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Dengue

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Title: Dengue


1
Dengue
  • Professor.Shivaprasad

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Dengue
  • The word dengue is derived from African word
    denga meaning fever with hemorrhage .
  • Is caused by virus transmitted of bites of
    mosquito aedes.

6
DEFINITION
  • Dengue Fever is a benign syndrome caused by
    several arthropod borne viruses, is
    characterized by biphasic fever, Myalgia, or
    Arthralgia, rash, Leukopenia and lymphadenopathy.

7
History
  • Over the last two hundred years dengue was known
    to the physician as a self limiting benign
    febrile condition.
  • The first outbreak that resembles a disease now
    recognized as dengue fever was that described by
    Benjamn Rush in Philadelphia, Pennsylvania in
    1780.
  • Epidemics probably due to dengue were common from
    the eighteenth to the twentieth centuries among
    the inhabitants of the Atlantic coast of the
    United States.

8
History
  • Dengue viruses almost certainly were the cause of
    the 5 and 7 day fevers that occurred among
    European Colonists in Tropical Asia.
  • In 1905 Aedes Aeggpti was identified as a dengue
    vector by Bancroft Ashburn and C raig.

9
History
  • When Dengue viruses were isolated in the
    laboratory mice in 1943 and 1944, the modern era
    of dengue research began.
  • In the beginning only two different dengue
    viruses named dengue virus type I and II.
  • During most of the previrologic era, dengue
    viruses were thought to be the cause of a
    generally benign self limited febrile exanthema.

10
History
  • In 1956 Philippine hemorrhage fever was
    associated with dengue when types 3 and 4 were
    recovered.
  • It now has become endemic through out tropical
    Asia since 1967 the term dengue hemorrhagic fever
    and DSS have come in to general use.

11
Problem statement
  • Dengue fever is the most common arthropod borne
    viral disease.
  • Dengue fever is one of the most important
    emerging disease of the tropical and sub tropical
    regions, affecting urban and pre urban areas.
  • The geographical distribution of the disease has
    greatly expanded and the number of cases has
    increased dramatically in the past 30 Years

12
Problem statement
  • The increase of Dengue and DHF is due to
    uncontrolled population growth and urbanization
    with out appropriate water management, to the
    global spread of dengue in a travel and trade and
    to erosion of vector control programme.
  • By 1997 most of the countries have experienced
    large out breaks of the disease, currently DF /
    DHF is endemic in Bangladesh , India, Indonesia,
    Maldives, Srilanka, Thailand approximately 1.3
    billion people are leaving in endemic areas

13
Problem statementIndia
  • Dengue / DHF is widely prevelent in India and all
    the 4 serotype are found. There has been a
    decline in dengue incidence after 1996.
  • However during 2001 out breaks have been reported
    from Rajasthan (1433 cases and 33 deaths),
    Tamilnadu (761 cases and 8 deaths), Karnataka
    (161 cases) Gujarath (46 cases)

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ETIOLOGY VIRUS
  • Dengue virion are spherical particles
    approximately 50 nm in diameter.
  • contains a single plus strand of RNA. Surrounded
    by a lipid bilayer.
  • Mature virions are composed of 6 RNA, 9
    carbohydrate, and 17 lipid.
  • Because of the lipid envelope, flavviviruses are
    readily inactivated by organic solvents and
    detergents.

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ETIOLOGY VIRUS
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ETIOLOGY VIRUS
  • Three viral proteins are associated with virions.
  • The E (envelop), M (membrane) and C (capsid)
    proteins.

17
VIRUS
  • The E protein is the major surface protein of the
    viral particle probably interacts with viral
    receptors, and mediates virus-cell membrane
    fusion.
  • Antibodies that neutralize virus infectivity
    usually recognize this protein and mutations in E
    can affect virulence.

18
VIRUS
  • M protein is a small proteolytic fragment which
    is important for maturation of the virus into an
    infectious form.
  • C protein is a component nucleocapsid.

