Hepatitis in Children 2014

8/10/2019 Hepatitis in Children 2014

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HEPATITIS IN CHILDREN

Dr Hamza Bawumia(BSc. Biochem, MBChB)

Supervisor:

Dr Paabie

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Liver is divided histologically into lobules. The center of the

lobule is the central vein. At the periphery of the lobule are portal

triads.

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Liver physiology

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Metabolic Function

Synthesis

BreakdownOther functions

storage of vitamin

A,D,B12,

Excretionof waste

products from

bloodstream into bile

Storage functions

Protein metabolism

Synthesis of amino acids

Carbohydrate metabolismGluconeogenesis

Glycogenesis

Lipid metabolismCholesterol synthesis

Lipogenesis

Production of coagulation

factors I, II, V, VII, IX, X and XI, andprotein C, protein S andantithrombin

Produces insulin-like growth factor 1

(IGF-1), a polypeptide protein

anabolic effects

Production of thrombopoetin

Liver is a multitask organ


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Liver physiology

Produces albumin, the major osmolarcomponent of blood serum

Synthesizes angiotensinogen,

responsible for raising blood pressurewhen activated by renin.

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Breaks down insulinand other hormones

Glycogenolysis

Breaks down or modifies toxic substances

Converts ammoniato urea Storageof iron, vitamins and trace

elements

Others- Hematopoietic organ when required Excretory organ: bile salts, degraded drugs

/toxins /antibiotics

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HEPATITIS = inflammation of liver

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HEPATITISsymptoms and

signsACUTE:

Malaise

Muscle and join

ache Fever

Nausea or vomiting

Loss of apetiteAbdominal pain

Dark urine

Enlarged TenderLiver

CHRONIC:

Malaise, tiredness,

weakness

Weight loss Peripheral oedema

Ascites

Jaundice*

Chronic Hepatitis is defined as

sustained inflammatory

disease of the liver lasting for

more than 6 months.8


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Viral Hepatitis

Viral hepatitis is a systemic disease

with primary inflammation of the liver

by any one of a heterogenous group of

hepatotropic viruses.

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Hepatotropic Viruses

PRIMARY Hepatitis A Virus (HAV)

Hepatitis B Virus (HBV)

Hepatitis C Virus (HCV)

Hepatitis D Virus (HDV) Requires HBV co-infection

Hepatitis E Virus (HEV)

Hepatitis F Virus(controversial)

Hepatitis G Virus(pathogen?)

Others

SYSTEMIC Cytomegalovirus (CMV)

Epstein-Barr Virus (EBV)

HIV

Adenovirus Parvovirus B19

Rubella

Coxsackievirus B

Enteroviruses

Human Herpes Viruses

Herpes Simplex Virus (HSV)

HHV-6

Varicella Zoster Virus (VZV)

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Acute Viral Hepatitis

Acute hepatocellular injury/inflammation Reflected by elevated transaminases (AST or

SGOT, ALT or SGPT)

Clinical manifestations often include fever,

malaise, jaundice, RUQ pain, nausea/vomiting

Typically self-limiting and of short duration

Contrast with: chronic, fulminant

Causative agents HAV (50% of cases in U.S.), HEV

CMV, EBV, VZV

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Fulminant Hepatitis

Acute, massive hepatocellular necrosis Impaired synthetic, excretory, and detoxifying

functions of the liver Cholestasis, ascites, coagulopathy, encephalopathy,

multi-system failure Initially very elevated transaminases

Falling transaminases and rising bilirubin ominous

Hyperammonemia, hypoalbuminemia, prolonged PT, hypoglycemia

Viral agents (50% of cases) Most cases of fulminant hepatic failure are caused by

unidentified agent, presumably viral HAV, HBV+/-HDV, HCV, HEV

HSV, enteroviruses, EBV, CMV, HHV-6, VZV

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Chronic Hepatitis

Prolonged necroinflammatory process Elevated transaminases for > 6 months

Insidious clinical manifestations

Can include cholestasis (jaundice, pruritus),ascites, hypoalbuminemia, coagulopathy,encephalopathy

Can progress to fibrosis and then cirrhosis

Viral agents: HBV (+/- HDV), HCV Other causes include autoimmune, metabolic

disorders (Wilsons, CF, alpha-1 antitrypsin deficiency),drug/toxin-mediated, idiopathic

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Type of Hepatitis

A B C D E

Source of

virus

Feces Blood

Blood derived

Body fluids

Blood

Blood derived

Body fluids

Blood

Blood derived

Body fluids

Feces

Route of

Transmission

Feco-oral Percutaneous

Permucosal

Percutaneous

Permucosal

Percutaneous

Permucosal

Feco-

oral

Chronic

Infection

No Yes Yes Yes No

Prevention Pre Post

Exposure

Immunization

Pre Post

Exposure

Immunization

Blood donor

screening

Blood donor

screening

Pre Post

Exposure

Immunization

Ensure

Safe

Drinking

water


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HepatitisA

Transmission: faecal-oral

Incubation: 2-6weeks

High-risk countries:Eastern Europe,Africa, Asia, South America

In these regions almost every child comes into

contact with the hepatitis A virus before the age of 10

The proportion of symptomatic forms

and complications increase with age

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HepatitisA

Diagnosis: AST, ALT, IgM, IgG

Prevention:hygienic measurespassive immunization ( gives


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HepatitisB:

ACUTE CHRONIC- 5-10%

(infection >6months)

Worldwide (W.H.O. estimates) More than 2 BILLION people alive today have

been infected with HBV at some time in their

lives. Of these, about 350 million remain infected

chronically and become carriersof the virus.

