acute hepatitis.pdf

Pediatrics acute hepatitis

1. Dr. VirendraKumar Gupta
MD Pediatrics
Fellowship In pediatric Gastroentero-Hepatology& Liver Transplantation
Assistant Professor
Department Of pediatrics
NIMS Medical College & Hospital , Jaipur

2. Hepatitis

3. Hepatitis
•Definition:
Acute hepatitis is defined as less than 6
months of liver inflammation, and chronic
hepatitis indicates an inflammatory process
which has been present for 6 or more months.

4. Causes
1-Viral: HAV, HBV, HCV, HDV, HEV, EBV,
CMV, HIV, Yellow fever
2-Non viral: Toxoplasmosis, Q fever &
Leptospiraiclerohaemorrhagua
3-Alcohol
4-Drugs & poisons: Paracetamol, Halothane,
A.T.T, CCLY, Aspirin (Reyes)
5-Metabolic: Wilson's, alpha-one anti-trypsin
deficiency
6-Ischemic: shock, Budd-chiari

6. Pathology
1-Depends on the cause
2-In viral & drug hepatitis :
-Pathology throughout the liver, specially
centrilobular. Lobules affected variably
-Damaged hepatocyte are swollen & granular,
while dead ones are shrunken & deeply
stained acidophilic
-Mononuclear cell infiltration
-Polymorph infiltration & fatty change in
some cases of tetracycline & CCL4 poisoning

7. -Severe damage collapse of reticulinframe
work ,particularly between central veins &
portal tract linking them together (briding).
Very severe damage massive necrosis & FHF
-Cholestasis+_

8. •EPIDEMIOLOGY:
•70% to 80% of all new cases of viral hepatitis are
related to HAV,
•5% to 30% are related to HBV,
•and 5% to 15% are related to HCV.
•The major risk factors for HBV and HCV are injection
drug use, frequent exposure to blood products
(hemophilia, organ transplants, chronic renal failure),
and maternal infection.
•HBV and HCV cause chronic infection, which may lead
to cirrhosis and is a significant risk factor for
hepatocellularcarcinoma and represents a persistent
risk of transmission.
Hepatitis

9. •CLINICAL MANIFESTATIONS :
•There is considerable overlap in the characteristic clinical courses
for HAV, HBV, and HCV .
•The preictericphase, which lasts approximately 1 week, is
characterized by headache, anorexia, malaise, abdominal
discomfort, nausea, and vomiting and usually precedes the onset of
clinically detectable disease.
•Jaundice and tender hepatomegalyare the most common physical
findings and are characteristic of the ictericphase. Prodromal
symptoms, particularly in children, may abate during the icteric
phase.
•Asymptomatic or mild, nonspecific illness without icterusis
common with HAV, HBV, and HCV, especially in young children.
•Hepatiticenzymes may increase 15-fold to 20-fold.
•Resolution of the hyperbilirubinemiaand normalization of the
transaminasesmay take 6 to 8 weeks.

10. Clinical picture of viral hepatitis
1-Prodromalsymptoms preceedclinical
Jaundice by 1-2 W
2-Hepatomegalywhich is tender
3-Rarely spleenomegaly& lymphoadenopathy
in children
4-Arthralgia, vasculitis, rash, myocarditisand
G.N specially with HBV
5-Yellow sclerae& dark urine.
6-Pale stool with cholastasis

11. 7-Most (95%) recover in 3-6 W
8-Few relapse
9-An icterichepatitis occur in 65%
10-Massive hepatic necrosis occur in 1%
causing F.H.F

12. 1-High ALT & AST(> 400U/L)
2-High Serum bilirubin
3-ALP rarely > 250U/L except in cholastasis
4-Normal serum alb
5-Prolong PT
6-Bilirubinuria.
7-Normal or low TWC with lymphsytosis
8-Viral markers
9-Mild proteinuria
LABORATORY AND IMAGING STUDIES

13. •Hepatitis A : The diagnosis of viral hepatitis is confirmed by
characteristic serologic testing .
•The presence of IgM-specific antibody to HAV with low or
absent IgGantibody to HAV is presumptive evidence of
HAV.
•There is no chronic carrier state of HAV.
•Hepatitis C :
•Seroconversionafter HCV infection may occur 6 months
after infection.
•A positive result of HCV ELISA should be confirmed with the
more specific recombinant immunoblotassay, which
detects antibodies to multiple HCV antigens.
•Detection of HCV RNA by PCR is a sensitive marker for
active infection, and results of this test may be positive 3
days after inoculation.

