Dengue

 Professor.Shivaprasad

Dengue

 The word dengue is derived from African word denga: meaning

fever with hemorrhage

.

 Is caused by virus transmitted of bites of mosquito aedes.

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.

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.

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.

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.

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.

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

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 ;

Problem statement India

 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)

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.

ETIOLOGY

VIRUS

ETIOLOGY VIRUS

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

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.

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.

Etiology Types

 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

Etiology

Dengue like fever

 Three other arthropod born viruses cause similar febrile diseases with rash.

 Chikungunya, Onyong-nyong and West Nile Fever

Etiology

Dengue like fever

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

Etiology

Dengue 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.

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.

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.

Vector

 Aedes mosquitoes (Tiger mosquito): distinguished by white stripes on black body.  Important members aedes family:A. aegypty, A.vittatus and A. albopictus.

 They are most abundent during rainy season.

Vector

 Lays egg singly, and eggs are cigar shaped.

 Female mosquito acts as vector.

 They do not fly over long distance <100mts(110yards), this factor facilitates its eradication.

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.

Transmission

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

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

Pathogenesis

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

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.



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.

Pathology Microscopy

 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.

Pathology Microscopy

 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.

Pathology Microscopy

 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.

Pathology Microscopy

 Kidney: There 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.

Dengue Classification

 Dengue fever  Dengue hemorrhagic fever  Dengue shock syndrome

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.

CLINICAL PROFILE OF DENGUE IN CHILDREN

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.

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.

Materials & methods SETTING:

Vani vilas children’s hospital, Bangalore.

STUDY DESIGN :

Institution based case series study.

Materials &methods

 Children with

clinically suspected dengue infection

between September2002 & September2003.

 38 cases recorded

IgM positive

for dengue by ELISA (NIV, Bangalore)

Materials &methods



Case records were reviewed for –

 Age & sex distribution  Signs and symptoms – Typical & Atypical  Haematological parameters  Clinical course of the illness  Outcome

Materials &methods

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

Age & sex distribution

10 8 6 4 2 0 1 2 <1 yr 7 4 9 8 3 4 1-5 yrs 5-10 yrs >10 yrs Male Female

25 20 15 10 5 0 11

Population distribution

22 6 Rural Urban slum Urban

30 20 10 0 16 9

Manifestations

20 Dengue fever DHF DSS

Fever

20 15 10 5 0 14 15 7 7 <5 days 5-10 days >10 days Biphasic

Symptoms- Typical

20 15 10 5 0 16 2 6 12 Myalgia Arthralgia Retro-orbital pain Head ache

12.5

12 11.5

11 10.5

Symptoms - Typical

12 Flushing Rashes 11

Atypical symptoms

2 1 4 3 0 2 3 1 1 Seizures Altered sensorium Acute liver failure Acute renal failure

25 20 15 10 5 0 10 17 20 9

Signs

Restlessness/ lethargy Cold extremities Hypotension Bleeding

30 20 10 0 25 7 8

Signs

Hepatomegaly Pleural effusion/Ascites Acalculous cholecystitis

20 15 10 5 0

LAB

7 12 19

Platelet counts

<20,000 20,000-50,000 50,000-1,00,000 >1,00,000

Hematocrit

10 8 6 4 2 0 9 1 1 1 5 5 3 v <20 20-25 25-30 30-35 35-40 40-45 >45

15 10 5 0

Recovery - Hypotension

14 2 1 3 1 day 2 days 3days >3days

Recovery - Platelets

8 2 0 6 4 2 7 4 5 1 1day 2days 3days 4days >4days

3 2 1 0 6 5 4

Recovery – Rhythm abnormalities

5 1 Bradycardia Arrhythmia

Outcome

40 30 20 10 0 35 3 Recovered Died

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  Retro–orbital pain(16%) and biphasic fevers(18%) were seen in only a minority.

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, 3 rd an infant, terminally ill referred for ventilator care.

 Unusual manifestations  Seizures  Altered sensorium  Acalculous cholecystitis  Acute liver failure  Acute renal failure.

Conclusions

Conclusions

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

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.

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.

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.

Diagnosis D.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.

Diagnosis



D.H.F

WHO Criteria For DHF :  Fever, Minor or Major Hemorrhagic manifestations.

 Thrombocytopenia ( < 100000 / mn3)  Objective evidence of increased capillary permeability (hematocrit increased > 20%) X ray pleural effusion  Hypoalbuminemia.

 DSS : Above mentioned criteria plus hypo tension and narrow pulse pressure ( < 20 mm of Hg)

Diagnosis D.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.

Diagnosis D.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

Diagnosis D.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.

DF /DHF

DF 

Grad e

DHF DHF DHF I II III DHF IV

Symptoms Laboratory

Fever with two or more of the following signs; headache, retro orbital pain, Myalgia, arthralgia. Above signs plus positive tourniquet test. Above signs plus spontaneous bleeding Luecopenia occasionally Thromocytopenia may be present, no evidence of plasma leakage. Thrombocytopenia <100,000 HCt rise>20% Thrombocytopenia <100,000, HCt rise>20%. Above signs plus circulatory failure (rapid weak pulse, pressure, cold clammy skin, restlessness and capillary refill time >3sec) Profound shock with undectable blood pressure and pulse Thrombocytopenia <100,000, Het rise >20% Thrombocytopenia <100,000, rise >20%.

D/D D.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

D/D D.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.

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.

         

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 > 3 seconds.

Narrowing of pulse pressure (<20 mm Hg) or Hypo tension.

Hematocrit of 40 or rising hematocrit. Platelet count of < 1,00000/ mm3 Acute abdominal pain Evidence of Plasma leakage. Eg. Pleural effusion /Ascities

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 < 400C.

Analgesics and mild sedation may be required to control pain

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.

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.

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.

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.

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.

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.

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.

DHF

Fluid Management

DHF Fluid 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

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.

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.

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.

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.

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

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.

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.

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

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.

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).

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.

Management Blood 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.

Management Platelet 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.

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).

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.

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.

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.

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.

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

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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

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.

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