19
EtiologyTypes
  • Four distinct antigenically related serotypes (
    1to 4) of dengue virus of the family flaviviridae
    are etiologically responsible.
  • Infection in human by one serotypes produces life
    long immunity against re-infection by the same
    serotype.
  • subsequent infection with other serotypes may
    result in a severe illness ie., DHF or DSS

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EtiologyDengue like fever
  • Three other arthropod born viruses cause similar
    febrile diseases with rash.
  • Chikungunya, Onyong-nyong and West Nile Fever

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EtiologyDengue like fever
  • Dengue like diseases may also occur in epidemics.
  • Epidemiological features depends on the vector
    and their geographic distribution.

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EtiologyDengue like fever
  • Chikungunya Virus is wide spread in the most
    areas of the world. In Asia A Aegypti is the
    principal vector. In South East Asia dengue and
    Chikungunya outbreaks occurs concurrently
  • Outbreaks of onyong-nyong and West Nile Fever
    usually involve villages or small towns in
    contrast to the urban outbreaks of dengue and
    chikungunya.

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EPIDOMIOLOGY
  • Dengue outbreaks in urban areas infested with
    A.aegypti may be explosive upto 70-80 of
    population may be involved.
  • During epidemic most disease occur in older
    children and adults because A.aegypti has a
    limited range spread, epidemic occurs mainly
    through viremic human beings and follows the main
    lines of transportation .
  • Where dengue is endemic children and susceptible
    foreigners may be the only persons to acquire
    overt disease adults having become immune.

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EPIDOMIOLOGY Vector
  • Dengue viruses are transmitted by mosquitoes of
    the stegomyia family.
  • Acdes aegypti a day time biting mosquito is the
    principal vector and all 4 types of virus have
    been recovered from it.

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Vector
  • Aedes mosquitoes (Tiger mosquito) distinguished
    by white stripes on black body.
  • Important members aedes familyA. aegypty,
    A.vittatus and A. albopictus.
  • They are most abundent during rainy season.

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Vector
  • Lays egg singly, and eggs are cigar shaped.
  • Female mosquito acts as vector.
  • They do not fly over long distance-
    lt100mts(110yards), this factor facilitates its
    eradication.

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Transmission
  • In most tropical areas A-aegypti is highly
    urbanized.
  • They breed in fresh water like water stored for
    drinking or bathing and in rain water collected
    in any container.
  • Dengue viruses have also been recovered from
    Aedes- Albopictus.

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Transmission
  • Outbreaks in the Pacific area have been
    attributed to several other Aedes species.
  • These species breed in water trapped in
    vegetation.

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Pathogenesis
  • In experimental studies of dengue virus infection
    in rhesus monkeys, after subcutaneous
    inoculation, virus was disseminated rapidly to
    regional lymph nodes and then to lymphatic tissue
    through out the body.

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Pathogenesis
  • Early in the viremic period virus could be
    recovered only from lymphonodes.
  • 2-3 days later there will be evidence of
    dissemination of skin and other tissues
  • Virus was recovred from skin, lymphonodes and
    several leukocyte rich tissues for up to 3 days
    after termination of Viremia.

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Pathogenesis
  • The number of sites of virus recovery greater as
    the infection progresses. Intra cellular
    infection is terminated abruptly 2-3 days after
    viremia ceases.
  • Animals infected with dengue virus type, 1,3
    4 and then infected with dengue virus type 2
    circulated virus at higher titer than when the
    strain was inoculated on to susceptible animals.

34
Pathogenesis
  • Epidemiological , Clinical and virologic studies
    of DHF / DSS in humans have shown a significant
    association between severe illness and infection
    in presence of circulating dengue antibody.
  • If tissue culture or suckling mice are used for
    virus recovery, dengue virus almost invariably is
    absent in tissues at the time of death. Tissue
    suspension contain large qualities of dengue
    neutralizing substances.

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Pathogenesis
  • Prospective study of dengue virus infection in
    Thai children
  • DHF / DSS occurred in children who were
    circulating enhancing antibodies from a previous
    single dengue virus infection. But did not occur
    in children whose first infection left them with
    low levels of cross reactive Dengue virus type-2
    neutralizing antibodies at the time of second
    dengue virus infections.

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Pathogenesis
  • In vitro studies of dengue virus type-2
    demonstrated enhanced growth in cultures of
    human mononuclear phagocytes that were
    supplemented with very small qualities of dengue
    antibodies.
  • It has been proposed that the number of infected
    mono nuclear phagocytes in individuals with
    naturally or passively acquired antibody may
    exceed that in non immune individuals.

