The document discusses liver cirrhosis, including its causes, pathophysiology, clinical presentation, diagnostic evaluation, complications, treatment, and nursing management. Specifically, it notes that liver cirrhosis results from chronic liver damage and regeneration that disrupts the liver's normal structure and function. Common causes include alcohol, hepatitis viruses, and other liver diseases. Patients may experience fatigue, abdominal pain, jaundice, easy bruising, fluid retention, and hepatic encephalopathy. Treatment focuses on managing complications, lifestyle changes, and potentially liver transplantation in severe cases. Nursing care emphasizes activity and nutrition, injury prevention, skin integrity, and addressing individual patient needs and complications.

1. GIT Medical Nursing
by :
Dr. Alshazaly abdoalghfar
BSN, RN, MSN, CNE PhD.

2. Liver Cirrhosis
Lecture 9
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3. Objectives
By the end of this lecture all of us well be able to
 Understanding the Liver Cirrhosis and his
pathophysiology and the complication for it.
 Identify the assessment and diagnostic test used to
detect Liver Cirrhosis .
 Formulate the nursing process as a framework for care
of patients with Liver Cirrhosis.

4. Liver Cirrhosis

5. Liver Functions:
 Metabolism – Carbohydrate, Fat & Protein
 Secretary – bile, Bile acids, salts & pigments
 Excretory – Bilirubin, drugs, toxins
 Synthesis – Albumin, coagulation factors
 Storage – Vitamins, carbohydrates etc.
 Detoxification – toxins, ammonia, etc.

6. Chronic liver disease(CLD) and Cirrhosis
 CLD
 Is liver damage occurring for >6 months.
 Results in progressive fibrosis and eventually cirrhosis.
 Cirrhosis
 necrosis & fibrotic liver damage with regeneration nodule
formation leading to diffusely abnormal liver architecture.
 This results in portal hypertension and impaired liver function.
 Sometimes called end-stage liver disease because it happens
after other stages of damage from conditions that affect the
liver, such as hepatitis.

7. Cirrhosis

8. Etiology of Cirrhosis
 Alcoholic liver disease 60-70%
 Viral hepatitis 10%
 Biliary disease 5-10%
 Primary hemochromatosis 5%
 Cryptogenic cirrhosis(hidden) 10-15%

9. Pathogenesis:
 Hepatocyte injury leading to necrosis.
 Alcohol, virus, drugs, toxins, genetic etc..
 Chronic inflammation - (hepatitis).
 Fibrosis.
 Regeneration of remaining Hepatocyte Proliferate as
round nodules.
 Loss of vascular arrangement results in regenerating
Hepatocyte ineffective.

10. Types
 Micronodular cirrhosis:
 Regeneration nodules <3mm and liver is uniformly involved.
Due to alcohol or Biliary disease.
 Macronodular cirrhosis:
 Variable sized nodules with normal acini within larger
nodules. Due to viral hepatitis.

11. Clinical features
 May be none, features of CLD or features of
complications/ decompensation.
 CLD features:
 Wasting, tiredness, loss of body hair, jaundice,
encephalopathy, spider naevi, leuconiychia, Dupuytren’s
contracture, testicular atrophy, edema and ascites,
hepatomegally, splenomegally.

12. leuconiychia

13. spider
naevi

14. Dupuytren’s contracture

15. 15
Diagnostic Evaluation
 LFT(More than 70% of the liver parenchyma damaged to become
abnormal).
 Serum enzyme activity (i.e., alkaline phosphates, lactic
dehydrogenize, serum aminotransferases), serum
concentrations of proteins (albumin and globulins), bilirubin, ammonia,
clotting factors, and lipids.
 U/S: to assess size and shape of liver and detect HCC.
 GI endoscopy: OGD
 Liver biopsy: to assess type and severity of liver disease.
 To determine cause:
 Viral markers.
 Autoantibody.
 Copper.

16. 16
LIVER BIOPSY

17. Treatment Options
 The major goals of treating the cirrhotic patient include:
 Slowing or reversing the progression of liver disease
 Preventing superimposed insults to the liver
 Preventing and treating the complications
 Determining the optimal timing for liver transplantation

18. Management
 Life style change (Avoid Aspirin, NSAIDs and alcohol).
 Dietary management (Eat a healthy, balanced diet, Low
salt intake
 Management of complications
 U/S and α- feto protein 6 monthly to detect HCC.

