Dengue

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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.

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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.

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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.

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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.

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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.

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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.

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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

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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

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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.

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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.

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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.

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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.

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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
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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

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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.

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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

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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.

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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.

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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

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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.

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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).

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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.

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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.

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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.

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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).

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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.

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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.

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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.

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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.

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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

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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