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Pathogenesis
  • Increase production of infected cells may
    contribute to shock, possibly through the release
    of cytokines, themselves the products of the
    immune elimination of virus infected, mononuclear
    phagocytes through cell mediated mechanisms.

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Pathogenesis
  • It is thought that the reduced risk to DHF / DSS
    of protein calorie malnourished children is
    consistent with hypothesis that a competent
    immune elimination system generates the cytokines
    that produce DHF / DSS.

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Pathogenesis
  • Early in the acute stage of secondary dengue
    virus infection, there is rapid activation of the
    complement system.
  • During shock
  • Blood levels of C1q, C3, C4, C5, C6,
    C7, C8 and C3 proactivator are depressed.
  • C3 catabolic rates elevated.
  • The blood clotting and
    fibrinolytic system are activated.

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Pathogenesis
  • Recent studies suggest a role for
    tumor necrosis factor and interferon gamma.
  • As yet neither the mediator of
    vascular permiability nor complete mechanism of
    bleeding has been identified.

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Pathogenesis
  • Capillary damage allows fluid electrolytes,
    protein, and in some instances red blood cell to
    leak in to intra vascular spaces. This internal
    redistribution of fluid together with deficit due
    to fasting, thirsting and vomiting results in
    hemo concentration, hypovolemia, increased
    cardiac work, tissue hypoxia, metabolic acidosis
    and hyponatremia.

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Pathogenesis
  • A mild degree of DIC plus liver damage and
    thrombocytopenia Could contribute additively to
    produce haemorrhage.

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Pathology
  • Pathologic examination there usually are no gross
    or microscopic lesions found that might account
    for death.
  • In rare instances death may be due to gastro
    intestinal or intra cranial hemorrhages.
  • Haemorrhages are seen in Upper GI tract
    intra ventricular septum of heart, on the
    pericardium. And on the subserosal surfaces of
    major viscera.

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Pathology
  • Focal hemorrhages occasionally seen in the lungs,
    liver, adrenals, sub arachniod space.
  • The liver is usually is enlarged often with fatty
    changes.
  • Yellow watery at times blood tinged effusions
    are present in serous cavities in about ¾ of
    patient and retro peritoneal tissues are markedly
    edematous.

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PathologyMicroscopy
  • Perivascular edema in the soft tissues and wide
    spread of diapedesis of RBC.
  • There may be maturational arrest of
    megakaryocytes in the bone marrow and increased
    numbers of them are seen in capillaries of lungs,
    in renal grlomeruli and in sinusoids of the
    liver and spleen.

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PathologyMicroscopy
  • Proliferation of lymphoid and plasma cytoid
    cells, lymphocytolysis and lymphophagocytosis
    occurs in the spleen and lymphonodes.
  • In the spleen malpighian corpuscle germinal
    centres are necrotic there is a depletion of
    lymphocytes in the thymus.

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PathologyMicroscopy
  • Liver there are varying degrees of
  • Falty metamorphosis,
  • Focal midzonal necrosis
  • Hyperplasia of the Kupffer
    Cells.
  • Non nucleated cells with
    vacuolated acidophilic cytoplasm resembling
    councilmanbodies are seen in the sinusoids.

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PathologyMicroscopy
  • KidneyThere is a mild proliferative glamerulo
    nephritis .
  • Skin Biopsies of the rash reveal swelling and
    minimal necrosis of endothelial cells.
    Subcutaneous deposits of fibrinogen and in a few
    cases dengue antigen in extra vascular
    mononuclear cells and on blood vessel walls.

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DengueClassification
  • Dengue fever
  • Dengue hemorrhagic fever
  • Dengue shock syndrome

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Classification Dengue fever
  • Dengue fever is an acute febnile viral illness
    presenting with Headache, bone (Back break
    fever), or joint (chikungunya or o-nyony-nyong)
    and muscular pains, rash and leucopenia caused by
    arthropod borne viruses.

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CLINICAL PROFILE OF DENGUE IN CHILDREN
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Introduction
  • Dengue is one of the ten leading causes of
    hospitalization and death in children.
  • Globally - 20 million cases/yr
  • - 24,000 deaths/yr.
  • It is important to know the typical and atypical
    presentations in dengue fever for early diagnosis
    and treatment.

