Cirrhosis is a chronic liver disease characterized by fibrosis, degeneration of liver cells, and impaired liver function. It affects millions worldwide, with significant mortality linked to causes like hepatitis B and C, and alcohol consumption. The document covers its definition, causes, pathophysiology, clinical manifestations, diagnostic measures, management strategies, and nursing care considerations.

1. CIRRHOSIS
Shashi Prakash
M.Sc. Nursing, II Year
CON, ILBS

2. CONTENT
• Definition
• Epidemiology
• Causes
• Pathophysiology
• Clinical manifestations
• Diagnostic measures
• Management
• Complications
• Nursing Management

3. INTRODUCTION
• The word "cirrhosis" is a neologism derived from
Greek kirrhós meaning "yellowish, tawny" and
the suffix - osis, i.e. "condition" in medical
terminology.

4. INTRODUCTION
• End-stage Liver disease
• Chronic in nature
• Liver does not function properly due to long-term
damage.
• Replacement of normal liver tissue by scar
tissue.

5. INTRODUCTION
• The cost of cirrhosis in terms of human suffering,
hospital costs, and lost productivity is high.

6. DEFINITION
• A chronic liver disease characterized by fibrotic
changes and the formation of dense connective
tissue within the liver, subsequent degenerative
changes, and loss of functioning cells.
• A chronic progressive disease of the liver
characterised by extensive degeneration and
destruction of the liver cells.

7. EPIDEMIOLOGY
• Cirrhosis affected about 2.8 million people and
resulted in 1.3 million deaths in 2015.
• Of these deaths, alcohol caused 3, 48, 000,
hepatitis C caused 326,000, and hepatitis B
caused 3, 71, 000.
• Cirrhosis is the 12 leading cause of death due to
disease in the United States (NIH).

8. EPIDEMIOLOGY
• In the United States, more men die of cirrhosis than
women.
India
• Around 10 lakh clients of liver cirrhosis are newly
diagnosed every year
• Liver disease may affect every one in 5 Indians.
• Liver disease is the tenth most common cause of
death (WHO)

9. EPIDEMIOLOGY
• Established cirrhosis has a 10 year mortality of
34- 66 %.
• Largely dependent on the cause of the cirrhosis
• Alcoholic cirrhosis has a worse prognosis than
primary biliary cholangitis and hepatitis.

10. CAUSES
• More than one cause is present in the same
person.
• Globally, 57% of cirrhosis is attributable to either
hepatitis B (30%) or hepatitis C (27%).
• Alcohol consumption is another major cause,
accounting for about 20% of the cases.

11. CAUSES
• Alcoholism
• Chronic viral hepatitis
Hepatitis B
Hepatitis C
• Autoimmune hepatitis
• NASH

12. CAUSES
• Biliary cirrhosis
Primary biliary cirrhosis
Primary Sclerosing cholangitis
• Autoimmune cholangiopathy
• Cardiac cirrhosis
• Inherited metabolic liver disease

13. CAUSES
Hemochromatosis
Wilson’s disease
• Cystic fibrosis
• Cryptogenic cirrhosis

14. PATHOPHYSIOLOGY OF LIVER
CIRRHOSIS
Liver insult, Alcohol ingestion, Viral hepatitis, Exposure to toxins
Liver necrosis
Hepatocyte damage
Liver inflammation
Alterations in blood and lymph flow
Decreased
ADH and
aldosterone
detoxification
Decreased
androgen and
estrogen
detoxification
Decreased
metabolism
of protein and
carbohydrate
Decreased
vitamin K
absorption
Decreased
bilirubin
metabolism
and biliary
tree damage
or obstruction

15. Oedema Palmar erythema,
spider angiomas
Ascites,
Hypoglycaemia
Bleeding
tendencies
Jaundice.
Clay-colored stools,
Dark urine
Liver fibrosis and scarring
Liver failure
PATHOPHYSIOLOGY OF LIVER
CIRRHOSIS

16. CLASSIFICATION
Micronodular Macronodular
Mixed

17. MICRONODULAR
• Alcohol
• Hemochromatosis
• Hepatic venous outflow obstruction
• Chronic biliary obstruction
• Jejunoileal bypass

18. MACRONODULAR
• Hepatitis B
• Hepatitis C
• Primary biliary cholangitis.

19. TYPES
Alcoholic
Cirrhosis
Post-necrotic
Cirrhosis
Biliary
Cirrhosis
Cardiac
Cirrhosis

20. ALCOHOLIC CIRRHOSIS
• Previously called Laennec’s cirrhosis
(René Laennec)
• Also called Portal or nutritional cirrhosis.
• Alcoholic cirrhosis develops for 10-20% of
individuals who drink heavily for a decade or
more.

