CASE REPORT

“Dengue fever”

PRECEPTOR:

dr. Hj. Ihsanil Husna, Sp.PD

BY:
Muhamad Irsyad
(2014730058)

MEDICAL PROFESSION PROGRAMME

DEPARTMENT OF INTERNAL MEDICINE
JAKARTA ISLAMIC HOSPITAL CEMPAKA PUTIH
FACULTY OF MEDICINE UNIVERSITY OF
MUHAMMADIYAH JAKARTA
2019
 PREFACE

AssalamualaikumWr. Wb.

Alhamdulillah, All praise to Allah SWT the almighty and the most merciful.
Shalawat and salaam to Rasulullah Muhammad Peace be Upon Him which bring us
from the darkest of time into the lights.

The writer also wish to express his deep and sincere gratitude for those who
have guided in completing this case report paper with the tittle “Geriatric Syndrome”
to fulfill the criteria for completing Medical Profession Programme in Internal
Medicine Department of Jakarta Islamic Hospital Cempaka Putih, Faculty of
Medicine University of Muhammadiyah Jakarta.

The writer wish this paper to be useful and add another dimension of
knowledge for the writer himself, medical profession student, and anyone else who
never stop in learning.

The writer acknowledge in the process of making this paper, there are a lot of
mistake and far from perfect, cause perfection are only belong to Allah SWT. All the
critics and advice are needed for the writer for the better of ourselves in this journey
to be the long life learner.

previously thank you to Dr. Ihsanil who had the opportunity to attend the guidance
this time. In here, I will present a presentation about case report with Dengue fever.
With all pleasure

WassalamualaikumWr. Wb

Jakarta, 12 April 2019

Muhamad Irsyad
 CHAPTER I
PATIENT’S IDENTITY

A. PATIENT’S IDENTITY
• Name : Mr. r
• Age : 21 years old
• Marital Status : Single
• Occupation : college student
• Religion : Moslem
• Date of Admission : April 2th 2019
• MR Number : 00 92 57 **

B. ANAMNESIS (AUTOANAMNESIS)
a. Chief Complaint :
Patients treated day 2 with fever.
Another Complaint :
Vomitus(+), muscle and joint pain, headache(+),coughing(+).
b. History of Present Illness
Patient treated day 2 with Fever. It cames accidentally since 6
days ago in the morning and the temperature getting higher in the
night. Vomitus +2 in a day since 2 days ago. Epigastric pain(+)
Coughing(+) since 6 days ago and theres no sputum. Rash(-),coated
tongue(-).
c. History of Past Illness
Never feels this kind of symptomps before.
d. History of Family
Patient has no history of family’s disease
e. History of Allergy
Patient has no allergy to food, drugs and weather
f. History of Treatment
• Paracetamol 3x500mg
• Ranitidine 2 x 150mg
 • g. Habits
Smoking Habits and alchohol: Denied
C. PHYSICAL EXAMINATION
• Generalis Status : Average ill
• Consciusness : Compos mentis, GCS E4M6V5
• Vital Sign
• Temperature 37,7oC
• RR 20x/minutes
• HR 82x/minutes
• BP 110/80 mmHg
Anthropometric Status
- Body weight : 50 kg
- Body high : 158 cm
- BMI : 20 (Normoweight)
GENERAL PHYSICAL EXAMINATION
• Head : Normocephal, Deformity (-)
• Eyes : Anemic Conjungtiva (-/), Icteric Sclera (-/-)
• Nose : Epistaksis (-/-), Secret (-/-), Deviated Septum (-/-)
• Mouth : The Oral Mucosa normal, Cyanosis (-)
• Neck : Palpable Mass (-), Lymphadenopathy (-).
• Ear : decubitus ulcer (-/-)
Thorax
• Inspection : The movement of the chest symmetrical
• Palpation : Same vocal fremitus in dextra and sinistra
• Percussion : Sonor
• Auscultacion : Vesicular breath sounds + / +, Ronkhi -/-, Wheezing - / -
Heart
• Inspection : Ictus cordis seen in ICS V LMCS
• Palpation : Ictus cordis palpable ICS V LMCS
• Percussion : Right heart margin: Sternalis line sinistra ICS-V
Left heart margin: Midclavicula line sinistra ICS-V.
• Auscultation : Regular 1st & 2nd heart sounds, Murmur (-), Gallop (-)
Abdomen
 Inspection : Supple, scar (-), darm contour (-) darm steifung (-)
 Auscultation : Bowel Sound (+)
 Palpation : Epigastric Pain (+), Hepar enlargement (-) spleen
enlargement (-)
 Percussion : Tympanic in all abdominal fields
Extremities
• Superior : Edema (- / -), Warm acral (+ / +), RCT <2 seconds (+ / +)
• Inferior : Edema (-/ -), Warm acral (+ / +), RCT <2 seconds (+ / +)

