Lakshmi V Paed KIMSB 2013

I
A STUDY ON CLINICAL PROFILE IN CORRELATION WITH

LABORATORY INVESTIGATIONS AND RADIOLOGICAL
FINDINGS IN DENGUE FEVER.
By
Dr. LAKSHMI.V M.B.B.S,

Dissertation submitted to the
Rajiv Gandhi University of Health Sciences, Bangalore, Karnataka
In partial fulfillment of the requirements for the degree of
DOCTOR OF MEDICINE
IN
PAEDIATRICS

Under the Guidance of
Dr. CHANDRAKALA.P. M.D.,
Associate Professor

DEPARTMENT OF PAEDIATRICS
KEMPEGOWDA INSTITUTE OF MEDICAL SCIENCES
K.R.ROAD, BANGALORE, KARNATAKA
2013

II

RAJIV GANDHI UNIVERSITY OF HEALTH SCIENCES,
BANGALORE, KARNATAKA
DECLARATION BY THE CANDIDATE
I hereby declare that this dissertation/thesis entitled A STUDY ON CLINICAL
PROFILE IN CORRELATION WITH LABORATORY
INVESTIGATIONS AND RADIOLOGICAL FINDINGS IN DENGUE
FEVER is a bonafide and genuine research work carried out by me under the
guidance of Dr.CHANDRAKALA.P M.D, Associate Professor of Paediatrics,
KIMS, Bangalore.

Date:
Place: Bangalore Dr. LAKSHMI.V

III

CERTIFICATE BY THE GUIDE

This is to certify that the dissertation entitled A STUDY ON CLINICAL
FEVER is a bonafide research work done by Dr. LAKSHMI.V, Postgraduate
student, Department of Pediatrics, Kempegowda Institute of Medical Sciences,
Bangalore, in partial fulfillment of the requirement for the degree of DOCTOR
OF MEDICINE IN PAEDIATRICS.

Dr. CHANDRAKALA.P. M.D,
Associate Professor of Paediatrics
Kempegowda Institute of Medical
Sciences and Research Centre
Date: Bangalore
Place: Bangalore

IV

ENDORSEMENT BY THE HOD, PRINCIPAL/HEAD OF THE
INSTITUTION

This is to certify that the dissertation entitled A STUDY ON CLINICAL
FEVER is a bonafide research work done by Dr. LAKSHMI.V Postgraduate
Student in Pediatrics, Kempegowda Institute Of Medical Sciences, Bangalore,
under the guidance of Dr. CHANDRAKALA.P M.D, Associate Professor of
Paediatrics, Kempegowda Institute of Medical Sciences and Research Centre ,
Bangalore

Signature and Seal of HOD Signature and Seal of Dean
Dr. A.C.RAMESH M.B.B.S., M.D.,DCH

Dr. M.K. SUDARSHAN

M.D (BHU), FAMS
Professor and Head of Department Dean And Principal
Department of Paediatrics Kempegowda Institute of Medical Sciences
Kempegowda Institute of Medical Sciences and Research Centre
and Research Centre Bangalore.
Bangalore.

Date : Date :
Place : Bangalore Place : Bangalore

V

COPYRIGHT

DECLARATION BY THE CANDIDATE

I hereby declare that the Rajiv Gandhi University of Health Sciences,
Karnataka shall have the rights to preserve, use and disseminate this dissertation /
thesis in print or electronic format for academic / research purpose.

Date:

Rajiv Gandhi University of Health Sciences, Karnataka

VI

ACKNOWLEDGMENT
I consider it my utmost privilege and honour to owe my immense gratitude
and respect to my mentor and guide Dr. CHANDRAKALA.P, Associate
Professor of Paediatrics, Kempegowda Institute of Medical Sciences and
Research Centre, Bangalore, who has long and steadfastly encouraged, constantly
guided and supported me. Her efforts, wise expertise and counsel have had an
indelible impact on me throughout my post-graduate course and on the final form
and quality of this dissertation.
I am extremely thankful to Dr. M. K. SUDARSHAN, Dean, Principal
and Professor of Community Medicine, Kempegowda Institute of Medical
Sciences, Bangalore for giving me an opportunity to conduct this study.
I immensely thank our beloved Head of Department of Pediatrics,
Dr.A.C.RAMESH who has been a friend, philosopher and a guide throughout
my course for his valuable support.
I thank Dr. SURESH., Medical Superintendent, Dr.(Capt.)
G.S.VENKATESH, Medical Director and Dr. VEERANNA, AMO, for allowing
me to conduct this study in this Institute and for their valuable support during the
study period.
It is with a humble sense of gratitude that I express my heartfelt thanks to
Dr. NISARGA.R, Dr. S.R. KESHAVAMURTHY, Dr. SRINIVASA.S,
Dr.YASHODHA.H.T, Professors in department of Paediatrics for their help and
guidance throughout my course.

VII

I also thank Dr. MURALI.B.H, Dr. POORNIMA SHANKAR,
Associate Professors in department of Paediatrics for their professional guidance
and encouragement during my post-graduate course.
I am immensely thankful to Dr.MADHU.G.N, Dr.H.S.RAMYA,
Dr.HARISH.J, Dr.SIVASHARANAPPA, Dr.GIRISH and Dr.SUSHANTH,
Assistant Professors in department of Paediatrics for their kind guidance during
the course.
I thank Dr.MOHAN KUMAR, Dr.DEEPASHRI, Dr.TANVIR AND
Dr.SHYLAJA, Senior residents in the department of Paediatrics for their
valuable support.
I thank Dr.NARESH, Dr.JAYAPRAKASH, Dr.SNEHA,
Dr.ARCHANA and all my other Post graduate colleagues for their wholehearted
support.
On a personal note, special thanks to my Husband MR. KARTHIK.J.
LINGAM , a dear friend, for his endless patience, constant encouragement and
unconditional moral support in this process of learning.
My most regardful thanks and I am ever grateful to my Father Mr.
S.VENKATESHA, my Mother Mrs. VIBHA.V, my Brother Mr. NAVEEN
KUMAR.V and my IN-LAWS, who have been a constant motive force and
support behind everything I do in my life. It is their love, prayers and sacrifice
that has made my education possible.
My sincere thanks to all the patients and their parents who have
participated in this study, without whose valuable time and co-operation, this
study would have been just a dream.
VIII

I also thank the Nursing staff, Dept Steno Mr. BABU and Dept Attender
Mr. PURANDAR for their help and encouragement during my PG course.
I thank M/s CYBER GARDEN for their meticulous typing and styling of
this script.
Above all, I thank the Almighty for showering me with His love and for
having blessed me to pursue the PG course in the most noble subject of the most
noble profession i.e. Paediatrics.

Date:

IX

ABSTRACT
Background: Dengue is the most important emerging tropical viral disease of
humans in the world today. It is estimated that there are between 50 and 100
million cases of dengue fever (DF) and about 500,000 cases of dengue
hemorrhagic fever (DHF) each year which require hospitalization. Over the last
10-15 years, DF/DHF has become a leading cause of hospitalization and death
among children in the South-East Asia Region of WHO, following diarrhoeal
diseases and acute respiratory infections. Earlier it was prevalent in those areas
with humid atmosphere and plenty of rains with changing monsoon pattern this
disease becoming prevalent in deccan land scape including Karnataka. Dengue is
a mosquito-borne disease, caused by serologically related but antigenically
distinct single-strand positive sense RNA viruses; the viruses have been grouped
into four serotypes (DENV-1 through DENV-4) belonging to the genus Flavivirus
(family Flaviviridae). Aedes aegypti is the primary mosquito vector; however,
other species from the genus Aedes ,such as Aedes albopictus , can also be
vectors of dengue virus transmission. It is important to recognise the clinical
signs and symptoms, alterations in the biochemical parameters, radiological
findings and the multi system involvement pattern to manage dengue cases
effectively. The current study is undertaken to study the various clinical
presentation , laboratory parameters and radiological features of Dengue Fever
and to evaluate common modes of clinical presentation and complications of
dengue in our hospital and to correlate these features with lab findings and the
various factors affecting the prognosis which may help us in early diagnosis and
better case management.
X
Aim: To assess various clinical manifestations of Dengue fever, to describe the
atypical presentation and complications, to establish the diagnosis of dengue fever
based on dengue antigen (NS 1) and antibody (IgM , IgG) and to find the
association between the clinical findings with laboratory investigations and
radiological findings.
Methods: 100 cases of suspected cases of dengue infection i.e. children below 18
yrs of age with clinical features suggestive of Dengue infection and children
presenting with fever of acute onset (<2wks), pain abdomen, vomiting, rash,
flushed appearance and bleeding manifestation admitted to KIMS, Bangalore
between December 2010 to April 2012 were studied. A detailed clinical history
and physical examination was done and baseline investigations were performed .
The cases were followed-up daily for the clinical and laboratory parameters.
WHO classification and case definition was used to classify Dengue Fever,
Dengue Hemorrhagic Fever and Dengue Shock Syndrome. And were treated
according to WHO guidelines. The data related to each of these cases was
collected, compiled and analysed.
Results: Out of 100 children in this study 36% cases belongs to DF, 33% cases
belongs to DHF, 15% cases belongs to DSS group and 16% cases belongs to DLI.
Conclusion: The clinical manifestation, examination finding, laboratory
parameters and radiological evidences in this study was similar to other Indian
studies.
In our present study classical dengue fever was most common presentation
followed by DHF and DSS.
XI
In children importance should be given to symptoms like, fever, vomiting,
abdominal pain, retro orbital pain, bleeding, musculoskeletal pain and flushing
during an epidemic of dengue fever.
If these associated with positive tourniquet test, hepatomegaly, elevated liver
enzymes, elevated PTT, thickened gall bladder on USG abdomen, pleural effusion
on chest X-ray, a strong possibility of dengue fever should be considered.
Platelet count does not correlate with severity of the disease.
During epidemics, differential diagnosis of dengue fever to be strongly considered
in a child with fever.
A focused history , detailed clinical examination and appropriate relevant
investigations can aid for early diagnosis and treatment. Proper evaluation of the
progress of the disease is a key in the management of disease.

Keywords : Dengue fever; Dengue Hemorrhagic Fever; Dengue Shock
Syndrome; Thrombocytopenia; Epistaxis; Liver enzymes; Shock; Bleeding;
WHO; Tourniquet test; Hematocrit.

XII

LIST OF ABBREVIATIONS USED
+/ - Present or absent
ADE Antibody-dependent enhancement
ARDS Acute Respiratory Distress Syndrome
ALT Alanine transaminase
ALK Alkaline phosphatase
APTT Activated partial thromboplastin time
ARBO Arthropod-borne
AST Aspartate transaminase
BT Bleeding time
C Complement
CD Cluster of Differentiation
CMV Cytomegalovirus
CNS Central nervous system
CT Clotting time
CVS Cardiovascular System
Cu.mm Cubic millimeter
CXR Chest X-ray
DEN Dengue
DF Dengue fever
DHF Dengue hemorrhagic fever
DIC Disseminated intravascular coagulation
DNA Deoxyribose Nucleic Acid
DSS Dengue shock syndrome
XIII
EBV Epstein Barr Virus
ELISA Enzyme linked immunosorbent assay
GB Guillain Barre Syndrome
GIT Gastrointestinal Tract
Hb Haemoglobin
HCT Hematocrit
HLA Human Leucocyte Antigen
IFN Interferon
IgM/IgG Immunoglobulin M/Immunoglobulin G
IL Interleukin
JEV Japanese encephalitis virus
KD Kilo Dalton
LN Lymphadenopathy
LFT Liver function test
MAC ELISA IgM Antibody Capture Enzyme linked immunosorbent assay
MRI Magnetic resonance imaging
NS Nonstructural protein
NSAIDs Non steroidal anti inflammatory drugs
ORS Oral Rehydration Solution
PCR Polymerase chain reaction
PT Prothrombin time
RBC Red blood corpuscles
RNA Ribo nucleic acid
ROP Retro orbital pain
RR Respiratory Rate
XIV
RS Respiratory system
SA Serum Albumin
SGOT Serum glutamate oxaloacetate transaminase
SGPT Serum glutamate pyruvate transaminase
SLEV Saint Louis encephalitis virus
TC/TLC Total leucocyte count
TNF Tumour necrosis factor
USG Ultra sonography
WBC White blood corpuscles
WHO World health organization
WNV West Nile virus
YFV Yellow fever virus

XV
TABLE OF CONTENTS
SI No. PARTICULARS
Page
No.
1 INTRODUCTION 1
2 OBJECTIVES 2
3 REVIEW OF LITERATURE 3 - 54
3.1 INTRODUCTION 3
3.2 HISTORY 3
3.3 EPIDEMIOLOGY 8
3.4 PATHOLOGY 20
3.5 PATHOGENESIS 23
3.6 CLINICAL FEATURES 30
3.7 DIAGNOSIS 44
3.8 MANAGEMENT 47

3.9 VECTOR SURVEILLANCE AND
CONTROL
52
4 METHODS AND MATERIALS 55 - 58
4.1 SOURCE OF DATA 55

4.2 METHODS OF COLLECTION OF
DATA
55
4.3 SAMPLE SIZE AND DESIGN 55
4.4 METHODOLOGY 56
5 RESULTS 59 - 95
6 DISCUSSION 96 - 107
7 CONCLUSION 108 - 109
XVI
8 SUMMARY 110 - 111
9 BIBLIOGRAPHY 112 - 124
10 ANNEXURES

10.1 ETHICAL CLEARANCE FOR
DISSERTATION STUDY
125
10.2 CLINICAL PHOTOGRAPHS 126
10.3 PROFORMA 127
10.4 KEY TO MASTER CHART 133
10.5 MASTER CHART

XVII
LIST OF TABLES

SI
N
o.
TABLE
PAGE
NO
1
DIAGNOSIS CLINICAL SPECTRUM OF
CASES
59
2 AGE DISTRIBUTION OF PATIENTS 60
3
AGE DISTRIBUTION OF PATIENTS
ACCORDING TO CLINICAL SPECTRUM
61
4 GENDER DISTRIBUTION OF PATIENTS 62
5
GENDER DISTRIBUTION OF CASES
63
6 SYMPTOMATOLOGY OF CASES 64
7 ANALYSIS OF SYMPTOMATOLOGY 65
8 SIGNS IN PATIENTS 67
9 TEMPERATURE 68
10
DISTRIBUTION OF SIGNS ACCORDING
TO CLINICAL SPECTRUM
69
11 RESPIRATORY SYSTEM EXAMINATION 70
12
DISTRIBUTION OF AIR ENTRY
(RESPIRATORY SYSTEM)
ACCORDING TO CLINICAL SPECTRUM OF
CASES
71
13
RELATIONSHIP BETWEEN VARIOUS SITES
OF BLEEDING AND DENGUE FEVER
72
14
RELATIONSHIP BETWEEN VARIOUS SITES
OF
BLEEDING AND DENGUE FEVER
73
XVIII
ACCORDING
TO CLINICAL SPECTRUM
15 TYPES OF SKIN RASHES 74
16
DISTRIBUTION OF TYPES OF SKIN RASHES
75
17 TOURNIQUET TEST 76
18
ANALYSIS OF TOURNIQUET TEST RESULTS
77
19 PLATELET COUNT 78
20 PLATELET COUNT 78
21
HAEMOGLOBIN LEVELS ACCORDING TO
CLINICAL SPECTRUM OF CASES
79
22 HAEMOGLOBIN LEVELS (Hb g%) 79
23
HEMATOCRIT (PACKED CELL VOLUME)
ACCORDING TO CLINICAL SPECTRUM OF
CASES
80
24 HEMATOCRIT (PCV%) 80
25
TOTAL LEUCOCYTE COUNT ACCORDING
TO CLINICAL SPECTRUM OF CASES
81
26
TOTAL LEUCOCYTE COUNT (TLC in cells/cu
mm)
81
27
PROTHROMBIN TIME ACCORDING TO
CLINICAL
SPECTRUM OF CASES
82
28 PROTHROMBIN TIME (PT in seconds) 82
29
ACTIVATED PARTIAL THROMBOPLASTIN
TIME ACCORDING TO CLINICAL SPECTRUM
OF CASES
83
30
ACTIVATED PARTIAL THROMBOPLASTIN
TIME
83
XIX
(APTT in seconds)
31
BLOOD UREA ACCORDING TO CLINICAL
SPECTRUM OF CASES
84
32 BLOOD UREA 84
33
SERUM CREATININE ACCORDING TO
CLINICAL
SPECTRUM OF CASES
85
34 SERUM CREATININE 85
35
LIVER FUNCTION TESTS- SERUM
GLUTAMATE OXALOACETATE
TRANSAMINASE (SGOT)
87
36
SERUM GLUTAMATE PYRUVATE
TRANSAMINASE (SGPT)
87
37
SERUM ALBUMIN ACCORDING TO
CLINICAL SPECTRUM OF CASES
88
38 SERUM ALBUMIN (g/dl) 88
39 SERUM ELECTROLYTES 89
40 DENGUE SEROLOGY 90
41
DENGUE SEROLOGY ACCORDING TO
CLINICAL
SPECTRUM OF CASES
91
42 CHEST X-RAY 92
43
CHEST X-RAY FINDINGS ACCORDING TO
CLINICAL SPECTRUM
93
44 ULTRASONOGRAPHY 94
45
ULTRASONOGRAPHY FINDINGS
95

XX

LIST OF FIGURES
SI
No.
FIGURES
PAGE
NO
1
ANNUAL WORLDWIDE INCIDENCE OF
DENGUE FEVER
5
2
WORLD WIDE DISTRIBUTION OF DENGUE
FEVER
6
3 EMERGENCE OF DEN/DHF 6
4 FLAVIVIRUS VIRION STRUCTURE 10
5 DENGUE VIRUS 11
6 FLAVIVIRUS GENOME 12
7 AEDES AEGYPTI MOSQUITO 13
8 LIFE CYCLE OF AEDES AEGYPTI MOSQUITO 14
9 TRANSMISSION OF DENGUE VIRUS 20
10
MECHANISM OF ACTION OF DENGUE
VIRUS
28
11 COURSE OF DENGUE ILLNESS 34
12 COMPARISON OF DIAGNOSTIC TESTS 44
13
PRIMARY & SECONDARY DENGUE
INFECTION
44
14 RASH IN CASE OF A DENGUE FEVER 126
15
RIGHT SIDED PLEURAL EFFUSION IN CASE
OF DENGUE FEVER
126

1
INTRODUCTION
Dengue fever is an arthropod borne viral fever. It is acquiring epidemic
proportion in this part of the world.
The geographical distribution has greatly expanded over the last 30 years,
because of increased potential for breeding of Aedes aegypti. This has been prompted
by demographic explosion, rapid growth of urban centers with strain on public
services, such as potable water and rainwater harvesting. Dengue fever (DF) with its
severe manifestations such as Dengue Hemorrhagic Fever (DHF) and Dengue Shock
syndrome (DSS) has emerged as a major public health problem of international
concern.
1
Today, Dengue ranks as one of the most important mosquito-borne viral
disease in the world. In the past 50 years, its incidence has increased 30-fold with
significant outbreaks occurring in five of six WHO regions. Current estimates report
that, atleast 112 countries are endemic for Dengue and about 40% of the world
populations (2.5-3 billion people) are at risk in tropics and sub-tropics. Estimates
suggest that annually 100 million cases of dengue fever and half a million cases of
dengue haemorrhagic fever (DHF) occur in the world with a case fatality in Asian
countries of 0.5%3.5%. 90% of DHF subjects are less than 15 years of age. Early
recognition and prompt initiation of treatment are vital if disease related morbidity
and mortality are to be controlled.
2
Dengue fever is caused by an RNA virus of the family Flaviviridae;
genus Flavivirus. It has 4 closely related serotypes DEN 1 ,DEN 2 , DEN 3 , DEN4
which bear partial cross reactivity with each other. The viruses are transmitted to man
by the bite of infective mosquitoes, mainly Aedes aegypti.
2
OBJECTIVES

1. To assess various clinical manifestations of Dengue fever.
2. To describe the atypical presentation and complications.
3. To establish the diagnosis of dengue fever based on dengue antigen (NS 1)
and antibody ( IgM , IgG )
4. To find the association between the clinical findings with laboratory
investigations and radiological findings.