21. ALCOHOLIC CIRRHOSIS
• Ethanol alcohol dehydrogenase acetaldehyde
• Acetaldehyde acetaldehyde dehydrogenase
acetate
• Increases intracellular accumulation of
triglycerides by increasing fatty acid uptake and
by reducing fatty acid oxidation and lipoprotein
secretion.

22. Formation of protein-acetaldehyde adducts
Interfere with specific enzyme activities, including
microtubular formation and hepatic protein
trafficking
Hepatocyte damage
Reactive oxygen species activate Kupffer species

23. Production of profibrogenic cytokines
Perpetuate stellate cell activation
Production of excess collagen,
extracellular matrix

24. POST-NECROTIC CIRRHOSIS
• It is a complication of viral, toxic or idiopathic
(autoimmune hepatitis).
• Broad bands of scar tissue forms within the liver.
BILIARY CIRRHOSIS
• Biliary cirrhosis is associated with chronic biliary
obstruction and infection.
• There is diffuse fibrosis of the liver with jaundice as
a main feature.

25. CARDIAC CIRRHOSIS
• It results from long standing, severe right-sided
heart failure in clients with cor-pulmonale,
constrictive pericarditis, and tricuspid
insufficiency.

26. CARDIAC CIRRHOSIS
• Elevated venous pressure transmitted via the
inferior vena cava and hepatic veins to the sinusoids
of the liver, which become dilated and engorged with
blood.
• The liver becomes enlarged and swollen
• With long-term passive congestion and relative
ischemia due to poor circulation, hepatocytes can
become necrotic, leading to fibrosis.

27. PATHOPHYSIOLOGY

28. PATHOPHYSIOLOGY
• The progression rate from fibrosis to cirrhosis and
the morphology of cirrhosis vary from person to
person.
• Presumably, the reason for such variation is the
extent of exposure to the injurious stimulus and the
individual’s response.
 Hepatic fibrosis
 Regenerating liver cells

29. Hepatocyte injury and loss
Growth regulator- cytokines
Hepatic growth factors – epithelial growth factor,
hepatocyte growth factor, transforming growth
factor-alpha, tumor necrosis factor
Hepatocellular hyperplasia and angiogenesis

30. Clinical picture of a client with liver dysfunction

31. CLINICAL MANIFESTATIONS
Early manifestations
• Onset of cirrhosis is usually insidious.
• Occasionally there is abrupt onset of symptoms.
• GI disturbances are common.

32. EARLY MANIFESTATIONS
• Anorexia
• Dyspepsia
• Flatulence
• Nausea and vomiting
• Change in bowel habits (Diarrhoea and
constipation)

33. EARLY MANIFESTATIONS
• Abdominal pain
• Fever
• Lassitude
• Slight weight loss
• Liver and spleen enlargement

34. LATER MANIFESTATIONS
It may be severe and result from liver failure and
its complications.
• Jaundice
• Skin lesions
Spider angiomata and Palmer erythema

36. LATER MANIFESTATIONS
• Haemotological probems: Thrombocytopenia,
leukopenia, anaemia, and coagulation disorders.
• Coagulation problems manifested by epistaxis,
purpura, petechiae, easy bruising, gingival
bleeding, and heavy menstrual bleeding.
• Peripheral neuropathy

37. LATER MANIFESTATIONS
Endocrine problems
• Men: Gynecomastia, loss of axillary, pubic hair,
testicular atrophy, impotence with loss of libido.
• Younger women: amenorrhoea
• Older women: vaginal bleeding
• Hyperaldosteronism causes sodium and water
retention and potassium loss.