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Objectives
  1. To study the modes of presentation of DF, DHF,
    DSS.
  2. To know the clinical course of Dengue infections.
  3. To analyze the outcome of Dengue in children.

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Materials methods
  • SETTING
  • Vani vilas childrens hospital, Bangalore.
  • STUDY DESIGN
  • Institution based case series study.

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Materials methods
  • Children with clinically suspected dengue
    infection between September2002 September2003.
  • 38 cases recorded IgM positive for dengue by
    ELISA (NIV, Bangalore)

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Materials methods
  • Case records were reviewed for
  • Age sex distribution
  • Signs and symptoms Typical Atypical
  • Haematological parameters
  • Clinical course of the illness
  • Outcome

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Materials methods
  • Standard definitions were used to define
  • Dengue fever
  • Dengue haemorrhagic fever
  • Dengue shock syndrome
  • Standard WHO treatment guidelines were
  • followed in treatment

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Age sex distribution
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Population distribution
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Manifestations
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Fever
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Symptoms- Typical
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Symptoms - Typical
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Atypical symptoms
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Signs
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Signs
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Platelet counts
  • LAB
  • PLATELET COUNTS

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Hematocrit
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Recovery -
Hypotension
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Recovery - Platelets
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Recovery Rhythm abnormalities
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Outcome
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Conclusions
  • Dengue is one of the most important re-emerging
    infections.
  • In the present study also commonest manifestation
    was fever high grade with rash/ flushing
  • Retroorbital pain(16) and biphasic fevers(18)
    were seen in only a minority.

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Conclusions
  • Other typical symptoms and signs continue to be
    common but
  • ATYPICAL features are also seen.
  • 35 out of 38 children recovered.
  • 2 had co - morbid conditions, 3rd an infant,
    terminally ill referred for ventilator care.

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Conclusions
  • Unusual manifestations
  • Seizures
  • Altered sensorium
  • Acalculous cholecystitis
  • Acute liver failure
  • Acute renal failure.

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Conclusions
  • Early recognition, careful monitoring and
    appropriate therapy reduces mortality.
  • Health care providers must have thorough update
    regarding the various presentations of dengue
    infection.

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DHF
  • Circum oral and peripheral cyanosis.
  • Respiration is rapid and often labored.
  • Pulse is weak, rapid and thready.
  • Heart sounds faint.
  • The liver may enlarge in 4-6 cm below the costal
    margin and is usually firm and some what tender.

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DHF
  • Approximately 20-30 of cases of dengue H.F. are
    complicated by shock (DSS)
  • Fewer than 10 of patients have gross echymosis
    or gastro intestinal bleeding usually after a
    period of corrected shock.

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DHF
  • After a 24 to 36 hrs period of crisis,
    convalescence is fairly rapid in children who
    recover.
  • The temperature may return to normal before or
    during the stage of shock.
  • Bradycardia and ventricular extrasystoles are
    common during convalescence.

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DiagnosisD.F
  • Clinical diagnosis (High suspicion)
  • Knowledge of the geographic distribution.
  • Environmental cycles of causal viruses.
  • The term dengue like disease should be used until
    a specific diagnosis is established.

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DiagnosisD.H.F
  • WHO Criteria For DHF
  • Fever, Minor or Major Hemorrhagic manifestations.
  • Thrombocytopenia ( lt 100000 / mn3)
  • Objective evidence of increased capillary
    permeability (hematocrit increased gt 20) X-ray
    pleural effusion
  • Hypoalbuminemia.
  • DSS Above mentioned criteria plus hypo tension
    and narrow pulse pressure ( lt 20 mm of Hg)

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DiagnosisD.H.F
  • Virologic diagnosis can be established by
    serologic tests or by isolation of the virus
    from blood leukocytes or serum.
  • Both in primary and second dengue infections,
    there is relatively transient appearance of anti
    dengue immunoglobulin IgM antibodies. These
    antibodies disappear after 6-12 weeks which can
    be used to time a dengue infection.

