Weight lossWeight loss
Enlarged liver or spleenEnlarged liver or spleen

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Clinical ManifestationsClinical Manifestations
Late ManifestationsLate Manifestations
Two causative mechanismsTwo causative mechanisms
–Hepatocellular failureHepatocellular failure
–Portal hypertensionPortal hypertension

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Clinical ManifestationsClinical Manifestations
JaundiceJaundice
Occurs because of insufficient Occurs because of insufficient
conjugation of bilirubin by the liver conjugation of bilirubin by the liver
cells, and local obstruction of cells, and local obstruction of
biliary ducts by scarring and biliary ducts by scarring and
regenerating tissueregenerating tissue

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Clinical ManifestationsClinical Manifestations
JaundiceJaundice
Intermittent jaundice is Intermittent jaundice is
characteristic of biliary cirrhosischaracteristic of biliary cirrhosis
Late stages of cirrhosis the patient Late stages of cirrhosis the patient
will usually be jaundicedwill usually be jaundiced

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Clinical ManifestationsClinical Manifestations
SkinSkin
Spider angiomas ( spider nevi)Spider angiomas ( spider nevi)
Palmar erythemaPalmar erythema

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Clinical ManifestationsClinical Manifestations
Endocrine DisturbancesEndocrine Disturbances
Steroid hormonesSteroid hormones of the adrenal of the adrenal
cortex (aldosterone), testes, and cortex (aldosterone), testes, and
ovaries are metabolized and ovaries are metabolized and
inactivated by the normal liverinactivated by the normal liver

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Clinical ManifestationsClinical Manifestations
Endocrine DisturbancesEndocrine Disturbances
Alteration in hair distributionAlteration in hair distribution
–Decreased amount of pubic hairDecreased amount of pubic hair
–Axillary and pectoral alopeciaAxillary and pectoral alopecia

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Clinical ManifestationsClinical Manifestations
Hematologic DisordersHematologic Disorders
Bleeding tendencies as a result of Bleeding tendencies as a result of
decreased production of hepatic decreased production of hepatic
clotting factors (II, VII, IX, and X)clotting factors (II, VII, IX, and X)

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Clinical ManifestationsClinical Manifestations
Hematologic DisordersHematologic Disorders
Anemia, leukopenia, and Anemia, leukopenia, and
thrombocytopenia are believed to thrombocytopenia are believed to
be result of hypersplenismbe result of hypersplenism

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Clinical ManifestationsClinical Manifestations
Peripheral NeuropathyPeripheral Neuropathy
Dietary deficiencies of thiamine, Dietary deficiencies of thiamine,
folic acid, and vitamin Bfolic acid, and vitamin B
1212

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ComplicationsComplications
Portal hypertension and Portal hypertension and
oesophageal varicesoesophageal varices
Peripheral oedema and ascitesPeripheral oedema and ascites
Hepatic encephalopathyHepatic encephalopathy
Fetor hepaticusFetor hepaticus

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ComplicationsComplications
Portal HypertensionPortal Hypertension
Characterized by:Characterized by:
–Increased venous pressure in portal Increased venous pressure in portal
circulationcirculation
–SplenomegalySplenomegaly
–Oesophageal varicesOesophageal varices
–Systemic hypertensionSystemic hypertension

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ComplicationsComplications
Portal HypertensionPortal Hypertension
Primary mechanism is the Primary mechanism is the
increased resistance to blood flow increased resistance to blood flow
through the liverthrough the liver

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ComplicationsComplications
Portal HypertensionPortal Hypertension
SplenomegalySplenomegaly
Back pressure caused by portal Back pressure caused by portal
hypertension hypertension ®® chronic passive chronic passive
congestion as a result of increased congestion as a result of increased
pressure in the splenic veinpressure in the splenic vein

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ComplicationsComplications
Portal HypertensionPortal Hypertension
Oesophageal Oesophageal Varices Varices
•Increased blood flow through the Increased blood flow through the
portal system results in dilation portal system results in dilation
and enlargement of the plexus and enlargement of the plexus
veins of the esophagus and veins of the esophagus and
produces varicesproduces varices

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ComplicationsComplications
Portal HypertensionPortal Hypertension
Oesophageal Oesophageal Varices Varices
•Varices have fragile vessel walls Varices have fragile vessel walls
which bleed easilywhich bleed easily

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ComplicationsComplications
Portal HypertensionPortal Hypertension
Internal HemorrhoidsInternal Hemorrhoids
•Occurs because of the dilation of Occurs because of the dilation of
the mesenteric veins and rectal the mesenteric veins and rectal
veinsveins

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ComplicationsComplications
Peripheral Oedema and AscitesPeripheral Oedema and Ascites
•Ascites:Ascites:
- - Intraperitoneal accumulation of Intraperitoneal accumulation of
watery fluid containing small watery fluid containing small
amounts of proteinamounts of protein

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ComplicationsComplications
Peripheral Oedema and AscitesPeripheral Oedema and Ascites
•Factors involved in the pathogenesis Factors involved in the pathogenesis
of ascites:of ascites:
-HypoalbuminemiaHypoalbuminemia
-­­ Levels of aldosteroneLevels of aldosterone
-­­ Portal hypertensionPortal hypertension

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ComplicationsComplications
Hepatic EncephalopathyHepatic Encephalopathy
Liver damage causes blood to Liver damage causes blood to
enter systemic circulation without enter systemic circulation without
liver detoxificationliver detoxification