3
REVIEW OF LITERATURE
3.1 INTRODUCTION
Dengue is the most rapidly spreading mosquito-borne viral disease in the
world. In the last 50 years, incidence has increased 30-fold with increasing geographic
expansion to new countries and, in the present decade, from urban to rural settings.
An estimated 50-100 million dengue infections occur annually and approximately 2.5
billion people live in dengue endemic countries.
3.2 HISTORY OF DENGUE
Dengue fever (DF) is an old disease; the first record of a case of probable
dengue fever is in a Chinese medical encyclopedia from the J in Dynasty (265420
AD) which referred to a water poison associated with flying insects.
6
As the global
shipping industry expanded in the 18th and 19th centuries, port cities grew and
became more urbanized, creating ideal conditions for the principal mosquito vector,
Aedes aegypti. Both the mosquitoes and the viruses were thus spread to new
geographic areas causing major epidemics. Because dispersal was by sailing ship,
however, there were long intervals (10-40 years) between epidemics. In the aftermath
of World War II, rapid urbanization in Southeast Asia led to increased transmission
and hyperendemicity. The first major epidemics of the severe and fatal form of
disease, dengue haemorrhagic fever (DHF), occurred in Southeast Asia as a direct
result of this changing ecology.
In the last 25 years of the 20th century, a dramatic global geographic
expansion of epidemic DF/DHF occurred, facilitated by unplanned urbanization in
tropical developing countries, modern transportation, lack of effective mosquito
control and globalization. As we go into the 21st century, epidemic DF/DHF is one of
4
the most important infectious diseases affecting tropical urban areas. Each year there
are an estimated 50-100 million dengue infections, 500000 cases of DHF that must be
hospitalized and 20000-25000 deaths, mainly in children. Epidemic DF/DHF has an
economic impact on the community of the same order of magnitude as malaria and
other important infectious diseases. There are currently no vaccines nor antiviral
drugs available for dengue viruses; the only effective way to prevent epidemic
DF/DHF is to control the mosquito vector, Aedes aegypti.
3
The first definite clinical report of Dengue is attributed to Benjamin Rush in
1789.
4

Since the geographical distribution of Dengue fever is world-wide, involving
nearly all tropical and subtropical countries, it has many names like-dandy fever,
Denguero, denga, dunga,break-bone fever, bouguet, seven day fever, bonon,
chapenonada, Knieueble, Tokkive-ana, Mal de genoux, homa mguu, and coup-d-
barre.
5
The origins of the word dengue are not clear, but one theory is that it is
derived from the Swahili phrase "Ka-dinga pepo", meaning "cramp-like seizure
caused by an evil spirit". The Swahili word "dinga" may possibly have its origin in
the Spanish word "dengue" meaning fastidious or careful, which would describe the
gait of a person suffering the bone pain of dengue fever . Alternatively, the use of the
Spanish word may derive from the similar-sounding Swahili. Slaves in the West
Indies who contracted dengue were said to have the posture and gait of a dandy, and
the disease was known as "Dandy Fever".
The first recognized Dengue epidemics occurred almost simultaneously in
Asia, Africa, and North America in the 1780s, after the identification and naming of
the disease in 1779.
5
Benjamin Rush coined the term "breakbone fever" because of the symptoms
of myalgia and arthralgia. The viral etiology and the transmission by mosquitoes
were only deciphered in the 20
th
century. Nowadays, about 2.5 billion people, or 40%
of the worlds population, live in areas where there is a risk of dengue transmission .
Dengue spread to more than 100 countries in Asia, the Pacific, the Americas, Africa,
and the Caribbean.

Fig 1: ANNUAL WORLDWIDE INCIDENCE OF DENGUE FEVER.
The appellation of break-bone fever for dengue is attributed to the popular
name given to the disease in the first described epidemic of an illness that is clinically
compatible with dengue in Philadelphia in 1780.
6

Dengue hemorrhagic fever has been recognized as a separate disease entity
from classical dengue fever since the second half of twentieth century with the first
out break called Philippine Hemorrhagic fever in 1953. This was followed by out
break in Thailand in 1958, which was referred to as Thai hemorrhagic fever.The
term Dengue shock syndrome was coined to describe the cases of DHF with shock.
6
The clinical studies indicated that it was caused by increased vascular permeability
and resultant intravascular hypovolemia.
7

MAGNITUDE OF THE PROBLEM : WORLD SCENARIO

Fig 2 : WORLD WIDE DISTRIBUTION OF DENGUE FEVER

Fig 3 : EMERGENCE OF DEN/DHF
Dengue and dengue haemorrhagic fever are present in urban and suburban
areas in the Americas, South-East Asia, the Eastern Mediterranean and the Western
Pacific and dengue fever is present mainly in rural areas in Africa.
7
Several factors have combined to produce epidemiological conditions in
developing countries in the tropics and subtropics that favour viral transmission by the
main mosquito vector, Aedes aegypti:
rapid population growth,
rural-urban migration,
inadequate basic urban infrastructure (eg. unreliable water supply
leading householders to store water in containers close to homes),
increase in volume of solid waste, such as discarded plastic containers
and other abandoned items which provide larval habitats in urban
areas.
Geographical expansion of the mosquito has been aided by
international commercial trade particularly in used tyres which easily
accumulate rainwater.
Increased air travel and breakdown of vector control measures have
also contributed greatly to the global burden of dengue and DHF.
8

WHO has reported that a temperature rise of 12 C could result in an increase
of the risk population by several hundred million, with 20,000 30,000 more fatal
cases annually.
9
MAGNITUDE OF THE PROBLEM : INDIAN SCENARIO

India is one of the seven identified countries in the South-East Asia region
regularly reporting incidence of DF/DHF outbreaks and may soon transform into a
major niche for dengue infection in the near future.
10

The first recorded outbreak of dengue fever in India was in 1812.
5
The dengue virus was isolated for the first time almost simultaneously in
J apan and Calcutta in 1963.
12
After the first virologically proved epidemic of dengue
8
fever along the East Coast of India in 1963-1964, it spread to all over the country.
DEN-2 virus strains were isolated from patients with severe haemorrhagic
manifestations . Further outbreaks occurred in 1965, 1967 and 1968. All four
serotypes of Dengue viruses have been isolated form various parts of India. New
Delhi, reported outbreaks of Dengue fever in 1967, 1970 and 1982,1996,2003. DEN-
2 were isolated during the 1970 epidemic. An explosive outbreak of Dengue fever
occurred between August and October 1982.
15
The first full-blown epidemic of the
severe form of the illness,the dengue haemorrhagic fever/dengue shock syndrome
occurred in North India in 1996.
11
DHF was first reported in Calcutta (Kolkata), West Bengal in 1963 , again in
1964 . Since then, there are numerous studies from the Indian subcontinent
investigating DHF in various parts of the country.
13

In 1960, DEN-1 was isolated in Vellore, in the south, without any association
with hemorrhagic diathesis.
14
3.3 EPIDEMIOLOGY
DHF first emerged as a public health problem in 1954, when the first epidemic
occurred in Manila. This gradually spread to other countries in the region. Major
epidemics occurred in other regions of the world in the 1980s and 1990s and were
caused by all four dengue viral serotypes. While the predominant serotype in the
1980s and the early 1990s was DEN-2, in recent years it has changed to the DEN-3
serotype. In 1998, a pandemic of dengue viral infections occurred, where 1.2 million
cases of dengue fever and DHF were reported from 56 countries worldwide. The
world population was exposed to a new subtype of the DEN-3 virus (subtype III),
which originated in the Indian subcontinent and later spread to involve other
9
continents. Exposure of a non-immune population to this new subtype of DEN-3 may
have been the cause of this pandemic. A situation of comparable magnitude was also
seen in 200102.
Microevolution of the dengue virus may have also contributed to the spread of
more virulent strains around the world. In fact there is evidence that the more virulent
genotypes of the virus are replacing the less virulent genotypes, which may explain
the global emergence of dengue infections.
EPIDEMIOLOGICAL TRENDS IN SOUTH ASIA
The first major epidemic of DHF occurred in Sri Lanka in 1989. Since then
regular epidemics have been occurring in Sri Lanka. As yet, no cases of DHF have
been reported from Nepal or Bhutan, endemicity is uncertain.
2
AGENT THE DENGUE VIRUS

DEN-II was isolated by Sabin and his co workers in 1944.
15
In 1956 Hammon
and coworkers isolated two new serotypes of Dengue virus, designated DEN-3 and
DEN-4, as well as the previously recognized DEN-1 and DEN-2 during epidemics of
severe hemorrhagic in the Philippines.
16
STRUCTURE OF DENGUE VIRUS:

Dengue virus belong to a larger, heterogeneous group of viruses called
arboviruses. This is an ecological classication, which implies that transmission
between vertebrate hosts including humans is dependent upon haematophagous
(blood-sucking) arthropod vectors.

The known natural hosts for Dengue virus are man, lower primates, and
mosquitoes.
17
Dengue virus (DENV) is a member of the genus Flavivirus in the
family Flaviviridae.
18
10
Flaviviridae are enveloped viruses with positive-strand RNAgenomes that
have been grouped into three genera, Hepacivirus, Pestivirus, and Flavivirus.
19

There are over 70 antigenically related viruses in the genus Flavivirus,
including the type species, Yellow fever virus. The genus includes several antigenic
complexes, including the dengue complex, the J apanese encephalitis complex and the
tick-borne encephalitis complex. The J apanese encephalitis complex includes several
well known disease pathogens of humans, including J apanese encephalitis, Murray
Valley encephalitis, St Louis encephalitis, West Nile, Kunjin, Zika and other viruses,
all of which are transmitted by mosquitoes. The tick-borne aviviruses include Tick-
borne encephalitis, Omsk haemorrhagic fever and Kyasanur Forest disease viruses.
20

Fig 4: FLAVIVIRUS VIRION STRUCTURE
11

Fig 5: DENGUE VIRUS
The structural proteins are included in mature virion, whereas the NS proteins
play various roles in virus replication and polypeptide processing.
NS1 a glycoprotein is detected in high titres in patients with secondary dengue
infection. Its function is unknown.
NS2 codes for 2 proteins (NS2A and NS2B), which play a role in polyprotein
processing.
NS3 the viral proteinase functions in the cytosol.
NS4 this region codes for two small hydrophobic proteins involved in the
membrane bound RNA replication complex establishment.
NS5 most conserved flavivirus protein. This protein is assumed to be the virus
encoded RNA dependent RNA polymerase.
NS6 and NS7 function yet to be found.
12

Fig 6: FLAVIVIRUS GENOME
Infection with one serotype is thought to produce lifelong immunity to that
serotype but only a few months immunity of the others. Humans and mosquitoes
(aedes aegypti) are the principal hosts of Dengue virus; the mosquito remains infected
for life, but the viruses are only known to cause illness in humans. In forest and
enzootic cycles in Africa and Asia, the virus is probably sustained through vertical
(transovarial) transmission in the mosquito with periodic amplification in non-human
primates.
21

13
VECTOR : MOSQUITO

Fig 7: AEDES AEGYPTI MOSQUITO
14

Fig 8: LIFE CYCLE OF AEDES AEGYPTI MOSQUITO

Transmission by Aedes aegypti which belongs to Stegomyia family, first
described by Bancroft in 1906, was later proved by Silver et al and Simmons et al.
22

Aedes aegypti, considered the most effective vector, originated in the forests
of Africa and is found in between 35 degrees north and 35 degrees south latitude.
The characteristic features of the Aedes aegypti are:
It is highly susceptible to Dengue virus.
It feeds preferentially on human blood.
Rest indoor, maximizes man- vector contact.
It is a daytime feeder.
Its bite is almost imperceptible.
It is a container breeder like flower vases, uncovered barrels, buckets, and
discarded tyres, but the most dangerous areas are wet shower floors and toilet
tanks.
15
It is restless mosquito as the slightest movement interrupts feeding, thus
several people may be bitten in a short period for one blood meal.
The female mosquito feeds during the daytime, with peak activity in the
mornings and late afternoons.
Flight range studies suggest that most female Ae. aegypti may spend their lifetime
in or around the houses where they emerge as adults and they usually fly an average
of 400 metres. This means that people, rather than mosquitoes, rapidly move the virus
within and between communities and places.
Unlike most mosquitoes, A aegypti takes more than one blood meal during a
gonotropic cyclethat is, before the eggs are laid. In many areas, dengue epidemics
occur during the warm, humid, rainy seasons, which favour abundant mosquitoes and
shorten the extrinsic incubation period.
23
Dengue transmission is largely confined to tropical and subtropical regions
because
freezing temperatures kill overwintering larvae and eggs of Ae. aegypti mosquitoes .
Also, temperature strongly affects pathogen replication, maturation, and period of
infectivity, as laboratory data suggest that the extrinsic incubation period (or viral
development rate) shortens nonlinearly with higher temperatures, increasing the
proportion of mosquitoes that become infectious at a given time . Also, elevated
temperatures can shorten insect survival time or disrupt pathogen development.
24

The average lifespan of an Aedes mosquito in Nature is 2 weeks
The mosquito can lay eggs about 3 times in its lifetime, and about 100 eggs
are produced each time.
The eggs can lie dormant in dry conditions for up to about 9 months, after
which they can hatch if exposed to favourable conditions, i.e. water and food
16
After feeding on a viraemic individual, the mosquito may transmit the
virus directly by change of host, or after 8 to 10 days during this time the virus
multiplies in the salivary glands. The infected mosquito then remains capable
of transmission for its entire life. Transovarian transmission of Dengue virus
has been documented and A.aegypti eggs are highly resistant to desiccation
and can survive for extended periods.
25

Aedes albopictus is indigenous to Southeast Asia, feeds during the day and has
been shown to have a higher biting frequency than A.aegypti. It was introduced into
Nigeria, Europe and the United States, probably by shipments of used automobile
tyres.
Aedes aegypti Index is the ratio expressed as percentage of the number of houses
in a well defined limited area in surrounding of which breeding places of Aedes
aegypti has been identified to the total number of houses surveyed in that area.
Breteau Index: Number of positive containers per 100 houses inspected.
Container Index : Percentage of water holding containers infested with larvae or
pupae.
House (premise) index : This is the percentage of houses infested with Aedes
aegypti larvae and/or pupae.
THE HOST: HUMAN
After an incubation period of 4--10 days, infection by any of the four virus
serotypes can produce a wide spectrum of illness, although most infections are
asymptomatic or subclinical . Primary infection is thought to induce lifelong
protective immunity to the infecting serotype . Individuals suffering an infection are
protected from clinical illness with a different serotype within 2--3 months of the
primary infection but with no long-term cross-protective immunity.
17
Individual risk factors determine the severity of disease and include secondary
infection, age, ethnicity and possibly chronic diseases (bronchial asthma, sickle cell
anaemia and diabetes mellitus). Young children in particular may be less able than
adults to compensate for capillary leakage and are consequently at greater risk of
dengue shock.
26

The high prevalence, lack of an effective vaccine, and absence of specific
treatment conspire to make dengue fever a global public health threat.
27

Air travel has enabled infected humans import viruses. These factors can
change a region form non-endemic (no virus present) to hypoendemic (one serotype
present) to hyperendemic (multiple serotypes present).
17

In South East Asia the mean number of annual cases of Dengue haemorrhagic
fever has increased to more than twenty fold in the past forty years. The same pattern
is now unfolding in the Americas.
28
The numbers of reported cases of imported
Dengue in countries outside
the tropics have also been increasing.
29,30
ENVIRONMENTAL CONDITIONS
Population growth in the tropics provides many susceptible hosts.
Uncontrolled urbanization leads to inadequate management of water and waste,
providing a range of large water stores and disposable, non-biodegradable containers
that become habitats for the larvae. Few control programmes are effective against the
mosquitoes.
31

The monsoon and post-monsoon surge of the disease is very well documented,
largely due to an effective breeding opportunity for the mosquito vector.
5
The
incidence increases from the monsoon season, reaches a peak in the post-monsoon
season before declining. The reasons for dramatic global emergence of Dengue fever
18
or DHF as a major public health problem are complex and not very well understood.
However, several important factors can be identified.
Major global demographic changes have occurred, the most important of
which have been uncontrolled urbanization and concurrent population growth.
These demographic changes have resulted in substandard housing and
inadequate water, sewage, and waste management systems, all of which
increase A.aegypti population densities and facilitate transmission of
A.aegypti borne disease.
Effective mosquito control is virtually nonexistent in most Dengue endemic
countries. Considerable emphasis for the past 25 years has been placed on
ultra-low-volume insecticide space sprays for adult mosquito control, a
relatively ineffective approach for controlling A.aegypti.
Increased travel by airplane provides the ideal mechanism for transporting
Dengue virus between population centers of the tropics, resulting in a constant
exchange of Dengue virus and other pathogens.
In most countries the public health infrastructure has deteriorated.
Limited financial and human resources and competing priorities have resulted
in a crisis mentality with emphasis on implementing so-called emergency control
methods in response to epidemics rather than on developing programmes to prevent
epidemic transmission. This approach has been particularly detrimental to Dengue
control, because in most countries, surveillance is very inadequate; the system to
detect increased transmission normally relies on reports by local physicians who often
do not consider Dengue in their differential diagnoses.
17
As a result, an epidemic has
often reached or passed transmission before it is detected.
19
Dengue has been linked to urbanization, explaining its maximum incidence in
middle class. The immediate microenvironment of the patient, consisting of artificial
collections of water within the house (as in flower vases, decorative plant pots within
the house), forms a fertile breeding place for the mosquito vector. This leads to
exposure to the mosquito bites and spread of Dengue.
Finally, international commercial trade has aided geographical expansion of
the mosquito, particularly in used tyres, in which rainwater easily accumulates.
Increased air travel and breakdown of vector control measures have also contributed
greatly to the global burden of Dengue fever.
32

ECONOMIC IMPACT OF DENGUE
Few studies on the economic impact of DF, DHF and DSS have been
conducted. For children suffering from dengue fever average hospital stays will be
about 5 10 days. Intensive care is required for severely ill patients, including
intravenous fluids, blood or plasma transfusion and medicines. Adults miss work in
order to attend to their childrens illness. Consequently, there are both direct and
indirect costs for each Dengue patient, ranging from inconvenience due to a sick child
with uncomplicated Dengue, to substantial costs for hospitalization and significant
disruption of earning potential. In addition, burden to local municipalities for vector
control activities, and often revenue is lost through reduced tourism. While the exact
cost of each epidemic is difficult to calculate, it is clear that Dengue and DHF/DSS
represent a significant economic burden on the society.
33

20
TRANSMISSION OF DENGUE VIRUS:
Dengue viruses are transmitted to humans through bite of infected female
Aedes Aegypti mosquitoes. Once infected, a mosquito remains infected for life
transmitting viruses to susceptible individuals during probing and feeding. Infected
female mosquito may also pass virus to next generation of mosquitoes by transovarian
transmission but this occurs infrequently and probably does not contribute
significantly to human transmission. Humans are main amplifying host of virus .The
virus circulates in blood of infected human at approximately time that they have
fever.
34

Fig 9: TRANSMISSION OF DENGUE VIRUS
3.4 PATHOLOGY
First attack of dengue virus in non immune individuals causes Classic Dengue.
Symptoms begin after 5 to 10 days of incubation period .The severe forms like DHF
and DSS usually occurs during a secondary Dengue infection in persons with pre-
existing, acquired immunity to a heterologous Dengue virus serotype .Illness begins
abruptly with a febrile episode of 2-4 days duration followed by rapid deterioration.
35
, 36
21
After inoculation, virus reaches the regional lymph nodes and disseminates to
the reticulo endothelial system where it multiples and enters the blood. The
pathological findings include endothelial swelling, Perivascular edema and
infilteration with mononuclear cells. Extensive extravasation of blood without
appreciable inflammatory reaction was observed in petechiae. Hemorrhages found in
skin and subcutaneous tissue, in mucosa of GIT, heart , liver. GI Hemorrhage may be
severe, but subarachnoid or cerebral hemorrhage is rarely seen. Serous effusion with a
high protein content (mostly albumin) commonly present in pleural and abdominal
cavity, pericardial cavity. In most severe cases, lymphocyte tissue shows an increased
activity of B lymphocyte system, with active proliferation of plasma cells and
lymphoblastoid cells and active germinal centres.
37

Pathological finding in other organ system:
LIVER: In liver, there is a focal necrosis of hepatic cells, swelling appearance of
Councillman bodies and hyaline necrosis and kupfer cells. Proliferation of
mononuclear leukocytes and less frequently polymorphonuclear leukocytes occurs in
sinusoids and occasionally in the portal areas.
At autopsy, dengue virus antigen has been found predominantly in liver,
spleen, lymph node and lung cells. The virus has also been isolated at autopsy from
bone marrow, brain, heart, kidney, liver, lungs, lymphnodes and GIT.
38
BONE MARROW: In bone marrow, depression of all haemopoetic cell is observed
which could rapidly improve as fever subsides.
KIDNEY: Studies in kidney has a mild immune-complex type of glomerulonephritis,
which could resolve after about 3 weeks with no residual change.

