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government sector. Another is the institution of universal insurance, with payrollcontributions from the employed and government-subsidized premiums for the poor.These should be combined with tighter supervision and quality control by thepanchayat to ensure more cost-effective health care delivery in the rural areas.

V. RAMAN KUlTYAchutha Menon Centre for Health Science Studies

Sree Chitra Tirunallnstitutefor Medical Sciences and TechnologyThiruvananthapuram

Kerala

REFERENCESI National Sample Survey Organization. Forty-second round. July 1986-June 1987. Report No. 364. Morbidity and

Utilization a/Medical Services. New Delhi:Department of Statistics. Government of India. 1989.2 National Council of Applied Economic Research. Household Survey a/Medical Care. New Delhi:NCAER. 1992.3 Kannan KP. Thankappan KR. Raman Kuny V. Aravindan KP. Health and Development in Rural Kerala.

Trivandrum:Kerala Sastra Sahitya Parishad, 1991.4 Rajaratnam J, Abel R, Duraisamy S, John KR. Morbidity pattern, health care utilization and per capita health

expenditure in a rural population of Tamil Nadu. Natl Med J India 1996;9:259-62.

Dengue Haemorrhagic Fever and Shock SyndromeDengue fever has been assuming progressively increasing public health importancein the tropical and SUbtropical countries during the past decade and this trend is likelyto continue unless effective measures to control the transmission of the infection areinstituted worldwide. IThe disease is caused by four serotypes ofthe dengue virus, anyof which may be responsible for an epidemic. Dengue haemorrhagic fever (DHF) anddengue shock syndrome (DSS) are serious clinical manifestations of the infection andmay be fatal in 40%-50% of untreated patients.' However, with appropriate treatment,the mortality can be brought down to 1%-5%.3

Dengue fever is a disease of uncontrolled urbanization resulting in overcrowding,and falling standards of sanitation and waste disposal.' Epidemic transmissionrequires a favourable temperature (>20 "C) and stagnant water for the breeding ofAedes aegypti. Outbreaks in urban areas infected with the Aedes mosquito may beexplosive with attack rates reaching up to 70% of the population+The environmentaltemperature affects the transmission dynamics of dengue infection; a higher temperaturewithin range of mosquito viability leads to more infectious mosquitoes which bitemore frequently."

The pathogenesis of DHFIDSS is not clear. It has been observed that sequentialinfection by any two of the four serotypes of dengue virus results in DHFIDSS inhyperendemic areas.' How a second dengue infection causes severe disease and whyonly some patients get a severe disease remains unclear. A recent study from Thailandsuggests that when the antibody residual from the first infection is able to neutralizea second virus type, even weakly, a secondary infection occurs but its severity isdownregulated and the disease is mild. When no cross-reactive neutralizing anti-bodies are present, a second infection is under the influence of enhancing antibodiesand the resulting infection and disease are severe. An alternative explanation is thatthe Southeast Asian dengue virus may be inherently more capable of supportingsevere antibody-enhanced infection than the virus in other geographic areas.'

The DHFIDSS remained a disease of children and young adults for two decadesafter its identification in the 1950s. In Singapore, the median age for DHF in 1973 was14 years and almost all the fatal cases were below 10 years of age." The median agein 1994 increased to 28 years and 9 of the 11 serologically confirmed cases were19 years or older," A similar experience has been reported from Malaysia'? and Fiji."

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In an outbreak of DHFIDSS in Delhi in 1988, children as well as adults wereaffected.":" In this year's epidemic in Delhi, more than half of the hospitalizedpatients were adults (unpublished data). The reasons for this change in the epidemiologyof DHF are not clear and need to be investigated further.

The diagnostic criteria for DHFIDSS include thrombocytopenia (platelets <100 000per cmm), haemoconcentration (change in haematocrit by more than 20% of thebaseline), haemorrhagic manifestations and/or hypotension.P By these criteria, apatient presenting with a history of fever, bleeding manifestations and thrombo-cytopenia but without haemoconcentration cannot be diagnosed as DHFIDSS. Thedocumentation of haemoconcentration presents certain difficulties since the baselinehaematocrit is often not available and may well be below normal on account ofnutritional factors. Further, severe bleeding may decrease the haematocrit by thetime the patient presents to a hospital. Sumarmo et at. I~ observed a lack of haemo-concentration in 9 of the 30 virologically confirmed fatal cases of dengue fever withthrombocytopenia and massive bleeding. In our experience, during the 1996 epi-demic in Delhi, about 10% of hospitalized children and a majority of adults admittedto the All India Institute of Medical Sciences, did not have evidence ofhaemoconcentration (unpublished data). In view of this, there is a need to redefineDHFIDSS and dengue fever with haemorrhagic manifestations.

