Cirrhosis of the Liver (relates to Chapter 42, “Nursing Management: Liver, Biliary Tract, and...

Cirrhosis of the LiverCirrhosis of the Liver

(relates to Chapter 42, “Nursing Management: Liver, Biliary Tract, and Pancreas Problems,” in

the textbook)

(relates to Chapter 42, “Nursing Management: Liver, Biliary Tract, and Pancreas Problems,” in

the textbook)

DescriptionDescription

• A chronic, progressive disease of the liver

– Extensive parenchymal cell degeneration

– Destruction of parenchymal cells

• A chronic, progressive disease of the liver

– Extensive parenchymal cell degeneration

– Destruction of parenchymal cells


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

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


• Normal lobular structure distorted by fibrotic connective tissue

• Lobules are irregular in size and shape with impaired vascular flow

• Insidious, prolonged course

• Normal lobular structure distorted by fibrotic connective tissue

• Lobules are irregular in size and shape with impaired vascular flow

• Insidious, prolonged course

StatisticsStatistics

• > 50% of liver disease in the US is directly related to alcohol consumption

• Of the estimated 15 million alcoholics in the USA 10-20% have or will develop cirrhosis

• > 50% of liver disease in the US is directly related to alcohol consumption

• Of the estimated 15 million alcoholics in the USA 10-20% have or will develop cirrhosis


• Growing number of cases related to chronic hepatitis C

• 4th leading cause of death in people between 35 and 54 years of age

• Growing number of cases related to chronic hepatitis C

• 4th leading cause of death in people between 35 and 54 years of age


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

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

Etiology and PathophysiologyEtiology and Pathophysiology

• Cell necrosis occurs

• Destroyed liver cells are replaced by scar tissue

• Normal architecture becomes nodular

• Cell necrosis occurs

• Destroyed liver cells are replaced by scar tissue

• Normal architecture becomes nodular


• Four types of cirrhosis:

– Alcoholic (Laennec’s) cirrhosis

– Postnecrotic cirrhosis

– Biliary cirrhosis

– Cardiac cirrhosis

• Four types of cirrhosis:

– Alcoholic (Laennec’s) cirrhosis

– Postnecrotic cirrhosis

– Biliary cirrhosis

– Cardiac cirrhosis


• Alcoholic (Laennec’s) Cirrhosis

– Associated with alcohol abuse

– Preceded by a theoretically reversible fatty infiltration of the liver cells

– Widespread scar formation

• Alcoholic (Laennec’s) Cirrhosis

– Associated with alcohol abuse

– Preceded by a theoretically reversible fatty infiltration of the liver cells

– Widespread scar formation


• Postnecrotic Cirrhosis

– Complication of toxic or viral hepatitis

– Accounts for 20% of the cases of cirrhosis

– Broad bands of scar tissue form within the liver

• Postnecrotic Cirrhosis

– Complication of toxic or viral hepatitis

– Accounts for 20% of the cases of cirrhosis

– Broad bands of scar tissue form within the liver


• Biliary Cirrhosis – Associated with chronic biliary

obstruction and infection

– Accounts for 15% of all cases of cirrhosis

• Biliary Cirrhosis – Associated with chronic biliary

obstruction and infection

– Accounts for 15% of all cases of cirrhosis


• Cardiac Cirrhosis – Results from longstanding severe

right-sided heart failure

• Cardiac Cirrhosis – Results from longstanding severe

right-sided heart failure

Manifestations of Liver CirrhosisManifestations of Liver Cirrhosis

Fig. 42-5

Clinical ManifestationsEarly Manifestations


• Onset usually insidious

• GI disturbances:

– Anorexia

– Dyspepsia

– Flatulence

– N-V, change in bowel habits

• Onset usually insidious

• GI disturbances:

– Anorexia

– Dyspepsia

– Flatulence

– N-V, change in bowel habits



• Abdominal pain

• Fever

• Lassitude

• Weight loss

• Enlarged liver or spleen

• Abdominal pain

• Fever

• Lassitude

• Weight loss

• Enlarged liver or spleen

Clinical ManifestationsLate Manifestations

Clinical ManifestationsLate Manifestations

• Two causative mechanisms

– Hepatocellular failure

– Portal hypertension

• Two causative mechanisms

– Hepatocellular failure

– Portal hypertension

Clinical ManifestationsJaundice


• Occurs because of insufficient conjugation of bilirubin by the liver cells, and local obstruction of biliary ducts by scarring and regenerating tissue

• Occurs because of insufficient conjugation of bilirubin by the liver cells, and local obstruction of biliary ducts by scarring and regenerating tissue



• Intermittent jaundice is characteristic of biliary cirrhosis

• Late stages of cirrhosis the patient will usually be jaundiced

• Intermittent jaundice is characteristic of biliary cirrhosis

• Late stages of cirrhosis the patient will usually be jaundiced

Clinical ManifestationsSkin

Clinical ManifestationsSkin

• Spider angiomas (telangiectasia, spider nevi)

• Palmar erythema

• Spider angiomas (telangiectasia, spider nevi)