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ComplicationsComplications
Hepatic EncephalopathyHepatic Encephalopathy
Main pathogenic toxin is NHMain pathogenic toxin is NH
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although other etiological factors although other etiological factors
have been identifiedhave been identified
Frequently a terminal complicationFrequently a terminal complication

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ComplicationsComplications
Fetor HepaticusFetor Hepaticus
Musty, sweetish odor detected on Musty, sweetish odor detected on
the patient’s breath the patient’s breath
From accumulation of digested by-From accumulation of digested by-
productsproducts

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Development of AscitesDevelopment of Ascites
Fig. 42-6

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Diagnostic StudiesDiagnostic Studies
Liver function testsLiver function tests
Liver biopsyLiver biopsy
Liver scanLiver scan
Liver ultrasoundLiver ultrasound

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Diagnostic StudiesDiagnostic Studies
EsophagogastroduodenoscopEsophagogastroduodenoscop
yy
Prothrombin timeProthrombin time
Testing of stool for occult Testing of stool for occult
bloodblood

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Collaborative CareCollaborative Care
RestRest
Avoidance of alcohol and Avoidance of alcohol and
anticoagulantsanticoagulants
Management of ascitesManagement of ascites

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Collaborative CareCollaborative Care
Prevention and management of Prevention and management of
oesophageal variceal bleedingoesophageal variceal bleeding
Management of encephalopathyManagement of encephalopathy

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Collaborative CareCollaborative Care
AscitesAscites
High carbohydrate, low protein, High carbohydrate, low protein,
low Na+ dietlow Na+ diet
DiureticsDiuretics
ParacentesisParacentesis

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Collaborative CareCollaborative Care
AscitesAscites
Peritoneovenous shuntPeritoneovenous shunt
–Provides for continuous reinfusion of Provides for continuous reinfusion of
ascitic fluid from the abdomen to the ascitic fluid from the abdomen to the
vena cavavena cava

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Peritoneovenous ShuntPeritoneovenous Shunt
Fig. 42-8

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Collaborative CareCollaborative Care
OesophagealOesophageal Varices Varices
Avoid alcohol, aspirin, and Avoid alcohol, aspirin, and
irritating foodsirritating foods
If bleeding occurs, stabilize patient If bleeding occurs, stabilize patient
and manage the airway, and manage the airway,
administer vasopressin (Pitressin)administer vasopressin (Pitressin)

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Collaborative CareCollaborative Care
Endoscopic sclerotherapy or Endoscopic sclerotherapy or
ligationligation
Balloon tamponadeBalloon tamponade
Surgical shunting procedures (e.g., Surgical shunting procedures (e.g.,
portacaval shunt, TIPS)portacaval shunt, TIPS)

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Sengstaken-Blakemore TubeSengstaken-Blakemore Tube
Fig. 42-9

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Portosystemic ShuntsPortosystemic Shunts
Fig. 42-11

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Drug TherapyDrug Therapy
There is no specific drug therapy for There is no specific drug therapy for
cirrhosiscirrhosis
Drugs are used to treat symptoms Drugs are used to treat symptoms
and complications of advanced liver and complications of advanced liver
diseasedisease

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Nutritional TherapyNutritional Therapy
Diet for patient without Diet for patient without
complications:complications:
–High in caloriesHigh in calories
v­­ CHOCHO
–Moderate to low fatModerate to low fat
–Amount of protein varies with degree of Amount of protein varies with degree of
liver damageliver damage

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Nutritional TherapyNutritional Therapy
Patient with hepatic Patient with hepatic
encephalopathyencephalopathy
–Very low to no-protein dietVery low to no-protein diet
Low sodium diet for patient with Low sodium diet for patient with
ascites and oedemaascites and oedema

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Nursing ManagementNursing Management
Nursing AssessmentNursing Assessment
Past health historyPast health history
Medications Medications
Chronic alcoholismChronic alcoholism
Weight lossWeight loss

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Nursing ManagementNursing Management
Nursing DiagnosesNursing Diagnoses
Imbalanced nutrition: less than body Imbalanced nutrition: less than body
requirementsrequirements
Impaired skin integrityImpaired skin integrity
Ineffective breathing patternIneffective breathing pattern
Risk for injuryRisk for injury

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Nursing ManagementNursing Management
PlanningPlanning
Overall goals:Overall goals:
–Relief of discomfortRelief of discomfort
–Minimal to no complicationsMinimal to no complications
–Return to as normal a lifestyle as Return to as normal a lifestyle as
possiblepossible

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Nursing ManagementNursing Management
Nursing ImplementationNursing Implementation
Health PromotionHealth Promotion
–Treat alcoholismTreat alcoholism
–Identify hepatitis early and treatIdentify hepatitis early and treat
–Identify biliary disease early and treatIdentify biliary disease early and treat

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Nursing ManagementNursing Management
Nursing ImplementationNursing Implementation
Acute InterventionAcute Intervention
–RestRest
–Oedema and ascitesOedema and ascites
–ParacentesisParacentesis
–Skin careSkin care
–DyspneaDyspnea
–NutritionNutrition

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Nursing ManagementNursing Management
Nursing ImplementationNursing Implementation
Ambulatory and Home CareAmbulatory and Home Care
–Symptoms of complicationsSymptoms of complications
–When to seek medical attentionWhen to seek medical attention
–Remission maintenanceRemission maintenance
–Abstinence from alcoholAbstinence from alcohol

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Nursing ManagementNursing Management
EvaluationEvaluation
Maintenance of normal body weightMaintenance of normal body weight
Maintenance of skin integrityMaintenance of skin integrity
Effective breathing patternEffective breathing pattern
No injuryNo injury
No signs of infectionNo signs of infection