22
SKIN: Biopsies of skin rashes have revealed perivascular oedema of
microvasculature of dermal papillae and infilteration of lymphocytes and monocytes.
Antigen bearing mononuclear phagocytes has been found in viscinity of this oedema.
Deposition of serum complements, immunoglobulin & fibrinogen on vessel walls has
been described.
The target cells include dendritic reticulum cells, monocytes, lymphocytes,
hepatocytes, and vascular endothelial cells.
39
Dengue hemorrhagic fever is distinguished from dengue by the presence of
increased vascular permeability, not by the presence of hemorrhage. Patients with
dengue may have severe hemorrhage without meeting WHO criteria for dengue
hemorrhagic fever. In these cases the pathogenesis probably derives from
thrombocytopenia or a consumptive co-agulopathy, not from the vascular leak
syndrome seen in dengue hemorrhagic fever. Dengue hemorrhagic fever may (grades
III and IV) or may not (grades I and II) include clinical shock, referred to as dengue
shock syndrome.
In primary and secondary infections, higher viral titres are associated with
more severe disease. Higher titres may result in an amplified cascade of cytokines and
complement activation causing endothelial dysfunction, platelet destruction, and
consumption of coagulation factors, which result in plasma leakage and hemorrhagic
manifestations.
23
All four serotypes have been associated with DHF . Variations in virus strains
within and between the four serotypes may influence disease severity. Secondary
infections (particularly with DEN-2) are more likely to result in severe disease and
dengue hemorrhagic fever.
23
The theory of immune enhancement, developed extensively by Halstead.
40
The
increased severity seen in secondary infections is due to antibody - dependent
enhancement (ADE) leading to increased replication in Fc receptor-bearing cells
41,
42,43
, where by cross reactive but non-neutralising antibodies from a previous
infection bind to the new infecting serotype and facilitate virus entry into cells
resulting in higher peak viral titres.

3.5 PATHOGENESIS OF DENGUE FEVER / DHF / DSS

These severe forms are characterized by
1) Increased vascular permeability that give rise to loss of plasma from vascular
compartment. This results in haemoconcentration, low pulse pressure and other signs
of shock.
2) Disorders in haemostasis involving vascular changes, thrombocytopenia and
coagulopathy.
After the bite of an infected mosquito, the dengue virus enters the body and
replicates within cells of the mononuclear phagocyte lineage (macrophages,
monocytes, and B cells). Additionally, infection of mast cells, dendritic cells, and
endothelial cells are known to occur. The incubation period of dengue infections is 7
10 days. A viraemic phase follows where the patient becomes febrile and infective.
Thereafter, the patient may either recover or progress to the leakage phase, leading to
DHF and/or dengue shock syndrome.
The mechanism of bleeding in dengue hemorrhagic fever is not known, but a
mild degree of disseminated intravascular coagulation, liver damage, and
thrombocytopenia may operate synergistically. Capillary damage allows fluid,
electrolytes, small proteins, and, in some instances, red cells to leak into extra
24
vascular spaces. This internal redistribution of fluid, together with deficits caused by
fasting, thirsting, and vomiting, results in haemoconcentration, hypovolemia,
increased cardiac work, tissue hypoxia, metabolic acidosis, and hyponatremia.
Antibody dependent enhancement is found to occur only in the presence of
subneutralising concentrations of dengue antibodies. DEN-1 immune sera at 1:250
dilution (subneutralising titre), but not at 1:10 dilution, enhances DEN-2 infection of
mononuclear leucocytes, in turn resulting in increased lymphocyte proliferation and
decreased interferon-c (IFN-c) production.
After primary dengue infection, antibodies form against both structural and
non-structural viral proteins. Although, the precise role of these different antibodies is
not known, antibodies against viral NS1 have been shown to induce endothelial cell
apoptosis in a caspase dependent manner.
Varying degrees of thrombocytopenia are common in DHF. Some of the
mechanisms responsible for this include: IgM type of antiplatelet antibodies, dengue
viral specific antibodies, bone marrow hypocellularity (leading to increases in
defective megakaryocytes), or destruction of platelets in the liver and spleen.
Immune complexes have been described in DHF but their role is not yet clear.
16 , 35
Dengue virus infected monocytes, B-lymphocytes, and mast cells produce
different cytokines. At present there is disagreement about the predominant cytokines
produced during dengue fever and DHF. According to Chaturvedi et al serum
concentrations of tumour necrosis factor-a (TNF-a), interleukin (IL)-2, IL-6, and IFN-
c are highest in the first three days of illness whereas IL-10, IL-5, and IL-4 tend to
appear later. IL-2 and IFN-c are Th1 and IL-5 and IL-4 Th2 type cytokines. Thus, it
has been suggested that Th1 responses are seen during the first 3 days and Th2
25
responses occur later. Increased levels of IL-13 and IL-18 have also been reported
during severe dengue infections, with highest levels seen in patients with grade IV
DHF. Serum IL-12 levels are highest in patients with dengue fever, but undetectable
in patients with grade III and IV DHF.
44
DHF patients have higher levels of TNF-a,
IL-6, IL-13, IL- 18, and cytotoxic factor compared with DF patients. These cytokines
have been implicated in causing increased vascular permeability and shock during
dengue infections. Moreover, cytotoxic factor, produced by CD4+T-cells, induces
macrophages to produce the pro inflammatory cytokines IL- 1a, TNF-a, and IL-8.
Levels of cytotoxic factor correlate with disease severity (being highest in patients
with grade IV DHF). Serum IL-6 concentrations are higher in patients with DHF and
dengue shock syndrome. IL-6 is produced mainly by mast cells and endothelial cells.
It is an endogenous pyrogen that also increases endothelial cell permeability.
Endothelial cells also produced IL-8, having potent proinflammatory and
chemoattractant activity. Levels of IL-8 are higher during severe dengue infections
and highest in those who died. Activated neutrophils release proteinases such as
elastase, which may facilitate neutrophil mediated endothelial injury, and activate the
complement, coagulation, and fibrinolytic systems. Since increased serum IL-8 and
elastase are found in patients with severe infections, they may have an important role
in pathogenesis of dengue infections.
The simultaneous activation of proteolytic enzymes of complement,
coagulation and possibly the Kinin systems may be expected to consume plasma
enzyme inhibitors. Partial depletion of these inhibitors may result in an imbalance
between activated enzymes and inhibitors and thus produce increased vascular
permeability and shock.
36 , 45

26
Dengue virus infected lymphocytes produce both IFN-a and IFN-c ; levels of
the former being higher than the latter. IFN-a inhibits infection of monocytes by the
dengue virus and hence is important in controlling primary dengue infections. IFN-c
is produced early in the course of infection. Peak levels occur on or before the day of
deferverscence and coincide with disappearance of viraemia.
Dengue virus infected dendritic cells produce high levels of TNF-a and IFN-a,
but low levels of IL-12.
46
TNF-a prolongs dendritic cell survival by up regulating
antiapoptotic factors within it. Prolonged survival of dengue virus infected dendritic
cells may contribute towards producing severe dengue infections. Serum
concentrations of serum TNF-a, IFN-c, IL-10, and soluble TNF receptor (sTNF-R )
are significantly higher in patients compared with normal controls. Increased levels of
TNF-a and IL-10 correlate with haemorrhagic manifestations and platelet decay
respectively. IL-10 may also down-regulate platelet function and thus contribute to
platelet defects associated with dengue infections. TNF-alpha and NO are produced
primarily by infected monocytes/macrophages and activate endothelial cells, which
can contribute to increased vascular permeability.
47 , 48
The dengue virus can infect both CD4+ and CD8+ T-cells.
36
Dengue
infections are associated with decreased numbers of CD4+T-cells, CD8+T-cells, and
natural killer cells. Reversal of CD4:CD8 ratios tend to occur around the sixth to 10th
day after the onset of fever, being seen more frequently in patients with DHF.

Generalised bone marrow suppression known to occur in dengue infections
may contribute to the absolute lymphopenia.
Early in the acute stage of secondary dengue infections, there is rapid
activation of the complement system. C1q, C3, C4, C5-C8, and C3 proactivators are
depressed, and C3 catabolic rates are elevated. These factors may interact at the
27
endothelial cell to produce increased vascular permeability through the nitric oxide
final pathway. The blood clotting and fibrinolytic systems are activated, and levels of
factor XII (Hageman factor) are depressed.
The model of original antigenic sin involving memory T-cell responses
postulates an inappropriate immune response to a secondary infection due to clonal
expansion of cross reactive memory T cells specic for the previous rather than a
current infection, resulting in delayed viral clearance and/or increased cytokine
secretion. There is evidence that this may occur during secondary DENV infections.
An imbalance in the regulation of coagulation and fibrinolysis, as in the
disseminated intravascular coagulation syndrome (DIC), in conjunction with the
characteristic thrombocytopenia may contribute to the bleeding tendency in DHF.
49

28

Fig 10 : MECHANISM OF ACTION OF DENGUE VIRUS

29
PLATELET DYSFUNCTION
Platelet defects may be both quantitative or qualitative,i.e in some circulating
platelet during acute phase of DHF may be exhausted (in capable of normal
function).Therefore even a patient with patients count greater than 1,00,000 / cu mm
may still have prolonged bleeding time.
Evidence for activation of blood coagulation system, occurrence of
intravascular coagulation is indicated by low fibrinogen level, decreased platelet
count and high proportion of considerable amount of fibrin and fibrinogen split
products. Further more activation of complement may affect platelet activation and
initiate blood coagulation.
5

Several hypotheses have emerged to explain why DHF occurs in some
individuals who are infected with Dengue virus. These include changes or differences
in viral virulence between serotypes and/or between strains within serotypes.
50

Interactions of Dengue virus with other environmental or infectious agent.
Age : usually children are more susceptible to develop DHF.
2

Sex : DHF is also reported to be more severe among females.
2

DHF tends to be commoner among patients suffering from other chronic
illnesses.
2

Differences in genetic susceptibility - Several human HLA class I and II
alleles are associated with development of DHF .Polymorphism in the tumor
necrosis factor alpha, Fc receptor, vitamin D receptor, CTLA-4, and
transforming growth factor genes has been associated with development of
DHF/DSS and certain host factors, such as glucose-6-phosphate
dehydrogenase (G6PD) deciency, may also contribute to increased
replication of DENV in monocytes.
51

30
The immunologic enhancement of Dengue infection by antibody acquired
from a previous infection with a different Dengue serotype.
Generally malnutrition predisposes to many infectious diseases (for example,
measles or tuberculosis) and tends to correlate positively with severity of disease.
However, malnutrition appears to be significantly uncommon among patients with
DHF, compared with patients with other infectious diseases or healthy children.
2

Entry of Dengue virus into mononuclear phagocytes, resulting in the increased
activation of complement and kinins and the release of mediators of vascular
permeability. This proposed mechanism has been supported by laboratory
investigation and several studies have shown that during outbreaks a majority of DHF
patients show secondary immune response patterns.
52

However, cases of DHF have been described in patients with primary Dengue
infection.
53
3.6 CLINICAL FEATURES
The clinical features of dengue vary with the age of the patient and in addition
to clinically inapparent infections, can be classified into five presentation:
Non-specific febrile illness,
Classic Dengue,
Dengue haemorrhagic fever,
Dengue haemorrhagic fever with Dengue shock syndrome,
Other unusual syndromes such as encephalopathy and fulminant liver
failure.
Three to Ten days after the bite of an infective mosquito, the patient typically
suffers sudden onset of headache, fever, retro-orbital pain, backache, bone and joint
31
pain, weakness, depression and malaise. Young children with Dengue often have an
undifferentiated febrile illness with a maculopapular rash. Upper respiratory
infections, especially pharyngitis are common. Classic Dengue is more commonly
seen among older children, adolescents, and adults. They are less likely to be
asymptomatic.
54

Dengue is abrupt in onset, typically with high fever accompanied by severe
headache, incapacitating myalgias and arthralgias, nausea and vomiting, sore throat,
cough, groin pain, hyperesthesia, dizziness, photophobia, eye pain and rash. The
decline in fever may be followed by 1 to 3 days later by a resurgence of fever and
symptoms, giving a saddleback appearance to the temperature curve.
55
The characteristic exanthem of DF is estimated to occur in 50-82% of patients
with DF. In DF, the initial rash is a transient flushing erythema of face that typically
occurs shortly before or within the first 24-48 hours of the onset of symptoms and is
thought to be the result of capillary dilatation. Some patients have an evanescent rash
over the thorax and joint flexures. There may be taste aberrations, anorexia and
abdominal pain.
Lymphadenopahty and hepatomegaly may occur but splenomegaly is
infrequent. Fever and associated symptoms may subside after 3 or 4 days and the
patient may recover completely. Recovery may be prolonged and include depression.
Dengue hemorrhagic fever is primarily a disease of children under 15 year of
age. Black populations may be at decreased risk. If major plasma leakage occurs, it
usually develops 24 hours before to 24 hours after defervescence. Patients may
develop effusions and ascites with a variable amount of bleeding. Enlargement and
tenderness of the liver has been reported in up to 40% of patients. As the fever begins
to drop around day 3 to 5, circulatory instability may develop with signs of decreased
32
peripheral perfusion. Profound shock may follow. Disseminated intravascular
coagulation and severe gastrointestinal hemorrhage have been described. Mortality
can be as high as 10-20% (over 40% if shock occurs) without early appropriate
treatment, but it is as low as 0.2% in hospitals with staff experienced in the disease.
Warning signs that Dengue shock syndrome is impending include:
Sustained abdominal pain.
Persistent vomiting,
Change in level of consciousness (irritability or somnolence),
Sudden change from fever to hypothermia,
Sudden decrease in platelet counts.
The second rash usually occurs 3-6 days after the onset of fever and it is
characterized by asymptomatic maculopapular or morbilliform eruption. In some
cases, individual lesions may coalesce and are then seen as generalized confluent
erythema with petechiae and rounded islands of sparing-white islands in a sea of
red and is thought to be due to an immune response to the virus. The generalized
rash characteristically starts on the dorsum of the hands and feet and spreads to the
arms, legs, and torso and it lasts for several days. The morbilliform, maculopapular
rash usually spares palms and soles. Severe itching, especially of the hands and feet,
may accompany this rash, which is sometimes followed by desquamation.
Hemorrhagic manifestations on the skin such as petechiae , purpura, or ecchymosis
are commonly seen in DHF and DSS and rarely in DF. Mucosal involvement is
estimated to occur in 15% to 30% of patients with dengue viral infections and more
commonly in patients with DHF than with DF. The mucosal manifestations noted in
dengue viral infections are conjunctival and scleral injection , small vesicles on the
soft palate, erythema and crusting of lips and tongue.
56
33
During the course of the illness there is often a relative or paradoxical
bradycardia in the face of increased temperature. Patients may have hemorrhagic
manifestations such as epistaxis or menorrhagia. J aundice is rare. Convulsions may
occur with the onset of fever. The spinal fluid is almost always clear with no elevation
of cell count but the pressure may be increased. Depression, weakness and blurred
vision may resolve slowly during convalescence. Patients may take several weeks to
recover completely. Although these symptoms characterize classical Dengue fever,
Dengue virus infection may also manifest a nonspecific febrile illness which can be
confused with influenza, measles or any nonspecific viral syndrome.
Significant Thrombocytopenia may occur in both DHF and classical
Dengue. A fall in platelet count associated with a rising hematorit may suggest the
development of DHF.
57
A negative tourniquet test may not be sufficient to exclude a diagnosis of DHF in a
febrile patient.
58

34

Fig 11 : COURSE OF DENGUE ILLNESS
3.7 DIAGNOSIS :
59

WHO has laid down the following criteria for the diagnosis of Dengue fever.
Diagnosis of Dengue fever and dengue haemorrhagic fever :
Dengue fever
Acute illness with two or more of :
Headache;
Retro-orbital pain;
Myalgia;
Arthralgia;
Rash;
Haemorrhagic manifestations;
Leucopenia.
35
Dengue haemorrhagic fever
All of following criteria must be present :
Fever, high degree and continuous of 2-7 days duration and occasionally
biphasic.
Haemorrhagic manifestations (shown by positive tourniquet test, petechiae,
ecchymoses or purpura, or bleeding from mucosa- epistaxis or bleeding from
gums , gastrointestinal tract- hematemesis or melena , injection sites, or other
locations)
Platelet count <100,000 /mm3
Objective evidence of plasma leakage due to increased vascular permeability
shown by either fluctuation of packed cell i.e.,
- A rise in Haematocrit equal to or greater than 20% above average for age, sex
and population;
- A drop in Haematocrit following volume replacement treatment equal to or
greater than 20% of baseline ,during the course of illness and recovery or
clinical signs of plasma leakage such as pleural effusion, ascites, or
hypoproteinaemia.
Other clinical manifestations suggestive of DHF are :
Hepatomegaly (which may be tender)
Circulatory disturbances (restlessness, cool extremities, capillary refill time >3 sec.,
tachycardia)
A fall in haematocrit following volume replacement

36
Dengue shock syndrome
All of the above four criteria for DHF must be present, plus evidence of
circulatory failure manifested by
Rapid and weak pulse, and Narrow pulse pressure 20 mmHg (2.7 kpa) or
manifested by:
Hypotension for age(defined as systolic pressure <80 mm Hg for those aged
<5 years or <90 mm Hg for those aged >5 years) and
Cold, clammy skin and restlessness.
Who grading of dengue haemorrhagic fever :
Grade I : In the presence of haemoconcentration, fever and non-specific
constitutional symptoms, a positive tourniquet test is the only haemorrhagic
manifestation.
Grade II : Spontaneous bleeding in addition to the manifestation of Grade I
Grade III : Circulatory failure, pulse pressure less than 20 mm Hg but
systolic pressure is still normal plus manifestations of Grade II
Grade IV : Profound shock, hypotension or unrecordable blood pressure.
(Grades III and IV are classified as Dengue shock Syndrome (DSS)).
23 , 60

37

CRITERIA FOR DENGUE WARNING SIGNS
CRITERIA FOR
SEVERE DENGUE
Probable Dengue Warning signs
live in /travel to dengue
endemic area.
Fever and 2 of the
following criteria:
Nausea, vomiting
Rash
Aches and pains
Tourniquet test
positive
Leukopenia
Any warning sign
Laboratory-confirmed
Dengue (important when
no sign of plasma leakage)
Abdominal pain or
tenderness
Persistent vomiting
Clinical fluid
accumulation
Mucosal bleed
Lethargy, restlessness
Liver enlargment >2 cm
Laboratory: increase in
HCT
concurrent with rapid
decrease
in platelet count
Severe plasma leakage
leading to:
Shock (DSS)
Fluid accumulation with
respiratory
distress
Severe bleeding
as evaluated by clinician
Severe organ involvement
Liver: AST or ALT
>=1000
CNS: Impaired
consciousness
Heart and other organs

DIAGNOSTIC CLASSIFICATION:
73

Probable diagnosis

An acute febrile illness with two or more of the following manifestations
Headache
Retro - orbital pain
Myalgia
Arthralgia
38
Rash
Haemorrhagic manifestations
Leukopenia
thrombocytopenia (platelet count <100 000 cells/mm3),
rising haematocrit (5 10%);
And
Supportive serology (a reciprocal haemagglutination-inhibition antibody titre
>1280, a comparable IgG enzyme-linked immunosorbent assay (ELISA) titre or a
positive IgM antibody test on a late acute or convalescent-phase serum specimen); OR
- Occurrence at the same location and time as other combined cases of dengue fever.
Confirmed-a case confirmed by laboratory criteria (see below).
Reportable-any probable or confirmed case should be reported
Occurrence at same location and time as confirmed cases of Dengue fever.
Confirmed diagnosis :
Atleast one of following :
Isolation of dengue virus from serum , CSF or autopsy samples.
Fourfold or greater increase in serum IgG (by haemagglutination inhibition test) or
increase in IgM antibody specific to Dengue virus.
Detection of Dengue virus in tissue, serum or cerebrospinal fluid by
immunohistochemistry, immunofluorescence, or enzyme linked immunosorbent
assay.
Detection of Dengue virus genomic sequences by reverse transcription polymerase
chain reaction.