D. LATEST LABORATORY EXAMINATION

EXAMINATION VALUE UNITS NORMAL

Hemoglobin 16 g/dL 13,2 – 17,3

Hematocrit 44 % 40 - 52

Leukocyte 4.77 103/uL 3.8 – 10,6

Trombosit 120↓ 103/µl 150 - 440

Eritrosit 4,04 106/µl 4,4 – 5,9

MCV 79 Fl 80-100
MCH 29 pg 26-34

MCHC 337 g/dl 32-36

Examination Result Normal

BLEEDING-CLOTTING TIME

Bleeding Time 2 minutes 1 - 3 minutes

Clotting Time 4,3 minutes 4 – 6 minutes

Examination Result Normal

HEPAR

SGOT 24 U/L

SGPT 15 U/L

Examination Result Normal

BLOOD GLUCOSE

Blood glucose 94 mg/dl 70-200

Examination Result Normal

ELECTROLYTE

Kalium 3,1 mEq/L↓ 3,5 - 5

Natrium 141 mEq/L 135-147

Cl 100 mEq/L 94-111

Examination Result Normal

ELECTROLYTE

Dengue NS1 Antigen Positive Negative

E. RESUME

On Physical Examination
Compos mentia with GCS 15
Vital Sign
o Blood Pressure :
110/90 mmHg
o Heart Rate :
104 x/minute
o Respiratory Rate:
20 x/minute
o Temperature: 38,7 ° C
Laboratory Findings
- Trombocyte : 22, 93 103/uL
- Kalium : 2,4 mEq/L
F. PROBLEM LIST
• Fever
• Vomitus
• Muscle and joint pain
• caughing

G. ASSESMENT
1. Febris et cause Dengue Fever

2. Hypocalemia et causa vomitus

3.Common Cold

4. Dyspepsia Syndrome
Follow UP
 CHAPTER II
LITERATURE REVIEW
Dengue fever
Definition
Dengue (DENG-gey) fever is a mosquito-borne disease that occurs in tropical and
subtropical areas of the world. Mild dengue fever causes a high fever, rash, and
muscle and joint pain. A severe form of dengue fever, also called dengue
hemorrhagic fever, can cause severe bleeding, a sudden drop in blood pressure
(shock) and death.

Epidemiology
Indonesia is reported as the second largest with dengue fever cases among 30
endemic coun- tries. The number of cases of dengue fever is most prevalent in the
provinces of East Java, West Java, and Central Java. However, there are a number
of provinces that are vulnerable with its high incidence rate of dengue fever. In
1968, the first 58 dengue cases were reported in Indonesia from the city of Jakarta
(DKI Jakarta) and Surabaya (East Java) [16–19]. Since then, the sharp increasing
numbers of cases and spreading to many other geographical locations have been
reported [16, 17, 20–25]. The epidemiology of dengue fever in Indonesia has been
described mostly in the form of case series, reporting on single outbreaks, or
clinical and virological studies in confined geographical locations and selected
years [2].

A study in 2014 reported that the annual dengue fever incidence increased from
0.05/100,000 in 1968 to ~35–40/100,000 in 2013. The highest epidemic occurred
in 2010 with the incidence of 85.7/100,000 population. The data revealed
declining of case fatality rate (CFR) from 41% in 1968 to 0.73% in 2013. Dengue
cases increased among ages during the observation period up to 1998 with the
highest incidence of aged 5–14 years. From 1999 onward, the trend of dengue
incidence increased among those aged 15 years or over. This study indicates
incidence of dengue fever increased rapidly over the past 45 years in Indonesia
with peak incidence shift- ing from young children to older age groups [3].
The threat of dengue fever among children was emphasized clearly on a recently
published study among 3194 children aged 1 through 18 years who lived in 30
different urban neigh- borhoods. Children blood samples were drawn for
antibodies to dengue, an indication that someone has been infected with the virus
in the past, and found that 69.4% of all children tested positive for dengue
antibodies. Among the age groups, positive antibodies found 33.8% at the group
of 1–4 year olds, 65.4% at the group of 5–9 year olds, 83.1% at the group of 10–
14 year olds, and 89% at the group of 15–18 year olds. The first time to become
infected with dengue was at the age of 4.8 years as the median, and in addition,
13.1% of children on average get their first dengue infection each year. It was also
found that the more people in a household who had been diagnosed with dengue
since a child’s birth, the more likely the child were to test positive for dengue
antibodies [4].