39. Compensated cirrhosis Decompensated cirrhosis
• Intermittent mild fever
• Vascular spiders
• Palmar erythema
• Unexplained epistaxis
• Ankle edema
• Vague morning indigestion
• Flatulent dyspepsia
• Abdominal pain
• Firm, enlarged liver
• Splenomegaly
• Ascites
• Jaundice
• Weakness, Muscle wasting
• Weight loss
• Continuous mild fever
• Purpura
• Spontaneous bruising
• Epistaxis
• Hypotension
• Sparse body hair
• Gonadal atrophy

41. DIAGNOSIS
• The gold standard for diagnosis of cirrhosis is a
liver biopsy
• The best predictors of cirrhosis are ascites,
platelet count <160,000/mm3, spider angiomata,
and a Bonacini cirrhosis discriminant score
greater than 7.

42. Bonacini score
Score Platelet count x109 AST/ALT Ratio INR
0 > 340 > 1.7 < 1.1
1 280 - 340 1.2 - 1.7 1.1 - 1.4
2 220 - 279 0.6 - 1.19 > 1.4
3 160 - 219 < 0.6 ---
4 100 - 159 ... ...
5 40 - 99 ... ...
6 < 40 ... ...

43. LABORTAORY FINDINGS
• Thrombocytopenia
• Aminotransferases
• Alkaline phosphatase - slightly elevated but less
than 2–3 times the upper limit of normal.
• Gamma-glutamyltransferase- correlates with ALP
levels. Typically much higher in chronic liver disease
from alcohol.

44. LABORTAORY FINDINGS
• Bilirubin
• Albumin
• Prothrombin time
• Globulins- increased due to shunting of bacterial
antigens away from the liver to lymphoid tissue.
• Leukopenia and neutropenia
• Coagulation defects

45. LABORATORY FINDINGS
• Fibro scan (>14 kPa)
• USG : Small, nodular liver in advanced cirrhosis
along with increased echogenicity with irregular
appearing areas. Other liver findings suggestive
of cirrhosis are an enlarged caudate lobe,
widening of the fissures and enlargement of the
spleen.

46. Liver biopsy: Gold standard for
 Diagnosis of cirrhosis
 Sequential histological grading of inflammation and
staging of fibrosis can assess risk of progression
Microscopy
 The presence of regenerating nodules of
hepatocytes
 Presence of fibrosis

47. LIVER BIOPSY
• Chronic hepatitis B: infiltration of the liver
parenchyma with lymphocytes
• Cardiac cirrhosis: Erythrocytes and a greater
amount of fibrosis in the tissue surrounding the
hepatic veins
• Primary biliary cholangitis: fibrosis around the bile
duct, the presence of granulomas and pooling of bile

48. LIVER BIOPSY
• Alcoholic cirrhosis: infiltration of the liver with
neutrophils
Child- Pugh score
• Also known as Child-Turcotte-Pugh score or Child
Criteria
• Devised in 1964 by Child and Turcotte, and modified
in 1973 by Pugh and others

49. Child-Turcotte-Pugh Score
Measure 1 point 2 points 3 points
Total bilirubin, μmol/L
(mg/dL)
<34 (<2) 34- 50 (2–3) >50 (>3)
Serum albumin, g/dL >3.5 2.8- 3.5 <2.8
Prothrombin time,
prolongation (s)
< 4.0 4.0- 6.0 > 6.0
INR <1.7 1.7–2.3 > 2.3
Ascites None Mild
(or suppressed
with medication)
Moderate to
severe
(or refractory)
Hepatic encephalopathy None Grade I–II Grade III–IV

50. Child- Pugh score
Interpretation
Points Class One-year
survival
Two-year
survival
5–6 A 100% 85%
7–9 B 80% 60%
10–15 C 45% 35 %

51. COMPLICATIONS
Portal
hypertension
Esophageal &
gastric varices
Peripheral
edema
Ascites
Hepatic
Encephalopathy
Hepatorenal
Syndrome

52. PORTAL HYPERTENSION
• Because of the structural changes in the liver from
cirrhotic process, there is compression and destruction
of the portal and hepatic veins and sinusoids.
• These changes cause obstruction to the normal flow of
blood through the portal system, resulting in portal
hypertension.
• It is defined as HVPG greater than or equal to 5 mm Hg
and is considered to be clinically significant when HVPG
exceeds 10 to 12 mm Hg.