39
REPORTABLE CASES OF DHF OR DSS:
Patients with provisional diagnosis of DHF or DSS should be reported to the
health Authorities as case of DHF or DSS if there is:
Virological or serological evidence of acute dengue infection,or
History of exposure in dengue endemic or epidemic area( during a period of
epidemic transmission ,or significant levels of endemic transmission, it is unlikely
that many cases will have laboratory confirmation).
CASE DEFINITION FOR DENGUE FEVER:
The clinical diagnosis must be supported by laboratory tests .
LABORATORY CRITERIA FOR CONFIRMATION OF DENGUE FEVER
ARE:
Isolation of the dengue virus from serum
Demonstration of a four fold or greater change m reciprocal IgG or IgM antibody
titres to one or more dengue virus antigens in paired serum samples ; or
Demonstration of dengue virus antigen in autopsy tissue, serum or cerebrospinal fluid
samples by polymerase chain reaction(PCR).
Atypical variants :
Rare and unusual presentations of Dengue are protean. The atypical variants have
been encountered in various studies. To quote a few,
Acute abdominal pains, diarrhoea, severe gastrointestinal haemorrhage,
Irregular pulse and heart rate, acute renal failure, haemolytic uraemic
syndrome.
61

Severe headache, convulsions, altered sensorium, Encephalitic signs
associated with or without intracranial haemorrhage.
62

40
Fulminant hepatic failure, obstructive jaundice, raised liver enzymes,
Reyes syndrome
Disseminated intravascular coagulation.
63

Respiratory distress.
64

Vertical transmission in newborns.
65

Dengue virus has been isolated from CSF suggesting direct involvement of
the brain.
66

Multisystem involvement is increasingly being documented during the last
10 years.
Transient reverse in the CD4/CD8 ratio occurred at days 6-10 after the
onset of fever. These changes in immune parameters indicate aberrant
immune activation during Dengue virus infection.
67

The haemophagocytic syndrome is characterized by systemic proliferation
of non-neoplastic histiocytes showing haemophagocytosis resulting in
blood cytopenia. Bone marrow aspirations showed that platelets, red and
white blood cells were phagocyted by histiocytes.
68

Rare presentations of infection include severe haemorrhage, jaundice,
parotitis, cardiomyopathy and non-specific ECG changes like ST
elevations, premature ventricular complexes and bradycardia.
68

Unusual neurological presentations include mononeuropathies,
polyneuropathies, encephalitis, and transverse myelitis.
Guillain-Barre syndrome has been associated with Dengue.
Encephalopathy occurs occasionally and may result from cerebral edema,
cerebral haemorrahge, liver failure or electrolyte imbalances.
`23

41
Lymphoreticular/bone marrow: Infection associated haemophagocytic
syndrome (IAHS) or Haemophagocytic lymphohistiocytosis (HLH),
idiopathic thrombocytopenic purura , Spontaneous splenic rupture, Lymph
node infarction.
74

COMPLICATIONS AND UNUSUAL MANIFESTATIONS
CNS :
Peripheral nerve involvement occur in the form of mononeuritis. The patients
with encephalopathy progressing to the death.
The pathogenesis of dengue encephalopathy include cerebral edema, anoxia, micro
vascular or frank haemorrhages, hyponatraemia and fulminant hepatic failure (DEN 2
and DEN 3 frequently reported as cause of neurological disease) which may a part of
reye like syndrome.
69 , 70 , 35

Few patients may develop coma. Encephalopathy and Encephalitis can occur.
Hemorrhagic encephalopathy in DSS caused by type 3 Dengue virus.

GIT , AND LIVER
Hepatitis/fulminant hepatic failure, Acalculous cholecystitis, Acute
pancreatitis, Hyperplasia of Peyers patches, Acute parotitis are some of the
manifestations .Dengue fever may present with lower GI bleeding and colonoscopic
features of Acute inflammatory colitis, acute liver failure which may completely
recovers with supportive management, acute abdominal pain, diarrhoea, obstructive
jaundice, Reye's syndrome.
35 , 71

Liver involvement is in the form of hepatitis secondary to either direct viral
invasion or due to consequence of inflammatory reaction . Patient may develop
jaundice , with elevation of liver enzymes . Few cases may progress to fulminant
hepatic failure and lead to hepatic encephalopathy. Typical features of fever , upper
42
quadrant abdominal pain, abnormality of liver function tests, thickened GB wall
without stones and positive Murphy's sign and sonographic evidence can establish a
diagnosis of Acute acalculus cholecystitis.
72
Acalculus cholecystitis may be seen in
patients with DHF.
RESPIRATORY SYSTEM:
The increased permeability of alveolar capillary membrane may result in
Edema in alveoli and interstitial spaces and pulmonary hemorrhage which leads to a
deterioration in pulmonary function.
69

Dengue shock syndrome is reported to be third leading causes of ARDS in
pediatric intensive care setting in endemic area. There are two important implication
for this manifestation. First , Early restoration of adequate tissue perfusion is critical
to prevent progression of dengue shock syndrome to ARDS. However equal care must
be exercised to avoid excessive fluid infusion after adequate volume replacement
because fluid over load may result in ARDS. Second, this manifestation in children
requires early recognition and appropriate treatment by means of intermittent positive
pressure ventilation with positive end expiratory pressure.
OCULAR MANIFESTATIONS :
The ophthalmologic findings mainly included retinal hemorrhage as a sign of
increased vascular permeability and breakdown of inner blood retinal barrier and
cotton wool spots representing micro infarction of nerve fibre layer due to occulusion
of pre capillary arterioles.
37

Pan ophthalmitis is also seen. Optic neuritis is consistent with colour vision
impairment, in cases of severe exudative maculopathy, the visual recovery may be
prolonged or may remain visually impaired.

43
RENAL SYSTEM :
Acute renal failure and haemolytic uremic syndrome are the complications.
MUSCULOSKELETAL SYSTEM :
Myositis with raised creatine phosphokinase (CPK) and Rhabdomyolysis.
Individuals with DENV-3 had a higher prevalence of musculoskeletal and
gastrointestinal manifestations, whereas individuals with DENV-4 infection had a
higher prevalence of cutaneous and respiratory manifestations. The higher prevalence
of malaise with DENV-2 and DENV-3 compared with the other DENV serotypes was
also a novel finding. a higher pleural effusion index was found in DENV-2 compared
with DENV-1. DENV serotypes showed a common respiratory endpoint (combining
cough, rhinorrhea, nasal stuffiness, or sore throat) was more prevalent in DENV-3
than DENV-2. An increased prevalence of rhinorrhea with DENV-1 infection and an
increased prevalence of pharyngeal congestion with DENV-4 infection. The DENV-2
period tended to be more associated with mucosal or internal bleeding (e.g.,
hematemesis, melena, menorrhagia, gingival bleeding, and epistaxis), whereas the
milder signs, such as a positive torniquet test and petequiae, were significantly more
associated with the DENV-1 period .
75
DIFFERENTIAL DIAGNOSIS OF DENGUE.
23
Arboviruses - Chikungunya virus (this has often been mistaken for dengue in South
East Asia)
Viral diseases - Hantavirus; measles; rubella; enteroviruses; influenza; hepatitis A
Bacterial diseases - Meningococcaemia; scarlet fever; typhoid
Parasitic diseases - Leptospirosis; rickettsial diseases; malaria

44
3.7 DIAGNOSIS:

Fig 12 : COMPARISON OF DIAGNOSTIC TESTS

Fig 13 : PRIMARY & SECONDARY DENGUE INFECTION

45
COMMON LABORATORY FINDINGS
Increased Hematocrit (due to hemoconcentration)
Thrombocytopenia platelet count below 1,00,000 / cu mm, usually observed
in the period between day 3 and day 8 following the onset of illness.
57 , 76 , 77 , 79

Lymphocytosis with reactive lymphocytes
Leucopenia.
78

Elevated liver enzymes.
80

Increased capillary permeability and the presence of thrombocytopenia with
hemoconcentration differentiate DHF from classical dengue fever.
57 , 75 , 81
DIAGNOSIS OF DENGUE
Virus isolation : Detection of dengue virus by culture is definite diagnostic,
but practical consideration limits its use. During the febrile phase, dengue viruses can
be isolated from serum, plasma, or leucocytes. Ideally, blood should be collected
during the febrile period, preferably before the fifth day of illness (that is, before
formation of neutralising antibodies). And as noted above dengue virus is generally
heat labile and special precaution must be taken against thermal inactivation of
specimen. It takes two weeks to read the results and lastly virus culture is expensive.
The immunofluorescence assay is cheaper and provides results faster (2448 hours).
Molecular detection : The sensitivity, specificity, and rapid detection of
minute quantities of dengue viral material i.e. Dengue RNA in the patients serum
makes RT-PCR amplication assay useful for the detection of dengue infection early in
the disease when antibodies are not detected. RT-PCR is more sensitive than virus
isolation, allows for rapid detection of dengue infections (results are usually available
in 24 hours) and easier identification of the circulating serotype . Dengue RNA may
also be identified in individuals, Using In situ hybridization or immunocytochemistry.
46
Dengue virus antigen detection by immuno cytochemisty is simple and can be used
for routine diagnostic purpose.
Serological diagnosis : It involves detection of antibodies in patients serum.
Methods used for serological diagnosis of dengue infections include:
haemagglutination inhibition tests, enzyme linked immunosorbent assay (ELISA),
complement fixation test and neutralisation tests. The timing of specimen collection
can be more flexible because anti dengue antibody response lasts for at least several
weeks after onset of illness. Immunoglobulins are not easily inactivated by harsh
treatment of specimens.
Dengue specific IgM and IgG ELISA is widely used, as it is relatively
inexpensive, has good sensitivity, and is quick and simple to perform. Most patients
have measurable IgM antibodies by the fifth day of infection. On average, they
become undetectable 3060 days after the onset of illness. The sensitivity of IgM
ELISA range from 83.9%98.4% with a specificity of 100%.
The ability of dengue viruses to agglutinate goose erythrocytes is used in the
haemagglutination inhibition test. A fourfold or greater rise in antibody titres is
suggestive of a flavivirus infection (and not diagnostic of dengue infections).
However, a single antibody titre 1:2560 is accepted as indicating secondary dengue
infection if supported by a clinical history suggestive of dengue.
On other hand, serological tests may produce false positive results which may
be due to polyclonal B cell activation or cross reactive antibodies, antibodies elicited
by other flavi virus (eg. J apanese Encephalitis) may cross react with dengue virus.
In summary serological diagnosis is in general less specific than diagnosis by
culture. The serological diagnosis of dengue in population exposed to other
47
flavivirusis are the challenges. Some degree of uncertainly is inevitable. MAC ELISA
and Hemagglutination inhibition test improve quality of lab diagnosis.
Future challenges in the study of dengue and DHF include the application of
modern techniques such as nucleic acid chips, protein chips and now biomarkers to
avoid cross reaction among different serotypes of dengue virus and other
flavivirus. Plans are development for internationally standardized guidelines to
improve quality assurance of those advanced Laboratory tests.
74

A triad of thrombocytopenia, raised hematocrit and elevated liver enzymes can be
used for early diagnosis of Dengue.
80
3.8 MANAGEMENT
There is no specific treatment that exist for Dengue. Steroids, antivirals and
(which decreases capillary permeability) have no proven role. Assessment of the
patient's condition includes investigations such as haemoglobin, packed cell volume,
platelet count, liver function tests, prothrombin time, partial thromboplastin time,
electrolytes, and blood gas analysis , renal function tests , chest radiograph and
abdominal ultrasound. Tests may also be done to rule out other causes of acute febrile
illness prevalent in that particular geographic location such as malaria, enteric fever,
chikungunya, hepatitis A etc.
Oral hydration solution should be started early, since the disease can lead to
increased vascular permeability and shock. Paracetamol (aspirin and other non-
steroidal anti-inflammatory drugs should be avoided owing to Reye's syndrome and
haemorrahge) can be used for fever and analgesia. Volume replacement and
transfusion of blood products are essential in patients with shock and severe
haematological abnormalities. The choice of crystalloid or colloid solutions in
48
Dengue shock syndrome is under debate. The patient's clinical condition should be
monitored until at least 24 hours after defervescence because of the risk of shock.
Management of a child with suspected Dengue infection :
A child with continuous fever for 3 or more days with no focus of infection
identified. Criteria for admission (any of the following) in the presence of
suspicion of Dengue fever:
Restlessness or lethargy
Cold extremities or circumoral cyanosis
Bleeding in any form
Oliguria or reluctance to drink fluids
Rapid and weak pulse
Narrowing of pulse pressure (<20 mm Hg or hypotension)
Haematrocrit of 40 or rising
Platelet count of less than 100,000/mm3
Acute abdominal pain
Evidence of plasma leakage, e.g., pleural effusion, ascites
If patient refuses admission, parent should be advised to:
Encourage child to drink fluids
Observe for coldness / blueness of extremities
Administer paracetamol for fever 10-15 m/kg/dose 4-6 hourly (limit to 5 doses in 24
hours)
Tepid sponging as necessary

49
Parents must bring the child back immediately to the nearest hospital in the
presence of any one of the following situations:
Not drinking / feeding poorly
Passing less urine than usual
Abdominal pain
Bleeding in any form
In older children, inability to sit up, giddiness
Irritability, drowsiness, restlessness
Child continues to be unwell
Following are the criterias to consider a patient for hospitalization in case of
significant dehydration (>10% of normal body weight) has occurred . Signs of
significant dehydration include:
Increasedcapillary refill time (>2s)
Tachycardia
Cool,mottled or pale skin
Diminished peripheral pulses
Changes in mental status
Oliguria
Sudden rise in haematocrit or continuously elevated haematocrit
Narrowing of pulse pressure 20mmHg (2.7kPa))
Hypotension (a late finding representing uncorrected shock).
82

Pointers for early diagnosis of DHF:
Frequent vomiting during first one or two days of febrile illness
Leucopenia on day 2

50
Management of grades I and II DHF :
All cases are to be admitted
Encourage patient to drink fluids, ORS, fruit-juices
Start intravenous fluid (1/5 dextrose saline initially) for those with poor oral intake.
Paracetamol for high fever
Daily capillary haematocrit determination
Rise in haematocrit of 20% or more reflects a significant plasma loss and also
indicates need for intravenous fluid therapy
Monitor urine output, vital signs.
Management of Dengue shock syndrome (Grades III and IV DHF) :
Infuse 0.9% saline or Ringers lactate at 10-20ml/kg boluses as rapidly as
possible until vital signs return to normal. 2-3 boluses may be needed in profound
shock. When vital signs improve, change IV fluids to dextrose 5% and 0.45% saline
at a reduced rate, 1-2 times maintenance (3-6 ml/kg/hour), guided by haematocrit,
urine output and vital signs.
If there is not definite improvement in vital signs and if haematocrit remains
high, use plasma or plasma expanders. If there is no definite improvement in vital
signs and if haematocrit is low or has decreased, transfuse blood because this signifies
hemorrhage, occult or obvious. Sudden drop in haemoglobin level is also an indicator
of occult hemorrhage.
Continue replacement of further plasma losses with Dextrose 5% and 0.45%
saline over a period of 24-48 hours. Reduce or discontinue intravenous fluids between
24-48 hours after the onset of shock if vital signs are stable. Reduce intravenous fluids
earlier if patient has good urine output. (Pulmonary edema and massive pleural
effusion will occur if excessive intravenous fluids are given after this stage).
51
Hyponatraemia and acidosis occur commonly in DSS. These will correct with
fluid resuscitation with 0.9% saline. Periodic arterial blood gases and electrolytes
should be measured.
Blood transfusion :
Blood transfusion is indicated in significant clinical bleeding, most often
haematemesis and melena.
Persistent shock with rapidly declining haematocrit level despite adequate volume
replacement, indicates significant clinical bleeding which requires prompt treatment
with blood transfusion.
It may be difficult to estimate and recognize the degree of internal blood loss in the
presence of haemoconcentration.
Blood products like fresh frozen plasma, platelet concentrate, and cryoprecipitate
may be indicated in some cases, especially with consumptive coagulopathy causing
significant bleeding.
In the presence of disseminated intravascular coagulation (DIC), supportive therapy
consisting of maintaining circulatory volume, correcting acidosis with sodium
bicarbonate and hypoxia with oxygen are required in addition to the use of blood
products. Cryoprecipitate (1 unit per 5 kg body weight) followed by platelets of 10-20
ml/kg within one hour and fresh frozen plasma (FFP 10 to 20 ml/kg). Frequent
clinical assessment and regular coagulation profile (PT, PTT, fibrinogen, platelet and
FDP) are mandatory as indicated. The administration of heparin may need to be
considered in patients who develop DIC.

52
Signs of Recovery:
Stable pulse, blood pressure and breathing rate
Normal temperature
No evidence of external or internal bleeding
Return of appetite
No vomiting
Good urinary output
Stable haematocrit
Convalescent confluent petechiae rash
Criteria for Discharging Patients:
Absence of fever for at least 24 hours without the use of antipyretics
Return of appetite
Visible clinical improvement
Good urine output
Stable haematocrit
Minimum of three days after recovery from shock
No respiratory distress from pleural effusion and no ascites
Platelet count of more than 50,000/mm3
Based on case-definitions, all suspected, probable and confirmed cases of
DF/DHF should be reported to the District Health Officer.
82

3.9 VECTOR SURVEILLANCE AND CONTROL:
The most important vector of dengue virus is mosquito which should be the main
target of surveillance and control activities.

53
Vector Surveillance:
Entomological surveillance is used to determining changes in geographical
distribution and density of vector, obtain relative measurements of the vector
population over time , evaluate control programmes, and facilitate appropriate and
timely decision regarding interventions. Special attention should be given to
surveillance of sea ports, air ports, other points of entry,
Vector control:
1. Environmental control methods : include: reducing vector breeding sites,
solid waste management, modification of man made breeding sites, and
improvements in house design. Environmental management methods to
control Aedes Aegyptus, Aedes Albopticus include the improvement of water
supply and storage, solid waste management and modification of man made
larval habits. Naturally occurring repellents (citronella oil, lemon grass) or
chemical repellents (DEET) are available.
Emergency control measures are based primarily on applications of
insecticides and it is essential to monitor periodically vector's susceptibility to
insecticides. Most widely used are temephos, malathion, fenthion, and
fenithrothion.
2. Biological control of the vector : These methods are targeted against the
larval stages of the dengue vector. They include the use of larvivorous fish
such as Gambusia affinis and Poecilia reticulate, endotoxin producing bacteria
(Bacillus thuringiensis serotype H-14 and Bacillus sphaericus are currently
used), and copepod crustaceans.
54
3. Chemical control : This includes the application of larvicidal insecticides or
space spraying. Larvicidal or focal control of Aedes Aegypti is usually limited
to containers Maintained for domestic use that can't be eliminated. The
larvicidal agents most commonly used are 1% Temphos sand granules,Insect
growth regulator methoprene.
Dengue Vaccines:
The importance of critical subjects like pathogenesis of dengue haemorrhagic
fever and inadequacy of animal model adversely affected dengue vaccine
development. The efficacy and safety of some of new vaccines candidates have been
evaluated and proven in human preclinical or clinical trials.
A tetravalent vaccine should simultaneously immunize against all four dengue
virus (DENV) serotypes in order to reduce the theoretical risk of dengue hemorrhagic
fever from subsequent wild-type DENV infections.
108
Two live attenuated tetravalent
vaccine candidates are in Phase 2 clinical trials in DENV endemic regions. Numerous
other vaccine candidates including inactivated whole virus, recombinant subunit
protein, DNA and virus-vectored vaccines are also under development.

There are
possibilities that non-structural components of Dengue virion, such as NS1 could
serve as protective antigens in addition to structural ones such as E antigen. Anti-
idiotypic vaccine is also a hypothetical candidate. The advantage of having
recombinant genes for protective epitopes packed into a single carrier is apparent. The
candidate carriers may include , l7D yellow fever vaccine and J E vaccine. The DEN-2
candidate vaccine may also serve as the carrier for such a recombinant. The aim is to
obtain information on gene sequencing of different strains and types of Dengue virus
and to perform epitope mapping of these viruses using monoclonal antibodies.

