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    Hepatitis in Children: DR Hamza Bawumia

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    Hamza Bawumia
    This document provides an overview of hepatitis in children, including: 1. The liver's structure and functions, such as metabolism, protein synthesis, and excretion of waste. 2. The causes, symptoms, and types of hepatitis, whether acute, chronic, or fulminant. The major causes are viral hepatitis from viruses A-E. 3. Details on each viral hepatitis, including transmission routes, incubation periods, prevalence in different regions, prevention through vaccination or hygiene, and treatment options. Chronic hepatitis B and C can lead to cirrhosis if not properly managed.

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    Hepatitis in Children: DR Hamza Bawumia

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    Hamza Bawumia
    56 views36 pages
    This document provides an overview of hepatitis in children, including: 1. The liver's structure and functions, such as metabolism, protein synthesis, and excretion of waste. 2. The causes, symptoms, and types of hepatitis, whether acute, chronic, or fulminant. The major causes are viral hepatitis from viruses A-E. 3. Details on each viral hepatitis, including transmission routes, incubation periods, prevalence in different regions, prevention through vaccination or hygiene, and treatment options. Chronic hepatitis B and C can lead to cirrhosis if not properly managed.

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    Original Title

    Hepatitis in Children 2014

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    This document provides an overview of hepatitis in children, including: 1. The liver's structure and functions, such as metabolism, protein synthesis, and excretion of waste. 2. The causes, symptoms, and types of hepatitis, whether acute, chronic, or fulminant. The major causes are viral hepatitis from viruses A-E. 3. Details on each viral hepatitis, including transmission routes, incubation periods, prevalence in different regions, prevention through vaccination or hygiene, and treatment options. Chronic hepatitis B and C can lead to cirrhosis if not properly managed.

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    © All Rights Reserved
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    Download as ppt, pdf, or txt
    56 views36 pages

    Hepatitis in Children: DR Hamza Bawumia

    Uploaded by

    Hamza Bawumia
    This document provides an overview of hepatitis in children, including: 1. The liver's structure and functions, such as metabolism, protein synthesis, and excretion of waste. 2. The causes, symptoms, and types of hepatitis, whether acute, chronic, or fulminant. The major causes are viral hepatitis from viruses A-E. 3. Details on each viral hepatitis, including transmission routes, incubation periods, prevalence in different regions, prevention through vaccination or hygiene, and treatment options. Chronic hepatitis B and C can lead to cirrhosis if not properly managed.

    Copyright:

    © All Rights Reserved
    Download as PPT, PDF, TXT or read online from Scribd
    Download as ppt, pdf, or txt
    of 36

    HEPATITIS IN CHILDREN

    Dr Hamza Bawumia
    (BSc. Biochem, MBChB)

    Supervisor:
    Dr Paabie

    Liver is divided histologically into lobules. The center of the


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

    Liver physiology

    Liver is a multitask organ

    Metabolic Function
    Synthesis
    Breakdown
    Other functions
    storage of vitamin
    A,D,B12,
    Excretion of waste
    products from
    bloodstream into bile
    Storage functions

    Protein metabolism
    Synthesis of amino acids
    Carbohydrate metabolism
    Gluconeogenesis
    Glycogenesis

    Lipid metabolism
    Cholesterol synthesis
    Lipogenesis

    Production of coagulation
    factors I, II, V, VII, IX, X and XI, and
    protein C, protein S and antithrombin
    Produces insulin-like growth factor 1
    (IGF-1), a polypeptide protein
    anabolic effects

    Production of thrombopoetin
    3

    Liver physiology
    Produces albumin, the major osmolar
    component of blood serum
    Synthesizes angiotensinogen,
    responsible for raising blood pressure
    when activated by renin.

    Breaks down insulin and other hormones


    Glycogenolysis
    Breaks down or modifies toxic substances
    Converts ammonia to urea
    Storage of iron, vitamins and trace
    elements
    Others - Hematopoietic organ when required
    Excretory organ: bile salts, degraded drugs
    /toxins /antibiotics

    HEPATITIS = inflammation of liver

    HEPATITIS - causes

    ACUTE:
    Viral hepatitis
    Non-viral infection
    Alcohol*
    Toxins
    Drugs
    Ischemic hepatits
    Autoimmune
    Metabolic diseases

    CHRONIC:
    Viral hepatitis
    Alcohol*
    Drugs
    Non-alcoholic
    steatohepatitis
    Autoimmune
    Heredity

    HEPATITIS symptoms and


    signs

    ACUTE:
    Malaise
    Muscle and join
    ache
    Fever
    Nausea or vomiting
    Loss of apetite
    Abdominal pain
    Dark urine
    Enlarged Tender
    Liver

    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.