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DiagnosisD.H.F
  • In secondary infection most antibody is of the
    IgG class.
  • Serological diagnosis depends on a four fold or
    greater increase in IgG antibody titer in paired
    sera
  • By
  • Hemaglutination inhibition.
  • Complement fixation
  • Enzyme immunoassay
  • Neutralization tests

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DiagnosisD.H.F
  • Carefully standardized immunoglobulin IgM, and
    IgG capture enzyme immuno assays are now to
    identify the acute phase antibodies from
    patients with primary or secondary dengue
    infections in single serum samples. (IgG antibody
    concentrations are abundant in secondary but
    minimum in primary) usually such samples should
    be collected not earlier than 5 days nor later
    than 6 weeks after onset.

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DF /DHF Grade Symptoms Laboratory
DF Fever with two or more of the following signs headache, retro-orbital pain, Myalgia, arthralgia. Luecopenia occasionally Thromocytopenia may be present, no evidence of plasma leakage.
DHF I Above signs plus positive tourniquet test. Thrombocytopenia lt100,000 HCt risegt20
DHF II Above signs plus spontaneous bleeding Thrombocytopenia lt100,000, HCt risegt20.
DHF III Above signs plus circulatory failure (rapid weak pulse, pressure, cold clammy skin, restlessness and capillary refill time gt3sec) Thrombocytopenia lt100,000, Het rise gt20
DHF IV Profound shock with undectable blood pressure and pulse Thrombocytopenia lt100,000, rise gt20.

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D/DD.F
  • The DDS of DF includes viral respiratory and
    influenza like diseases. Early stages of Malaria
    , mild yellow fever, scrub typhus, viral
    hepatitis and leptospirosis.
  • Four arboviral diseases have dengue like courses
    but without rash Colorado Tick fever, sand fly
    fever, Rift valley fever and Ross river

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D/DD.H.F
  • Meningo Cocccemia , Yellow Fever other viral
    hemorrhagic fevers, many in rickettsial diseases
    and other severe illneses caused by a variety of
    agents may produce clinical picture similar to
    DHF.

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Management Dengue fever
  • There is no specific anti viral treatment and
  • The management is essentially supportive and
    symptomatic (Bedrest)
  • The key to success is frequent monitoring and
    changing strategies depending on clinical and
    laboratory evaluations.

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Management Indications of hospitalizations
  • Restlessness or lethargy frequent vomiting one or
    two days of febrile illness.
  • Cold extremities or circumoral cyanosis.
  • Bleeding in any form.
  • Rapid and weak pulse.
  • Capillary refill time gt 3 seconds.
  • Narrowing of pulse pressure (lt20 mm Hg) or Hypo
    tension.
  • Hematocrit of 40 or rising hematocrit.
  • Platelet count of lt 1,00000/ mm3
  • Acute abdominal pain
  • Evidence of Plasma leakage. Eg. Pleural effusion
    /Ascities

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Management Dengue fever
  • The management of dengue fever is symptomatic and
    supportive.
  • Bed rest is advisable during the acute febrile
    phase.
  • Antipyretics or cold sponging should be used to
    keep the body temperature lt 400C.
  • Analgesics and mild sedation may be required to
    control pain

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Management Dengue fever
  • Fluids and electrolyte replacement therapy is
    required when there are deficits due to sweating/
    fasting / thirsting / vomiting or diarrhea.
  • Because of the dengue hemorrhageic diathesis
    aspirin should not be given to reduce fever or
    control pain.

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Management Dengue Hemorrhagic Fever
  • Explicit recommendations for management of DSS
    have been made by a WHO expert committee. These
    plus earlier recommendations by ohen and halstead
    are the basis of this section.
  • Fluid intake by mouth should be as ample as
    tolerated.

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Management DHF
  • Electrolyte and dextrose Solution ( as used in
    diarrhea disease) or Fruit Juice or both are
    preferable to plain water.
  • With high fever there is a risk of convulsion and
    antipyretic drugs may be indicated.

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Management DHF
  • Acetaminophen is preferable at the following
    doses younger than year of age 60mg / dose, 1-3
    years 60-120mg/dose, 3-6 years 120 mg/dose,
    6-12 years 240mg /dose children should be
    observed closely for early signs of shock. The
    critical period is the transition from febrile to
    afebrile phase.
  • A rise in hematocrit value indicates significant
    plasma loss and a need for parenteral fluid
    therapy.

