2. Definition of cirrhosis
Cirrhosis is derived from Greek word kirros=orange or
tawny and osis=condition
-WHO 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.
14. In Whom Should We Suspect Cirrhosis?
Any patient with chronic liver disease
• Chronic abnormal aminotransferases and/or
alkaline phosphatase
Physical exam findings
• Stigmata of chronic liver disease (muscle
wasting, vascular spiders, palmar erythema)
• Palpable left lobe of the liver
• Small liver span
• Splenomegaly
• Signs of decompensation (jaundice, ascites,
asterixis)
DIAGNOSISOFCIRRHOSIS– CLINICALFINDINGS
15. Laboratory
• Liver insufficiency
• Low albumin (< 3.8 g/dL)
• Prolonged prothrombin time (INR >
1.3)
• High bilirubin (> 1.5 mg/dL)
• Portal hypertension
• Low platelet count (< 175 x1000/ml)
• AST / ALT ratio > 1
In Whom Should We Suspect Cirrhosis?
DIAGNOSISOFCIRRHOSIS– LABORATORYSTUDIES
16.
17. CT Scan in Cirrhosis
Liver with an irregular surface SplenomegalyCollaterals
DIAGNOSISOFCIRRHOSIS– CATSCAN
18. No
Yes
Diagnostic Algorithm
Patient with chronic liver disease and any of the following:
Variceal hemorrhage
Ascites
Hepatic encephalopathy
Liver biopsy not
necessary for the
diagnosis of cirrhosis
Physical findings:
Enlarged left hepatic lobe
Splenomegaly
Stigmata of chronic liver
Laboratory findings:
Thrombocytopenia
Impaired hepatic synthetic
function
Radiological findings:
Small nodular liver
Intra-abdominal collaterals
Ascites
Splenomegaly
Colloid shift to spleen and/or bone marrow
Yes No
disease
Yes No
Liver biopsy
DIAGNOSTICALGORITHM
19. Management of cirrhosis
-Specific treatment in some pre cirrhotic lesions:wilson disease—
Dpenicillamine,,hemochromatosis--- phlebotomy,,antiviral drugs for chronic viral hepatitis
-in established cirrhosis---treatment of complications
-screening for hepatocellular carcinoma
-liver transplantation
-maintenance of nutrition
20. CHILD-PUGH CLASSIFICATION OF PROGNOSIS IN
CIRRHOSIS
Score 1 2 3
Encephalopathy None Mild Marked
Bilirubin (mg/dl) <2.0 2.0-3.0 >3.0
Albumin (g/dl) >3.5 3.0-3.5 <3.0
Prothrombin time
(secondsprolonged)
<4 4-6 >6
Ascites None Mild Marked
Add the individual
scores:
<7 =Child'sA
7-9 =Child's B
>9 =Child's C
21. MELD SCORE
MELD = 3.8(SERUM BILIRUBIN –MG/DL)+11.2
IN INR + 9.6 IN SERUM CREATININE –
MG/DL+ 6.4
22. PORTAL HYPERTENSION
Definition:it is an increase in portal venous pressure.
-normal portal pressure:5-10mmHg.
-portal hypertension;>12mmHg
-normal portal blood flow:1-1.5L/minute
-- increased resistance to portal blood flow
• +hyperdynamic circulation-----formation of porto systemic
collaterals that diver blood to systemic circulation bypassing the
liver
23. Mechanisms of Portal Hypertension
Pressure (P) results from the interaction
of resistance (R) and flow (F):
P = R x F
Portal hypertension can result from:
• increase in resistance to portal flow and/or
• increase in portal venous inflow
MECHANISMSOFPORTALHYPERTENSION
27. CAUSES
CAUSES OF PORTAL HYPERTENSION
ACCORDING TO SITE OF
ABNORMALITY
• Budd-Chiari syndromeExtrahepatic post-sinusoidal
• Veno-occlusive diseaseIntrahepatic post-sinusoidal
• CirrhosisSinusoidal
•
•
•
Cystic liver disease
Partial nodular transformation of the liver Metastatic malignant disease
Intrahepatic pre-sinusoidal
• Schistosomiasis
• Sarcoidosis
• Congenital hepatic fibrosis
• Vinyl chloride
• Drugs
Extrahepatic pre-sinusoidal
• Portal vein thrombosis due to sepsis* (umbilical, portal pyaemia) or procoagulopathy (thrombotic diseases,
oral contraceptives, pregnancy), or secondary to cirrhosis
•
•
•
•
Abdominal trauma, including surgery Malignant
disease of pancreas or liver Pancreatitis
Congenital
28. Clinical complications of PHT
VARICES:esophageal,gastric,anorectal,retroperit oneal.
