The document outlines the management of hepatitis, cirrhosis, and portal hypertension, detailing various types of hepatitis (alcoholic, viral, drug-induced, autoimmune), their causes, symptoms, investigations, and treatments. It emphasizes the serious nature of cirrhosis, its complications, and the importance of liver function tests, while also discussing portal hypertension and its management strategies such as beta-blockers and endoscopic therapy. Additionally, it covers liver transplantation when necessary and the importance of monitoring for liver-related complications.

1. MANAGEMENT OF HEPATITIS,
CIRRHOSIS AND PORTAL
HYPERTENSION
-RAICHEL BABU

2. HEPATITIS
• hepatitis is a broad term that means inflammation of liver.
• it is most commonly caused by viruses but also be caused by drugs
(alcohol), chemicals, autoimmune diseases and metabolic
abnormalities.

3. TYPES OF HEPATITIS
• Alcoholic Hepatitis
• Viral Hepatitis
• Drug Induced Hepatitis
• Autoimmune Hepatitis

4. ALCOHOLIC HEPATITIS
• alcohol is a major risk factor for fatty liver disease which manifests as
hepatitis.
• c/f : may be asymptomatic or present with fever
rapid onset of jaundice,
abdominal discomfort, muscle wasting
portal HTN,ascites , without cirrhosis
hepatomegaly and splenomegaly

5. INVESTIGATION :
• Biochemical findings :AST, ALT raised
raised bilirubin,decreased albumin
• Hematological findings: prolonged prothrombin time, leukocytosis
• Liver biopsy
TREATMENT:
• Stop consumption of alcohol
• Severe hepatitis – bed rest
• Nutrition –fine bore nasogastric tube

6. • Treatment for encephalopathy and ascites
• Corticosteroids – prednisolone
• Antimicrobial therapies for bacterial and fungal infection
• N-acetylcysteine – antioxidants – reduce inflammation
• Liver transplantation

7. VIRAL HEPATITIS
• Causative agents : Hepatitis A virus
Hepatitis B virus
Hepatitis C virus
Hepatitis D virus
Hepatitis E virus

9. HEPATITIS B VIRUS
• Most common cause of chronic liver disease and hepatocellular
carcinoma
• Source of infection: human suffering from hepatitis or carriers
• Mode of transmission :
 vertical transmission
Horizontal transmission

10. INVESTIGATION :
• viral markers : surface antigen , e- antigen, viral load (PCR)
• Liver markers : elevated levels of AST ,ALT and rarely ALP
• Specific antibody in blood against viral antigen , an IGM antibody
indicates acute infection while IG-G antibody indicates development
of secondary immune response

11. MANAGEMENT OF ACUTE HEPATITIS B
• Full spontaneous recovery occurs in more than 95./. Adults with
acute HBV infection
• If fulminant liver failure present –life threatening and requires liver
transplantation
• Treatment is supportive with monitoring of acute liver failure
• Antiviral therapy –severe liver injury with coagulopathy
• Recovery occurs within 6 months with appearance of antibody to
viral antigen
• Persistence of HBeAg andHBsAg indicates chronic infection

12. MANAGEMENT OF CHRONIC HEPATITIS B
• Goals of treatment :HBeAg seroconversion, reduction in HBV-DNA,
normalisation of LFTs
• DIRECT ACTING NUCLEOSIDE /NUCLEOTIDE ANTIVIRAL AGENTS:
lamivudine, entecavir, tenofovir
• PEGYLATED INTERFERON –ALFA – acts by augmenting host immune
response
• Liver transplantation

13. PREVENTION AND PROPHYLAXIS
• AVOIDING RISK FACTORS
• ACTIVE IMMUNIZATION: Recombinant vaccines (containing HBsAg)
dosage regimen – given into deltoid muscle at 0,1,6 months
for high risk groups and children
• Combined prophylaxis : vaccination and immunoglobulin

14. DRUG INDUCED HEPATITIS
• Drug and toxin induced hepatotoxicity- any degree of
liver injury by drugs and toxins
• Examples: acetaminophen, alcohol, carbon tetrachloride,
chloroform,
heavy metals, phosphorus
TREATMENT:
• Withdrawal of offending drug
• N-acetylcysteine – in paracetamol toxicity
• Supportive therapy for specific type of liver injury