55
METHODS AND MATERIALS
4.1 Source of Data: Suspected cases of Dengue fever in Outpatients and admitted as
Inpatient in Kempegowda Institute of Medical Sciences and Research Centre ,
Bangalore.
4.2 Method of collection of data: Definition of Study Subjects- 100 cases of
suspected Dengue fever children who fulfilled the inclusion criteria were selected.
Pretest counseling was given to parents / guardian. After taking written informed
consent from parents ,case was enrolled ,data was collected in a predesigned semi-
structured questionnaire .Blood samples were collected from children with suspected
Dengue infection for complete blood count, haematocrit , liver function tests,
prothrombin time, activated partial thromboplastin time, Dengue viral Ag, IgG &
IgM, and other relevant investigations who are admitted to Kempegowda Institute of
medical sciences as inpatient and also as Out-patients .WHO classification and case
definition was used to classify Dengue Fever, Dengue Hemorrhagic Fever, Dengue
Shock Syndrome and Dengue like illness.
4.3 Sample size : 100
4.3 Study design : Hospital based descriptive study.
Duration of study : one and a half year.
Inclusion criteria:
1. All children below 18 yrs of age with clinical features suggestive of Dengue
infection admitted as inpatients and outpatients in Kempegowda Institute of
Medical Sciences, Bangalore.
2. Child presenting with fever of acute onset (<2wks), pain abdomen, vomiting,
rash, flushed appearance and bleeding manifestation.
56
Exclusion criteria:
1. Febrile illness of >2wks duration.
2. Patients with any identified specific infection like Malaria, Typhoid, UTI,
etc..
4.4 Methodology :
The present study was conducted at Kempegowda Institute of Medical
Sciences hospital, Bangalore , a tertiary care pediatric hospital.
An alarmingly increasing epidemic of dengue was noticed in this part of state, with
more number of admissions in the pediatric age group. Hence the following study was
conducted to find out the early clinical manifestation and its outcome in dengue fever.
Hundred children in the paediatric age group (<18yrs) presenting with symptoms and
signs suggestive of dengue fever as per WHO criteria were included in the study,
between December 2010 to April 2012.
Written consent was taken from parents before enrolling in study. A detailed
demographic data, clinical history, physical examination and relevant baseline
investigations were undertaken as per the proforma. Patients with an identified
bacterial focus or any other identified specific infection were excluded during the
Study. Serum samples were obtained on an average of 5 to 7 days after DF symptoms
had appeared. The cases were followed-up daily for the clinical and laboratory
parameters. The patients were treated with IV fluids, paracetamol ,antacids, blood
products and inotropics as per WHO criteria for treatment of dengue. These cases
were stratified based on the presence or absence of complications like shock and
haemorrhage in to various dengue types. The frequency of various signs and
symptoms and the values of laboratory tests were compared. The results were
tabulated and correlated. The outcome was recorded in every subject. The criteria
57
defined by WHO as mentioned previously, were followed for the inclusion of subjects
in to the study.
Investigations :
1. Complete blood count,
2. Blood test (Serology) for Dengue fever,
3. Urine routine,
4. Serum electrolytes,
5. Random blood sugar,
6. QBC for MP,
7. WIDAL/ Blood culture,
8. Liver enzymes- SGOT, SGPT, Serum albumin,
9. Chest x ray,
10. Ultrasound abdomen,
11. PT, APTT.
If necessary-
12. Blood urea, serum creatinine,
13. CSF analysis,
14. 2D echo,
15. CT scan brain/MRI.
All the hundred children registered in the study were treated at KIMS,
Bangalore as per the WHO algorithm on dengue fever.

58
Method of Statistical Analysis:
The following methods of statistical analysis have been used in this study. The Excel
and SPSS (SPSS Inc, Chicago) software packages were used for data entry and
analysis.
The results were presented in numbers and percentage for categorical data in
Table and Figure.
1) Proportions were compared using Chi-square test of significance
Chi-Square (
2
) test for (r x c tables)
a,b..h are the observed numbers. N is the Grand Total
2
=
+ + +

1
1
....... ..........
1 1
1 1
2
1
2
1
1 2
2
1
1
c c
i r i
c
i
n
h
t n
b
t n
a
t
N
DF=(r-1)*(c-1), where r=rows and c=columns
DF=Degrees of Freedom (Number of observation that are free to vary after
certain . Restriction have been placed on the data)
2) One way analyses of variance were used to test the difference between groups.
When comparing more than two means, an ANOVA F-test tells you whether the
means are significantly different from each other. Comparison of Two variance Sa2
and Sb2 , estimated for two group Na and Nb subjects respectively. Uses F test

2
2
Sb
Sa
F =
with Na-1 and Nb-1 degrees of freedom.
In the above test a p value of less than 0.05 was accepted as indicating
statistical significance.
59
RESULTS
Out of the 100 children the study group, the following characteristics
were noted.
1. DIAGNOSIS CLINICAL SPECTRUM OF CASES.

Diagnosis
Frequency(N=100) Percentage
DF 36 36.0
DHF 33 33.0
DLI 16 16.0
DSS 15 15.0
Total 100 100.0

Out of total 100 cases studied, 36 children met WHO specified criteria for DF, 33
children with DHF, 15 children with DSS and 16 children with DLI.

60
2. AGE DISTRIBUTION OF PATIENTS.

Age groups
Frequency(N=100) Percentage
<1 yr 3 3.0
1-4 yrs 16 16.0
5-8 yrs 31 31.0
9-12 yrs 26 26.0
>12 yrs 24 24.0
Total 100 100.0

In the present study highest number of cases were found in age group of 5 to 8yrs
(31% ), followed by in age group of 9-12yrs (26%).

61
3. AGE DISTRIBUTION OF PATIENTS ACCORDING TO CLINICAL
SPECTRUM.
Age distribution of patients
<1
yr
1-4
yrs
5-8
yrs
9-12
yrs
>12
yrs
Total
2

value
p
value
DF 1 7 6 12 10 36
DHF 1 2 15 5 10 33
DLI 0 4 6 3 3 16
DSS 1 3 4 6 1 15
3 16 31 26 24 100 Total
3.0% 16.0% 31.0% 26.0% 24.0% 100.0%
15.856 0.198

In the present study highest number of cases were found in age group of 5 to 8yrs
(31% ), followed by in age group of 9-12yrs (26%).
62
4. GENDER DISTRIBUTION OF PATIENTS.

Gender
Frequency( N=100) Percentage
Male 66 66.0
Female 34 34.0
Total 100 100.0

Out of the 100 children 66 were male and 34 were female. The ratio M:F =1.94:1.

63
5. GENDER DISTRIBUTION OF CASES ACCORDING TO CLINICAL
SPECTRUM.
Gender
distribution

Male Female
Total
2

value
p
value
28 8 36 DF
77.8% 22.2% 100.0%
19 14 33 DHF
57.6% 42.4% 100.0%
11 5 16 DLI
68.8% 31.3% 100.0%
8 7 15 DSS
53.3% 46.7% 100.0%
66 34 100 Total
66.0% 34.0% 100.0%
4.395 0.222

Out of the 100 children 66 were male and 34 were female. The ratio M:F =1.94:1.
64
6. SYMPTOMATOLOGY OF CASES.
Symptomatology Present
Fever 96
Abdominal pain 42
Vomiting 49
Headache 12
Myalgia 7
J oint pain 4
Edema 3
R O Pain 1
Diarrhea 7
Cold 3
Cough 10
Convulsion 2
Menorrhagia 1
Symptomatology
96
42
49
12
7
4
3
1
7
3
10
2
1
0 20 40 60 80 100
Fever
Abdominal pain
Vomiting
Headache
Myalgia
J oint pain
Edema
R O Pain
Diarrhea
Cold
Cough
Convulsion
Menorrhagia
Menorrhagia
Convulsion
Cough
Cold
Diarrhea
R O Pain
Edema
J oint pain
Myalgia
Headache
Vomiting
Abdominal pain
Fever
96 (96%) children presented with fever as the predominant complaint.
65
7. ANALYSIS OF SYMPTOMATOLOGY.

DF(N=36)
DHF
(N=33)
DLI
(N=16)
DSS
(N=15)
Symptoms
n % n % n % n %
2

value
p
value
Fever 35 97.2% 33 100.0% 14 87.5% 14 93.3% 4.803 0.187
Abdominal
Pain
14 38.9% 13 39.4% 9 56.3% 6 40.0% 1.593 0.661
Vomiting 20 55.6% 16 48.5% 7 43.8% 6 40.0% 1.285 0.733
Headache 3 8.3% 3 9.1% 3 18.8% 3 20.0% 2.322 0.508
Myalgia 4 11.1% 2 6.1% 1 6.3% 0 0.0% 2.122 0.547
J oint Pain 1 2.8% 1 3.0% 2 12.5% 0 0.0% 3.856 0.277
Edema 1 2.8% 1 3.0% 1 6.3% 0 0.0% 1.051 0.789
Retro Orbital
Pain
0 0.0% 0 0.0% 0 0.0% 1 6.7% 5.724 0.126
Diarrhea 2 5.6% 3 9.1% 0 0.0% 2 13.3% 2.466 0.482
Cold 1 2.8% 2 6.1% 0 0.0% 0 0.0% 2.027 0.567
Cough 5 13.9% 3 9.1% 1 6.3% 1 6.7% 1.070 0.784
Convulsion 0 0.0% 1 3.0% 0 0.0% 1 6.7% 2.907 0.406
Menorrhagia 0 0.0% 1 3.0% 0 0.0% 0 0.0% 2.051 0.562

66

96 (96%) children presented with fever as the predominant complaint followed
by vomiting 49 (49%), Abdominal pain 42 (42%), Headache 12 (12%), Cough 10
(10%), Diarrhea 7 (7%), Myalgia 7 (7%), Joint pain 4 (4%), Edema 3 (3%), Cold
3 ( 3%), Convulsion 2 (2%), Retro orbital pain 1 (1%), Menorrhagia 1 (1%).

67
8. SIGNS IN PATIENTS.

Signs Present Absent
Conjunctival congestion 18 82
Facial puffiness 28 72
Pedal edema 21 79
Hepatomegaly 53 47
Splenomegaly 8 92
Ascites 13 87

The most common signs were Hepatomegaly(53%), followed by Facial
puffiness(28%), Pedal edema(21%), Conjunctival congestion(18%),
Ascites(13%), Splenomegaly (8%).
68
9. TEMPERATURE

Temperature Frequency
Febrile 12
Afebrile 88

12% of children in the study group had fever.

69
10. DISTRIBUTION OF SIGNS ACCORDING TO CLINICAL
SPECTRUM.

DF(N=36)
DHF
(N=33)
DLI
(N=16)
DSS
(N=15)
Signs
n % n % n % n %
2

value
p
value
Conjunctival
congestion
3 8.3% 8 24.2% 1 6.3% 6 40.0% 9.566 0.023
Facial
Puffiness
2 5.6% 14 42.4% 1 6.3% 11 73.3% 31.447 <0.001
Pedal edema 1 2.8% 11 33.3% 1 6.3% 8 53.3% 21.782 <0.001
Temp (Febrile) 6 16.7% 0 0.0% 4 25.0% 2 13.3% 7.828 0.050
Hepatomegaly 13 36.1% 25 75.8% 5 31.3% 10 66.7% 15.147 0.002
Splenomegaly
3 8.3% 3 9.1% 1 6.3% 1 6.7% 0.162 0.984
Ascites
1 2.8% 7 21.2% 1 6.3% 4 26.7% 8.415 0.038

The most common sign was Hepatomegaly (53%).
70
11. RESPIRATORY SYSTEM EXAMINATION.

Air entry Frequency
Normal 73
Decreased 27

On respiratory system examination , 27% of cases were observed to have
decreased air entry.

71
12. DISTRIBUTION OF AIR ENTRY (RESPIRATORY SYSTEM)
ACCORDING TO CLINICAL SPECTRUM OF CASES.

DF(N=36)
DHF
(N=33)
DLI
(N=16)
DSS
(N=15)
Air entry
n % n % n % n %
2

value
p
value
Normal 32 88.9% 19 57.6% 15 93.8% 7 46.7%
Decreased 4 11.1% 14 42.4% 1 6.3% 8 53.3%
17.367 0.001

On respiratory system examination , 27% of cases were observed to have
decreased air entry.

72
13. RELATIONSHIP BETWEEN VARIOUS SITES OF BLEEDING AND
DENGUE FEVER.

Site of bleeding Present Absent
Rashes 12 88
Melaena 0 100
Hematuria 2 98
Hematemesis 4 96
Epistaxis 4 96
Gum bleeds 2 98

Bleeding was noted in 24% of total number of cases. The skin bleeds were the
most common manifestation noted in 12 cases (12%) followed by GIT bleeding
like hematemesis 4 cases (4%) followed by epistaxis 4 cases (4%) ,hematuria 2
cases (2%) and gumbleeds 2 cases (2%). The bleeding manifestations were more
in DHF, DSS group than DF group.
73
14. RELATIONSHIP BETWEEN VARIOUS SITES OF BLEEDING AND
DENGUE FEVER ACCORDING TO CLINICAL SPECTRUM.
DF(N=36)
DHF
(N=33)
DLI
(N=16)
DSS
(N=15) Site of
Bleeding
n % n % n % n %
2

value
p
value
Rashes 0 0.0% 8 24.2% 0 0.0% 4 26.7% 14.830 0.002
Melaena 0 0.0% 0 0.0% 0 0.0% 0 0.0%
Hematuria 0 0.0% 2 6.1% 0 0.0% 0 0.0% 4.143 0.246
Hematemesis 0 0.0% 4 12.1% 0 0.0% 0 0.0% 8.460 0.037
Epistaxis 1 2.8% 3 9.1% 0 0.0% 0 0.0% 3.659 0.301
Gum Bleeds 0 0.0% 2 6.1% 0 0.0% 0 0.0% 4.143 0.246

Bleeding was noted in 24% of total number of cases. The skin bleeds were the
most common manifestation noted in 12 cases (12%) followed by GIT bleeding
like hematemesis 4 cases (4%) followed by epistaxis 4 cases (4%) ,hematuria 2
cases (2%) and gumbleeds 2 cases (2%). The bleeding manifestations were more
in DHF, DSS group than DF group.
74
15. TYPES OF SKIN RASHES

Skin rashes Present Absent
Flushing 54 46
Macular rash 21 79
Petechiae 33 67
Ecchymosis 11 89

Most common type of skin rash observed in the present study was Flushing 54%,
followed by Petechiae 33% , Macular rash 21% and Ecchymosis in 11% of cases.

75
16. DISTRIBUTION OF TYPES OF SKIN RASHES ACCORDING TO
CLINICAL SPECTRUM.

DF(N=36)
DHF
(N=33)
DLI
(N=16)
DSS
(N=15)
Skin rashes
n % n % n % n %
2

value
p
value
Flushing 15 41.7% 22 66.7% 6 37.5% 11 73.3% 8.347 0.039
Macular
rash
0 .0% 14 42.4% 0 .0% 7 46.7% 28.909 <0.001
Petechiae 0 .0% 23 69.7% 0 .0% 10 66.7% 53.401 <0.001
Ecchymosis 0 .0% 4 12.1% 0 .0% 7 46.7% 25.960 <0.001

Most common type of skin rash observed in the present study was Flushing 54%,
followed by Petechiae 33% , Macular rash 21% and Ecchymosis in 11% of cases.

76
17. TOURNIQUET TEST.
Tourniquet test Frequency
Positive 43
Negative 57

Tourniquet test (Hess capillary resistance test) was performed by placing the
sphygmomanometer cuff around the upper arm and raising the pressure midway
between systolic and diastolic pressure for 5 7 minutes. The test was considered
positive when more than 20 petechiae developed in an area of 1 sq. inch on the flexor
aspect of forearm. Tourniquet test is performed by inflating a blood pressure cuff on
the upper aspect of arm to a point midway between systolic and diastolic pressures for
5 minutes. The test is considered positive when >20 petechiae/2.5 cm
2
are observed.
Hemorrhagic manifestations usually appear 4-5 days after the onset of fever. This test
is a very useful screening test in suspected cases of Dengue fever.
The tourniquet test was positive in 43% of cases.

77
18. ANALYSIS OF TOURNIQUET TEST RESULTS ACCORDING TO
CLINICAL SPECTRUM.

DF(N=36)
DHF
(N=33)
DLI
(N=16)
DSS
(N=15) Hess
Test
n % n % n % n %
2

value
p
value
Positive 0 0.0% 30 90.9% 1 6.3% 12 80.0%
Negative 30 100.0% 3 9.1% 15 93.8% 3 20.0%
75.256 <0.001

The tourniquet test was positive in 43% of cases.

78
19. PLATELET COUNT.
DF(N=36) DHF (N=33) DLI (N=16) DSS (N=15)
Platelet Count
(cells/cu mm)
n % N % n % n %
<20000 2
5.6%
18 50.0% 16 44.4% 0 0.0%
20000-50000 12
36.4%
12 36.4% 8 24.2% 1 3.0%
500001-100000 1 6.3% 8 50.0% 7 43.8% 0 0.0%
>100000 7 46.7% 6 40.0% 2 13.3% 0 0.0%
20. PLATELET COUNT.

Parameter Platelet count
(cells/cu mm)
Mean 41870
SD 31459.98

A mean value of Platelet count was 41870 cells/cu mm. The WHO criteria of
low platelet count of < 1,00,000 cells/cu mm was seen in most of the cases (85%).
With maximum number of cases having platelet count in the range of <20000 cells/cu
mm in DHF and DLI groups.
79
21. HAEMOGLOBIN LEVELS ACCORDING TO CLINICAL SPECTRUM
OF CASES.

DF(N=36)
DHF
(N=33)
DLI
(N=16)
DSS
(N=15)

n % n % n % n %
2

value
p
value
Hb(g%) <=15 31 86.1% 24 72.7% 16 100.0% 13 86.7%
>15 5 13.9% 9 27.3% 0 0.0% 2 13.3%
6.366 0.095

22. HAEMOGLOBIN LEVELS (Hb g%).

N Mean SD Min. Max. f
value
p
value
DF 36 12.831 1.6570 9.3 15.9
DHF 33 13.158 2.5024 6.8 18.9
DLI 16 11.956 1.4339 9.3 14.3
Hb
DSS 15 12.313 2.7823 6.5 15.4
1.364 0.258

TOTAL 100 12.721 2.14 6.5 18.9

The hemoglobin level ranges from 6.518.9 gm%, with a mean level of 12.721
gm%.

80
23. HEMATOCRIT (PACKED CELL VOLUME) ACCORDING TO
CLINICAL SPECTRUM OF CASES.

DF(N=36)
DHF
(N=33)
DLI
(N=16)
DSS
(N=15)

n % n % n % n %
2

value
p
value
<=45 34 94.4% 28 84.8% 16 100.0% 13 86.7%
PCV
(%)
>45 2 5.6% 5 15.2% 0 0.0% 2 13.3%
3.973 0.264

24. HEMATOCRIT (PCV%)

value
p
value
DF 36 38.147 4.4575 27.9 48.0
DHF 33 38.739 6.9912 19.2 54.2
DLI 16 36.550 4.0678 27.2 40.4
PCV
DSS 15 36.653 7.8856 18.7 45.7
0.737 0.533

TOTAL 100 37.86 5.91 18.7 54.2

The hematocrit ranged from 18.7 54.2% with a mean value of 37.86%.

81
25. TOTAL LEUCOCYTE COUNT ACCORDING TO CLINICAL
SPECTRUM OF CASES.
DF(N=36)
DHF
(N=33)
DLI
(N=16)
DSS
(N=15)
n % n % N % n %
2

value
p
value
<4000 13 36.1% 15 45.5% 2 12.5% 6 40.0%
4000-
11000
21 58.3% 14 42.4% 13 81.3% 7 46.7%
Total
count
(cells/cu
>11000 2 5.6% 4 12.1% 1 6.3% 2 13.3%
7.835 0.250

26. TOTAL LEUCOCYTE COUNT (TLC in cells/cu mm)

valu
e
p
value
DF 36 5786.11 3377.417 1600 19200
DHF 33 5778.79 4286.079 1400 18900
DLI 16 6362.50 3019.023 3400 15700
TLC
DSS 15 6710.00 5097.766 2400 22000
0.278 0.841

TOTAL 100 6014.5 3893.197 1400 22000

Normal : 4000 11000 cells/cu mm.
The range of total leukocyte count varied from 1400 22000 cells/cumm with a mean
count of 6014.5 cells/cu mm.36 (36%) patients had leucopenia i.e. <4000 cells/cu
mm.

