1. ACUTE HEPATITIS
Dr Manoj K Ghoda M.D., M.R.C.P
Consultant Gastroenterologist
Visiting Faculty at GCS Hospital
2. 18 yrs F
3 days h/o
Fever
Malaise and body ache,
Nausea
Vomiting
RUQ pain
CBC: Normal
LFT:
Bil: 4.5( 70% conjugated)
ALT: 1500
ALP: 125
PT: 18/13 sec
USG: Diffuse hypoechoic liver parenchyma
GB: Collapsed with mild perichocystic fluid
3. Hepatitis: Diffuse inflammation of liver parenchyma from any cause.
Etiology:
•Viral: Type- A, B, C, E, Cytomegalo, Epstein- Barr virus, HSV.
•Alcoholic.
•Drug induced, e.g. Pyrizinamide, isoniazide, rifampicin, paracetamol and
many more.
•Autoimmune.
•Metabolic, e.g.,Wilson’s disease.
Hepatitis like picture is also seen in enteric fever, falciparum malaria,
leptospirosis and Dengue fever. This is important in tropical countries where
such diseases are more common than or as common as hepatitis
6. HAV or HBV are not directly cytopathic, the damage is immune
mediated
Antibodies
Disposed
off
7. Hepatitis A or B viruses are not directly cytopathic;
damage is due to antigen- antibody reaction
8. Drug induced liver injury is of two types
• Dose dependent; as in Paracetamol injury
• Idiosyncratic; as in anti-tuberculous drugs
induced injury
x
N-Acetyl Cystein
9. Acetaldehyde is formed by various pathways from
Ethanol. This is the reactive molecule responsible for
hepatotoxicity
12. •Anorexia, nausea and vomiting, are cardinal symptoms of
hepatitis.
• Sometimes there is abhorrence to the food and sight, smell, noise or even thought
of food could bring on nausea and vomiting.
•This is followed by jaundice and dark urine, within 1 to 2
weeks.
•In a large number of children, there may be an anicteric infection, with mild or no
symptoms at all, subsiding fairly quickly.
•Altered sensorium or hepatic coma
•Edema and ascites
•Bruising
Presence or absence of above mentioned symptoms and their severity depends
upon the liver parenchymal damage
Symptoms originating from Liver parenchymal
damage
13.
14. •Malaise,
•body ache,
•joint pain,
•fatigue,
•weakness.; and sometimes
•Fever;
are common prodromal symptoms.
•Fever has no particular pattern but could range from mild to
high grade fever.
•Occasional patient has diarrhea also.
These are mainly features of viremia
and therefore not seen in acute
hepatitis of non-viral origin
15.
16. Symptoms not originating from Liver parenchymal
damage (Secondary symptoms)
•Right upper quadrant pain.
•Itching may appear with onset of jaundice and sometimes mainly nocturnal
only. Itching could be quite severe and responsible for poor well being of a patient
who is otherwise quite well.
21. Differentiating Acute liver disease from chronic
liver disease
Acute liver disease
Clinical context
No edema
No ascites
No stigmata of CLD
Liver and spleen are just
enlarged
Liver is soft and tender
USG : Diffuse parenchymal
hypoechogenecity, PV and SV
are normal, no collaterals
A/ G ratio normal or if albuin is
decreased then Globulin still
normal
Chronic Liver diseases
Clinical context
Edema
Ascites may be present
Stigmata of CLD
Liver and spleen may be significantly
enlarged and liver may be firm or
with irregular surface
USG: Coarse echopattern of liver
parenchyma, may be shrunken,
portal vein and splenic vein may be
dilated
A/G ratio is reversed
22. Progression:
•In a majority, viral hepatitis runs a benign course, from a few
days to several weeks and then there is a recovery.
•About 10% of adult and 90% neonates go on to become
chronically infected with hep-B and about 80% of the adults
become chronically infected following hep-C infection.
23. Recovery is generally complete within 6 months or
early in a majority of the patients.
In a tiny minority of the patients symptoms progress
relentlessly and the patient becomes comatose or
develops ascites and edema, the subacute liver
failure.
24. •Absence of fever,
• Return of appetite and
•Disappearance of malaise are good clinical markers of recovery
from acute hepatitis.
Acute viral hepatitis is generally of a shorter duration in children
but could be prolonged in adolescent and elderly, as much as 3
months, and abnormal transaminases may persist up to 6
months.