-portal hypertensive gastropathy and colopathy.
-caput medusae
-ascites
-congestive splenomegaly
-hepatic encephalopathy
29. Small varices Large varicesNo varices
7-8%/year 7-8%/year
Varices Increase in Diameter Progressively
Merli et al. J Hepatol 2003;38:266
VARICESINCREASEIN DIAMETERPROGRESSIVELY
30. Predictors of hemorrhage:
• Variceal size
• Red signs
• Child B/C
Variceal hemorrhage Varix with red signs
PROGNOSTICINDICATORSOFFIRSTVARICEALHEMORRHAGE
31. Treatment of portal hypertension
-treatment of complications:variceal
bleeding,,,ascites…
-endoscopic procedures:sclerotherapy +band
ligation+prophylactic propranolol
32. Treatment of Acute Variceal Hemorrhage
General Management:
• Iv acess and fluid resuscitation
• Do not overtransfuse (hemoglobin ~ 8 g/dL)
• Antibiotic prophylaxis
Specific therapy:
• Pharmacological therapy: terlipressin,
somatostatin and analogues, vasopressin +
nitroglycerin
• Endoscopic therapy: ligation, sclerotherapy
• Shunt therapy: TIPS, surgical shunt
TREATMENTOFACUTEVARICEALHEMORRHAGE
33. Endoscopic Variceal Band
Ligation
Bleeding controlled in 90%
Rebleeding rate 30%
Compared with sclerotherapy:
• Less rebleeding
• Lower mortality
• Fewer complications
• Fewer treatment sessions
ENDOSCOPICVARICEALBANDLIGATION
35. Management of Uncomplicated
Ascites
Definition:
in
Ascites responsive to diuretics the
absence of infection and renal
dysfunction
Sodium restriction
• Effective in 10-20% of cases
• Predictors of response: mild or moderate ascites,
Urine Na excretion > 50 mEq/day
Diuretics
• Should be spironolactone-based
• A progressive schedule (spironolactone à
furosemide) requires fewer dose adjustments than a
combined therapy (spironolactone + furosemide)
MANAGEMENTOFUNCOMPLICATEDASCITES
36. Diuretic Therapy
Dosage
• Spironolactone 100-400 mg/day
• Furosemide (40-160 mg/d) for inadequate weight loss or if hyperkalemia
develops
Increase diuretics if weight loss <1 kg in the first week and < 2
kg/week thereafter
Decrease diuretics if weight loss >0.5 kg/day in patients without
edema and >1 kg/day in those with edema
Side effects
• Renal dysfunction, hyponatremia, hyperkalemia, encephalopathy, gynecomastia
Management of Uncomplicated Ascites
MANAGEMENTOFUNCOMPLICATEDASCITES:DIURETICTHERAPY
37. Early Diagnosis of SBP
Diagnostic paracentesis:
• If symptoms / signs of SBP occur
• Unexplained encephalopathy and / or renal
dysfunction
• At any hospital admission
Diagnosis based on ascitic fluid
PMN count >250/mm3
Rimola et al., J Hepatol 2000; 32:142
EARLYDIAGNOSISOFSPONTANEOUSBACTERIALPERITONITIS(SBP)
38. Treatment of Spontaneous Bacterial
Peritonitis
Recommended antibiotics for initial empiric therapy
• i.v. cefotaxime, amoxicillin-clavulanic acid
• oral nofloxacin (uncomplicated SBP)
• avoid aminoglycosides
Minimum duration: 5 days
Re-evaluation if ascitic fluid PMN count has not
decreased by at least 25% after 2 days of treatment
Rimola et al., J Hepatol 2000; 32:142
TREATMENTOFSPONTANEOUSBACTERIALPERITONITIS(SBP)
40. Type C Hepatic Encephalopathy is
the Encephalopathy of Cirrhosis
Neuropsychiatric complication of cirrhosis
Results from spontaneous or surgical / radiological
portal-systemic shunt + chronic liver failure
Failure to metabolize neurotoxic substances
Alterations of astrocyte morphology and function
(Alzheimer type II astrocytosis)
TYPECHEPATICENCEPHALOPATHYISTHEENCEPHALOPATHYOFCIRRHOSIS
43. Hepatic Encephalopathy Is A Clinical
Diagnosis
Clinical findings and history important
Ammonia levels are unreliable
Ammonia has poor correlation with diagnosis
Measurement of ammonia not necessary
Number connection test
Slow dominant rhythm on EEG
HEPATICENCEPHALOPATHYISACLINICALDIAGNOSIS