Medical Surgical Nursing - I UNIT: IV -Nursing Management of Patients With Disorder of Digestive System "Cirrhosis of liver" the topic covers - the stages, Pathophysiology and clinical manifestation of Cirrhosis of liver - diagnostic evaluation and complication of Cirrhosis of liver - medical, surgical and nursing management of patient with Cirrhosis of liver

1. Medical Surgical Nursing - I
UNIT: IV -Nursing Management of
Patients With Disorder of Digestive
System
Cirrhosis of liver
Mrs.SARANYA.R,M.Sc(N),
Associate Professor,
SRM Trichy College of Nursing,

2. OBJECTIVES
At the end of the class the students are able to,
- define Cirrhosis of liver
- List out types of Cirrhosis of liver
- describe the risk factor, etiology of Cirrhosis of liver
- Explain the stages, Pathophysiology and clinical manifestation of
Cirrhosis of liver
- Discuss the diagnostic evaluation and complication of Cirrhosis
of liver
- enumerate medical, surgical and nursing management of patient
with Cirrhosis of liver

3. ANATOMY AND PHYSIOLOGY
The liver is located in the upper right-hand portion of the abdominal
cavity, beneath the diaphragm, and on top of the stomach, right kidney,
and intestines. Shaped like a cone, the liver is a dark reddish-brown
organ that weighs about 3 pounds

4. FUNCTION OF LIVER
Metabolism –Carbohydrate, Fat & Protein
Secretory –bile, Bile acids, salts & pigments
Excretory –Bilirubin, drugs, toxins
Synthesis –Albumin, coagulation factors
Storage –Vitamins, carbohydrates etc.
Detoxification –toxins, ammonia, etc.

5. INTRODUCTION
The word "cirrhosis" is a neologism that derives from
Greek kirrhos, meaning "tawny" (the orange-yellow
colour of the diseased liver).
While the clinical entity was known before, it was
René Laennec who gave it the name "cirrhosis" in his
1819 work in which he also describes the stethoscope.

6. INTRODUCTION
Cirrhosis is a consequence of chronic liver disease
characterized by replacement of liver tissue by fibrous
scar tissue as well as regenerative nodules (lumps that
occur as a result of a process in which damaged tissue
is regenerated, leading to progressive loss of liver
function

7. TERMINOLOGY
• Necrosis. Cirrhosis is characterized by episodes of necrosis
involving the liver cells.
• Scar tissue. The destroyed liver cells are gradually replaced
with a scar tissue.
• Fibrosis. There is diffuse destruction and fibrotic regeneration
of hepatic cells.
• Alteration. As necrotic tissue yields to fibrosis, the disease
alters the liver structure and normal vasculature, impairs blood
and lymph flow, and ultimately causes hepatic insufficiency.

8. DEFINITION
A diffuse process characterized by liver necrosis and
fibrosis and conversion of normal liver architechture into
structurally abnormal nodules that lack normal lobular
organisation. WHO

9. DEFINITION
Cirrhosis of liver is a chronic, progressive disease
characterized by widespread fibrosis (scaring) & nodule
formation.
Cirrhosis occurs when the normal flow of
blood, bile, & hepatic metabolites is altered by fibrosis A
chronic disease of the liver marked by degeneration of cells,
inflammation, and fibrous thickening of tissue. It is typically a
result of alcoholism or hepatitis

10. INCIDENCES
Various types of cirrhosis may occur in different types of
individuals.
 The most common, Laennec’s cirrhosis, occurs in 30% to 50%
of cirrhotic patients.
 Biliary cirrhosis occurs in 15% to 20% of patients.
 Postnecrotic cirrhosis occurs in 10% to 30% of patients.
 Pigment cirrhosis occura in 5% to 10% of patients.
 Idiopathic cirrhosis occurs in about 10% of patients

11. TYPES
1. Alcoholic cirrhosis- Most common, due to chronic
alcoholism. Scar tissue characteristically surrounds the
portal area.
2. Postnecrotic cirrhosis- There are broad bands
of scar tissue due to late results of acute viral
hepatitis, postintoxication with industrial chemicals.

12. TYPES
3. Biliary cirrhosis- Scaring occurs around bile duct in
liver, Results from chronic biliary obstruction &
infection.
4. Cardiac cirrhosis- Associated with severe right
sided long term heart failure, fairly rare.

