6 Kuliah Liver Cirrhosis

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Liver Cirrhosis

What is Liver Cirrhosis?


 Diffuse fibrosis of the liver with
nodule formation
 Abnormal response of the liver to
any chronic injury
Introduction
 12th leading cause of death in the united
states
 On average about 27,000 deaths per year
 Patients with cirrhosis are susceptible to
a variety of complications and their life
expectancy is markedly reduced
Causes of Cirrhosis
1. Chronic viral hepatitis
2. Metabolic: hemochromatosis, Wilson dis,
alfa-1-antitrypsin, NASH
3. Prolonged cholestasis (primary biliary
cirrhosis, primary sclerosing cholangitis)
4. Autoimmune diseases (autoimmune
hepatitis)
5. Drugs and toxins
6. Alcohol
Pathophysiology
 Irreversible chronic injury of the hepatic
parenchyma
 Extensive fibrosis - distortion of the
hepatic architecture
 Formation of regenerative nodules
Clinical Manifestations
 Spider angiomas
 Palmar erythema
 Nail changes
 Muehrcke's nails
 Terry’s nails
 Gynecomastia
 Testicular atrophy
Clinical Manifestations
 Muehrcke's nails  Terry’s nails
Clinical Manifestations
 Fetor hepaticus  Hepatomegaly
 Jaundice  Splenomegaly
 Asterixis  Caput medusa
 Pigment gallstones
 Parotid gland
enlargement
Laboratory Studies
 most common measured laboratory test
classified as LFTs include
the enzyme tests (principally the serum
aminotransferases, alkaline phosphatase, and
gamma glutamyl transpeptidase), the serum
bilirubin
tests of synthetic function (principally the
serum albumin concentration and prothrombin
time)
Diagnosis
 Liver biopsy
 Obtained by either a percutaneous,
transjugular, laparoscopic, or radiographically-
guided fine-needle approach
 Sensitivity of a liver biopsy for cirrhosis is in
the range of 80 to 100 percent depending upon
the method used, and the size and number of
specimens obtained
Diagnosis
 not necessary if the clinical, laboratory, and
radiologic data strongly suggest the presence of
cirrhosis
 liver biopsy can reveal the underlying cause of
cirrhosis
Histopathology
Histopathology
Histopathology
Morphologic Classification
Micronodular cirrhosis
Nodules less than 3 mm in diameter
Believed to be caused by alcohol,
hemochromatosis, cholestatic causes of
cirrhosis, and hepatic venous outflow
obstruction
Morphologic Classification
 Macronodular
cirrhosis

 Nodules larger than 3


mm
 Believed to be
secondary to chronic
viral hepatitis
Morphologic Classification
 Relatively nonspecific with regard to etiology
 The morphologic appearance of the liver may change as
the liver disease progresses
 micronodular cirrhosis usually progresses to macronodular
cirrhosis
 Serological markers available today are more specific than
morphological appearance of the liver for determining the
etiology of cirrhosis
 Accurate assessment of liver morphology may only be
achieved at surgery, laparoscopy, or autopsy
Anatomy of the portal venous system
Complications of
Portal Hypertension
1. Varices
Collaterals
Varices
Esophagus
Gastric
Colo-rectal
Portal hypertensive gastropathy
Varices
Diagnosis
 History : Hematemases, melena
 Physical examination
 Ultrasound abdomen
 Endoscopy
Varices
Management-General
 ABC
2 IV Lines
 Type and cross match
 Resuscitation
IVF
Blood
 Platelet transfusion (platelet <75,000)
 Fresh frozen plasma (Correct Pt)
Varices
Management-Specific
 IV vasoconstrictors (Octreotide)
 Endoscopic therapy
Banding
Sclerotherapy
 Shunting
Surgical
TIPS
Variceal Banding
Types of Shunts

Surgical shunt

TIPS (Transjugular intrahepatic


portosystemic shunt)
Varices
Prevention
Treat underlying disease
Endoscopic banding protocol
B-blockers
Shunt surgery (only if no cirrhosis)
Liver transplantation
2. Ascites
Ascites

 Definition: fluid in the


peritonial cavity
Mechanism of Ascites
Causes of Ascites
1. Liver disease: cirrhosis
2. Right sided heart failure
3. Kidney disease (nephrotic syndrome)
4. Low albumin (malnutrition, bowel loss)
5. Peritonial infection (TB…)
6. Peritonial cancer
Presentation
History:
 Increased abdominal girth
 Increased wt

Physical exam:
 Bulging flanks
 Shifting dullness
 Fluid wave
Diagnosis
 Physical examination
 Ultrasound
 Ascitic tap
WBC (>250 PMN: SBP)
RBC
SAAG (serum albumin to ascitic fluid
albumin gradient)
>11 mg/dl : portal hypertension
<11 mg/dl : Other
Portal hypertension Peritonial disease

or heart failure or kidney disease


Treatment-General
Treat the underlying disease
Salt restriction (<2gm/d)
Diuretics
Loop diuretic (Lasix)
Aldosterone inhibitor (Spironolactone)
Treatment-Resistant
Recurrent tapping
Peritoneal-venous shunt
TIPS
Liver transplantation
Spontaneous Bacterial Peritonitis

Infection of ascitic fluid


Usually gram negative (E.Coli)
Presentation variable
Mortality is high
Dx: ascitic tap = PMN>250
Treatment : third generation
cephalosporin IV
3. Hepatic
Encephalopathy
Hepatic
Encephalopathy
Reversible decrease in neurological
function secondary to liver disease
Acute: seen with acute liver failure
Acute on chronic: established
cirrhosis
Hepatic Encephalopathy
Mechanism
Hepatic Encephalopathy
Clinical features
 Reversal of sleep pattern
 Disturbed consciousness
 Personality changes
 Intellectual deterioration
 Fetor hepaticus
 Astrexis
 Fluctuating
Flapping Tremor
Drawing Tests
Hepatic Encephalopathy
Diagnosis
 Clinical
(most important)
 The drawing tests
 EEG
 CT/MRI may show cerebral atrophy
Hepatic Encephalopathy
Exacerbating factors
Hepatic Encephalopathy
Treatment
 Identifyand treat precipitation factor
 Treat underlying liver disease
 Normal protein diet
 Antibiotics (Neomycin, metronidazole)
 Lactolose
 Transplantation
4. Hepatorenal
Syndrome
Hepatorenal
Syndrome
Progressive renal failure
Type 1 : rapidly progressive, high
mortality
Type 2: slower progression
R/O volume depletion secondary to
diuretics
IV vasoconstrictors
Summary
1. Mechanical compression of blood flow
plus hemodynamic changes leads to portal
hypertension
2. Common complications of portal
hypertension are:
Collateral formation (Varices)
Ascites
Hepatic encephalopathy
Summary
3. The most important step in variceal bleed
management is resuscitation

4. The most important step in management of


hepatic encephalopathy is the identification
of the precipitating factor

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