19. Complications/effects of cirrhosis
 Portal hypertension/ GI haemorrhage
 Ascites
 Portosystemic encephalopathy
 Renal failure (hepatorenal syndrome)
 HCC
 Bacteraemias and infections
 Malnutrition

20. Hepatic decompensation
 Jaundice
 Bleeding
 Ascites
 Portal Hypertension
 Hepatic encephalopathy

22. Portal hypertension/ GI haemorrhage
 Liver cirrhosis can develop esophageal varices and
gastric varices.
 Diagnosis by endoscopic
 Treat by:
 Beta blocker, such as propranolol, to reduce the chance of
the varices bleeding, or to help control bleeding.
 Endoscopic intervention for a variceal haemorrhage
 A blood product called plasma, to prevent or treat bleeding.
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23. Edema and ascites
 Is A build-up of fluid in the tummy area (ascites) or legs and
ankles (peripheral oedema)
 Treated by:
 Dietary sodium restriction (no added salt diet)
 Fluid restriction: (if hypoNa <128mm
 Diuretic, such as spironolactone or furosemide.
 Antibiotics if appear infection in ascetic fluid
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24. Hepatic Encephalopathy
 Is a reversible neuropsychiatric syndrome occurring in patients
with advanced liver failure.
 Can occur in patients with acute fulminant liver failure (acute
encephalopathy).
 HE is often triggered by an inciting event that results in a rise in
the serum ammonia level
 HE develops in 50% to 70% of patients with cirrhosis.

25. Clinical Features
 Fetor hepaticus(Breath odder),result from volatile aromatic
substance that accumulate- ammonia in the breath.
 Asterixis (course flapping tremor).
 Feeling sleepy, and problems concentrating
 Slow slurred speech, irritability and confusion.
 Coma in advance disease.
 Hypertonia and hyperreflexia

26. 1. Empty bowel: laxatives e.g. Lactulose
 Lactulose reduces intestinal pH, thereby inhibiting ammonia absorption.
2. Give antibiotics: e.g. metronidazole orally
 Modify the intestinal flora and lower stool pH to enhance the excretion of
ammonia.
 Are used as second-line agents after Lactulose or in patients who are
intolerant of non absorbable disaccharides.
3. Diet:
 Adequate nutrition and calories (glucose)
 Vitamins & minerals containing diet.
4. Treat infections.
5. Maintain hydration.
6. Management of other complications e.g. i.v. Vit K
Management

27. Liver Transplantation
 Is the definitive treatment for patients with decompensated
cirrhosis
 Depends upon the severity of disease, quality of life and the
absence of contraindications
 Minimal criteria for listing cirrhotic patients on the liver
transplantation list include:
 A child-Pugh score 7
 Less than 90 percent chance of surviving one year without a transplant
 An episode of gastrointestinal hemorrhage related to portal hypertension
 An episode of spontaneous bacterial peritonitis

28. Vaccinations
 Hepatitis A and B
 Pneumococcal vaccine
 Influenza vaccination

29. Nursing management
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30. Nursing Assessment
 Focuses on the onset of symptoms and a history of precipitating
factors.
 The patient’s past and current patterns of alcohol use (duration
and amount) are assessed and documented.
 Document any exposure to toxic agents encountered in the
workplace or during recreational activities
 Documents and reports exposure to potentially hepatotoxic
substance (medications, inhalants) or general anesthetic agent.
 assesses the patient’s mental status by orientation to person,
place, and time

31.  ND 1:
 Activity intolerance related to fatigue, general debility, muscle
wasting, and lack of energy .
 P.E.O.C:
 Client will maintain a balance b/w rest & activity as evidenced by the
absence of fatigue & problems associated with immobility
 Imp:
 The patient with active liver disease requires rest and other supportive
measures to permit the liver to reestablish its functional ability.
 Oxygen therapy may be required in liver failure.
 Rest reduces the demands on the liver and increases the liver’s blood
supply
 Because the patient is susceptible to the hazards immobility, efforts to
prevent respiratory, circulatory, and vascular disturbances are
initiated
 When nutritional status improves and strength increases, encourages
the patient to increase activity gradually.

32.  ND2:
 Nutrition altered, less than body requirements, related to chronic
gastritis, decreased liver function( anorexia /vomiting) .
 P.E.O.C:
 The client will take adequate nutrition as evidenced by no weight loss
& no signs of malnutrition.
 Imp:
 The patient with cirrhosis without complication high-protein diet if
tolerated, supplemented by vitamins of the B complex and others as
indicated (including vitamins A, C, K and folic acid).
 Encourage oral intake
 Provide small, frequent meals are better than three large meals.
 Consider pt preferences
 Sodium restriction is also indicated to prevent ascites

33.  ND 3:
 Risk for injury and bleeding related to altered clotting Mechanisms
 P.E.O.C:
 Decreased potential for injury.
 Imp:
 Protects the patient with cirrhosis from falls and other injuries.
 The side rails should be in place and padded with blankets in case
the patient becomes agitated or restless.
 Orients the patient to time and place and explains all procedures.
 Instructs the patient to ask for assistance to get out of bed.
 Use an electric rather than a safety razor
 Used a soft-bristled toothbrush
 Applied pressure to all venipunctur sites

34.  ND 4:
 Impaired skin integrity related to compromised immunologic
status, edema, and poor nutrition.
 P.E.O.C:
 To maintain skin intact.
 Imp:
 Providing careful skin care is important because of subcutaneous
edema, the patient’s immobility, jaundice, and increased
susceptibility to skin breakdown and infection.
 Frequent position changes are necessary to prevent pressure
ulcers .
 It is important to avoid irritating soaps and the use of adhesive
tape to prevent trauma to the skin.

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36. Thank you
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