acute hepatitis

35
ACUTE HEPATITIS Dr Manoj K Ghoda M.D., M.R.C.P Consultant Gastroenterologist Visiting Faculty at GCS Hospital

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Page 1: Acute hepatitis

ACUTE HEPATITIS

Dr Manoj K Ghoda M.D., M.R.C.P

Consultant GastroenterologistVisiting Faculty at GCS Hospital

Page 2: Acute hepatitis

18 yrs F

3 days h/o FeverMalaise and body ache,NauseaVomitingRUQ pain

CBC: Normal

LFT: Bil: 4.5( 70% conjugated)ALT: 1500ALP: 125PT: 18/13 sec

USG: Diffuse hypoechoic liver parenchymaGB: Collapsed with mild perichocystic fluid

Page 3: Acute hepatitis

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

Page 4: Acute hepatitis

Pathogenesis:

Page 5: Acute hepatitis

Viral causes and acute hepatitis

Page 6: Acute hepatitis

HAV or HBV are not directly cytopathic, the damage is immune mediated

Antibodies

Disposed off

Page 7: Acute hepatitis

Hepatitis A or B viruses are not directly cytopathic; damage is due to antigen- antibody reaction

Page 8: Acute hepatitis

Drug induced liver injury is of two types

• Dose dependent; as in Paracetamol injury• Idiosyncratic; as in anti-tuberculous drugs induced injury

xN-Acetyl Cystein

Page 9: Acute hepatitis

Acetaldehyde is formed by various pathways from Ethanol. This is the reactive molecule responsible for hepatotoxicity

Page 10: Acute hepatitis

Symptoms of acute hepatitis

Page 11: Acute hepatitis

Symptoms may vary according to the etiology

Page 12: Acute hepatitis

•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•BruisingPresence or absence of above mentioned symptoms and their severity depends upon the liver parenchymal damage

Symptoms originating from Liver parenchymal damage

Page 13: Acute hepatitis
Page 14: Acute hepatitis

•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

Page 15: Acute hepatitis
Page 16: Acute hepatitis

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.

Page 17: Acute hepatitis

Physical findings:

•Jaundice•Fever•Scratch marks

• Altered sensorium• Edema• Ascites

•Liver enlarged and tender•Spleen +

Page 18: Acute hepatitis

Investigations:

Diagnostic:ALTS. Bilirubin,

Monitoring: Blood sugar, Prognostic:

PT, repeatedly and after vit K

ammoniaIf in doubt: USG upper abdomen

Etiological diagnosis:

Page 19: Acute hepatitis

Actually, I am a donkey!!

ALT has a diagnostic value only and has no prognostic value!

It is obvious the way you order tests!!

Page 20: Acute hepatitis

Differential diagnosis: Cholecystitis.Gastritis.Liver abscess.Hepatic amebiasis.

Page 21: Acute hepatitis

Differentiating Acute liver disease from chronic liver disease

Acute liver disease

Clinical contextNo edemaNo ascitesNo stigmata of CLDLiver and spleen are just enlargedLiver is soft and tenderUSG : Diffuse parenchymal hypoechogenecity, PV and SV are normal, no collateralsA/ G ratio normal or if albuin is decreased then Globulin still normal

Chronic Liver diseases

Clinical contextEdemaAscites may be presentStigmata of CLDLiver and spleen may be significantly enlarged and liver may be firm or with irregular surfaceUSG: Coarse echopattern of liver parenchyma, may be shrunken, portal vein and splenic vein may be dilatedA/G ratio is reversed

Page 22: Acute hepatitis

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.

Page 23: Acute hepatitis

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.

Page 24: Acute hepatitis

•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.

Page 25: Acute hepatitis

LFT: Bil:

4.5( 70% conjugated)

ALT: 1500ALP: 125PT: 18/13

sec

LFT: Bil:

2.0( 70% conjugated)

ALT: 75ALP: 125PT: 15/13

sec

LFT: Bil: 3.5( 70%

conjugated)ALT: 750ALP: 125PT: 14/13 sec

18 F with hepatitis Story

continues………HAV IgM : reactive

Day 0 Day 15 Day 40

Page 26: Acute hepatitis

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

Page 27: Acute hepatitis

LFT: Bil:

4.5( 70% conjugated)

ALT: 1500ALP: 125PT: 18/13

sec

LFT: Bil:

12.0( 70% conjugated)

ALT: 75ALP: 125PT: 15/13

sec

LFT: Bil: 23.5( 70%

conjugated)ALT: 40ALP: 125PT: 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.

Page 28: Acute hepatitis

LFT: Bil:

4.5( 70% conjugated)

ALT: 1500ALP: 125PT: 18/13

sec

LFT: Bil:

12.0( 70% conjugated)

ALT: 575ALP: 125PT: 59/13

sec

LFT: Bil: 13.5( 70%

conjugated)ALT: 750ALP: 125PT: 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%

Page 29: Acute hepatitis
Page 30: Acute hepatitis
Page 31: Acute hepatitis

LFT: Bil:

4.5( 70% conjugated)

ALT: 1500ALP: 125PT: 18/13

secAlb: 3.5

LFT: Bil:

12.0( 70% conjugated)

ALT: 575ALP: 125PT: 59/13

secAlb: 2.9

LFT: Bil: 13.5( 70%

conjugated)ALT: 750ALP: 125PT: 56/13 secAlb: 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

Page 32: Acute hepatitis

.

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.

Page 33: Acute hepatitis

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

Page 34: Acute hepatitis

•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.

Page 35: Acute hepatitis

Any questions?

Dr Manoj K Ghoda M.D., M.R.C.P. (England)

Consultant GastroenterologistVisiting faculty at GCS Hospital

This Lecture is available on facebook: Gujaratgastrogroup