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Chronic Hepatitis B

2 types

Chronic persistent hepatitis

Chronic active hepatitis

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Chronic Persistent Hepatitis

a) Histology- Normal hepatic lobular architecture with

infiltration of monocytes in portal areas

b) Elevated plasma transaminase levels withnormal PT, Alkaline phosphate, albumin,globulin, GGT

Treatment

Close observation

Excellent prognosis ( rarely progresses toCAH or cirhosis)

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Chronic Active Hepatitis

Histology-Patchy hepatocellular necrosis with

destruction of lobular architecture andregenerating hepatocytes with multiple nuclei

-Raised transaminase, bilirubin, ANA(75%)Treatment

Immunosuppresive therapy

- Prednisolone- Azathioprine

- Interferon for Hep B

These may prevent progression to serious liver damage and cirhosis

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Transmission: blood and body fluids, iv drugabusers, sexual transmission

Incubation: 1-6 months

Hepatitis B virus primarily interferes with functions

of the liver by replicating in liver cells

During HBV infection, the host immune response

causes both hepatocellular damage and viralclearance

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HBV Diagnosis

Hochman J, Balistreri WF. Pediatr Rev. 2003; 24: 399-410.

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HBV Treatment

Lin KW, Kirchner JT.Am Fam Physician 2004; 69:75-82.

Interferon-alfa

Lamivudine

Adefovir

GOALS of TREATMENT- Suppress HBV replication

- Seroconversion from eAg to e Ab

- Prevent long-term sequelae 26


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Prevention: vaccination

Treatment: chronic- interferon-2, antiviraldrugs (lamivudine...)

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When HBV infection is acquired at birth (vertical

transmission) or early childhood there is a high

level of immunological tolerance and cellularimmune response does not occur, thus chronic

infection is the norm.

This immune tolerant phase is characterized byminimal hepatic inflammatory activity and normal or

near normal serum ALT despite positive Hbe Ag

and high levels of HBV replication.

This phase persists for 2-3 decades before an

active hepatitis develops that might lead to fibrosis

and cirrhosis.

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ROUTE AND SITE OF


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AGE PICTURE VACCINES DOSE

ROUTE AND SITE OF

ADMINISTRATION

BCG 0.05ml intra-dermal, right upper arm

OPV 0 2 drops oral

Hepatitis B 0.5ml intra-muscular, right thigh

OPV 1 2 drops oral

DPT-HepB-Hib 1 0.5ml intra-muscular, left thigh

Pneumococcal 1 0.5ml intra-muscular, right thigh

Rotavirus 1 1.0ml oral

OPV 2 2 drops oral



Rotavirus 2 1.0ml oral

OPV 3 2 drops oral



6 months Vitamin A 100,000 I.U oral

Measles 1 0.5ml sub-cutaneous, left upper arm

Yellow Fever 0.5ml sub-cutaneous, right upper ar

12 months Vitamin A 200,000 I.U oral

Measles 2 0.5ml sub-cutaneous, left upper arm

Vitamin A 200,000 I.U oral

18 months

Long Lasting

Insecticidal Net

(LLIN)

6 weeks

At Birth

NB: After 18 months vitamin A will be given every six months till child is five years old

10 weeks

14 weeks

9 months

18 months

Immunizationschedule

in

Ghana

Showing Hep Bimmunization

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Hepatitis D

Subviral satellite because it can propagate only inthe presence of hepatitis B

coinfection superinfection

Transmission: parenteral (intravenous druguse mostly)

> 60% develop cirrhosis

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Hepatitis C

ACUTE CHRONIC 50-80%first 6 months after infection more than 6 months

60-70% asymptomatic often asymptomaticmost patients develop chronic 1/3 progress to cirrhosis in 20y

HCV

Infects 3-4 million people per year worldwide.

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Hepatitis C

Transmission: blood

Incubation: 2weeks - 6months

No vaccine!

35% of patients infected with HIV are also infected

with hepatitis C virus.

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Thank you

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References

Nelsons Textbook of Pediatrics Essentials of clinical medicine Kumar and Clark

http://www.emedicinehealth.com/hepatitis

http://www.hepatitis.org/hepatalcool_angl.htm

Oxford handbook of clinical medicine

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North American Society for PediatricGastroenterology, Hepatology and Nutrition

www.naspghan.org

www.cdhnf.org

www.hepb.org

www.aasld.org

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http://www.naspghan.org/http://www.cdhnf.org/http://www.hepb.org/http://www.aasld.org/http://www.aasld.org/http://www.hepb.org/http://www.hepb.org/index.htmlhttp://www.cdhnf.org/http://www.naspghan.org/http://www.cdhnf.org/


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Acknowledgement

Dr Paabie

Documents

Hepatitis in Children 2014