14. •Hepatitis B:
•The presence of HB
sAgsignifies acute or chronic infection with HBV.
•Antigenemiaappears early in the illness and is usually transient, but
also is diagnostic of the carrier state.
•Hepatitis B e antigen (HBeAg) appears in the serum with acute HBV.
•The continued presence of HB
sAgand HB
eAgin the absence of
antibody to e antigen (anti-HBe) indicates high risk of
transmissibility that is associated with ongoing viral replication.
•Clearance of HB
sAgfrom the serum precedes a variable window
periodfollowed by the emergence of the antibody to surface
antigen (anti-HBs), which indicates development of lifelong
immunity.
•Antibody to core antigen (anti-HBc) a useful marker for recognizing
HBV infection during the window phase (when HB
sAghas
disappeared, but before the appearance of anti-HB
s).
•Anti-HB
eis useful in predicting a low degree of infectivity during the
carrier state.

15. Typical course of hepatitis B infection. After exposure to hepatitis B virus (HBV; arrow), the
earliest detectable serum marker is a rise in HBsAg, which may appear at any time (weeks 1 to
10) postexposure; HBV DNA and HBAgfollow closely. HBeAgis detectable 2 to 8 weeks before the
onset of the symptomatic phase, which is heralded by an increase in alanineaminotransferase
(ALT) levels, serum bilirubinconcentrations, and constitutional signs. Clearance of HBsAgby
immune aggregation with anti–hepatitis B core antigen (HBc) occurs by 6 to 8 months
postinfection; those who fail to clear are termed HBsAgcarriers. Anti-HBc, which appears just
before the symptomatic phase, is the first detectable, host-induced immunologic marker of
hepatitis B infection. Anti-HBcof the IgMclass may be the only marker of HBV infection in serum
after clearance of HBsAgand before a rise in anti-HBs. Anti-HBcis not a neutralizing antibody and
therefore, in contrast to anti-HB, is not protective.

16. TREATMENT
•The treatment of acute hepatitis is largely supportive
and involves rest, hydration, and adequate dietary
intake.
•Hospitalization is indicated for persons with severe
vomiting and dehydration, a prolonged prothrombin
time, or signs of hepatic encephalopathy.
•When the diagnosis of viral hepatitis is established,
attention should be directed toward preventing its
spread to close contacts.
•For HAV, hygienic measures include hand washing and
careful disposal of excreta, contaminated diapers or
clothing, needles, and other blood-contaminated
items.

17. •Chronic HBV infection may be treated with
interferon alfa-2b or lamivudine,
•and HCV may be treated with interferon alfa
alone or more often in combination with oral
ribavirin.
TREATMENT

18. 1-F.H.F
2-Relapsing hepatitis (biochem. OR clinical)
3-Cholestasis
4-Post-hepatic syndrome
5-Unconjugated hyperbilirubinaemia(Gilbert)
6-A plastic anaemia(HAV, HCV, HEV)
7-Connective tissue disease
8-G.N & renal failure
9-H.Sch. purpura
10-Papularacrodermatitis
11-Chronic hepatitis, liver cirrhosis and HCC
wzHBV &HCV.
COMPLICATIONS

19. PROGNOSIS
•Most cases of acute viral hepatitis resolve without specific therapy,
with less than 0.1% of cases progressing to fulminanthepatic
necrosis.
•HBV, HCV, and HDV may persist as chronic infection with chronic
inflammation, fibrosis, and cirrhosis and the associated risk of
hepatocellularcarcinoma.
•Five percent to 10% of adults with HBV develop persistent infection,
defined by persistence of HB
sAgin the blood for more than 6
months compared with 90% of children who acquire HBV by
perinataltransmission.
•Approximately 85% of persons infected with HCV remain chronically
infected, which is characterized by fluctuating transaminaselevels.
•Approximately 20% of persons with chronic infection develop
cirrhosis, and approximately 25% of those develop hepatocellular
carcinoma.