15. AUTOIMMUNE HEPATITIS
• Chronic and progressive hepatitis
• Associated with circulating autoantibodies and
hypergammaglobulinemia
INVESTIGATIONS :
o biochemical findings : raised serum transferases, ALP, bilirubin
serum gamma globulin, low serum albumin
oProthrombin time, autoantibodies, liver biopsy

16. TREATMENT:
• Prednisolone 30 mg given orally (2 wks) maintenance
dose 10-15mg for 2yrs after LFT becomes normal
• Azathioprine – dose 1-2mg/kg daily
• Immunosuppressive agents: cyclosporin ,tacrolimus
• Duration of tx : lifelong
• Liver transplantation if treatment fails

17. CIRRHOSIS
• End stage of any chronic liver disease
• Diffuse process characterised by fibrosis and conversion of normal
architecture to structurally abnormal regenerating nodules of liver
cells
• 3 main characteristics: fibrosis
regenerating nodules
loss of architecture of entire liver

18. PATHOGENESIS
• Chronic liver injury results in inflammation & widespread necrosis of
liver cells and eventually fibrosis ( due toactivation of stellate cells
by many cytokines)
• Extensive fibrosis results in loss of liver architecture.
• Regenerating nodules produced due to hyperplasia of remaining
surviving liver cells. Destruction and distortion of hepatic vasculature
by fibrosis leads to obstruction of blood flow
• Ascites and hepatic encephalopathy (hepatocellular insufficiency)

20. CAUSES OF CIRRHOSIS
• Alcohol
• Chronic viral hepatitis (B or C)
• Non alcoholic fatty liver
disease
• Immune : primary sclerosing
cholangitis
autoimmune liver
disease
• Biliary : primary biliary
cholangitis
• Genetic :haemochromatosis
wilson’s disease
alpha 1 antitrypsin deficiency
• Cryptogenic
• Chronic venous outflow obstruction
• Any chronic liver disease

21. SYMPTOMS
• Some are asymptomatic (diagnosed at ultrasound)
• Weakness, fatigue, muscle cramps ,weight loss, anorexia, upper
abdominal discomfort
• Also present as shortness of breath due to large right pleural
effusion

22. CLINICAL FEATURES OF CIRRHOSIS
• Hepatomegaly (although may be small )
• Jaundice
• Ascites
• Circulatory changes :spider telangectasia, palmar erythema,
cynosis
• Endocrine changes :loss of libido, hair loss
men – gynaecomastia, testicular atrophy
women – breast atrophy, amenorrhoea
• Hemorrhagic tendency : bruises , purpura, epistaxis
• Portal hypertension: splenomegaly, collateral vessels ,variceal
bleeding

23. COMPLICATIONS
• Portal hypertension
• Hepatic encephalopathy
• Ascites
• Renal failure

24. MANAGEMENT
INVESTIGATIONS:
• LIVER FUNCTION TESTS :
o hyperbilirubinemia
oSerum proteins: reversal of A:G ratio (hypoalbuminemia due to
reduced synthesis by liver)(hyperglobulinemia- stimulation of
reticuloendothelial system)
oSerum transaminases- AST,ALT raised, ALP slightly elevated
oProthrombin time prolonged

25. • Hematological tests- peripheral blood picture,serological markers
• Other biochemical markers- serum electrolytes blood ammonia
• Imaging – usg ,CT scan, MRI , endoscopy
• Liver biopsy- uses- to confirm diagnosis, assess severity and type

26. TREATMENT
• No treatment available to arrest or reverse the cirrhotic changes in
liver
• Liver transplantation is the specific treatment
• Progression can be halted by:
treatment of underlying cause, removal of causative agents –
drugs and alcohol, nutrition , treatment of complications

27. • . Diet : daily calorie intake – 35kcal/kg
daily protein intake -1.2-1.5g/kg
• Avoid hepatotoxic drugs
• Follow up- 6 monthly ultrasound and serum alpha
fetoprotein for detection of HCC

28. PROGNOSIS
• COMPENSATED CIRRHOSIS- good prognosis with median
survival >12 yrs
• DECOMPENSATED cirrhosis – median survival around 2 yrs
• Poor prognostic factors :
raised bilirubin, low albumin, prolonged PT, renal dysfunction,
hyponatremia