53. • Collateral circulation develops
• These collateral and systemic circulations
communicate to develop varicosities such as
esophageal, gastric, caput medusa and
haemorrhoids

54. ESOPHGAEAL & GASTRIC
VARICES
• These collateral vessels contain little elastic
tissue and are quite fragile. They tolerate high
pressure poorly resulting in distension and bleed
easily.

55. PERIPHERAL EDEMA
• Edema results from decreased colloidal oncotic
pressure from impaired liver synthesis of
albumin and increased portacaval pressure from
PHTN.
• Peripheral edema occurs as ankle and presacral
edema.

56. ASCITES
• When blood pressure is elevated in the liver as occurs in
cirrhosis, proteins move from the blood vessels via the
large pores of the sinusoids (capillaries) into the lymph
space.
• When the lymph system is unable to carry off the excess
proteins and water, they leak through the liver capsule
into the peritoneal cavity.
• The osmotic pressure of the proteins pulls additional fluid
into the peritoneal cavity.

57. ASCITES
• Hypoalbuminemia causes decreased colloidal oncotic
pressure.
• Damaged hepatocytes does not metabolise aldosterone.
The increased level of aldosterone causes increased
sodium reabsorption by the renal tubules and therfore
additional water retention.
• Because of edema formation there is decreased
intravascular volume and subsequently decreased renal
flow and glomerular filteration.

58. HEPATORENAL SYNDROME
• Functional renal failure with advancing
azometia, oliguria, and intractable ascites
without structural abnormality of the kidneys

59. HRS
• Type 1 HRS is characterized by a progressive
impairment in renal function and a significant reduction in
creatinine clearance within 1–2 weeks of presentation.
• Type 2 HRS is characterized by a reduction in
glomerular filtration rate with an elevation of serum
creatinine level, but it is fairly stable and is associated
with a better outcome than that of Type 1 HRS.

60. Portal Hypertension
Splanchnic vasodilation
Decreased effective circulatory volume
Activation of renin-angiotensin-aldosterone system
Renal sodium activity Renal vasoconstriction
Ascites Hepatorenal Syndrome

61. COMPLICATIONS
Malnutrition
Abnormalities
in
coagulation
Bone
diseases
Hematological
Abnormalities

63. MANAGEMENT
Stop
the
progression
Manage
complications
Nutritional
Therapy
Treat cause

64. Ascites
• Sodium restriction
• Based on the degree of ascites.
• Initially sodium intake to 2g/day
• Severe ascites : sodium intake to 250-500 mg/day.
• Diuretic therapy: A high potency loop diuretic such as
furosemide in combination with potassium sparing
diuretic such as spironolactone.
• Paracentesis

65. Portosystemic shunt

66. Complications
• Thrombosis formation at the venous tip of the
shunt
• Infection
• Shunt occlusion

67. Esophageal & gastric varices
• Avoid ingesting alcohol, aspirin, irritating foods, prompt
treatment of upper respiratory infections and controlled
cough
• Drug therapy (Somatostatin analog octreotide,
vasopressin, nitroglycerine, and beta adrenergic
blockers such as propranolol)
• Endoscopic therapies include sclerotherapy, ligation of
varices

68. Hepatic encephalopathy
Lactulose
• Lactulose in the colon is split into lactic acid and acetic
acid which decreases pH from 7 to 5. The acidic
environment discourages bacterial growth.
• Also, it traps the ammonia in the gut and the laxative
effect of the drug expels the ammonia from the colon.
• Antibiotics such as metronidazole, vancomycin, rifaximin
to reduce the bacterial flora of the colon.

69. Drug Mechanism
Vasopressin Hemostasis and control of bleeding in
esophageal varices, constriction of
splanchnic arterial bed.
Propranolol Reduction of portal venous pressure,
reduction of esophageal varices bleeding
Vitamin K Correction of clotting abnormalities
Histamine receptor blockers and proton
pump inhibitors
Decreases gastric acidity
Diuretics
Spironolactone
Furosemide
Blocks action of aldosterone, potassium
sparing
Acts on distal tubule and loop of Henle
to prevent reabsorption of sodium and
water
Fat soluble vitamins, Thiamine, Zinc
supplementations

70. DRUG THERAPY
Acetylcysteine N-acetylcysteine (NAC) is a
hepatoprotective agent that turns into
the amino acid L-cysteine when
ingested. In turn, L-cysteine helps
produce glutathione (GSH) that helps
produce the antioxidant glutathione,
which plays a key role in protecting the
liver from damage.

