Approach to liver disease

1. CLINICAL APPROACH TO
PATIENT WITH LIVER DISEASE

2. LIVER DISEASES
 Cholestasis: bile duct damage from stones or
tumour, primary biliary cirrhosis
 Infection: hepatitis A, B, C, EBV, CMV
 Chemical damage: drugs and alcohol
 Hereditary: Wilsons disease, haemochromatosis
 Vascular damage: Budd-Chiari
 Autoimmunity: autoimmune hepatitis, primary
sclerosing cholangitis
 Congenital anomalies: biliary atresia,
Caroli'sdisease
 Metabolic disease: galactosemia, fatty liver
disease

3. EVALUATION
 Establishing the etiologic diagnosis: hepatocellular,
cholestatic or mixed
 Estimating the disease severity (grading): active or
inactive, mild to severe
 Establishing the disease stage: acute or chronic,
pre-cirrhotic, cirrhotic, or end stage

4. CLINICAL EXAMINATION OF THE ABDOMEN FOR
LIVER AND BILIARY DISEASE

5. CLINICAL SYMPTOMATOLOGY
 Jaundice
 Fatigue
 Weakness
 Pruritus
 RUQ pain
 Anorexia
 Dark urine
 Light stools
 Asymptomatic

6. PORTAL HYPERTENSION
 Ascites
 Prominent superficial veins
 Edema
 Weight loss

7. CLINICAL HISTORY
 Prodromal symptoms
 Use of parenteral illicit drugs
 Maternal history of hepatitis
 Exposure to jaundiced patients
 Use of medications (including herbal meds)
 Sexual history (multiple partners, same sex)
 Blood transfusion
 Family history: Wilson’s disease, hemochromatosis
 Alcohol abuse

8. HEPATIC FAILURE
(ENCEPHALOPATHY)
ALTERED SLEEPING PATTERNS
MENTAL DULLNESS
ALTERED SENSORIUM – DISORIENTATION,
CONFUSION,
STUPOR, COMA
FETOR HEPATICUS
 ASTEREXIS

9. INVESTIGATION OF LIVER AND
HEPATOBILIARY DISEASE
Investigations play an important role in the
management of liver disease in three settings:
 identifying the presence of liver disease
 establishing the aetiology
 understanding disease severity (in particular,
identification of cirrhosis with its complications).

10. LIVER BLOOD BIOCHEMISTRY
 Bilirubin and albuminThe degree of elevation of
bilirubin can reflect the degree of liver damage.Serum
albumin levels are often low in patients with liver
disease.
 Alanine aminotransferase(ALT) and aspartate
aminotransferase(AST) Large increases of
aminotransferase activity favour hepatocellular damage
 Alkaline phosphatase and γ-glutamyl transferase
large increases in ALP and GGT activity favours biliary
obstruction and is commonly described as cholestatic or
obstructive
 Hepatitis serology
 Autoimmune markers

11. OTHER BIOCHEMICAL TESTS
 Hyponatraemia occurs in severe liver disease due to
increased production of vasopressin
 Serum urea may be reduced in hepatic failure, whereas
levels of urea may be increased following gastrointestinal
haemorrhage.
 When high levels of urea are accompanied by raised
bilirubin, high serum creatinine and low urinary sodium,
this suggests hepatorenal failure, which carries a grave
prognosis.
 Significantly elevated ferritin suggests
haemochromatosis.Modest elevations can be seen in
inflammatory disease,NAFLD and alcohol excess.

12. DISEASE DIAGNOSTIC TEST
Hepatitis A Anti HAV IgM
Hepatitis B
Acute
Chronic
HBsAg and anti-HBc IgM
HBsAg and HBeAg and/or HBV
DNA
Hepatitis C Anti-HCV and HCV RNA
Hepatitis D HBsAg and anti-HDV
Hepatitis E Anti-HEV
Autoimmune hepatitis ANA or SMA, elevated IgG levels,
and compatible histology

13. DISEASE DIAGNOSTIC TEST
Alcoholic liver disease History of excessive alcohol intake
and compatible histology
Nonalcoholic steatohepatitis Ultrasound or CT evidence of fatty
liver and compatible histology
Wilson disease Decreased serum ceruloplasmin and
increased urinary copper; increased
hepatic copper
level
Hepatocellular cancer Elevated-fetoprotein level >500;
ultrasound or CT image of mass

14. DIAGNOSTIC IMAGING
 Ultrasonography
 CT Scan
 MRI/MRCP
 ERCP
 Hepatic Elastography

15. LIVER BIOPSY
 Gold standard
 Etiology, Grading, Staging of the disease
 Monitoring response to therapy
 Core biopsy, 1.5 to 2.0 cm specimen length
 Replaced by fibrosis markers, elastography

16. MANAGEMENT

17. MANAGEMENT OF ASCITES
 Low-sodium diet
 Diuretics Such as aldactone (aldosterone blocking
agent) first line therapy. Lasix may be added
 Bed rest
 Paracentesis
 Administration of salt-poor albumin
 Transjugular intrahepatic portosystemic shunt
(TIPS)

18. MANAGEMENT OF HEPATIC
ENCEPHALOPATHY
 Eliminate precipitating cause
 Lactulose to reduce serum ammonia levels
 IV glucose to minimize protein catabolism
 Protein restriction
 Reduction of ammonia from GI tract by gastric
suction, enemas, oral antibiotics
 Discontinue sedatives analgesics and tranquilizers
Monitor for and promptly treat complications and
infections

19. MANAGEMENT OF HEPATITIS
 Prevention- Good hand washing, safe water, and
proper sewage disposal (feco oral transmission
Hepatitis A)
 Screening of blood,Prevention of needle sticks for
health care workers (Blood transmission Hepatitis
B,C)
 Vaccine
 Immunoglobulin for contacts to provide passive
immunity
 Bed rest during acute stage
 Nutritional support

20. MANAGEMENT OF CIRRHOSIS
 Based on presenting symptoms
 Monitor for complications
 Maximize liver function
 Antiacids to decrease gastric distress and minimize
the possibility of gastric bleeding
 Adequate rest, Vitamins and nutritional support to
promote healing of damaged liver cell
 Potassium sparing diuretics
 Avoidance of alcohol- adequate calories and
protein
 Colchicine

21. NONSURGICAL MANAGEMENT OF
LIVERCANCER
 Underlying cirrhosis, which is prevalent in patients
with liver cancer, increases risks of surgery
 Major effect of nonsurgical therapy may be
palliative
 Radiation therapy
 Chemotherapy
 Percutaneous biliary drainage
 Other nonsurgical treatments

22. SURGICAL MANAGEMENT OF LIVER CANCER
 • Treatment of choice for HCC if confined to one
lobe and liver function is adequate
 Liver has regenerative capacity
 Types of surgery
 Lobectomy
 Cyrosurgery
 Liver transplant

23. THANK YOU…