29. PORTAL HYPERTENSION
• Increased portal pressure or sinusoidal pressure
• Normal hepatic venous pressure gradient is 5-6mmhg
• Portal HTN is present when >10mmhg
• Risk of variceal bleeding increase beyond gradient of 12 mmhg

31. PATHOLOGY
CAUSE : lobules of liver being replaced by nodules
separated by fibrous septations which compress sinusoids
(increased resistance)
portal pressure = flow X resistance
Increased resistance reduction in blood flow to liver
simultaneously development of
collateral
vessels
portal blood bypass liver and enter

32. CLINICAL FEATURES
• Splenomegaly is a cardinal finding . Spleen is rarely
enlarged more than 5 cm below the left costal margin in
adults but more marked splenomegaly can occur in
childhood and adolescence.
• Thrombocytopenia
• collateral vessels may be visible on the anterior
abdominal wall and occasionally several radiate from the
umbilicus to form a ‘caput medusae’ -
cruveilhier Baumgarten syndrome -venous hum from

33. • Ascites – partly due to portal HTN and mainly due to liver cell failure
(sodium retention)
• Variceal bleeding –from osephagial varices

34. COMPLICATIONS OF PORTAL HTN
• Variceal bleeding:
oesophageal,
gastric,other
• Congestive gastropathy
• Hypersplenism
• Ascites
• Iron deficiency anaemia
• Renal failure

35. INVESTIGATIONS
• diagnosis is often done clinically
• Portal venous pressure measurement –balloon catheter via
transjugular route
• Thrombocytopenia
• endoscopy is the most useful investigation to determine whether
gastro-oesophageal varices are present

36. • ultrasonography - splenomegaly and collateral vessels, and can
sometimes indicate the cause, such as liver disease or portal vein
thrombosis.
• ct and magnetic resonance angiography can identify the extent of
portal vein clot and are used to identify hepatic vein patency

37. MANAGEMENT
focused on the prevention and/or control of variceal haemorrhage.
• NON-BLEEDING VARICES : non selective β-adrenoceptor
antagonist (β-blocker) therapy : propranolol (80–160 mg/day) or
nadolol (40–240 mg/day)
reduce the heart rate by 25% has been shown to be effective in the
primary prevention of variceal bleeding.

38. • carvedilol: a non-cardioselective vasodilating β-blocker (6.25–12.5
mg/day).

39. FOR ACUTE VARICEAL BLEEDING
• Antibiotics – iv cephalosporin or piperacillin/ tazobactum
• Vasoactive medications- terlipressin-
• Endoscopic therapy( banding)
• Balloon tamponade
• Transjugular intrahepatic portosystemic stent shunt

40. • TERLIPRESSIN - synthetic vasopressin analogue
• given by intermittent injection rather than continuous infusion
• reduces portal blood flow &resistance ,hence decrease portal HTN
• is 2 mg iv 4 times daily until bleeding stops, and then 1 mg 4 times
daily for up to 72 hours
• caution - severe ischaemic heart disease or peripheral vascular
disease

41. VARICEAL LIGATION (‘BANDING’)
• stops variceal bleeding in 80% of patients and can be repeated if
bleeding recurs.
• band ligation involves the varices being sucked into a cap placed on the
end of the endoscope, allowing them to be occluded with a tight rubber
band.
• the occluded varix subsequently sloughs with variceal obliteration.
banding is repeated every 2–4 weeks until all varices are obliterated.

42. BALLOON TAMPONADE
• this technique employs a Minnesota tube which consists of 2
balloons – positioned in the fundus of the stomach and in the lower
oesophagus, respectively.
• additional lumens allow contents to be aspirated from the stomach
and from the oesophagus
• life-threatening haemorrhage

43. TIPSS :
• this technique uses a stent placed between the portal vein and the
hepatic vein within the liver to provide a portosystemic shunt and
therefore reduce portal pressure.
• it is carried out under radiological control via the internal jugular
vein

44. SECONDARY PREVENTION OF VARICEAL BLEEDING
•
• beta-blockers prevent recurrent variceal bleeding
• following successful endoscopic therapy

45. THANK YOU