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Management DHF
  • In grade I and II volume replacement can be given
    in a period of 12-24 hours.
  • Patients with any signs of bleeding and
    persistently high hematocrit values dispite being
    given volume replacement should be admitted to
    hospital.

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Management DHF
  • The volume and type of fluid should be similar to
    that used in the treatment of diarrhea with
    moderate isotonic dehydration but the rate should
    be carefully titrated. The required volume should
    be charted on a 2 3 hours basis and the rate
    of administration adjusted throughout the 24 48
    hours period of leakage.

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Management DHF
  • Serial haemetocrit determination every 4 6
    hours and frequent recording of vital signs are
    recorded for adjusting the fluid replacement. In
    order to assume adequate volume replacement and
    avoid over transfusion.

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DHFFluid Management
103
DHFFluid Management
  • Formula
  • ml / hr (drop / min) x 3
  • The fluid replacement should be the minimum
    volume i.e. sufficient to maintain effective
    circulation during the period of leakage.
  • Excessive replacement will cause respiratory
    distress (from massive pleural effusion and
    ascites). Pulmonary congestion and edema

104
D H F Fluid management
  • The type of fluid used are 1) Crystalloid and 2)
    Colloidal
  • I. Crystalloid
  • 1/3 to ½ of the total fluid as physiologic saline
    solution (NS)
  • ½ to 2/3 of the remainder as 5 glucose in water.
  • For acidosis ¼ of the total fluid should be 1/6
    molar sodium bicarbonate.

105
D H F Fluid management
  • 5 dextrose in ringer lactate solution
  • 5 dextrose in ringer acetate solution
  • 5 dextrose in half strength NS.
  • 5 dextrose in NS solution.

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Fluid management Colloids
  • Dextran 40 and plasma
  • Management of Shock
  • DSS is a medical emergency that requires prompt
    and vigorous volume replacement therapy.
  • There are also electrolytes (sodium) and acid
    base disturbances it must be consider that there
    is a high potential for developing DIC. And
    stagnant acidemia. Blood will promote and or
    enhance DIC which may lead to sever hemorrhage
    and or irreversible shock.

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The replacement of plasma loss
  • Immediate replacement of plasma loss with
    isotonic salt solution (5 dextrose in ringer
    acetate solution or 5 dextrose in NS) at the
    rate of 10-20ml / kg body weight are in case of
    profound shock (grade-4) as a bolus of 10ml/kg
    body weight (1-2 times) should take place.

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The replacement of plasma loss
  • In case of continued or propound shock (with high
    haematocrit values) colloidal fluid (dextran or
    medium molecular weight in NSS or plasma) should
    be given the following initial fluid at a rate of
    10-20ml/kg body weight / hour.
  • Blood transfusion is indicated in cases with
    profound and persistent shock dispite declining
    hematocrit values after initial fluid replacement

109
The replacement of plasma loss
  • When improvement is apparent the rate of I/V
    fluid replacement should be reduced and adjusted
    1-2 hourly throughout the 24 hours period.
  • Colloidal fluid is indicated in cases with
    massive leakage and to whom a large volume of
    crystalloid fluid as been given.

110
The replacement of plasma loss
  • In small children 5 dextrose in a half strength
    normal saline solution (5 dextrose / ½ NSS )
    initial resuscitation and 5 dextrose in ½ NSS
    may be used in infants under 1 year age. If the
    serum sodium is normal.

111
D H F Discontinuation of IV fluids
  • WHEN
  • The hematocrit reading drops to around 40
  • Vital signs are stable.
  • A good urine out flow indicates sufficient
    circulate renal volume.
  • A return of appetite and diuresis are signs of
    recovery

112
D H F Discontinuation of IV fluids
  • It is extremely important to emphasize that a
    drop in heamatocrit reading at this stage should
    not be interpreted as a sign of internal
    hemorrhage.
  • Strong pulse, BP with wide pulse pressure and
    diuresis are good vital signs during this
    re-absorption phase.

113
D H F Management (contd)
  • Sedations are needed in some cases because of
    marked agitation.
  • Hepatotoxic drugs should be avoided.
  • Chloral hydrate orally or rectally recommended in
    a dose of 30 50 mg/kg as a single hypotonic
    dose (maximum dose 1gram).