72. MANAGEMENT
Nutritional Therapy
• Without complications: High in calories
(3000 kcal/day) with high carbohydrate content
and moderate to low fat levels.
• Hepatic encephalopathy: Protein restriction
• Ascites & edema: Low sodium diet

73. MANAGEMENT
• Alcoholic cirrhosis: High in protein, calorie
• Enteral formulas
Liver Transplantation
• It is considered in patients with recurring hepatic
encephalopathy and end-stage liver disease.
• It depends upon factors - cause of the cirrhosis and
other systemic medical problems.

74. NURSING
MANAGEMENT

76. Horta’s Conceptual Model

77. NURSING ASSESSMENT
•Assess for presence of haemorrhage, hypovolemia and oliguria
•Assess the client’s respiratory, renal and hemodynamic status.
•Fluid and electrolyte imbalances, hypoglycaemia.
•Manifestations of infections (fever, increased white blood cells).
•Pain levels.
•Mental status of the client.

80. NURSING MANAGEMENT
• Ineffective breathing pattern related to ascites
and restriction of thoracic excursion secondary
to ascites, abdominal distention, and fluid in the
thoracic cavity.
• Chronic pain and discomfort related to enlarged
tender liver and ascites

81. NURSING MANAGEMENT
• Haemorrhage related to bleeding tendency
secondary to altered clotting factors and rupture
of esophageal or gastric varices.

82. NURSING MANAGEMENT
• Fluid volume excess related to ascites and edema
formation.
• Disturbed thought processes related to deterioration
of liver function and increased serum ammonia
level.
• Imbalanced nutrition: less than body requirements,
related to abdominal distention, discomfort and
anorexia.

83. NURSING MANAGEMENT
• Activity intolerance related to fatigue, lethargy,
and malaise.
• High risk for injury related to altered clotting
mechanisms and altered level of consciousness.

84. EXERCISES FOR LIVER
CIRRHOTIC PATIENTS

85. DIETARY PATTERN IN LIVER
CIRRHOSIS
• Low-sodium diet
• Adequate protein intake to prevent muscle wasting.
• Omega-6 fatty acids should be avoided as it can lead to toxic lipid
metabolites.
• Fluid-restricted diet.
• A nighttime snack of approximately 700 calories and approximately 25
grams of protein
• Vitamin A, D, Zinc and Magnesium supplementation.
• Branched-chain amino acids (BCAAs)
• Oral and enteral nutritional supplementation
• Probiotic treatment
• Coffee consumption

86. HEALTH EDUCATION
• Cirrhosis of the liver is a life-threatening chronic
illness, which is ultimately terminal without
transplantation. However, the management of
some cirrhosis cases may be improved with diet,
thorough compliance with prescribed
medications, and abstinence from alcohol.

87. SUMMARY

88. CONCLUSION
Cirrhosis is defined as the histological development of
regenerative nodules surrounded by fibrous bands in
response to chronic liver injury, that leads to portal
hypertension and end stage liver disease.
Alcoholic liver disease and hepatitis C are the most
common causes in the Western world, while hepatitis B
prevails in most parts of Asia and sub-Saharan Africa.
The ultimate therapy for cirrhosis and end stage liver
disease is liver transplantation.

89. BIBLIOGRAPHY
Bacon, B. R. (2018). Cirrhosis and Its Complications. Longo,
D.L., Kasper, D.L., Jameson, J.L., Fauci, S. A., Hauser, S.L., Fishman,
A.R., & Loscalzo, J (Eds.), Harrison Principals of Internal Medicine (pp.
2592- 2602). New Delhi: MacGraw Hill.
Cirrhosis. 2019. Retrieved May 22, 2019 from
https://en.wikipedia.org/wiki/Cirrhosis.
Schuppan, D., & Afdhal, N. H. (2008). Liver Cirrhosis. Lancet,
371(9615), 838–851. doi: 10.1016/S0140-6736(08)60383-9

90. BIBLIOGRAPHY
Smeltzer, C. S., Bare, G. B., Hinkle, L. J., & Cheever, H. K.
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91. Thankyou