LIVER CIRRHOSIS

Dr. Imran Masood, Ph.D

drimranmasood@iub.edu.pk
 CONTENTS
 Definition
 Diagrammatic evaluation
 Epidemiology
 Classification
 Causes
 Sign & symptoms
 Diagnosis
 Complications
 Treatment & management
 DEFINITION
Cirrhosis is derived from Greek word
KIRROS : ORANGE OR TAWNY
OSIS : CONDITION
A chronic disease of the liver marked by degeneration of
parenchymal cells , inflammation , and fibrous thickening of tissue.
 WHO DEFINITION:

“A diffused process characterized by liver necrosis and fibrosis

and conversion of normal liver architecture into structurally
abnormal nodules that lack normal lobular organization.”
DIAGRAMMATIC EVALUATION
PATHOPHYSIOLOGY OF
LIVER CIRRHOSIS:
 Damage to the hepatic parenchyma (due to inflammation)

Activation of stellate cells

Extensive fibrosis - distortion of the hepatic architecture

Obstructs hepatic blood

Formation of regenerative nodules

Development of scar tissue that replaces normal parenchyma

 EPIDEMIOLOGY
15th leading cause of death ages 45 – 54 & 12 th leading cause of death
in adults .
 Predominant age: peak incidence ages 40-50
 Predominant sex: male > female; but more female get cirrhosis from
alcohol abuse
 CLASSIFICATION OF LIVER CIRRHOSIS
1) Cirrhosis can be classified histologically into two types.

• Micronodular cirrhosis: characterized by small nodules about 1mm in

diameter and seen in alcoholic cirrhosis.

• Macronodular cirrhosis: characterized by large nodules of various sizes .

areas of previous collapse of the liver architecture are evidenced by large
fibrous scars .
CLASSIFICATION ON THE BASIS OF CAUSATIVE AGENT

 Laennac’s cirrhosis:
Associated with alcohol abuse& malnutrition.
Post necrotic cirrhosis:
Due to results of acute viral hepatitis , post intoxication
with industrial chemical.
Biliary cirrhosis:
Scaring occur around the bile duct in liver, results from
chronic biliary obstruction and infection
 CAUSES OF CIRRHOSIS
 Genetic
Haemochromatosis:
Normal role of hepridine is disturbed.
Wilson’s disease:
Copper overload in liver, brain and eye.
Αlpha₁ - antitrypsin deficiency:
Accumulation of excess protein molecules in
hepatocytes.
 CAUSES OF CIRRHOSIS
 Alcohol
 Chronic viral hepatitis ( B or C )
Nonalcoholic steatohepatitis:
Type of non-alcoholic fatty liver disease.
 Autoimmune liver disease:
Immune system of the body started attacked the liver cell
 CAUSES OF CIRRHOSIS
Primary biliary cirrhosis:
Slow progressive destruction of the small bile ducts
Cystic fibrosis:
Bile become thick and tenacious thus difficulty getting
out of the liver.
 SIGN & SYMPTOMS
SIGNS
Skin changes
• Spider – angiomata , xanthoma
• Hyperpigmentation
• Jaundice
Organomegaly
• Hepatomegaly ( if fatty liver , alcohol , or viral)
• Spleenomegaly
Central obesity
Gynecomastia
 SYMPTOMS

Fatigue, malaise, weakness, anorexia

Weight loss (gain if ascites / edema)
Right upper abdominal tenderness
Tea-colored urine
 Clay- colored stools
Abdominal swelling / bloating
Abdominal bleeding
Pruritus
 DIAGNOSIS
Physical findings
 Lab findings
 Imaging techniques
a) Ultrasonography
B) MRI
C) CT scan
 Liver biopsy
 PHYSICAL FINDINGS
O Jaundice
O Ascites
O Spider angiomatous
O Palmer erythema
O Gynecomastia
O Encephalopathy
O Terry's nails
O Muehrcke’s lines
O Clubbing
 LAB FINDINGS:
Most common measured laboratory test classified as LFT’s include:
Enzyme tests
• Serum aminotransferases
• Alkaline phosphatase
• Gamma glutamyl transpeptidase

Tests of synthetic function

• Serum albumin concentration
• Serum bilirubin
• Prothrombin time
 LABORATORY ABNORMALITIES

Hypoalbumenemia
Elevated prothrombin time
Hyperbilirubinemia
Thrombocytopenia
Elevated alkaline phosphatase
Elevated aspartate transaminase (AST), alanine transaminase (ALT) ,
and ɤ-glutamyl trans peptidase(ggt)
 IMAGING TECHNIQUES
Ultrasonography
CT scan
MRI
• Imaging techniques can provide useful information regarding the
presence of liver disease.
• These imaging test detect hardening and stiffening of liver.
• Ultrasonography is also used to detect the size of liver.
 LIVER BIOPSY
• Biopsy of the liver is the needle aspiration of a core of tissue for
histologic analysis.
• Purpose: it helps to identify hepatic disorders after imaging studies
have failed to detect them.
 TREATMENT

Cirrhosis is an irreversible condition.