82
27. PROTHROMBIN TIME ACCORDING TO CLINICAL SPECTRUM
OF CASES.

DF(N=36)
DHF
(N=33)
DLI
(N=16)
DSS
(N=15)

n % n % n % n %
2

value
p
value
10-
13
0 .0% 7 21.2% 0 0.0% 1 6.7%
>13 1 2.8% 25 75.8% 1 6.3% 14 93.3%
PT (in
seconds)
ND 35 97.2% 1 3.6% 15 93.5% 0 0.0%
92.032 <0.001

28. PROTHROMBIN TIME (PT in seconds)

value
p
value
DF 1 24.000 . 24.0 24.0
DHF 32 17.856 4.8536 11.6 32.1
DLI 1 13.600 . 13.6 13.6
PT
DSS 15 21.063 10.1666 12.5 54.0
1.096 0.361

TOTAL 49 18.88 6.98 11.6 54.0

PT - Normal 10-13 sec.
The prothrombin time ranged from 11.6-54 sec with a mean of 18.88 sec.

83
29. ACTIVATED PARTIAL THROMBOPLASTIN TIME ACCORDING
TO CLINICAL SPECTRUM OF CASES.

DF(N=36)
DHF
(N=33)
DLI
(N=16)
DSS
(N=15)

n % n % n % n %
2

value
p
value
26-
36
1 2.8% 8 24.2% 0 0.0% 3 20.0%
>36 0 0.0% 24 72.7% 1 6.3% 11 73.3%
APTT
(in
seconds)
ND 35 97.2% 1 3.0% 15 93.8% 1 6.7%
85.127 <0.001

30. ACTIVATED PARTIAL THROMBOPLASTIN TIME (APTT in
seconds)

value
p
value
DF 1 35.700 . 35.7 35.7
DHF 32 43.366 8.5671 28.2 60.4
DLI 1 47.000 . 47.0 47.0
APTT
DSS 15 45.336 11.1144 31.0 69.0
0.434 0.730

TOTAL 49 43.86 9.22 28.2 69.0

APTT Normal 26-36 sec.
The activated partial thromboplastin time ranged from 28.2-69.0 sec with a
mean of 43.86 sec.

84
31. BLOOD UREA ACCORDING TO CLINICAL SPECTRUM OF CASES.
DF(N=36)
DHF
(N=33)
DLI
(N=16)
DSS
(N=15)

N % n % n % n %
2

value
p
value
5-18 0 0.0% 0 0.0% 1 0.0% 0 0.0%
>18 2 5.6% 7 21.2% 1 6.3% 9 60.0%
B.Urea
(in
mg/dl)
ND 34 94.4% 26 78.8% 14 87.5% 6 40.0%
27.457 <0.001

32. BLOOD UREA.

value
p
value
DF 2 35.00 5.657 31 39
DHF 7 49.71 40.194 25 136
DLI 2 26.50 17.678 14 39
B.Urea
(mg/dl)
DSS 9 43.00 32.592 19 114
0.284 0.836

TOTAL 20 42.9 32.056 14 136

The range for Blood urea was 14-136 mg/dl with a mean of 42.9 mg/dl.

85
33. SERUM CREATININE ACCORDING TO CLINICAL SPECTRUM OF
CASES.
DF(N=36)
DHF
(N=33)
DLI
(N=16)
DSS
(N=15)

N % n % n % n %
2

value
p
value
0.3-
0.7
1 2.8% 4 12.1% 1 6.3% 7 46.7%
>0.7 1 2.8% 3 9.1% 1 6.3% 2 13.3%
S.Creatinine
(in mg/dl)
ND 34 94.4% 26 78.8% 14 87.5% 6 40.0%
22.605 0.001

34. SERUM CREATININE.

valu
e
p
valu
e
DF 2 0.750 0.0707 0.7 0.8
DHF 7 0.700 0.1633 0.4 0.9
DLI 2 0.650 0.3536 0.4 0.9
S.Creatinine
(mg/dl)
DSS 9 0.778 0.4147 0.4 1.8
0.128 0.942

TOTAL 20 0.735 0.299 0.4 1.8

The range for Serum creatinine was 0.4 1.8 mg/dl with a mean of 0.735 mg/dl.

86
DistributionofLabparametervalues
8
6
.
1
%
1
3
.
9
%
9
4
.
4
%
5
.
6
%
3
6
.
1
%
5
8
.
3
%
5
.
6
%
0
.
0
%
2
.
8
%
9
7
.
2
%
2
.
8
%
0
.
0
%
9
7
.
2
%
7
2
.
7
%
2
7
.
3
%
8
4
.
8
%
1
5
.
2
%
4
5
.
5
%
4
2
.
4
%
1
2
.
1
%2
1
.
2
%
7
5
.
8
%
3
.
6
%
2
4
.
2
%
7
2
.
7
%
3
.
0
%
1
0
0
.
0
%
0
.
0
%
1
0
0
.
0
%
0
.
0
%
1
2
.
5
%
8
1
.
3
%
6
.
3
%
0
.
0
%6
.
3
%
9
3
.
5
%
0
.
0
%6
.
3
%
9
3
.
8
%
8
6
.
7
%
1
3
.
3
%
8
6
.
7
%
1
3
.
3
%
4
0
.
0
%
4
6
.
7
%
1
3
.
3
%
6
.
7
%
9
3
.
3
%
0
.
0
%
2
0
.
0
%
7
3
.
3
%
6
.
7
%
0.0%
20.0%
40.0%
60.0%
80.0%
100.0%
120.0%
<
=
1
5
>
1
5
<
=
4
5
>
4
5
<
4
0
0
0
4
0
0
0
1
1
0
0
0
>
1
1
0
0
0
1
0
1
3
>
1
3
N
D
2
6
3
6
>
3
6
N
D
Hb(%) PCV(%) Totalcount(cells/cumm) PT(inseconds) PTT(inseconds)
DF(N=36)
DHF(N=33)
DLI(N=16)
DSS(N=15)

87
LIVER FUNCTION TESTS
35. SERUM GLUTAMATE OXALOACETATE TRANSAMINASE (SGOT).

value
p
value
DF 36 122.81 111.275 10 596
DHF 31 144.39 60.918 50 298
DLI 16 84.50 81.310 12 298
SGOT
(IU/L)
DSS 15 340.47 324.793 35 1072
9.397 <0.001

TOTAL 98 156.69 168.58 10 1072

SGOT - Normal 1-55 IU/lt.
The range for SGOT was 10-1072 IU/lt with a mean of 168.58 IU/lt.
36. SERUM GLUTAMATE PYRUVATE TRANSAMINASE (SGPT).

value
p
value
DF 36 60.11 62.910 7 268
DHF 33 112.48 121.982 23 481
DLI 16 73.81 49.872 6 200
SGPT
(IU/L)
DSS 15 188.33 245.011 24 829
4.080 0.009

TOTAL 100 98.82 130.37 6 829

SGPT - Normal 5-45 IU/lt.
The range for SGOT was 6-829 IU/lt with a mean of 98.82 IU/lt.

88
37. SERUM ALBUMIN ACCORDING TO CLINICAL SPECTRUM OF
CASES .
DF(N=36)
DHF
(N=33)
DLI
(N=16)
DSS
(N=15)

n % n % n % n %
2

value
p
value
<3.4 14 38.9% 26 78.8% 8 50.0% 14 93.3%
3.4-
5.4
22 61.1% 4 12.1% 8 50.0% 1 6.7%
S.Albumin
(g/dl)
ND 0 0.0% 3 9.1% 0 0.0% 0 0.0%
29.856 <0.001

38. SERUM ALBUMIN (g/dl) .

value
p
value
DF 36 3.381 0.5019 2.2 4.2
DHF 30 2.883 0.4160 1.9 3.6
DLI 16 3.056 0.6511 1.9 3.8
S.Alb
DSS 15 2.620 0.6405 1.0 3.5
9.017 <0.001

TOTAL 97 3.066 0.58 1.0 4.2

SA Normal 3.4 5.4 gm%. The range for serum albumin was 1.0 4.2 gm% with a
mean of 3.066 gm%. Serum albumin of <3.4 gm% was seen in 62% of children,
more in DHF and DSS group. It is statistically significant. (
2
=29.856, P =
<0.001).

89

39. SERUM ELECTROLYTES

N Mean SD Min. Max. f value p value
DF 2 132.00 2.828 130 134
DHF 8 135.25 6.497 122 144
DLI 2 134.00 1.414 133 135
DSS 8 135.38 6.116 130 148
0.199 0.896
Na
TOTAL 20 134.85 5.57 122 148
DF 2 4.200 0.4243 3.9 4.5
DHF 8 4.525 0.8481 3.7 6.3
DLI 2 4.850 1.2021 4.0 5.7
DSS 8 4.075 0.7146 2.8 4.8
0.727 0.551
K
TOTAL 20 4.35 0.78 2.8 6.3
DF 2 98.00 2.828 96 100
DHF 8 100.38 6.116 91 107
DLI 2 98.00 0.000 98 98
DSS 8 97.00 4.629 90 102
0.598 0.626
Cl
TOTAL 20 98.55 4.96 90 107

Na Normal 136-146 meq/l. The range for serum sodium was 122-148 meq/l
with a mean of 134.85 meq/l. K Normal 3.5-5.0 meq/l. The range for serum
potassium was 2.8-6.3 meq/l with a mean of 4.35 meq/l. Cl Normal 98-106 meq/l.
The range for serum chloride was 90-107 meq/l with a mean of 98.55 meq/l.

90

40. DENGUE SEROLOGY.

Test component Frequency
Antigen 43
IgM 58
IgG 22

Dengue Ag was positive in 43 cases (43%), IgM was positive in 58 cases (58%)
and IgG was positive in 22 cases (22%) in this study.

91

41. DENGUE SEROLOGY ACCORDING TO CLINICAL SPECTRUM OF
CASES .

DF(N=36)
DHF
(N=33)
DLI
(N=16)
DSS
(N=15)
Test
component

n % n % n % n %
2

value
p
value
Positive. 16 44.4% 21 63.6% 0 0.0% 6 40.0%
Antigen
Negative. 20 55.6% 12 36.4% 16 100.0% 9 60.0%
17.890 <0.001
Positive. 24 66.7% 21 63.6% 0 0.0% 13 86.7%
IgM
Negative. 12 33.3% 12 36.4% 16 100.0% 2 13.3%
28.696 <0.001
Positive. 9 25.0% 8 24.2% 0 0.0% 5 33.3%
IgG
Negative. 27 75.0% 25 75.8% 16 100.0% 10 66.7%
5.921 0.116

Dengue Ag was positive in 43 cases (43%), IgM was positive in 58 cases (58%)
and IgG was positive in 22 cases (22%) in this study.
92
42. CHEST X-RAY.

Chest x-ray Frequency
Normal 62
Effusion 38

Chest x-ray was done in all the 100 cases, in 38 children (38%) there was pleural
effusion.

93
43. CHEST X-RAY FINDINGS ACCORDING TO CLINICAL SPECTRUM.

DF(N=36)
DHF
(N=33)
DLI
(N=16)
DSS
(N=15)
Chest X-
ray
Findings
n % n % n % n %
2

value
p
value
Normal 29 80.6% 15 45.5% 14 87.5% 4 26.7%
Effusion 7 19.4% 18 54.5% 2 12.5% 11 73.3%
21.460 <0.001

Chest x-ray was done in all the 100 cases, in 38 children (38%) there was pleural
effusion.
In the DHF and DSS group the number of cases were more compare to DF and
DLI group. (
2
= 21.460 , P<0.001) It was statistically significant.

94
44. ULTRASONOGRAPHY.

Ultra sonography Frequency
Normal 47
Gall bladder wall thickening 33
Acalculous cholecystitis 14
Pleural effusion 37
Ascites 32
Hepatomegaly 8
Splenomegaly 12

About 33 patients had gall bladder wall thickening, 37 patients had
pleuraleffusion, 32 patients had ascites, 14 patients had acalculous cholecystitis.
95
45. ULTRASONOGRAPHY FINDINGS ACCORDING TO CLINICAL
SPECTRUM.
DF(N=36)
DHF
(N=33)
DLI (N=16)
DSS
(N=15)
Diagnosis
n % n % n % n %
Normal 26 14.4%
5 3.0% 14
17.5% 2 2.7%
Gall bladder wall
thickening
8 4.4% 16 9.7%
1 1.3% 8 10.7%
Acalculous
Cholecystitis
2 1.1% 8 4.8%
0 0.0% 4 5.3%
Pleural Effusion 7 3.9% 18 10.9% 2 2.5% 10 13.3%
Ascites 4 2.2% 20 12.1% 0 0.0% 8 10.7%
Hepatomegaly 0 0.0% 5 3.0% 0 0.0% 3 4.0%
Splenomegaly 1
.6%
7 4.2% 1 1.3% 3 4.0%

About 33 patients had gall bladder wall thickening, 37 patients had
pleuraleffusion, 32 patients had ascites, 14 patients had acalculous cholecystitis.
96
DISCUSSION
Dengue fever is the most important arboviral infection of humans and has
become a major global public health problem. It is one of the most important tropical
infectious disease in the world.
In India, epidemics are becoming more frequent. Involvement of younger age
group and increasing in the frequency of epidemics are indicators of higher incidence
of infection. Classical dengue fever is an acute febrile illness but in a small percentage
of Dengue infection, a more severe form of disease known as DHF occurs. Early
recognition and meticulous management are very important to save precious lives
from this killer disease.
INCIDENCE
In the present study of 100 cases - 36% cases belongs to DF, 33% cases
belongs to DHF, 15% cases belongs to DSS group and 16% cases belongs to DLI.
AGE DISTRIBUTION
Although high incidence of degree has been described in children, very few
studies have been exclusively studied on them. The 5-11 year age group dominated
the Present study, accounting for 54% of the total.
The present study correlate with the previous studies in the age incidence.
Among the subgroup, there is a tendency for DSS to occur at younger age.
However previous studies have not noted any difference in age between dengue with
or without shock. The youngest child in the present study was 8 months old.

97
The following table gives incidence in the age group of 5 11 years among other
studies.
Sl. No. Study Place Year %
1 WHO meta
analysis
28
SEAR 1978-88 54
2 Narayanan et al
83
Chennai 2002 45
3 Gomber et al
84
Delhi 2001 78.9
4 Present study Bangalore 2010-12 54
GENDER DISTRIBUTION :
The incidence of male children that were affected is slightly more in our study,
the ratio being 1.94:1. Similar observation were made by others also showed
increased preponderance among boys as in WHO study in 1999 due to increased
outdoor activities of male children.
Sl. No. Study Year No. of
cases
Place M:F ratio
1 Chandrakanta et
al
85
2008 80 Lucknow 1.6:1
2 Cam et al
86
2001 27 Denmark 1.7:1
3 Pancharoen et al
87
2001 80 Thailand 1.1:1
4 Gurdeep S.D et
al
88
2008 81 North India 1.89:1
5 Kumar et al
74
2002-08 466 Karnataka 1.8:1
6 Sajid et al
89
2011 35 Pakistan 1.33:1
7 Present study 2010-12 100 Bangalore 1.94:1
98
SYMPTOMATOLOGY
In the present study fever (96%) was the predominant symptoms followed by
vomiting (49%), abdominal pain (42%%), bleeding (24%), Rashes (24, retro-orbital
pain (28%).
The following pattern of symptoms have been observed in other studies.
SI
No.
Study No of
cases
Fever Vomiti
ng
Abd
Pain
Headac
he
Bleeding ROP
1
Narayana
n et al
83
59 98.3% 83% 23.7% 28.8% 66.1% 11.9%
2
Anuradh
a et al
90
515 100% 8% 10.2% - 52.6% -
3
Misra et
al
91
17 100% 58% - 52.5% - -
4
Kankira
watana
et al
92
8 100% 62.5% - 62.5% - -
5
Solomon
et al
66
9 100% 45% - 55% - -
6
Kumar et
al
46
466 99.1% 47.6% 37.6% 47.6% 21.7% -
7
Sajid et
al
89
35 100% 34% 51% - - -
8
Present
study
100 96% 49% 42% 12% 24% 1%
99
EPIDEMIOLOGICAL CHARACTERISTICS :
The evaluation of immediate micro and macroenvironments of the patients
habitat revealed following observations.
Storage of water in containers was present.
Artificial storage of water as in flower vases, plant pots and ceiling hung
plants, coconut shell were also noticed.
The scope for mosquito breeding was present. Those children got infected in
the immediate monsoon or post monsoon months, being responsible for the
increase in the number of cases in that period.
Efforts were made to educate parents about disease from which their children
was suffering and the possible modes of spread, the environmental factors that might
have been responsible, the ways and means to prevent spread of disease, like keeping
surrounding clean using mosquito curtain etc, as a long term measures.
CLINICAL EXAMINATION :
Of the 100 children in the study 96% children had fever and no child was in
category of hyperpyrexia.
BLEEDING :
In the present study bleeding manifestations were found in 24% of cases.
Apart from petechiae, which usually associated with bleeding manifestations,
Hematemesis and epistaxis were the predominant modes of bleeding. Hematemesis
was the most common bleeding manifestation reported in other Indian studies.

100
Other studies have noted following pattern of bleeding.
SI. No. Study Place Year Bleeding Type
1 Kumar et
al
94
Lucknow 2000 31.2% Hematemesis
2 Anuradha et
al
90
New Delhi 1998 52.6% Epistaxis
3 Rahman et
al
95
Bangladesh 2002 46% Maelena
4 Present
study
Bangalore 2010-12 24% Hematemesis

TOURNIQUET TEST :
The platelet count and tourniquet test did not consistently correlate with each
other. The tourniquet test was positive in 43% of cases. Other studies have noted
varying results in this test.
Tourniquet test is not a reliable test for diagnosis as observed in many other
Indian studies.
SI No. Study Place Year Test positive
1 Kabra et al
96
New Delhi 1999 40%
2 Nimmannitya et
al
97
SEAR 1969 83.9%
3 Gomber et al
84
New Delhi 2001 25%
4 Present study Bangalore 2010-12 43%

101
SYSTEMIC EXAMINATION :
The systemic examination revealed non specific signs, as like any other viral
illness. Hepatomegaly was been in 53 children (53%) in the present study. Other
studies also reported hepatomegaly in significant percentage.
SI. No. Study Place Year Hepatomegaly
1 Narayanan et
al
83
Chennai 2002 52.5%
2 Nimmannitya et
al
97
SEAR 1969 90%
3 Mohan et al
98
New Delhi 2000 74%
4 J agadish kumar
et al
99
Mysore 2008-10 79%
5 Present Study Bangalore 2010-12 53%

INVESTIGATIONS :
The mean hemoglobin and hematocrit in the present study were 12.721 gm%
and 37.86 % respectively.
In a study done by Gurdeep S.D et al; the mean hematocrit value was 35.5 % .
88

There was no significant statistical correlation between hematocrit and
severity of disease among the clinical subgroups of dengue.
83
Narayanan et al reported the same to be 10.8 gm% and 33.2% respectively.
The classical description of > 20% rise in the hematocrit is difficult to
establish, as the reference standards have not been established for Indian children.
Hence the rise in hematocrit was not taken as a diagnostic criteria.
102
Leucopoenia has been reported in a number of studies, the present study had
36 (36%) patients with leucopenia i.e. <4000 cells/cu mm.and mean total leukocyte
count of 6014.5 cells/cumm. The highest and lowest TLC was 22000 and 1400
cells/cu mm respectively.
Nazish Butt et al, in their series found that, out of 104 patients ,55 (52.8%) had
leucopenia. The mean leucoycte count was 5200 cells/cu.mm , which almost correlates
with the present study.
80
Thrombocytopenia and dysfunctional platelets remains a central hallmark of
dengue fever, surprisingly little is known about the interaction of dengue virus with
platelets.
100

Platelets counts carry one of the most important key for diagnosis. On taking
the WHO limit of <100000/cmm for low platelet count, 85 % had thrombocytopenia
in the present study.
The mean platelet in the present study was 41870 cells/cmm. The platelet
counts at the admission was neither an indicator of prognosis nor of bleeding
tendencies or progression of the disease. This suggest that other factors like platelet
dysfunction or disseminated intravascualr coagulation may have role in bleeding in
dengue fever cases. However studies which include only DHF cases shows correlation
between low platelet count and bleeding manifestations.
101
The studies by Gomber et al and Narayanan et al have documented the same
opinion.
83 , 84

A study done in Hong-Kong during 1998-2005 among 126 patients with 123
(98%) being dengue fever and 3 (2%) had dengue hemorrhagic fever,
thrombocytopenia, was present in 86%of patients.
78

103
But platelet count provides a very useful means of diagnosis at the screening
level. Hence the platelet count was a sensitive indicator for diagnosis but it did not
correlated with the outcome. Bleeding manifestations are more frequent with low
platelet count.
Nazish Butt et al study found that history, clinical examination and triad of
thrombocytopenia, haematocrit and elevated liver enzymes useful in early diagnosis
of Dengue hemorrhagic fever without waiting for Dengue serology.
.
In Nazish Butt et
al study, 100% of the patients had thrombocytopenia.
80

In Larreal et al study, laboratory test findings showed leucopenia in 72.5% in
both forms of dengue, and of patients with DHF severe thrombocytopenia (<
50,000/mm
3
platelets) in 70.9% .
102
Faridi et al study found that children presented with fever and hepatomegaly,
had a platelet count of between 20,000 /mm3 and 50,000/mm3, bleeding
manifestations were not related to platelet count.
103
The present study findings concurred with the previous studies and we found
that thrombocytopenia was the most commonly associated finding.
PROTHROMBIN TIME AND ACTIVATED PARTIAL THROMBOPLASTIN
TIME :
Few studies have documented utility of PTT as a diagnostic indicator.
PT is a sensitive indicator of synthetic function of liver. The prolonged APTT in the
acute phase may be due to hepatic injury and a low grade disseminated intravascular
coagulation.