25. LFT:
Bil: 4.5( 70%
conjugated)
ALT: 1500
ALP: 125
PT: 18/13 sec
LFT:
Bil: 2.0( 70%
conjugated)
ALT: 75
ALP: 125
PT: 15/13 sec
LFT:
Bil: 3.5( 70%
conjugated)
ALT: 750
ALP: 125
PT: 14/13 sec
18 F with hepatitis
Story continues………
HAV IgM : reactive
Day 0 Day 15 Day 40
26. Biochemical or symptomatic relapse is seen
in up to 15% of patients of acute hepatitis A,
between 30-70- days but it has no adverse
effect on recovery
27. LFT:
Bil: 4.5( 70%
conjugated)
ALT: 1500
ALP: 125
PT: 18/13 sec
LFT:
Bil: 12.0( 70%
conjugated)
ALT: 75
ALP: 125
PT: 15/13 sec
LFT:
Bil: 23.5( 70%
conjugated)
ALT: 40
ALP: 125
PT: 14/13 sec
18 F with hepatitis
Similar patient……
HAV IgM : reactive
Day 0 Day 15 Day 40
Cholestatic hepatitis usually seen in type-A and E.There is severe itching and deep
jaundice. It responds to corticosteroids, sometimes dramatically. Rifampicin,
Cholestyramine and ursodeoxycholic acid are useful.These drugs are given if itching is
intolerable, otherwise supportive measures like taking cold bath, applying calamine lotion
or taking anti-histaminic could suffice.
28. LFT:
Bil: 4.5( 70%
conjugated)
ALT: 1500
ALP: 125
PT: 18/13 sec
LFT:
Bil: 12.0( 70%
conjugated)
ALT: 575
ALP: 125
PT: 59/13 sec
LFT:
Bil: 13.5( 70%
conjugated)
ALT: 750
ALP: 125
PT: 94/13 sec
38 F with hepatitis
Story continues………
HEV IgM : reactive
Day 0 Day 5 Day 6
Drowsy but
rousable
Gr IV coma
Acute fulminant hepatitis is uncommon with viral hepatitis with incidence of around 0.1%.
However in Pregnancy, HEV could lead to acute liver failure with mortality up to 20%
29.
30.
31. LFT:
Bil: 4.5( 70%
conjugated)
ALT: 1500
ALP: 125
PT: 18/13 sec
Alb: 3.5
LFT:
Bil: 12.0( 70%
conjugated)
ALT: 575
ALP: 125
PT: 59/13 sec
Alb: 2.9
LFT:
Bil: 13.5( 70%
conjugated)
ALT: 750
ALP: 125
PT: 56/13 sec
Alb: 2.0
58 m with hepatitis
Story continues………
HEV IgM : reactive
Day 0 Day 15 Day 36
Mild edema
feet
Gross ascites
An occasional patient with Hep-B and Hep-E may go on to develop sub-acute liver failure
with ascites, edema and occasionally hepatic coma.This usually happens in patients above
55 years of age
32. .
Chronic hepatitis: 80% of type C and 10% of type B go on to
develop chronic hepatitis.
Bone marrow depression.
Hepato-renal syndrome: Here there is associated kidney failure.
Prognosis is grave.
Cecal ulceration.
33. Management:
•Mainly supportive.
•Most of the patients are not acutely ill and reassurance, together with
palatable diet, is all that is required. Vitamins or glucose is not necessary and
may increase nausea and vomiting.
•Persistent vomiting, fever, drowsiness and prolonged prothrombin time
requires admission.
•Maintenance of nutrition and fluid and electrolyte balance.
•For nausea metochlopromide /domperidone in half dose.
•Fever to be tackled by cold sponging or low dose paracetamol.
•Glucose infusion if hypoglycemia occurs. Avoid large amount of glucose
orally
34. •Mannitol if cerebral edema is suspected.This is the most frequent cause of death in
hepatic encephalopathy. If cardiac status permits, Pentothal sodium could also be
given. Hyperventilation may also help by washing off CO2, decreasing vasodilatation
leading to decreased intracranial pressure.
•Antibiotics and anti-fungal may be required, if the patient develop gram negative
septicemia or fungemia.
•Lactulose to remove toxic products from bowel and decrease production of
ammonia.The dose is 30 ml. every two hourly till diarrhea establishes and then the
dose could be reduced to produce 2-3 loose motions per day. If patient is not taking
orally, then lactulose retention enema could be given as well.
•L-ornithine-L aspartate orally or as intravenous infusion is useful in patients with
very high ammonia level. Sodium benzoate, 5 gm. twice a day is equally effective and
cheaper alternative.
•Fresh frozen plasma for very high PT or with actual bleeding.
•Liver transplant may be the last recourse if everything fails.
35. Any questions?
Dr Manoj K Ghoda M.D., M.R.C.P. (England)
Consultant Gastroenterologist
Visiting faculty at GCS Hospital
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