Treatment goals are to slow the progression of liver damage and
reduce the risk of further complications.
There are currently no drug available to treat liver scaring.
 TREATMENT OF UNDERLYING CAUSES
Biliary cirrhosis
Ursodeoxycholic acid 10mg/kg PO daily
Wilson’s disease
Penicillamine 1-3g/ day or Tetrathiomolybdate 100-400 mg /day. After one
year zinc acetate alone 250mg b.i.d for maintenance.
Autoimmune liver disease
Prednisone 5-20mg /day with or without Azathioprine (immunosuppressant)
0.5-1mg/kg for at least two years.
 MANAGEMENT

GENERAL MEASURES
• Treat the underlying cause, if possible
• Patient must abstain from alcohol
• Immunize for pneumococcal disease , hepatitis A&B and influenza
• Weight reduction , exercise , control of lipid and diabetes
 DIETARY CHANGES

• Maintain nutritious diet, high fiber, daily multivitamins (without iron)

• Restrict dietary salts
• 1-1.5 g protein per kg of body weight
 COMPLICATIONS OF CIRRHOSIS

The major complications of cirrhosis that require therapeutic intervention

include:
Portal hypertension
• Variceal bleeding
• Ascites
• Hepatic encephalopathy
Spontaneous bacterial peritonitis
Hepatorenal syndrome
 SPONTANEOUS BACTERIAL PERITONITIS

• Spontaneous bacterial infection is defined as the spontaneous

infection of the acetic fluid in the absence of identified intra-
abdominal source of infection or inflammation.
• This condition has a mortality rate of 30%-50%
 SYMPTOMS OF SBP
• Fever,
• Changes in mental status,
• Abdominal tenderness,
• Gastrointestinal (GI) bleeding,
• Chills,
• Nausea or vomiting.
 DIAGNOSIS OF SBP
• Diagnosis of SBP is defined by a polymorphonuclear cell count
(PMN) (250/mcl or more)
• A protein concentration of 1 g/dl (10 g/L) or less, corresponding to
decreased ascitic opsonic activity.
• Cultures of ascites give the highest yield—80–90% positive—using
specialized culture bottles inoculated at the bedside.
 TREATMENT OF SPONTANEOUS BACTERIAL PERITONITIS

Antibiotics will be given, without waiting for culture results.

Patient with ascites have high WBC’s count should receive IV antibiotic
therapy (usually cefotaxime 2g t.i.d) or oral antibiotic therapy with
ofloxacin.
In addition to antibiotics, infusions of albumin are usually administered.
Paracentesis may be repeated after 48 hours to ensure control of
infection.
After recovery from a single episode of SBP, patient should be
treated with long- term antibiotic therapy of norfloxacin 400mg Per
Oral daily
or trimethoprim / sulphamethoxazole double strength tablet daily to
prevent further infection.
 HEPATORENAL SYNDROME

• Hepatorenal syndrome (often abbreviated HRS) is a life-threatening

medical condition that consists of rapid deterioration in kidney
function in individuals with cirrhosis or fulminant liver failure.
• HRS is a relatively common complication of cirrhosis, occurring in
18% of people within one year of their diagnosis, and in 39% within
five years of their diagnosis.
 SYMPTOMS OF HEPATORENAL
SYNDROME
• Jaundice,
• Altered mental status
• Evidence of decreased nutrition
• The presence of ascites.
 DIAGNOSIS

• Hepatorenal syndrome is diagnosed only when other causes of acute

kidney injury (including prerenal azotemia and acute tubular
necrosis) have been excluded.
• Diagnostic criteria for hepatorenal syndrome in cirrhosis
1. Cirrhotic patients with ascites
2. Serum creatinine >133 μmol/L (1.5 mg/dl)
3. No improvement of serum creatinine (↓ to a level of ≤133 μmol/L)
After at least 2 days along with
A. Diuretic withdrawal and
B. Volume expansion with albumin (1 g/kg of body weight per day
up to a maximum of 100 g/d)
• 4. The absence of shock
• 5. No current or recent treatment with nephrotoxic drugs
• 6. The absence of parenchymal kidney disease as indicated by
• A. Proteinuria >500 mg/d
• B. Microhematuria (>50 red blood cells per high-power field)
• C. And/or abnormal renal ultrasonography
 TREATMENT OF HEPATORENAL
SYNDROME:

• Treatments for HRS are still investigational

• The definitive treatment for HRS is liver transplantation.
 LIVER TRANSPLANT

When liver cirrhosis progresses to end-stage

liver disease , patient may be candidates for
liver transplantation.