The DHFIDSS predominantly affects the blood vessels, bone marrow, liver andskin. Its clinical manifestations include skin and mucosal bleeding, hypotension,hepatomegaly, hypovolaemic shock and serous or haemorrhagic effusions in theserous cavities of the body. Occasionally, it may be associated with hepatitis,encephalitis and glomerulonephritis.F:"

The treatment of DHFIDSS consists of administration of crystalloids by the intra-venous route. In unresponsive patients, colloids orplasma infusions are recommended.Blood transfusions are required in the presence of massive haemorrhage or a fallinghaernatocrit." The role of platelet infusions in severely thrombocytopenic patientswith or without severe bleeding, in the absence of randomized clinical trials, remainsuncertain. They seem to have a role in patients with massive bleeding and severethrombocytopenia. However, their effect on survival in patients with less severeforms of bleeding needs to be evaluated. This is important, particularly duringepidemics, as the availability of platelet concentrates is unlikely to match the demand.In a double-blind, placebo-controlled trial, high dose methyl prednisolone failed toshow any benefit in established DSS.19High dose intravenous immunoglobulin hasnot been tried in the management of DSS, but is unlikely to be a practical propositionin view of the high costs involved.

Close monitoring and appropriate fluid therapy of patients with DHFIDSS hasresulted in considerable reduction in mortality from these serious complications.However, further work is required to elucidate the mechanism of DHFIDSS and todevise simpler interventional strategies to tackle this growing public health problem.

REFERENCESI Halstead SB. The twentieth century dengue pandemic: Need for surveillance and research. World Health Stat

Quart 1992;45:292-8.2 BensonAS (ed). Control of communicable diseases in man. Washington DC:American Public HealthAssociation,

1990.3 Halstead SB. Global epidemiology of dengue: Health system in disarray. Trop Med 1993;35: 137-46.4 Horton R. The infected metropolis. Lancet 1996;347:134-5.5 Gubler OJ, Trent DW. Emergence of epidemic dengue/dengue hemorrhagic fever as a public health problem in

America. Infect Agent Dis 1994;2:383-93.6 Patz JA, Epstein PR, Burke TA, Balbus M. Global climate change and emerging infectious diseases. lAMA

19%;275:217-23.7 Halstead SB. Dengue haemorrhagic fever. In: Gear JHS (ed). Handbook of viral and rickettsial haemorrhagic

fevers. Boca Raton, Florida:CRC Press, 1988:85-94.8 Chan KL, Ng SK, Chow LM. The 1973 dengue hemorrhagic syndrome in Singapore and its control. Sing Med 1

1977;18:81-93.9 Goh KT. Changing epidemiology of dengue in Singapore. Lancet 1995;346: I098.

10 Dengue and dengue haemorrhagic fever in Malaysia. Wkly Epidemiol Rec 1995;70:243-4.II Fagbaml AH, Mataika JV, Shrestha M, Gubler DJ. Dengue type I epidemic with haemorrhagic manifestations In

Fiji. Bull World Health Organ 1995;73:291-7.12 Kabra SK, Verma IC. Arora NK, Jain Y, Kalra V. Dengue haemorrhagic fever in children in Delhi. Bull World

Health Organ 1992;70: I05-8.

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13 Acharya SK. Buch P, Irshad M. Gandhi BM. Joshi YK. Outbreak of dengue fever in Delhi. Lancet 1988;2:I485-{i.

14 Srivastava SK. Suri S, Bhasin A. Srivastava L. Bhardwaj M. An epidemic of dengue haemorrhagic fever anddengue shock syndrome in Delhi: A clinical study. Ann Trop Pediatr 1990;10:329-34.

15 World Health Organization. Dengue haemorrhagic fever: Diagnosis, treatment and control. Geneva:WorldHealth Organization, 1986.

16 Sumanno HW. Jahja E, Gubler DJ, Suharyono W, Sorensen K. Clinical observations on virologically confirmedfatal dengue infections in Jakarta, Indonesia. Bull World Health Organ 1983;61:693-701.

17 Lum Le, Lam SK. Choy YS. George R. Harun F. Dengue encephalitis: A true entity. Am J Trop Med Hyg1996;54:256-9.

18 Nimmannitya S, Thisyakorni U. Hemschehan V. Dengue haemorrhagic fever with unusual manifestations. SouthAsian J Trop Med Public Health 1987;18:398-406.

19 Tassniyom S, Vasanawathan S, Chirawatkal A. Rojanasuphot S. Failure of high dose methyl prednisolone inestablished dengue shock syndrome: A placebo-controlled, double blind study. Pediatrics 1993;92:111-15.

1. N. PANDE

Department of MedicineAll India Institute of Medical Sciences

New Delhi

S.K. KABRA

Department of PaediatricsAll India Institute of Medical Sciences

New Delhi