Advanced Concept of Nursing- IIUNIT- V

Advance Nursing Management of GITdiseases.

LIVER CIRRHOSIS

In The Name of God

(A PROJECT OF NEW LIFE HEALTH CARE SOCIETY, KARACHI)

UNIT- VAdvance Nursing Management of GIT

diseases.LIVER CIRRHOSIS

Shahzad BashirRN, BScN, DCHN,MScN (Std.DUHS)

InstructorNew Life College of NursingUpdated on June 08, 2016

Objectives

Define liver cirrhosis. Enlist the causes of Liver Cirrhosis. List the types of liver cirrhosis. Understand the pathophysiology of liver

cirrhosis. Identify the clinical features of liver cirrhosis Elaborate the investigations of liver cirrhosis Discuss the medical and nursing management

of liver cirrhosis

Define liver cirrhosis. Enlist the causes of Liver Cirrhosis. List the types of liver cirrhosis. Understand the pathophysiology of liver

cirrhosis. Identify the clinical features of liver cirrhosis Elaborate the investigations of liver cirrhosis Discuss the medical and nursing management

of liver cirrhosis

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Normal Liver

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Histology of Liver

Lobule– Hepatocytes radiating from central vein– Sinusoids

Reticuloendothelial (Kupffer) cells– Stationary phagocytes

Lobule– Hepatocytes radiating from central vein– Sinusoids

Reticuloendothelial (Kupffer) cells– Stationary phagocytes

Liver Cirrhosis

Cirrhosis is a chronic disease characterized byreplacement of normal liver tissue with diffusefibrosis.

It disrupts the structure and function of the liver.

1. Complete loss of normal architecture,2. Replaced by extensive fibrosis with,3. Regenerating parenchymal nodules.

Cirrhosis is a chronic disease characterized byreplacement of normal liver tissue with diffusefibrosis.

It disrupts the structure and function of the liver.

1. Complete loss of normal architecture,2. Replaced by extensive fibrosis with,3. Regenerating parenchymal nodules.

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Liver Cirrhosis Extensive scarring of the liver caused by necrotic

injury or a chronic reaction to inflammation over aprolonged period of time

A chronic progressive disease of the livercharacterized by diffused damage to cells withfibrosis and nodular regeneration.

Repeated destruction of hepatic cells causes theformation of scar tissues.

Extensive scarring of the liver caused by necroticinjury or a chronic reaction to inflammation over aprolonged period of time

A chronic progressive disease of the livercharacterized by diffused damage to cells withfibrosis and nodular regeneration.

Repeated destruction of hepatic cells causes theformation of scar tissues.

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Etiology of Liver Cirrhosis.

Alcoholism.Viral hepatitis.Toxic reactions to drugs and chemicals.Biliary obstruction.Cardiac disease.Hemochromatosis (i.e., iron deposition).Wilson’s disease (i.e., copper deposition).

Alcoholism.Viral hepatitis.Toxic reactions to drugs and chemicals.Biliary obstruction.Cardiac disease.Hemochromatosis (i.e., iron deposition).Wilson’s disease (i.e., copper deposition).

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Types of Liver Cirrhosis.

There are four types of Livercirrhosis.– Laennec’s (Alcohol induced)

cirrhosis– Post necrotic cirrhosis– Biliary cirrhosis– Cardiac

There are four types of Livercirrhosis.– Laennec’s (Alcohol induced)

cirrhosis– Post necrotic cirrhosis– Biliary cirrhosis– Cardiac

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Pathophysiology

Irreversible chronic injury of the hepaticparenchyma.

Extensive fibrosis - distortion of the hepaticarchitecture.

Formation of regenerative nodules

Irreversible chronic injury of the hepaticparenchyma.

Extensive fibrosis - distortion of the hepaticarchitecture.

Formation of regenerative nodules

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Pathophysiology

Liver insultAlcoholic Ingestion, Viral hepatitis

Exposure to toxins

Hepatocytedamage

PainIncrease

WBCHepatocyte

damage

Alterations inblood and

lymph flow

LiverInflammation

Pain

Fever

AnorexiaNauseaVomiting

Fatigue

IncreaseWBC

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Livernecrosis

LLiveriverfailurefailure

Liver fibrosisLiver fibrosisAnd scarringAnd scarring

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DEATHDEATH

Dec.androgen/Estrogen p.

Decrease ADH

Dec.met.of CHONAnd Carb./

Dec.Fat

PlasmaCHON

Spiderangiomas

Testicularatrophy Gyneco

mastia

PalmarErythema

Loss ofBody hair

Menstrualchanges

Edema

Hypoglycemia AcitesEdema

Bile

Vit.k absop.