    Viral Hepatitis

    Viral hepatitis is a systemic disease


    with primary inflammation of the liver
    by any one of a heterogenous group of
    hepatotropic viruses.

    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)
    10

    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
    11

    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

    12

    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
    13

    Type of Hepatitis
    A

    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

    Fecooral

    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

    14

    Hepatitis A
    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

    15

    Hepatitis A

    Diagnosis:

    AST, ALT, IgM, IgG

    Prevention: hygienic measures


    passive immunization ( gives <3 months
    immunity to those at risk)
    active immunization

    Treatment: nonspecific, dietary food and long rest

    CHRONIC

    LIVER DISEASE DOES NOT OCCUR with


    Hepatitis A infection.
    16

    Hepatitis B:
    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 carriers of the virus.
    17

    18

    Chronic Hepatitis B
    2 types
    Chronic persistent hepatitis
    Chronic active hepatitis

    19

    Chronic Persistent Hepatitis


    Histology
    - Normal hepatic lobular architecture with
    infiltration of monocytes in portal areas
    b) Elevated plasma transaminase levels with
    normal PT, Alkaline phosphate, albumin,
    globulin, GGT
    Treatment
    Close observation
    Excellent prognosis ( rarely progresses to
    CAH or cirhosis)
    a)

    20

    21

    Chronic Active Hepatitis


    Histology
    -Patchy hepatocellular necrosis with
    destruction of lobular architecture and
    regenerating 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
    22

    23

    Transmission: blood and body fluids, iv drug


    abusers, 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 viral
    clearance

    24

    HBV Diagnosis

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


    25

    HBV Treatment

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

    GOALS of TREATMENT

    - Suppress HBV replication


    - Seroconversion from eAg to e Ab
    - Prevent long-term sequelae

    Interferon-alfa
    Lamivudine
    Adefovir
    26

    Prevention: vaccination
    Treatment: chronic- interferon-2, antiviral

    drugs (lamivudine...)

    27

    When HBV infection is acquired at birth (vertical


    transmission) or early childhood there is a high
    level of immunological tolerance and cellular
    immune response does not occur, thus chronic
    infection is the norm.

    This immune tolerant phase is characterized by


    minimal 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.
    28

    AGE

    At Birth

    Immunization
    schedule
    in
    Ghana
    Showing Hep B
    immunization

    6 weeks

    10 weeks

    14 weeks

    6 months
    9 months

    12 months
    18 months

    18 months

    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

    DPT-HepB-Hib 2

    0.5ml

    intra-muscular, left thigh

    Pneumococcal 2 0.5ml

    intra-muscular, right thigh

    Rotavirus 2

    1.0ml

    oral

    OPV 3

    2 drops

    oral

    DPT-HepB-Hib 3

    0.5ml

    intra-muscular, left thigh

    Pneumococcal 3 0.5ml

    intra-muscular, right thigh

    Vitamin A

    100,000 I.U

    oral

    Measles 1

    0.5ml

    sub-cutaneous, left upper arm

    Yellow Fever

    0.5ml

    sub-cutaneous, right upper arm

    Vitamin A

    200,000 I.U

    oral

    Measles 2

    0.5ml

    sub-cutaneous, left upper arm

    Vitamin A
    Long Lasting
    Insecticidal Net
    (LLIN)

    200,000 I.U

    oral

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

    29

    Hepatitis D

    Subviral satellite because it can propagate only in


    the presence of hepatitis B
    coinfection

    superinfection

    Transmission: parenteral (intravenous drug


    use mostly)

    > 60% develop cirrhosis

    30

    Hepatitis C
    ACUTE

    CHRONIC 50-80%

    first 6 months after infection


    60-70% asymptomatic
    most patients develop chronic
    HCV

    more than 6 months


    often asymptomatic
    1/3 progress to cirrhosis in 20y

    Infects 3-4 million people per year worldwide.

    31

    Hepatitis C
    Transmission: blood
    Incubation: 2weeks - 6months

    No vaccine!

    35% of patients infected with HIV are also infected


    with hepatitis C virus.

    32

    Thank you

    33

    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

    34

    North American Society for Pediatric


    Gastroenterology, Hepatology and Nutrition

    www.naspghan.org

    www.cdhnf.org

    www.hepb.org

    www.aasld.org
    35

    Acknowledgement

    Dr Paabie

    36

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