114
D H F Management (contd)
  • In cases without pulmonary complications
    paraldehyde 0.1ml/kg I.M. (maximum dose 10ml)
    also be use.
  • Oxygen therapy should be given to all patients in
    shock. The oxygen mask or tent may increase
    apprehension.

115
ManagementBlood transfusion
  • Transfusion with fresh whole blood is preferable
    and the amount to given should be such that
    normal RBC concentration is not exceeded.
  • Fresh Frozen Plasma (FFP) may be indicated in
    cases where consumptive coagulopathy causes
    massive bleeding. DIC is usual in sever shock and
    may play an important part in the development of
    massive bleeding or lethal shock.

116
ManagementPlatelet transfusion
  • Platelet transfusion in cases of DHF / DSS is
    also surrounded with controversies. Mild
    reductions in platelet counts are usually not
    associated with significant bleeding.
  • Secondly thrombocytopenia in DHF / DSS is a short
    lived phenomenon with platelets returning to
    normal by 7 to 9 days.

117
Management Platelet transfusion
  • Platelet transfusions are recommended only for
    children with platelet count of 50,000 / mm3 and
    having significant bleeding manifestations.
  • Prophylactic platelet concentrate is indicated
    when platelet count is less than 10000-20000 /
    mm3 (10 to 20ml / kg of platelet).

118
Polyserosities
  • Need the insertion of intercostal tube or ascitic
    drainage respectively.
  • Caution must be taken before drainage as the
    chances of sever hemorrhages are high.
  • Patients should be haematologically stabilized
    first with use of fresh whole blood, FFP or
    platelet concentrates and drainage of these
    fluids should be done slowly to prevent sudden
    circulatory collapse.

119
Polyserosities
  • Large pleural effusions during the recovery phase
    after 48 hours may need small doses of frusemide
    (0.25 to 0.5 mg / kg B/w 6th hourly) with these
    method it may possible to avoid insertion of
    intercostal drains.
  • Generally steroids do not shorten the duration of
    disease or improve the prognosis in children
    receiving careful supportive therapy.

120
Monitoring
  • Patients should be monitored constantly until
    there is a reasonable certainly that the danger
    as passed in practice.
  • Pulse, BP, RR Temp. be taken every 15 to 30
    minutes are more often until the shock resolves.

121
Monitoring
  • Hematocrit or Hb studies should be performed
    every two hours for the first six hours then
    every four hours thereafter until the patient is
    stable.
  • Accurate record of intake and output including
    the type of fluid given should be made.

122
Management of Epidemic Dengue Hemorrhagic Fever
  • During epidemics, outpatient and inpatient
    facilities may be overwhelmed.
  • It is essential that only children requiring
    hospital care be admitted.
  • A recently elevated body temperature and positive
    tourniquet test are sufficient to suggest DHF

123
Management of Epidemic Dengue Hemorrhagic Fever
  • When possible, a microhematocrit and platelet
    count should be done in the outpatient
    department.
  • Patients with thrombocytopenia and elevated
    hematocrit counts should be sent to a rehydration
    ward or, if hematocrit does not fall or rises in
    the face of fluid therapy, admitted to hospital.

124
Management of Epidemic Dengue Hemorrhagic Fever
  • . If a patient lives a long distance from the
    hospital and nearby accommodations are not
    available, admission for observation may be
    necessary.

125
Regulatory Measures
  • Dengue diseases are not subject to international
    surveillance regulations. An intensive and
    effective voluntary reporting system has been
    devised by the regional offices of the World
    Health Organization.

126
Prognosis
  • Children who develop profound shock rapidly with
    no detectable diastolic pressure or with
    unobtainable blood pressure.
  • Children in shock with delayed admission to
    hospital.
  • Children in shock with gastrointestinal
    hemorrhage have a poor prognosis.
  • Mortality rates may exceed 50 per cent in these
    groups.

127
PREVENTION
  • Tissue culture-based vaccines for dengue virus
    types 1, 2, 3 and 4 are immunogenic but not
    available for general use.
  • Prophylaxis depends on use of insecticides,
    repellents, body protective clothing, and
    screening of houses to avoid the bite of the
    mosquito.
  • Destruction of A. aegypti breeding sites also is
    effective.