HyperbilirubinemiaBilirubin metabolism

Bilirubin excretionIn urine

Clay- coloredstool

Dark urine

Jaundice

Bleedingtendencies

Hypoglycemia Acites

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Liver fibrosisLiver fibrosis Portal HPN

Ascites

BleedingHemorrhoids

SuperficialAbdominal

varices

Esophagealvarices

Edema

AnemiaThrombocytopenia

Leukopenia

Splenomegaly

SuperficialAbdominal

varices

Infection

DelayedWoundhealing

Bleeding

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Liver failureLiver failureInability toMetabolizeammonia

Hepaticencephalopathy

Increaseserum

ammoniaAlterations

Insleep

Foul breath

Inability toMetabolizeammonia

Confusion toHepaticcoma

DEATHDEATH

Asterexis

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Types of Liver Cirrhosis.

1. Laennec’s (Alcohol induce) Cirrhosis:

Alcoholic cirrhosis in which the scar tissue

characteristically around central veins & the portal

areas.

This is most frequently due to chronic alcoholism

& malnutrition.

It is the most common type of cirrhosis.

1. Laennec’s (Alcohol induce) Cirrhosis:

Alcoholic cirrhosis in which the scar tissue

characteristically around central veins & the portal

areas.

This is most frequently due to chronic alcoholism

& malnutrition.

It is the most common type of cirrhosis.

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Alcoholic Fatty Liver

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Alcoholic Cirrhosis

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Conti

2. Post necrotic cirrhosis

Caused by massive hepatic cell necrosis, usually

from acute viral hepatitis

Post necrotic cirrhosis, in which there are broad

bands of scar tissue.

Late result of a previous bout of acute viral

hepatitis & massive induced drugs.

2. Post necrotic cirrhosis

Caused by massive hepatic cell necrosis, usually

from acute viral hepatitis

Post necrotic cirrhosis, in which there are broad

bands of scar tissue.

Late result of a previous bout of acute viral

hepatitis & massive induced drugs.

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3. Biliary cirrhosis

Caused by chronic biliary obstruction, bile stasisand inflammation. The liver becomes fibrotic.

Biliary cirrhosis, in which scarring occurs in theliver around the bile ducts.

This type usually is the result of chronic biliaryobstruction and infection (cholangitis)

It is much less common than the other two types.

Caused by chronic biliary obstruction, bile stasisand inflammation. The liver becomes fibrotic.

Biliary cirrhosis, in which scarring occurs in theliver around the bile ducts.

This type usually is the result of chronic biliaryobstruction and infection (cholangitis)

It is much less common than the other two types.8/22/2016 22

4.Cardiac

Caused by severe or chronic HF. Theliver becomes enlarged and congestedwith venous blood, resulting in cellnecrosis from anoxia. Withouttransplant, usually fatal

Caused by severe or chronic HF. Theliver becomes enlarged and congestedwith venous blood, resulting in cellnecrosis from anoxia. Withouttransplant, usually fatal

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Clinical Manifestation

Early complaints including: Fatigue Anorexia Epistaxis Weight loss Edema Fever

Early complaints including: Fatigue Anorexia Epistaxis Weight loss Edema Fever

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In later disease:

Chronic dyspepsia, constipation and diarrhea. Esophageal varices Hepatomegaly Splenomegaly Portal Obstruction Ascites Vitamin Deficiency ( Vit: A, Vit: K, Vit C) Anemia Impaired GI functions Malabsorption of fat Elevated blood ammonia level

Chronic dyspepsia, constipation and diarrhea. Esophageal varices Hepatomegaly Splenomegaly Portal Obstruction Ascites Vitamin Deficiency ( Vit: A, Vit: K, Vit C) Anemia Impaired GI functions Malabsorption of fat Elevated blood ammonia level

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CirrhosisClinicalFeatures

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Nursing AssessmentCirrhosis of the Liver Monitor vital signs LOC-Neuro Pulmonary GI Integumentary GU Coagulation defects Fetor hepaticus -liver breath-end stage

Monitor vital signs LOC-Neuro Pulmonary GI Integumentary GU Coagulation defects Fetor hepaticus -liver breath-end stage

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Nursing Assessment Petechiae red pinpoint and red-purple lesions,

Ecchymosis, nose bleeds, hematemesis

Spider angiomas red spider -like lesions of face, upperthorax, and shoulders

Dependent peripheral edema of extremities and sacrum

Asterixis- tremors liver flapping tremor of the wrist andfingers

Complications of portal hypertension

Petechiae red pinpoint and red-purple lesions,

Ecchymosis, nose bleeds, hematemesis

Spider angiomas red spider -like lesions of face, upperthorax, and shoulders

Dependent peripheral edema of extremities and sacrum

Asterixis- tremors liver flapping tremor of the wrist andfingers

Complications of portal hypertension

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Management of CirrhosisNon-surgical