• Palmar erythema

Clinical Manifestations Endocrine DisturbancesClinical Manifestations Endocrine Disturbances

• Steroid hormones of the adrenal cortex (aldosterone), testes, and ovaries are metabolized and inactivated by the normal liver

• Steroid hormones of the adrenal cortex (aldosterone), testes, and ovaries are metabolized and inactivated by the normal liver

Clinical Manifestations Endocrine DisturbancesClinical Manifestations Endocrine Disturbances

• Alteration in hair distribution

– Decreased amount of pubic hair

– Axillary and pectoral alopecia

• Alteration in hair distribution

– Decreased amount of pubic hair

– Axillary and pectoral alopecia

Clinical Manifestations Hematologic Disorders


• Bleeding tendencies as a result of decreased production of hepatic clotting factors (II, VII, IX, and X)

• Bleeding tendencies as a result of decreased production of hepatic clotting factors (II, VII, IX, and X)



• Anemia, leukopenia, and thrombocytopenia are believed to be result of hypersplenism

• Anemia, leukopenia, and thrombocytopenia are believed to be result of hypersplenism

Clinical Manifestations Peripheral Neuropathy

Clinical Manifestations Peripheral Neuropathy

• Dietary deficiencies of thiamine, folic acid, and vitamin B12

• Dietary deficiencies of thiamine, folic acid, and vitamin B12

ComplicationsComplications

• Portal hypertension and esophageal varices

• Peripheral edema and ascites

• Hepatic encephalopathy

• Fetor hepaticus

• Portal hypertension and esophageal varices

• Peripheral edema and ascites

• Hepatic encephalopathy

• Fetor hepaticus

Complications Portal Hypertension


• Characterized by:

– Increased venous pressure in portal circulation

– Splenomegaly

– Esophageal varices

– Systemic hypertension

• Characterized by:

– Increased venous pressure in portal circulation

– Splenomegaly

– Esophageal varices

– Systemic hypertension



• Primary mechanism is the increased resistance to blood flow through the liver

• Primary mechanism is the increased resistance to blood flow through the liver


Splenomegaly


Splenomegaly

• Back pressure caused by portal hypertension chronic passive congestion as a result of increased pressure in the splenic vein

• Back pressure caused by portal hypertension chronic passive congestion as a result of increased pressure in the splenic vein

Complications Portal Hypertension Esophageal Varices


• Increased blood flow through the portal system results in dilation and enlargement of the plexus veins of the esophagus and produces varices

• Increased blood flow through the portal system results in dilation and enlargement of the plexus veins of the esophagus and produces varices



• Varices have fragile vessel walls which bleed easily

• Varices have fragile vessel walls which bleed easily


Internal Hemorrhoids


Internal Hemorrhoids

• Occurs because of the dilation of the mesenteric veins and rectal veins

• Occurs because of the dilation of the mesenteric veins and rectal veins


Caput Medusae


Caput Medusae

• Collateral circulation involves the superficial veins of the abdominal wall leading to the development of dilated veins around the umbilicus

• Collateral circulation involves the superficial veins of the abdominal wall leading to the development of dilated veins around the umbilicus

Complications Peripheral Edema and Ascites


• Ascites:- - Intraperitoneal accumulation of

watery fluid containing small amounts of protein

• Ascites:- - Intraperitoneal accumulation of

watery fluid containing small amounts of protein



• Factors involved in the pathogenesis of ascites:

- Hypoalbuminemia Levels of aldosterone Portal hypertension

• Factors involved in the pathogenesis of ascites:

- Hypoalbuminemia Levels of aldosterone Portal hypertension

Complications Hepatic Encephalopathy


• Liver damage causes blood to enter systemic circulation without liver detoxification

• Liver damage causes blood to enter systemic circulation without liver detoxification



• Main pathogenic toxin is NH3 although other etiological factors have been identified

• Frequently a terminal complication

• Main pathogenic toxin is NH3 although other etiological factors have been identified

• Frequently a terminal complication

Complications Fetor HepaticusComplications Fetor Hepaticus

• Musty, sweetish odor detected on the patient’s breath

• From accumulation of digested by-products

• Musty, sweetish odor detected on the patient’s breath

• From accumulation of digested by-products

Development of AscitesDevelopment of Ascites

Fig. 42-6

Diagnostic StudiesDiagnostic Studies

• Liver function tests

• Liver biopsy

• Liver scan

• Liver ultrasound

• Liver function tests

• Liver biopsy

• Liver scan

• Liver ultrasound

Diagnostic StudiesDiagnostic Studies

• Esophagogastroduodenoscopy

• Prothrombin time

• Testing of stool for occult blood

• Esophagogastroduodenoscopy

• Prothrombin time

• Testing of stool for occult blood

Collaborative CareCollaborative Care

• Rest

• Avoidance of alcohol and anticoagulants

• Management of ascites

• Rest

• Avoidance of alcohol and anticoagulants

• Management of ascites

Collaborative CareCollaborative Care

• Prevention and management of esophageal variceal bleeding

• Management of encephalopathy

• Prevention and management of esophageal variceal bleeding

• Management of encephalopathy

Collaborative Care Ascites


• High carbohydrate, low protein, low Na+ diet

• Diuretics

• Paracentesis

• High carbohydrate, low protein, low Na+ diet

• Diuretics

• Paracentesis



• Peritoneovenous shunt

– Provides for continuous reinfusion of ascitic fluid from the abdomen to the vena cava