13. CAUSES
1. Drugs and toxins
– Alcohol, methotrexate, isoniazid,
– methyldopa
2. infections
– Hepatitis B and C , Schistosoma japonicum
3. autoimmune
– PBC, autoimmune hepatitis, PSC
4. metabolic
– Wilson’s disease, haemochromatosis, alpha
1 antitrypsin, porphyria

14. CAUSES
5. Biliary obstruction
– Cystic fibrosis, atresia, strictures, gall stones
6. vascular
– Chronic right heart failure, Budd Chiari
– syndrome
7. miscellaneous
– Sarcoidosis, intestinal by- pass surgery for
– obesity
8. unknown
– cryptogenic

15. STAGES OF LIVER DAMAGE

16. PATHOPHYSIOLOGY
Primary event is injury to hepatocellular elements
Initiates inflammatory response with cytokine
release->toxic substances
Destruction of hepatocytes, bile duct cells, vascular endothelial cells
Repair through cellular proliferation and regeneration
Formation of fibrous scar

17. PATHOPHYSIOLOGY

18. SIGN AND SYMPTOMS
 Hepatomegaly (although liver may also be small)
 Jaundice
 Ascites
 Circulatory changes
Spider telangiectasia, palmar erythema, cyanosis
 Endocrine changes
Loss of libido, hair loss
Men: gynaecomastia, testicular atrophy, impotence
Women: breast atrophy, irregular menses, amenorrhoea

19. SIGN AND SYMPTOMS
 Haemorrhagic tendency
– Bruises, purpura, epistaxis, menorrhagia
 Splenomegaly, collateral vessels, variceal bleeding, fetor
hepaticus
 Hepatic (portosystemic) encephalopathy
 Asterixis
 Other features
– Pigmentation, digital clubbing
 Hypertrophic osteoarthropathy
 Dupuytren's contracture

20. SIGN AND SYMPTOMS
Nail changes.
 Muehrcke's nails - paired horizontal bands separated by normal
color due to hypoalbuminemia (low production of albumin).
 Terry's nails - proximal two thirds of the nail plate appears white
with distal one-third red, also due to hypoalbuminemia
 Clubbing - angle between the nail plate and proximal nail fold >
180 degrees

21. DIAGNOSTIC EVALUATION
 History collection
 Physical Examination
 Liver biopsy detects destruction and fibrosis of hepatic tissue.
Liver scan shows abnormal thickening and a liver mass.
 CT scan determines the size of the liver and its irregular
nodular surface.

22. DIAGNOSTIC EVALUATION
 Esophagoscopy to determine esophageal varices.
 Paracentesis to examine ascitic fluid for cell, protein, and
bacterial counts.
 PTC differentiates extrahepatic from intrahepatic obstructive
jaundice.
 Laparoscopy and liver biopsy permit direct visualization of the
liver.
 Serum liver function test results are elevated.

23. COMPLICATION
 Bruising and bleeding due to decreased production of
coagulation factors.
 Jaundice due to decreased processing of bilirubin.
 Itching (pruritus) due to bile products deposited in the skin.
 Ascites - fluid leaks through the vasculature into the abdominal
cavity.
 Esophageal varices - collateral portal blood flow through
vessels in the stomach and esophagus. These blood vessels
may become enlarged and are more likely to burst.

24. COMPLICATION
 Hepatic encephalopathy - the liver does not clear ammonia and
related nitrogenous substances from the blood, which are carried to
the brain, affecting cerebral functioning: neglect of personal
appearance, unresponsiveness, forgetfulness, trouble concentrating,
or changes in sleep habits.
 Sensitivity to medication due to decreased metabolism of the
active compounds.
 Hepatocellular carcinoma is primary liver cancer, a frequent
complication of cirrhosis. It has a high mortality rate.

25. MEDICAL MANAGEMENT
• Diuretic therapy, frequently with spironolactone (Aldactone), a
potassium-sparing diuretic that inhibits the action of aldosterone
on the kidneys. Furosemide (Lasix), a loop diuretic, may also be
used in conjunction with spironolactone to help balance
potassium depletion
• Symptomatic relief measures, such as pain medication and
antiemetics.
• Lactulose. Encephalopathy is treated with lactulose.
• Octreitide If required, octreotide may be prescribed for
esophageal varices.

26. MEDICAL MANAGEMENT
• Minimize further deterioration of liver function through the
withdrawal of toxic substances, alcohol, and drugs.
• Administration of albumin to maintain osmotic pressure.

27. NON MEDICAL MANAGEMENT
• Diet. The patient may benefit from a high-calorie and a
medium to high protein diet, as developing hepatic
encephalopathy mandates restricted protein intake.
• Sodium restriction is usually restricted to 2g/day.
• Fluid restriction. Fluids are restricted to 1 to 1.5 liters/day.
• Activity. Rest and moderate exercise is essential.