Diet- low Na, low protein, moderate fat restriction, highcarb, high calories, vitamins

TPN often necessaryMeds-Aldactone, Lactulose, Neomycin, antacidsParacentesisEsophagogastric balloon tamponadeInjection sclerotherapySTOP alcohol

SurgicalPeritovenous shunt or LaVeen shuntEndoscopic band ligation

Non-surgicalDiet- low Na, low protein, moderate fat restriction, highcarb, high calories, vitamins

TPN often necessaryMeds-Aldactone, Lactulose, Neomycin, antacidsParacentesisEsophagogastric balloon tamponadeInjection sclerotherapySTOP alcohol

SurgicalPeritovenous shunt or LaVeen shuntEndoscopic band ligation

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Investigations

Liver function test ( serum liver enzyme,)

Liver Biopsy(Detects cell destruction and fibrosis of hepatic disease )

Albumin test ( serum albumin)

CT Scan (Determines the size of the liver and its irregularnodular surface)

Ultrasound (Hepatomegaly).

Esophagoscopy( Determines the presence of esophagealvarices).

Percutaneous transhepatic cholangiography(Differentiates extrahepatic from intrahepatic obstructivejaundice).

Liver function test ( serum liver enzyme,)

Liver Biopsy(Detects cell destruction and fibrosis of hepatic disease )

Albumin test ( serum albumin)

CT Scan (Determines the size of the liver and its irregularnodular surface)

Ultrasound (Hepatomegaly).

Esophagoscopy( Determines the presence of esophagealvarices).

Percutaneous transhepatic cholangiography(Differentiates extrahepatic from intrahepatic obstructivejaundice).

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Complications of Cirrhosis Portal Hypertension Ascites Bleeding esophageal varices Coagulation defect Jaundice Hepatic encephalopathy Hepatorenal syndrome Congestive splenomegaly. Bleeding varices. Hepatocellular failure.

– Hepatic encephalitis / hepatic coma. Hepatocellular carcinoma.

Portal Hypertension Ascites Bleeding esophageal varices Coagulation defect Jaundice Hepatic encephalopathy Hepatorenal syndrome Congestive splenomegaly. Bleeding varices. Hepatocellular failure.

– Hepatic encephalitis / hepatic coma. Hepatocellular carcinoma.

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Bleeding esophageal varices

Hematemesis and melenaDx: endoscopy, CT, ultrasound, bariumswallow, LFTsTx: O2, IVF, Blood transfusions, I&O,Balloon tamponade, saline lavage,endoscopic tamponade, vasopressin(Pitressin)

Hematemesis and melenaDx: endoscopy, CT, ultrasound, bariumswallow, LFTsTx: O2, IVF, Blood transfusions, I&O,Balloon tamponade, saline lavage,endoscopic tamponade, vasopressin(Pitressin)

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Nursing Diagnoses

Altered mental statusIneffective breathing patternExcess fluid volumeRisk for impaired skin integrityRisk for infectionChronic painRisk for imbalanced nutrition

Altered mental statusIneffective breathing patternExcess fluid volumeRisk for impaired skin integrityRisk for infectionChronic painRisk for imbalanced nutrition

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Pharmacologic Interventions:

Provide asymptomatic relief measures such aspain medications and antiemetics.Diuretic therapy, frequently with

spironolactone, a potassium-sparing diuretic. I.V albumin to maintain osmotic pressure and

reduce ascites.Administration of lactulose or neomycin

through a nasogastric tube or retention enemato reduce ammonia levels during periods ofhepatic encephalopathy.

Provide asymptomatic relief measures such aspain medications and antiemetics.Diuretic therapy, frequently with

spironolactone, a potassium-sparing diuretic. I.V albumin to maintain osmotic pressure and

reduce ascites.Administration of lactulose or neomycin

through a nasogastric tube or retention enemato reduce ammonia levels during periods ofhepatic encephalopathy.

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Surgical Intervention:

Transjugularintrahepaticportosystemic shuntmay be performed inpatients whose ascitesprove resistant. Thispercutaneous procedurecreates a shunt from theportal to systemiccirculation to reduceportal pressure andrelieve ascites.

Transjugularintrahepaticportosystemic shuntmay be performed inpatients whose ascitesprove resistant. Thispercutaneous procedurecreates a shunt from theportal to systemiccirculation to reduceportal pressure andrelieve ascites.

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Surgical Intervention:

Orthotopic livertransplantation(OLT)may be necessary.

Orthotopic livertransplantation(OLT)may be necessary.