128
PREVENTION
  • If water storage is mandatory, a light-fitting
    lid or a thin layer of oil may prevent egg
    deposits or hatching.
  • A larvicide, such as Abate, available as a 1
    sand granule formulation and effective at a
    concentration of 1 part per million, may be added
    safely to drinking water.

129
EPIDEMIC MEASURES
  • World Health Organization recommendations are as
    follow
  • On the basis of epidemiologic and entomologic
    information, the size of the area that requires
    adult mosquito abatement should be determined.
  • With technical malathion or fenitrothion at 438
    ml/ha, two adulticidal treatments at a 10-day
    interval should be made by use of a
    vehicle-mounted or portable ultra-low-volume
    aerosol generator or mist blower.

130
EPIDEMIC MEASURES
  • Cities of moderate size should stockpile at least
    one vehicle-mounted aerosol generator, five mist
    blowers, 10 swing fog machines, and 1000 liters
    of ultra-low-volume insecticides to be prepared
    to carry out adulticidal operations over a 20-km2
    area rapidly.

131
EPIDEMIC MEASURES
  • With limited funds, such equipment and
    insecticides can be stockpiled centrally for
    rapid transportation where required. Priority
    areas for launching ground applications are those
    having a concentration of cases.

132
EPIDEMIC MEASURES
  • Special attention should be focused on areas
    where people congregate during daylight hours,
    for example, hospitals and schools. If necessary,
    ultra-low-volume insecticides may be applied from
    aircraft. C47 or similar aircraft, smaller
    agricultural spray planes, and helicopters have
    been used to make aerial applications.
  • During the early stages of epidemics,
    ultra-low-volume spray of 4 malathion in diesel
    oil or kerosene may be used to spray all houses
    within a 100-m radius of the residence of DHF
    patients.

133
Eradication and Control
  • A. aegypti was eradicated from countries and
    whole continents with use of the techniques
    pioneered by the Rockefeller Foundation.
  • With time, the species successfully reestablished
    itself in much of its former range.

134
Eradication and Control
  • An eradication campaign in the United States was
    abandoned and was replaced by a program of
    disease surveillance and containment of
    introduced virus.

135
Eradication and Control
  • Mosquito control or eradication programs require
    the simultaneous use of two approaches
  • Reduction in breeding sites
  • Application of larvicides
  • Alternatively, a significant reduction in
    population may be effected by closely spaced
    application of adulticides.

136
Reduction in breeding sites
  • Source reduction campaigns should be well
    organized, supervised, and evaluated.
  • Includes proper disposal of discarded cans,
    bottles, tires, and other potential breeding
    sites not used for storage of drinking or bathing
    water.
  • Drinking and bathing water storage containers
    and flower vases should be emptied completely
    once weekly.

137
Reduction in breeding sites
  • Water containers that can not be emptied should
    be treated with Abate 1 sand granules at dosage
    of 1 ppm (e.g., 10 g of sand to 100 L of water).
  • Treatments should be repeated at intervals of 2
    to 3 months.

138
Application of larvicides
  • Vehicles-mounted or portable ultra-low-volume
    aerosol generators or mist blowers can be used to
    apply technical grade malathion or fenitrothion
    at 438 mL/ha.
  • Three applications made at 1-week intervals can
    suppress. A aegypti populations for about 2
    months.

139
Health Education
  • A. aegypti control has been maintained
    effectively in some tropical areas through the
    simple expedient of emptying water containers
    once a week.
  • During the yellow fever campaigns, strong
    sanitary laws made the breeding of mosquitoes on
    premises a crime punishable by fine or jail

140
Health Education
  • In the modern era, Singapore and Cuba have
    adopted these measures successfully.
  • Health education through mass media or through
    the schools has been attempted in Burma,
    Thailand, Malaysia, and Indonesia without
    spectacular success.

141
REFERENCES
  • WHO Technical Guides for Diagnosis, Treatment,
    Surveillance, Prevention and Control of Dengue
    Hemorrhagic Fever, WHO. Geneva, 1975.
  • Management of Dengue Fever in ICU by Arun Soni,
    Krishan Chugh, Anil Sachdev Dhiren Gupta.
  • Pediatric text book of Nelson
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