104
Larreal et al study found that laboratory test findings showed prolonged PT and APPT
in 23.0% and 42.3% respectively.
102
TRANSAMINASES :
Although transaminases are said to be non specific for infections and stress, a
significant more than four fold rise was documented in some cases in this study. They
are not of any prognostic value, but serve as useful masker for diagnosis. Many
studies have noted high transaminases levels. Kalayanaroojs et al in 1997 in their
study at Bangkok reported higher levels of SGPT in patients of DHF than in DF.
1
The present study did not demonstrate a significant difference in the LFTs
between the clinical subgroup of dengue.
In epidemic or endemic areas, dengue fever infection should be considered in
the differential diagnosis of anicteric hepatitis. The high incidence of vomiting,
hepatomagaly and elevated liver enzymes can score as markers of suspicion of dengue
during an epidemic.
SI. No. Study Place Year No. of
cases
SGPT
levels
SGOT
levels
1 Chandrakanta
et al
85
Lucknow 2008 80 78 98
2 Kumar et al
94
Lucknow 2008 39 129 116
3 Pancharoen
et al
87

Thailand 2001 80 1503 597
4 Present study Bangalore 2010-12 100 98.82 168.58

105
Wahid et al study noted that ALT levels were significantly different in grade 2
or 4 DHF cases, indicating that the liver function derangement is related to the
severity of Dengue viral infection. DHF patients in the present study with
spontaneous hemorrhage had significantly higher ALT and ALP levels than those
without hemorrhage, suggests that DHF patients who bled had more severe
hepatocellular damage. Concluded that the liver is commonly involved in Dengue
viral infection, the presence of spontaneous bleeding may be useful in predicting the
extent of the hepatocellular damage observed in DHF.
104
Itha S et al study showed transaminases values being increased in 96% of
cases.
105
Larreal et al study showed that laboratory test findings showed Transaminase
values five fold higher than the normal values (p <0.005) were observed in 36.8%
and 74.4% of patients with CD and DHF respectively, AST was predominant in both
groups as their results suggest liver damage during the course of Dengue.
102
W.Petdachai in his study found that in children with Dengue shock syndrome,
AST levels were elevated in all cases and were more than ALT levels. Hepatic
dysfunction is common in Dengue infection and aminotransferase levels were useful
in predicting the occurrence of hepatic dysfunction.
106
J agadish kumar et al found a rise in AST in 93% and ALT in 78% of the
cases.
99
Luis et.al. In there study on Impact of Dengue on liver function as evaluated
by aminotransferase levels found that aminotransferase levels were high in
65.1% of patients.
107
106
Faridi et al study found that children had serum glutamic pyruvate
transaminase (SGPT) >40 IU/L and they concluded that hepatic dysfunction with
increased levels of serum enzymes was common in DHF.
103

SERUM ALBUMIN :
SI. No. Study Place Year No. Of
cases
Test
Positivity
1 Itha S, et
al
105
Uttar Pradesh 2005 45 76%
2 J agadish
kumar et al
99
Mysore 2008-10 110 66%
3 Present study Bangalore 2010-12 100 64%

Plasma leakage, which indicates that dengue causes hypoalbuminemia, is an
indicator of severity. In our study, albuminemia lesser than 3.4 g/dL was associated
with higher incidence of DHF. Usually high values of albuminemia may reflect the
integrity of the vascular endothelium, whereas albumin levels less than 3.4 g/dL may
be an early indicator of vascular permeability alteration. Therefore, this parameter
may be an early indicator of plasma leakage and a useful prognostic marker.
CHEST RADIOGRAPHY :
Out of 100 children in the study 38 (38%) showed evidence of right sided
pleural effusion, out of them 2 had bilateral effusion.
WHO has mentioned pleural effusion, especially on right side, as a consistent finding
of dengue. According to WHO, pleural effusion is a supporting evidence of plasma
leakage, the distinguishing feature of DHF. It also mentions that extent of pleural
107
effusion correlates with the severity of the disease and bilateral pleural effusion is
common in shock.
USG ABDOMEN :
The most striking USG-Abdomen finding in our study population was GB
wall thickening /edema that was seen in 33% of the patients. Splenomegaly,
hepatomegaly and ascites were also seen.
P M Venkata sai, R Krishnan, in their study on role of Ultrasound in Dengue
fever found that ultrasound of abdomen is an important adjunct to clinical profile in
diagnosing DF and may help direct further confirmatory investigations and during an
epidemic , ultrasound features of thickened GB wall, pleural effusion and ascites
strongly favour the diagnosis of Dengue fever.
108
J agadish kumar et al , in their study have demonstrated abnormal USG
abdomen findings in 65% of cases which included Gall bladder wall thickening.
99
DENGUE SEROLOGY:
The dengue Ag was positive in 43 children, IgM was tested positive in 58 children ,
IgG was positive in 22 cases in the study.
FINAL DIAGNOSIS:
The present study had DF 36 (36%), DHF 33 (33%), DSS 15 (15%) and DLI 16
(16%) cases among total of 100 cases.

108
CONCLUSION
Dengue is a major public health problem in Bangalore and surrounding
districts in the state of Karnataka in South India.
The present study had an objective of studying early clinical manifestation and
complications, hematological and hepatic dysfunction associated with the diseaseand
to correlate with other laboratory investigations and radiological findings in Dengue
fever.
In our present study classical dengue fever was most common presentation
followed by other complicated forms such as dengue hemorrhagic fever and dengue
shock syndrome.
Most of the patients presented with classical features such as fever, vomiting,
abdominal pain, headache, myalgia, arthralgia, oedema, low back ache, retro orbital
pain, rashes, bleeding manifestations. However few patients presented with atypical
presentations such as cough, diarrhoea, sore throat (cold).
Hypotension, hemorrhagic spots , positive tourniquet test , jaundice , pleural
effusion , ascites , neck stiffness are the common findings on examination associated
with complicated forms of dengue.
Bleeding , shock , hepatitis, polyserositis , meningitis, pneumonia are the
complications seen in severe forms.
On investigation Deranged liver function test, renal function test, secondary
dengue infection, thickened gall bladder wall , hepatosplenomegaly on ultrasound
abdomen, pleural effusion on chest radiogram are associated with DHF and DSS.
Platelet count does not correlate with severity of the disease.
109
In children, importance should be given to symptoms like fever, vomiting,
bleeding, musculoskeletal pain flushing and abdominal pain. If these are associated
with hepatomegaly, positive tourniquet test, low platelet count , elevated PTT and
elevated liver enzymes, a strong possibility of dengue to be considered, especially
during epidemic.
A positive torniquet test should prompt close observation and early hospital
referral, but a negative test does not excluded dengue infection.
During epidemic, dengue should be considered on the differential diagnosis of
any child presenting with fever.
Tourniquet test, low platelet count and chest radiograph for pleural effusion
are useful guides at primary health care level. Blood pressure should be monitered for
evaluating the progress of the disease. Bleeding tendencies should be closely watched.
Any evidence of disease progressing towards dengue hemorrhagic fever or dengue
shock syndrome, should be immediately referred to nearby referral centres.
A focused history , detailed clinical examination and appropriate relevant
investigations will aid for early diagnosis. The treatment of dengue is mainly
supportive, but early institution and meticulous monitoring are the corner stone for
positive outcome.

110
SUMMARY
The present study was undertaken to study various clinical manifestations and
acute complications of Dengue fever, including its complicated forms such as
DSS and DHF.
It involved prospective analysis of 100 cases of suspected cases of dengue
fever who were admitted at KIMS Hospital Bangalore from December 2010 to
April 2012 i.e. during the study period.
It was observed that the disease was common in age group of 5-11 yr (54%).
Most of the patients were male (66%) with an M: F ratio of 1.94:1.
The common presenting symptoms were fever(96%), vomiting(49%),
abdominal pain(42%), headache(12%), myalgia(7%), arthralgia(4%), retro
orbital pain(1%).
But few patients had unusual symptoms such as vomiting, diarrhoea, cough,
sore throat, breathlessness.
General physical examination revealed presence of hypotension, tachycardia,
rashes, facial puffiness (28%), pedal oedema (21%), and conjunctival
congestion (18%).
Tourniquet test was positive in 43 cases.
The skin bleeding was the most common manifestation noted in 12 cases
(12%) followed by GIT bleeding like hematemesis 4 cases (4%) followed by
epistaxis 4 cases (4%), hematuria 2 cases (2%) and gum bleeds 2 cases (2%).
On Systemic examination patients were found to have Hepatomegaly (53%),
Ascites (13%), Splenomegaly (8%), and pleural effusion (27%).
The mean hemoglobin and hematocrit in the present study were 12.721 gm%
and 37.86 % respectively.
111
36 (36%) patients in the study had leucopenia and mean total leukocyte count
of 6014.5 cells/cu mm. The highest and lowest TLC was 22000 and 1400
cells/cu mm respectively.
85 % cases had thrombocytopenia in the present study. The mean platelet in
the present study was 41870 cells/cu mm.
Elevated liver enzymes and elevated serum creatinine was found in
complicated forms of disease.
Out of total 100 cases studied 36 were classified as classical dengue fever, 33
as DHF, 15 as DSS, 16 as DLI.

112
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125
10.1 ETHICAL CLEARANCE FOR DISSERTATION STUDY

126
10.2 CLINICAL PHOTOGRAPHS

Fig 14 : RASH IN CASE OF A DENGUE FEVER.

Fig 15 : RIGHT SIDED PLEURAL EFFUSION IN CASE OF DENGUE
FEVER.

127
10.3 PROFORMA FOR A CASE OF DENGUE FEVER
SECTION A
1. NAME OF THE INSTITUTE : KEMPEGOWDA INSTITUTE OF
MEDICAL SCIENCES AND RESEARCH CENTRE, BLORE.
2. CASE INVESTIGATION No. :
3. NAME OF THE PATIENT :
4. AGE :
5. SEX : MALE / FEMALE
6. ADDRESS :
7. OCCUPATION :
8. RELIGION : HINDU /MUSLIM /CHRISTIAN /OTHERS
9. INFORMANT :
10. DATE OF ADMISSION :
11. DATE OF DISCHARGE :
12. IP / OP No. :
SECTION B
SYMPTOMS :
IF YES, DURATION:
1. Fever : Yes / No
2. Abdominal Pain : Yes / No
3. Vomiting : Yes / No
4. Headache : Yes / No
5. Myalgia : Yes / No
6. J oint Pains : Yes / No
7. Rashes : Yes / No
128
8. Petechiae : Yes / No
9. Ecchymosis : Yes / No
10. Melaena : Yes / No
11. Hematuria : Yes / No
12. Hematemesis : Yes / No
13. Epistaxis : Yes / No
14. Gum Bleeds : Yes / No
15. Edema : Yes / No
16. Retro Orbital Pain : Yes / No
17. Diarrhea : Yes / No
18. Constipation : Yes / No
19. Cold : Yes / No
20. Cough : Yes / No
21. Hurried Respiration : Yes / No
22. Convulsions : Yes / No
23. Altered Sensorium : Yes / No
24. Transient Weakness : Yes / No
25. H/O Recent Travel : Yes / No
129
GENERAL PHYSICAL EXAMINATION
General condition : Stable / Critical
Temperature :
Pulse Rate :
Blood Pressure :
Respiratory Rate :
Pulse pressure :
Tourniquet Test : Positive / Negative
Anthropometry :
PARAMETERS

OBSERVED

EXPECTED

REMARKS
Weight
Height / Length
Head Circumference
Chest Circumference
Mid Arm Circumference
SYSTEMIC EXAMINATION
PER ABDOMEN :
RESPIRATORY SYSTEM :
CARDIOVASCULAR SYSTEM :
CENTRAL NERVOUS SYSTEM:
DIAGNOSIS :
1. Dengue like illness :
2. Dengue Fever :
3. Dengue Hemorragic Fever Grade :
4. Dengue shock syndrome :
130
SECTION C
INVESTIGATIONS :
1. Date & Time
Hb (g/dl)
PCV (%)
Platelet
count(/cu mm)

2. Total count (TC) :
3. Differential Count (DC) :
4. ESR :
5. Peripheral Smear (PS) :
6. Urine Routine : Albumin -
Sugar -
Pus cells -
Epi cells
7. SGPT :
8. SGOT :
9. PT : INR:
10.aPTT :
11. Sr. Albumin :
12. Dengue Serology : Ag
Ig M
Ig G
13. RBS :
14. QBC For MP :
131
15. Widal Test /Blood c/s :
16. Chest X-Ray :
17. Ultrasound Abdomen :
OTHERS / IF NECESSARY :
18. Blood urea :
19. Serum Creatinine :
20. Serum Electrolytes :
21. ECG :
22. 2D ECHO :
23. CSF Analysis :
24. CT Scan Brain/MRI :
TREATMENT:
1. Supportive :
Fluid Therapy
10 ml/kg/hr : Yes / No
2. FFP Transfusion : Yes / No
3.Platelet Transfusion : Yes / No
4. Packed RBC Transfusion : Yes / No
5. Whole Blood Transfusion : Yes / No
6. Inotropes :
Dopamine
Dobutamine
132
7. Antibiotics : Yes / No
8. Ventilator Support : Yes / No

FINAL DIAGNOSIS :
OUTCOME OF THE PATIENT :

SIGN OF THE CANDIDATE / SIGN OF THE GUIDE :
INVESTIGATOR : DATE :
DATE :