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Nursing Management.1. Observe stools and emesis for color, consistency, and

amount, and test each one for occult blood.2. Monitor fluid intake and output and serum electrolyte

levels to prevent dehydration and hypokalemia, whichmay precipitate hepatic encephalopathy.

3. Maintain some periods of rest with legs elevated tomobilize edema and ascites. Alternate rest periods withambulation.

4. Encourage and assist with gradually increasing periods ofexercise.

5. Encourage the patient to eat high-calorie, moderateprotein meals and supplementary feedings. Suggest small,frequent feedings.

1. Observe stools and emesis for color, consistency, andamount, and test each one for occult blood.

2. Monitor fluid intake and output and serum electrolytelevels to prevent dehydration and hypokalemia, whichmay precipitate hepatic encephalopathy.

3. Maintain some periods of rest with legs elevated tomobilize edema and ascites. Alternate rest periods withambulation.

4. Encourage and assist with gradually increasing periods ofexercise.

5. Encourage the patient to eat high-calorie, moderateprotein meals and supplementary feedings. Suggest small,frequent feedings.

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Nursing Management.

6. Encourage oral hygiene before meals.7. Administer or teach self-administration of medications for

nausea, vomiting, diarrhea or constipation.8. Encourage frequent skin care, bathing with soap, and

massage with emollient lotions.9. Keep the patient’s finger nails short to prevent scratching

from pruritus.10. Keep the patient quiet and limit activity if signs of

bleeding are evident.11. Encourage the patient to eat foods high vitamin C content.12. Use small gauge needles for injections and maintain

pressure over injection site until bleeding stops.

6. Encourage oral hygiene before meals.7. Administer or teach self-administration of medications for

nausea, vomiting, diarrhea or constipation.8. Encourage frequent skin care, bathing with soap, and

massage with emollient lotions.9. Keep the patient’s finger nails short to prevent scratching

from pruritus.10. Keep the patient quiet and limit activity if signs of

bleeding are evident.11. Encourage the patient to eat foods high vitamin C content.12. Use small gauge needles for injections and maintain

pressure over injection site until bleeding stops.

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Nursing Management.

13. Protect from sepsis through good hand washing andprompt recognition and management of infection.

14. Pad side rails and provide careful nursing surveillance toensure the patient’s safety.

15. Stress the importance of giving up alcohol completely.16. Involve the person closest to the patient, because recovery

usually is not easy and relapses are common.

13. Protect from sepsis through good hand washing andprompt recognition and management of infection.

14. Pad side rails and provide careful nursing surveillance toensure the patient’s safety.

15. Stress the importance of giving up alcohol completely.16. Involve the person closest to the patient, because recovery

usually is not easy and relapses are common.

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Conclusions:Common end result of diffuse liver damage.

(Viral hepatitis, Alcohol, congenital, drugs, toxins & Idiopathic)

Characterised by diffuse loss of architecture.Fibrous bands & regenerating nodules distort

and abstruct blood flow. (Inefficient function)Hepatocellular insufficiency & portal

hypertension.Shrunken, scarred liver, ascitis,

spleenomegaly, liver failure, CNS toxicity.

Common end result of diffuse liver damage.(Viral hepatitis, Alcohol, congenital, drugs, toxins & Idiopathic)

Characterised by diffuse loss of architecture.Fibrous bands & regenerating nodules distort

and abstruct blood flow. (Inefficient function)Hepatocellular insufficiency & portal

hypertension.Shrunken, scarred liver, ascitis,

spleenomegaly, liver failure, CNS toxicity.

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Thank you andThank you andMay God beMay God beGlorifiedGlorified

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References Brunner, L. S., Suddarth, D. S., & Smeltzer, S. C.

(2008). Brunner & Suddarth's textbook of medical-surgical nursing (12th ed.). Philadelphia: LippincottWilliams & Wilkins.

Porth, MC. (6th ED). Pathophysiology. (2002).Philadelphia. USA. Lippincott Willams& Willkins,

A Wolters Kluwer Company

McPhee, J. S., & Papadakis, A. M. (2011). CurrentMedical Diagnosis and Treatment.(50th ED). Chicago. USA: Mc Graw Hill

Brunner, L. S., Suddarth, D. S., & Smeltzer, S. C.(2008). Brunner & Suddarth's textbook of medical-surgical nursing (12th ed.). Philadelphia: LippincottWilliams & Wilkins.

Porth, MC. (6th ED). Pathophysiology. (2002).Philadelphia. USA. Lippincott Willams& Willkins,

A Wolters Kluwer Company

McPhee, J. S., & Papadakis, A. M. (2011). CurrentMedical Diagnosis and Treatment.(50th ED). Chicago. USA: Mc Graw Hill

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