• Peritoneovenous shunt

– Provides for continuous reinfusion of ascitic fluid from the abdomen to the vena cava

Peritoneovenous ShuntPeritoneovenous Shunt

Fig. 42-8

Collaborative Care Esophageal Varices


• Avoid alcohol, aspirin, and irritating foods

• If bleeding occurs, stabilize patient and manage the airway, administer vasopressin (Pitressin)

• Avoid alcohol, aspirin, and irritating foods

• If bleeding occurs, stabilize patient and manage the airway, administer vasopressin (Pitressin)



• Endoscopic sclerotherapy or ligation

• Balloon tamponade

• Surgical shunting procedures (e.g., portacaval shunt, TIPS)

• Endoscopic sclerotherapy or ligation

• Balloon tamponade

• Surgical shunting procedures (e.g., portacaval shunt, TIPS)

Sengstaken-Blakemore TubeSengstaken-Blakemore Tube

Fig. 42-9

Portosystemic ShuntsPortosystemic Shunts

Fig. 42-11

Collaborative Care Hepatic EncephalopathyCollaborative Care

Hepatic Encephalopathy

• Goal: reduce NH3 formation– Protein restriction (0-40g/day)– Sterilization of GI tract with antibiotics

(e.g., neomycin)– lactulose (Cephulac) – traps NH3 in gut– levodopa

• Goal: reduce NH3 formation– Protein restriction (0-40g/day)– Sterilization of GI tract with antibiotics

(e.g., neomycin)– lactulose (Cephulac) – traps NH3 in gut– levodopa

Drug TherapyDrug Therapy

• There is no specific drug therapy for cirrhosis

• Drugs are used to treat symptoms and complications of advanced liver disease

• There is no specific drug therapy for cirrhosis

• Drugs are used to treat symptoms and complications of advanced liver disease

Nutritional TherapyNutritional Therapy

• Diet for patient without complications:

– High in calories CHO

– Moderate to low fat

– Amount of protein varies with degree of liver damage

• Diet for patient without complications:

– High in calories CHO

– Moderate to low fat

– Amount of protein varies with degree of liver damage

Nutritional TherapyNutritional Therapy

• Patient with hepatic encephalopathy

– Very low to no-protein diet

• Low sodium diet for patient with ascites and edema

• Patient with hepatic encephalopathy

– Very low to no-protein diet

• Low sodium diet for patient with ascites and edema

Nursing ManagementNursing Assessment

Nursing ManagementNursing Assessment

• Past health history

• Medications

• Chronic alcoholism

• Weight loss

• Past health history

• Medications

• Chronic alcoholism

• Weight loss

Nursing ManagementNursing Diagnoses

Nursing ManagementNursing Diagnoses

• Imbalanced nutrition: less than body requirements

• Impaired skin integrity• Ineffective breathing pattern• Risk for injury

• Imbalanced nutrition: less than body requirements

• Impaired skin integrity• Ineffective breathing pattern• Risk for injury

Nursing ManagementPlanning

Nursing ManagementPlanning

• Overall goals:

– Relief of discomfort

– Minimal to no complications

– Return to as normal a lifestyle as possible

• Overall goals:

– Relief of discomfort

– Minimal to no complications

– Return to as normal a lifestyle as possible

Nursing ManagementNursing ImplementationNursing ManagementNursing Implementation

• Health Promotion

– Treat alcoholism

– Identify hepatitis early and treat

– Identify biliary disease early and treat

• Health Promotion

– Treat alcoholism

– Identify hepatitis early and treat

– Identify biliary disease early and treat


• Acute Intervention– Rest– Edema and ascites– Paracentesis– Skin care– Dyspnea– Nutrition

• Acute Intervention– Rest– Edema and ascites– Paracentesis– Skin care– Dyspnea– Nutrition


• Acute Intervention

– Bleeding problems

– Balloon tamponade

– Altered body image

– Hepatic encephalopathy

• Acute Intervention

– Bleeding problems

– Balloon tamponade

– Altered body image

– Hepatic encephalopathy


• Ambulatory and Home Care

– Symptoms of complications

– When to seek medical attention

– Remission maintenance

– Abstinence from alcohol

• Ambulatory and Home Care

– Symptoms of complications

– When to seek medical attention

– Remission maintenance

– Abstinence from alcohol

Nursing ManagementEvaluation

Nursing ManagementEvaluation

• Maintenance of normal body weight

• Maintenance of skin integrity

• Effective breathing pattern

• No injury

• No signs of infection

• Maintenance of normal body weight

• Maintenance of skin integrity

• Effective breathing pattern

• No injury

• No signs of infection

Cirrhosis of the Liver (relates to Chapter 42, “Nursing Management: Liver, Biliary Tract, and...

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