28. NON MEDICAL MANAGEMENT
Paracentesis. Paracentesis may help alleviate ascites.

29. NON MEDICAL MANAGEMENT
Sengstaken-Blakemore or
Minnesota tube. The
Sengstaken-Blakemore or
Minnesota tube may also help
control hemorrhage by
applying pressure on the
bleeding site.

30. SURGICAL MANAGEMENT
Transjugular intrahepatic
portosystemic shunt may be
performed in patients whose
ascites prove resistant. This
percutaneous procedure
creates a shunt from the portal
to systemic cisculation to
reduce portal pressure and
relieve ascites.

31. SURGICAL MANAGEMENT
liver transplantation

32. NURSING DIAGNOSES
• Activity Intolerance related to fatigue, general debility, and
discomfort
• Imbalanced Nutrition: Less Than Body Requirements related
to anorexia and GI disturbances
• Impaired Skin Integrity related to edema, jaundice, and
compromised immunologic status
• Risk for Injury related to altered clotting mechanisms
• Disturbed Thought Processes related to deterioration of liver
function and increased serum ammonia level

33. PROMOTING ACTIVITY TOLERANCE
• Encourage alternating periods of rest and ambulation.
• Maintain some periods of bed rest with legs elevated to
mobilize edema and ascites.
• Encourage and assist with gradually increasing periods of
exercise.

34. IMPROVING NUTRITIONAL STATUS
• Encourage patient to eat high-calorie, moderate-protein meals
and to have supplementary feedings.
• Suggest small, frequent feedings and attractive meals in an
aesthetically pleasing setting at mealtime.
• Encourage oral hygiene before meals.
• Administer or teach self-administration of medication for
nausea, vomiting, diarrhea, or constipation

35. PROTECTING SKIN INTEGRITY
• Note and record degree of jaundice of skin and sclerae and
scratches on the body.
• Encourage frequent skin care, bathing without soap, and
massage with emollient lotions.
• Advise patient to keep fingernails short

36. PREVENTING INJURY THROUGH BLEEDING
• Observe stools and emesis for color, consistency, and amount;
test each one for occult blood.
• Observe for external bleeding: ecchymosis, leaking needle stick
sites, epistaxis, petechiae, and bleeding gums.
• Keep patient quiet and limit activity if signs of bleeding exhibited.
• Administer vitamin K as prescribed.
• Stay in constant attendance during episodes of bleeding.

37. • Institute and teach measures to prevent trauma:
– Maintain safe environment.
– Gentle blowing of nose.
– Use of soft toothbrush.
• Encourage intake of foods with high vitamin C content.
• Use small-gauge needles for injections, and maintain
pressure over site until bleeding stops.
PREVENTING INJURY THROUGH BLEEDING
cont..

38. PROMOTING IMPROVED THOUGHT
PROCESSES
• Restrict high-protein loads while serum ammonia is high to
prevent hepatic encephalopathy. Monitor ammonia levels.
• Protect from sepsis through good hand washing and prompt
recognition and management of infection.
• Monitor fluid intake and output and serum electrolyte levels to
prevent dehydration and hypokalemia (may occur with the use
of diuretics), which may precipitate hepatic coma.

39. PROMOTING IMPROVED THOUGHT
PROCESSES
• Keep environment warm and limit visitors.
• Pad the side rails of the bed and provide careful nursing
surveillance to ensure patient's safety.
• Assess LOC and frequently reorient as needed.
• Administer lactulose (Cephulac) or neomycin (through a
retention enema or nasogastric (NG) tube, as ordered, for
elevated ammonia levels and decreasing LOC.

40. HEALTH EDUCATION
• Stress the necessity of giving up alcohol completely.
• Urge acceptance of assistance from a substance abuse
program.
• Provide written dietary instructions.
• Encourage daily weighing for self-monitoring of fluid retention
or depletion.
• Discuss adverse effects of diuretic therapy.

41. HEALTH EDUCATION
• Emphasize the importance of rest, a sensible lifestyle, and an
adequate, well-balanced diet.
• Involve the person closest to the patient because recovery
usually is not easy and relapses are common.
• Stress the importance of continued follow-up for laboratory
tests and evaluation by a health care provider.

42. BIBLIOGRAPHY
 Brunner and suddarth’s (2004) “Text book of medical surgical
nursing”, 10th edition, published by Lippincott Williams and
Wilkins page no. 2079-2087.
 Lewis (2002), “Medical surgical nursing”, 6th edition, published
by Mosby page no 1635-1651.
 Black .J.M. & Hawks .J.H, (2004), “Medical Surgical Nursing” 7th
edition, New Delhi: Elsevier publication,