133
10.4 KEY TO MASTER CHART
M Male
F Female
P Present
A Absent
Abd Pain Abdominal Pain
R O Pain Retro-orbital Pain
1 Positive
2 Negative
3 Dengue Antigen Positive
4 Dengue IgM Positive
5 Dengue IgG Positive
6 Gall bladder wall thickened
7 Acalculous Cholecystitis
8 Pleural Effusion
9 Ascites
10 Hepatomegaly
11 Splenomegaly
N Normal
F Febrile
D Decreased
Na Sodium
K Potassium
Cl Chloride
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1 24488/10 SyedMuthaiyab 5yrs M P P P A A A A A A P A A A A A A A A A 1 A A A A A A A N 86 98/70 24 P A A N 15.3 43.9 20000 18900 6 366 17.7 36.8 1.19 4,5 N 6,8,9,10 DHF
2 24580/10 Archana 12Yrs F P P A A A A A A A A A P A A A A A A A 2 A A P A A A A N 88 82/64 28 A A A N 13.5 40 9000 2600 4 38 22 40 1.5 3 N 6,8,9,10 DHF
3 24609/10 Chandana 11yrs F P P A A A A A A A A A A A A A A P A A 2 A A A A A A A N 80 104/70 28 A A A N 11.5 32 35000 4900 12 298 200 2 N N DLI
4 24647/10 Harish 11yrs10mM P A P A A A A A A A P A A A A A A A A 1 P A P A A A A N 82 96/56 28 P A A N 13.3 37.2 7000 3800 12 50 49 16 42.5 1.11 5 N N DHF
5 24730/10 Dhanush 4yrs M P P A A A A A A A A A A A A A A A A A 2 A A A A A A A N 78 100/60 24 P A A N 9.5 29 100000 15700 44 247 147 1.9 N N DLI
6 24988/10 Gagana 10yrs F P A A A A A A A A A A A A A A A A A A 1 A A P A A A A N 96 100/64 28 P A P D 14.6 39.8 9000 4300 4 203 92 32.1 60.4 2.22 2.6 3,4 E 7,8,9 DHF
7 25077/10 ArifPasha 13yrs M P P P A A A A A A A A A A A A A A A A 1 P A A A A A A N 72 106/68 22 P A P D 18.9 54.2 6000 13300 20 255 379 28 50.5 1.93 2.9 3 E 7,10,11 DHF
8 25209/10 Prajwal 6yrs M P P A A A A A A A A A A A A A A A A A 1 A A P A A A A N 110 94/54 28 P A A N 12.4 37.2 52000 4500 20 298 90 20.3 43.1 1.37 3.2 3 N N DHF
9 25474/10 MdMannan 11yrs M P P P P P A A A A A A A A A A A A A A 1 A A P A A A A N 68 100/70 26 A A A N 12.1 36.1 54000 2700 7 102 98 20.2 40.2 1.37 2.9 3,4 N N DHF
10 25479/10 DilNawaz 6yrs M P A A A A A A A A A A A A A A A A A A 1 P A A A A A A N 98 90/60 40 A A A N 11.4 35 33000 3700 13 139 38 20.9 45 1.47 3.6 N 6,7,8 DHF
11 25522/10 Roshan 11yrs M P A A A A A A A A A A A A A A A A A A 1 A A A A A P A N 98 80/64 28 A A A N 14.7 43 17000 3400 6 36 24 21 40 1.39 2.6 E 6,8,9 DSS
12 26499/10 Ranjitha 8yrs F P P P A A A A A A A A A A A A A A A A 1 P P P P P P A N 108 80/64 22 P A A N 13.3 38 5000 3400 2 226 43 21 40.5 1.45 2.7 3,4,5 N N DSS
13 1666/11 Nadishk 8yrs M P A A A A A P A A A A P A A A A P A A 1 P P A A A P P N 104 98/72 22 P A A N 9.9 28.9 5000 11000 12 112 23 14.1 33.2 1.15 2.5 3,4 E 6,9 DHF
14 2134/11 Walahith 4yrs M P P A A A A A A A A A A A A A A A A A 2 P A A A A A A F 108 96/66 24 P A A N 12.6 40.2 48000 6200 7 62 78 2.9 4 N N DF
15 2334/11 Harshitha 7yrs F P A A A A A A A A A A A A A A A A A A 2 P A A A A A A N 92 98/68 20 A A A N 10.3 38.3 48000 3400 10 117 119 2.3 N N DLI
16 3834/11 Moulya 1.8yrs F P A A A A A A A A A A A A A A A A A A 2 A A A A A A A F 98 90/64 22 P P A A 13.6 39.6 25000 9600 12 84 44 3.2 3 N N DF
17 4431/11 SyedSalauddin 16yrs M P P A A P A A A A A A A A A A A A A A 2 A A A A A A A N 90 104/64 20 P A A N 13.5 40.1 26000 2500 5 454 267 2.7 3,4,5 E 7 DF
18 4596/11 Hoysala 7yrs M P P P A A A A A A A A A A A A A A A A 2 A A A A A A A N 78 100/70 18 A A A N 13.2 40.4 53000 6000 5 38 42 3.5 N N DLI
19 4860/11 Raghu 14yrs M P A A A A A A A A A A A A A A A P A A 2 A A A A A A A N 68 100/70 20 A A A N 11.9 34.8 99000 8300 24 102 32 4 4 N N DF
20 4957/11 Hema 13yrs F P A A P P A A A A A A A A A A A A A A 1 P P P A P P A N 98 104/78 26 P A A N 16.1 49.9 13000 2600 5 81 33 17 52 1.15 3.1 4,5 E 7,9,10,11 28 0.7 138 4.9 107 DHF
21 4988/11 SyedSalauddin 16yrs M P P A P A A A A A A A A A A A A A A A 1 P P P P A P A N 108 80/66 18 P A A N 13.5 40.1 26000 2500 5 454 267 18 42.5 1.02 2.7 3,4,5 E 7 28 0.7 DSS
22 5392/11 Gracy 8yrs F P A A A A P A A A A A A P A A A A A A 2 P A A A A A A N 82 94/64 18 A A A N 12.6 40 52000 4200 10 45 42 3.4 N N DLI
23 6227/11 Rekha 15yrs F P P P A A A A A A A A A A A A A A A A 1 P P P A A P A N 100 100/76 24 A A A N 15.5 43.2 13000 3700 4 107 71 17.7 55.4 1.2 3.6 4,5 N 7,9 DHF
24 6917/11 Thasmias 10yrs F P A P A A A A A A A A A A A A A A A A 2 P A A A A A A N 90 104/72 22 P A A N 11.6 34.7 65000 2100 24 101 61 4.2 3,4,5 N N DF
25 7155/11 Moheenkhan 8months M P A P A A A A A A A A A A A P A A P A 2 A A A A A P A N 120 90/60 30 P A A N 10.1 30.6 12000 4700 3 218 101 17.1 57.7 1.15 2.3 3,4 N 6,8 51 0.8 140 4.2 103 DHF
26 8007/11 Rizwana 14yrs F P A P A A A A A A A A A A A P A A A P 1 P A P A A A A N 92 100/70 20 P A A N 6.8 19.2 8000 1400 6 120 65 20 47.9 1.43 3 3 E 6,8,9,11 25 0.9 144 3.7 106 DHF
27 8043/11 MdRoshan 6yrs M P P P A A A A A A A A A A A A A A A A 2 A A A A A A A N 86 100/60 20 A A A N 15.5 43.8 48000 10000 32 112 32 2.6 4,5 E 6,8 DF
28 8107/11 Anirudh 2.6yrs M P P P A A A A A A A A A A A A A A A A 2 P A A A A A A F 104 90/62 18 P A A N 12.6 38.4 75000 4800 8 77 42 3.3 N N DLI
29 9180/11 Waseem 6yrs M P P P A A A P A P A A A A A A A A A A 1 P P P A P P P N 92 90/64 20 P P P D 15.8 45 43000 4100 9 146 48 23 39.6 1.49 3.2 4 E 6,8 DHF
30 9633/11 Arbiya 8yrs F P P A A A A A A A P A A A A A A A A A 1 A A A A A P P N 96 90/70 24 P A P D 14.9 43.4 34000 6700 12 173 82 18 54 1.2 3.2 4,5 E 8,9 134 5 104 DHF
31 10277/11 Punitha 1yrs F P A A A A A A A A A A A A A P A A A A 1 A A P A P P P N 86 70/54 34 P A P D 6.5 18.7 32000 2400 15 309 127 54 69 4.9 1.6 4 E 7,8,10,11 19 0.7 130 4.3 92 DSS
32 10527/11 Vinod 2yrs M P A A A A A A A A A A A A A A A A A A 2 A A A A A A A F 96 98/68 22 A A A N 13.2 35.7 75000 7800 7 44 46 3.4 N N DLI
33 10823/11 Rithesh 5yrs M A P P A A A A A A A A A A A A A A A A 2 A A A A A A A N 70 98/68 20 A A A N 10.4 35.4 32000 3800 10 40 78 3.5 N N DLI
34 11587/11 Jabeerk 11months M P A P A A A A A A A A A A A P A A A A 2 A A A A A A P N 90 90/70 28 P A A D 10.7 32.1 25000 8500 5 119 60 2.8 4 N 6,9 DF
35 11816/11 Nandini 12yrs F P A A A A A A A A A A A A A A A A A A 2 A A A A A A A F 114 110/70 26 P P P D 13.2 42.5 75000 2800 5 42 46 3.7 4 E 6,8,9 DF
36 13056/11 Somashekhar 14yrs M P A A A A A P A A A A A A A A A A A A 1 P P P A A A A N 100 98/68 20 P A A D 15.8 45.7 42000 3300 8 228 43 24 42.5 1.42 2.6 3 N 6,8,9 DHF
37 13677/11 Yashas 8yrs M P A P A A A A A A P A A A A A A A A A 1 P P P A A A P N 76 90/66 24 A A A D 14.4 39.5 31000 2600 10 101 42 12.5 32.5 0.88 2.99 3 E 6,8,9 DHF
38 14130/11 Sowmya 9yrs F P A A A A A A A A A A A A A A A A A A 2 A A A A A A A N 72 100/70 26 P A A N 12.4 36.2 50000 3500 4 42 38 2.6 4 N N DF
39 15051/11 Devika 7yrs F A P A P P A A A A A A A A A A A A A A 2 A A A A A A A N 72 110/74 22 A A A N 12.6 38.7 67000 4200 7 56 43 2.9 N N DLI
40 15140/11 Harshalam 8yrs M P A A A A A A A A A A A A A A A A A A 1 A A A A A A A N 70 100/70 18 P P A N 11.8 36.5 59000 5100 10 188 62 13.6 50.4 0.97 3 4,5 E 6,8,9 DHF
41 15630/11 AmitGowda 9yrs M P P A A A A A A A A A A A A A A A A A 2 A A A A A A A N 72 110/60 18 A A A N 12.6 38.4 82000 6200 12 48 45 3.8 4 N N DF
42 16142/11 Vijayk 13yrs M P A P A A A A A A A A A A A A A A A A 2 P A A A A A A N 92 108/70 20 P A A N 11.5 32.6 36000 7500 35 207 175 24 35.7 1.18 2.2 3 N N DF
43 16447/11 Suhas 16yrs M P A A A A A A A A A A A A A A A A A A 2 A A A A A A A N 80 110/70 22 P A A D 13.3 38 27000 3800 15 150 66 2.9 4,5 E 6,8 DF
44 16550/11 Rashmitha 14yrs F P P P A A A A A A A A A A A A A A A A 1 P A A A A A A N 92 102/68 20 P A A N 11.7 34.1 47000 5200 8 185 183 14.2 45.9 1.02 2.8 4 N 9,11 DHF
45 16553/11 Bindushree 11yrs F P A P P A A A A A A A A A A A A A A A 1 P A A A A A A N 94 104/64 22 P P A N 11.1 31.3 30000 11400 62 114 133 19.1 37.2 1.44 2.3 3,4 N N DHF
46 17946/11 Yashwanth 14yrs M P A P A A A A A A A A A P A A A A A A 2 A A A A A A A N 90 106/72 22 P A A N 12.3 35.4 90000 7300 5 86 79 3.8 4 N 6,8,11 DF
47 18062/11 Akhil 4yrs M A P P P P P A A A A A A A A A A A A A 2 P A A A A A A N 74 96/68 18 A A A N 11.4 37.4 78000 3500 7 164 44 3.2 3 N N DF
48 18092/11 Manasa 9yrs F P P P A A A A A A A A A A A A A A A A 1 P A A A A P P N 98 88/64 26 A A A N 12.6 37.3 15000 4800 14 122 98 30 45 1.45 3 4 N 8 DSS
49 18138/11 Tamim 6yrs M P A A A A A P A A A A A A A A A P A A 1 P A P P A A A N 102 70/52 30 P A A D 11.3 33 50000 7500 20 725 694 15.15 33.6 1.09 2.7 4,5 E 6 DSS
50 18770/11 Praveena 12yrs M P P P P A A P A A A A A A P A A A A A 1 P P P A A P P N 110 80/66 30 P A P D 15.4 45.7 6000 2850 3 280 75 16.2 50.3 1.28 3.2 4,5 E 6,8,9 29 0.9 132 4.8 102 DSS
51 20062/11 Sangeetha 11yrs F P A P A A A A A A A A A A A A A A A A 2 P A A A A A A F 110 120/70 24 A A A N 9.3 27.9 60000 5200 28 112 40 3.4 4 N N DF
52 21819/11 Praneeth 14yrs M P A P P A A A A A A A A A A A A A A A 2 A A A A A A A N 120 110/70 28 A A A N 15.3 44.7 14000 2900 8 82 60 2.9 4 N N DF
53 21998/11 Kousar 5yrs F P P A A A A A A A A A A A A A A A A A 2 P A A A A A A N 120 64 26 P A A N 13.5 44 13000 2700 8 82 36 22 40.2 1.3 2.9 3,4 E 6,8,9 26 0.7 136 3.6 102 DSS
54 21999/11 Yasin 4yrs F P P P A A A A A A A A A A A A A A A A 2 P A A A A A A N 88 110/80 22 P A A N 11.7 38.2 14000 7300 10 110 35 3.5 N N DLI
55 22181/11 Advitha 1yrs F P A A A A A P A A A A A A A A P A A A 1 P P P A A A A N 120 90/60 30 P A A N 15.9 45.8 43000 3400 8 226 43 24 40.5 1.45 2.6 3,4 N 6,8,9 DHF
56 22685/11 HeenaKhanum 10yrs F P P P A A A A A A A A A A A A A A A A 2 P A A A A A A A 90 110/70 20 A A A N 14.3 42.8 26000 5200 2 20 60 2.9 3 N N DF
57 22728/11 KiranK 3yrs M P A P A A A A A A A A A A A A A A A A 2 A A A A P P A N 116 96/60 28 A A A N 10.6 32.5 96000 3800 25 60 28 3.5 3,4 N N DF
58 22830/11 Venkatesh 5yrs M P A P A A A A A A A A A A A A A A A A 2 P A A A A A A N 124 100/60 26 A A A N 11.6 37.5 39000 8800 5 114 31 3.2 4,5 E 6 DF
59 22980/11 NoorAhmed 15Yrs M P A P P A A A A A A A A A A A A A A A 2 A A A A A A A F 120 120/80 40 P A A D 11.9 39.6 22000 7800 14 30 78 2.9 E 8 39 0.9 135 5.7 98 DLI
60 23142/11 SyedIsmail 11yrs M P A A P A A A A A A A A A A A A A A A 2 A A A A A A A F 96 110/70 20 A A A N 12.4 39.8 42000 6500 7 78 44 3.6 N N DLI
61 23143/11 SyedRehman 10yrs M P P P A A A A A A A A A A A A A A A A 2 P A A A p A A F 90 100/70 22 P A A N 14.8 42.5 32000 3900 6 10 47 4 3 N 6,8,9 DF
62 23460/11 VijayN 10yrs M P A A P A A A A A A A A A A A A A A A 2 P A A A p P P N 92 70 28 A A A D 14.9 42.1 9000 11100 2 35 110 18.3 31 1.37 1 4,5 E 7,8,9,10,1 28 0.7 131 4.8 90 DSS
63 23497/11 Thammanna 7yrs M P P P A A A A A A A A A A A A A A A A 1 P A A A p P P N 98 80/60 26 P A P N 9.3 27.2 47000 9700 18 117 119 13.6 47 0.97 2 E 6,8,11 14 0.4 133 4 98 DLI
64 23609/11 Ajay 14yrs M P A P A A A A A A A A A A A A A A A A 2 A A A A A A A N 92 120/80 22 A A A N 14.9 41.2 59000 3600 7 153 268 3.4 4,5 N 6,8 DF
65 23760/11 SaniyaKousar 6yrs F P A A A A A A A A A P A A A A A A A A 1 P P P P A P A N 100 104/80 30 P A A N 12.3 39.5 50000 2600 12 112 38 12.8 35 0.91 3.2 4 N 6,9 DHF
66 23978/11 Bhaskar 16yrs M P P A A A A A A A A A A A A P A A A A 1 A A P A P A A N 94 110/70 28 P A P D 17.6 49.6 6000 5300 2 92 33 19 35 0.99 3.4 3,4 E 6,8,9,10,11 DHF
67 24279/11 BharathK 14yrs M P P P A A A A A A A A A A A A A A A A 2 A A A A A A A N 64 98/68 22 A A A N 13.4 37.4 45000 5000 7 12 78 3.2 N N DLI
68 24809/11 ZahidK 2.2Yrs M P P P A A A A A A A A A A A A P P A A 2 A A A A P P A N 96 96/62 24 A A A N 15.9 48 52000 19200 5 89 26 3.4 4 N N DF
69 25772/11 Inchara 6yrs F P A A A A A A A A A A A A A A A A A A 1 P A P A A A A N 98 104/80 30 P A A N 12.4 39.5 50000 2700 10 116 38 12.8 35 0.921 3.4 4 N 6 DHF
70 25860/11 Abhishek 15Yrs M P A P A P A A A A A A A A A A A A A A 2 A A A A A A A N 60 110/72 20 A A A N 15.2 46.8 54000 5200 10 163 40 3.9 4 N N DF
71 25865/11 Pankaj 1yr M P A A A A A A A A A A A A A A A A A A 2 P A A A A A A F 126 90/64 26 A A A N 11.2 38.4 49000 7700 9 48 42 3.6 3 N N DF
72 26504/11 Pavan 10yrs M P A P A A A A A A A A A A A A A A A A 2 A A A A A A A N 110 80/66 34 A A A N 15.3 45.7 50000 6700 3 275 75 16.1 50.3 1.18 3.1 4,5 N N 130 4.6 97 DSS
73 26819/11 HemanthK 4yrs M P P P A A A A A A A A A A A A A A A A 2 A A A A A A A N 92 92/62 20 P A A N 14.1 40.8 14000 4400 3 596 183 3.4 3 N N DF
74 27275/11 Uma 9yrs F P A P A A A A A A A A A A A A A A A A 1 P P P P A P P N 120 80/60 28 A A A N 13.4 39.2 27000 10200 5 49 31 14.5 55.5 1.09 2.6 3 N 6,8 DSS
75 27432/11 AliyaAnjum 1yr F A A A A A A A A A A A A A A A A A P A 1 A A P A A A A N 120 84/66 40 P A A D 7.7 26.1 28000 22000 10 1072 829 25 42 1.7 3.5 4 E 6,9 28 0.7 138 3.5 101 DSS
76 28834/11 Mohan 10yrs M P A P A A A A A A A A A A A A A A A A 2 A A A A A A A N 80 120/78 20 A A A N 15.3 39.2 51000 6500 3 40 13 4.2 4 N N DF
77 29696/11 Sandhya 11yrs F P P P P A A A A A A A A A A A A A A A 2 P A A A A A A N 90 110/70 20 P P A N 11.4 35.6 65000 11800 20 56 37 4 4,5 N N DF
78 1165/12 Mayamma 13yrs F P A P A A A A A A A A A A A A A A A A 1 A A P A A A A N 74 96/70 34 A A A N 11.4 34.7 79000 6200 4 112 90 2.5 3,4,5 N N DHF
79 1712/12 Karuna 13yrs M P A A A A P A A A A A A A A A A A A A 2 A A A A A A A N 90 86/60 32 A P A N 12.4 34.3 67000 5500 35 21 6 3.8 N N DLI
80 2166/12 UdayK 2yrs M P A A A A A P A A A A A P A A A P A A 1 P P P P P P P N 120 90/60 30 P A A D 10.6 30.8 74000 17900 10 77 68 16.3 40.7 1.1 2.2 3,5 E 6,8,9 26 0.4 132 4.1 98 DHF
81 4057/12 Ravi 10yrs M P A A A A A A A A A A A A A A A A A A 2 P A A A A A A N 94 104/74 20 A A A N 14.3 40.4 25000 5200 2 22 62 3.7 N N DLI
82 5949/12 Rashmi 10yrs F P A A A A A A A A A A A A A A A A A A 2 A A A A A A A N 90 100/70 20 A A A N 13.6 35.4 20000 6000 10 56 15 3.2 3 N N DF
83 7240/12 Aishwarya 7yrs F P A A A A A A A A A A A A A A A A A A 1 P P P A P P P N 110 90/70 26 P A P D 15.3 43.9 19000 7100 6 220 52 16.5 54.7 1.21 1.89 4 E 8,9 56 0.8 122 6.3 91 DHF
84 8977/12 Prashanth 8yrs M P A P A A A A A A A A A A A A A A A A 1 A A P A A P P N 102 88/72 24 A A A D 12.3 38 43000 7000 20 115 43 12.1 53.2 0.84 3 3,4,5 E 11 136 0.7 136 4 102 DHF
85 10274/12 MdFardeen 13yrs M P A P A P A A A A A P A A A A A P A A 2 P A A A A A A N 86 110/70 20 A A A D 12.4 37 22000 1600 14 112 35 3.5 3 E N DF
86 10294/12 Harish 5yrs M P P A A A A A A A A A A A A A A A A A 2 P A A A A A A N 94 94/64 18 A A A N 12.6 37.1 36000 5600 12 170 12 4 4,5 E N DF
87 10564/12 B/ORamya 9months M P A A A A A A A A A A A A A P A A A A 1 P P P P P P P F 124 56 30 P P P D 8.4 26.5 9000 5500 10 285 90 16 >3min 1.25 2 3,4 E 7,8,9,10,1 114 1.8 148 2.8 94 DSS
88 12041/12 Santhosh 7yrs M P P A A A A A A A A A A A A A A P A A 2 A A A A A A A N 88 94/68 24 A A A N 12.9 37.1 86000 4600 8 114 14 3.4 3,4,5 N N DF
89 12616/12 Chandana 3.6yrs F P A A A A A P A A A A A A A A A A A A 1 P P P P P P P F 122 70 28 P A P D 11.4 33.2 26000 8600 7 937 256 12.5 32.5 0.88 2.9 4 E 6,8,9 32 0.4 138 4.2 98 DSS
90 12878/12 SyedGouse 10yrs M P P A A A A A A A A A A A A A A A A A 2 A A A A A A A N 88 104/74 20 A A A N 10.6 31.8 32000 4600 6 131 38 2.8 5 N N DF
91 13522/12 VasanthKumar 13yrs M P P P A A P P A P A P A A A A A A A A 1 P P P A P P P N 110 70/52 18 P A A D 11.9 37.7 17000 2200 7 79 241 11.9 52.8 0.77 2.5 3 E 7,8,11 DHF
92 13531/12 Jaswanth 8yrs M P P P A A A A A A A A A A A A A A A A 1 P P P P P P P N 92 80/50 20 P A A D 12.5 41.8 78000 2900 7 127 481 11.6 38 0.8 2.8 3,4 E 7,8 DHF
93 13560/12 Krishna 5yrs M P A A A A A A A A A A A A A A A A A A 2 P A A A A A A N 90 94/64 18 A A A N 12.6 37.1 38000 6600 12 170 12 3.5 3,4 N N DF
94 13594/12 NayeemPasha 14yrs M P A A A A A A A A A A A A A A P P A A 1 P A A A A A A N 90 110/72 18 A A A D 13.8 42.1 30000 3600 2 125 418 12.7 28.2 0.89 3 3,4,5 E 9 DHF
95 13798/12 Amar 5yrs M P P P A A A P A A A A A A A A A A A A 1 P P P P P P P N 110 70/52 20 P A A D 12.8 37.2 20000 7000 4 220 70 16.2 62.3 1.19 2.8 3,4,5 E 6,8,9 83 0.4 DSS
96 14094/12 Dilip 14yrs M P A A A A A A A A A A A A A A A P A A 2 P A A A A A A N 94 120/80 18 A A A N 13 40.7 36000 4800 17 170 53 3.4 3 N N 39 0.7 134 4.5 100 DF
97 14419/12 Sudeep 7yrs M P A A A A A A A A A A A A A A A A A A 2 A A A A A A A N 94 90/60 20 A A A N 10.3 31.6 34000 2200 6 112 36 3.6 4 N 7,8,9 DF
98 14678/12 Suhas 6yrs M P A A A A A P A A A A A A A A A A A A 1 P P P A A P P N 90 90/60 20 P A A D 10.3 30.6 245000 5100 17 74 70 19 34 1.01 3.2 3 E 6,9 DHF
99 14695/12 Shivananda 10yrs M P P P A A A A A A A A A A A P A A A A 2 P A A A A A A N 78 100/70 20 A A A N 13.9 41.8 72000 2300 6 70 7 3.9 3,4,5 N N 31 0.8 130 3.9 96 DF
100 14845/12 Harini 7yrs F P P P A A A P A A P A A A A A A A A A 2 P P P P P P P N 96 100/72 20 P A P D 12.5 33.7 33000 9100 5 181 61 15.2 33.8 1.1 3 3,5 E 7,8,9 26 0.6 136 4 92 DHF

Lakshmi V Paed KIMSB 2013

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