20. Prevention of hepatitis B
•HepatitisBvaccineandhepatitisB
immunoglobulin(HBIG)areavailablefor
preventionofHBVinfection.
•HepatitisBImmunoglobulin
•HBIGisindicatedonlyforspecificpostexposure
circumstancesandprovidesonlytemporary
protection(3-6mo).Itplaysapivotalrolein
preventingperinataltransmissionwhen
administeredwithin12hofbirth.

21. •Twosingleantigenvaccines(RecombivaxHBand
Engerix-B)areapprovedforchildrenandaretheonly
preparationsapprovedforinfants<6moold.
•Threecombinationvaccinescanbeusedfor
subsequentimmunizationdosingandenable
integrationoftheHBVvaccineintotheregular
immunizationschedule.
•Seropositivityis>95%withallvaccines,achievedafter
the2nddoseinmostpatients.The3rddoseservesasa
boosterandmayhaveaneffectonmaintaininglong-
termimmunity.
•Inimmunosuppressedpatientsandinfants<2,000g
birthweight,a4thdoseisrecommended,asischecking
forseroconversion.

22. HbsAg-positive mothers?
•Topreventperinataltransmissionthroughimprovedmaternalscreening
andimmunoprophylaxisofinfantsborntoHbsAg-positivemothers,infants
borntoHBsAg-positivewomenshouldreceivevaccineatbirth,1-2mo,
and6moofage.
•Thefirstdoseshouldbeaccompaniedbyadministrationof0.5mLofHBIG
assoonafterdeliveryaspossible(within12hr)becausetheeffectiveness
decreasesrapidlywithincreasedtimeafterbirth.
•Post-vaccinationtestingforHBsAgandanti-HBsshouldbedoneat9-
18mo.
•Iftheresultispositiveforanti-HBs,thechildisimmunetoHBV.
•IftheresultispositiveforHBsAgonly,theparentshouldbecounseledand
thechildevaluatedbyapediatricgastroenterologist.
•IftheresultisnegativeforbothHBsAgandanti-HBs,a2ndcomplete
hepatitisBvaccineseriesshouldbeadministered,followedbytestingfor
anti-HBstodetermineifsubsequentdosesareneeded.

23. Acute (Fulminat) hepatic failure
1-RareconditioninwhichBiochemicalevidenceof
acuteliverinjury(usually<8weekduration);no
evidenceofchronicliverdisease;andhepatic
basedcoaguolopathydefinedasaPT>15secor
INR>1.5notcorrectedbyvitaminKinthe
presenceofclinicalhepaticencephalopathy,ora
PT>20secorINR>2regardlessofthepresence
ofclinicalhepaticencephalopathy.
2-Ifitoccur8-12W=subacuteFHF
3-Rarebut90%mortalityfollowingacutehepatitis
fromanycause

24. 4-Causes include
-viral infection (HAV , HBV , HDV)
-drugs (pracetamol , aspirin , halothane ,
ATT)
-poisons (mushroom , CCL4)
-acute fatty liver of pregnancy
-shock & cardiac failure
-bud-chiari syndrome
-leptospirosis
-Wilson's disease

25. 5-Pathologically
-There is extensive liver cell necrosis with
severe fatty degeneration being characteristic
of tetracycline , pregnancy & Reyes
-There is cerebral aedema & disruption of
BBB
6-Clinically
Low alertness , poor conc. , restlessness ,
aggression, drowsiness , disorientation ,
change of sleep rhythm & coma

26. -Slurred speech , yawning , hiccough and
seizures.
-Asterixis (Flapping tremers) & foeter
hepaticus are other features
-Myoclonus , spalicity , decorticate rigidity
may be seen
-Papilla edema is very late (high I.C.P)
-Fever , vomiting , hypotension and
hypoglythemia may occur
-Jaundice & small liver size
-Fluid retention & spleenomegaly are
uncommon

27. 7-Investigation
Markedly deranged LFT , ECG ,CBC , BUN &
electrolytes , U/S ,viral markers , toxicity ,
screening , Auto-antibodies , CXR , se cu &
caeruloplasmin
8-Management
1-No specific treatment except liver transplant
2-Support life & monitor
3-Ranitol , vitK , H2RA ,antibiotics
4-Treatment of cardio-respiratory arrest & fail.
5-Exchange transfusion , plasmapheres &
charcoal haemoperfusion

28. Thank you 