The incidence rate (IR) for every 100,000 population in seven provinces were
found over 100 or are prone to dengue cases. The seven provinces are Bali (484),
East Kalimantan (306), DKI Jakarta (198.7), DI Yogyakarta (167.9), North
Kalimantan (158.3), Southeast Sulawesi (123.3), and South Kalimantan (101.1).
The lowest IR is achieved by Papua province (11.8) and West Kalimantan (12.1)
(Figure 1). The whole of Indonesia is high (IR is 78.0). In general, the increasing
number of dengue fever cases is more likely followed by the spread of the cities[4].
and districts infected in all of 34 provinces in Indonesia (Figure 2). From the total
of 497 cities and districts in Indonesia, about 80% have reported the dengue fever
cases in 2017. [4].

In the context of dengue fever mortality, as many as 1229 people died in 2015
from the disease caused by this dengue virus. Throughout the history of dengue
fever in Indonesia, the highest death rate occurred when first time the disease was
discovered in 1968 in Surabaya. Of the 58 people infected, 24 lives were lost. In
2016, the highest percentage of CFR was obtained in Maluku Province (6.0%),
Gorontalo (6.1%), and West Papua (4.6%). Provinces with the lowest CFR were
achieved by Papua (0%), DKI Jakarta (0.1%), and NTT (0.2%). In some
provinces, dengue disease was an outbreak in 1998 and 2004 that caused 79,480
people and 800 more deaths. In subsequent years, there has been reported a
decrease in the case of death but note that the number of cases continues to
increase. In 2008, there were 137,469 cases and 1187 deaths. In 2009, there were
[
154,855 cases and 1384 deaths
Transmission
The virus

Dengue virus (DEN) is a small single-stranded RNA virus comprising four

distinct serotypes (DEN-1 to -4). These closely related serotypes of the dengue
virus belong to the genus Flavivirus, family Flaviviridae.

The mature particle of the dengue virus is spherical with a diameter of 50nm
containing multiple copies of the three structural proteins, a host-derived
membrane bilayer and a single copy of a positive-sense, single-stranded RNA
genome. The genome is cleaved by host and viral proteases in three structural
proteins (capsid, C, prM, the precursor of membrane, M, protein and envelope, E)
and seven nonstructural proteins (NS).

Distinct genotypes or lineages (viruses highly related in nucleotide sequence)

have been identified within each serotype, highlighting the extensive genetic
variability of the dengue serotypes. Purifying selection appears to be a dominant
theme in dengue viral evolution, however, such that only viruses that are “fit” for
both human and vector are maintained. Among them, “Asian” genotypes of DEN-
2 and DEN-3 are frequently associated with severe disease accompanying
secondary dengue infections (43–45). Intra-host viral diversity (quasispecies) has
also been described in human hosts.

The vectors

The various serotypes of the dengue virus are transmitted to humans through the
bites of infected Aedes mosquitoes, principally Ae. aegypti. This mosquito is a
tropical and subtropical species widely distributed around the world, mostly

between latitudes 35 0N and 35 0S. These geographical limits correspond

approximately to a winter isotherm of 10 0C. Ae. aegypti has been found as far

north as 45 0N, but such invasions have occurred during warmer months and the
mosquitoes have not survived the winters. Also, because of lower temperatures,
Ae. aegypti is relatively uncommon above 1000 metres. The immature stages are
found in water-filled habitats, mostly in artificial containers closely associated
with human dwellings and often indoors. Studies suggest that most female Ae.
aegypti may spend their lifetime in or around the houses where they emerge as
adults. This means that people, rather than mosquitoes, rapidly move the virus
within and between communities. Dengue outbreaks have also been attributed to
Aedes albopictus, Aedes polynesiensis and several species of the Aedes scutellaris
complex. Each of these species has a particular ecology, behaviour and
geographical distribution. In recent decades Aedes albopictus has spread from
Asia to Africa, the Americas and Europe, notably aided by the international trade
in used tyres in which eggs are deposited when they contain rainwater. The eggs
can remain viable for many months in the absence of water (Chapter 3).

Chapter 1: Epidemiology, burden of disease and transmission

The host

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 (Chapter 2). Primary infection is thought to induce
lifelong protective immunity to the infecting serotype (46). 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.

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.

Seroepidemiological studies in Cuba and Thailand consistently support the role of

secondary heterotypic infection as a risk factor for severe dengue, although there
are a few reports of severe cases associated with primary infection (47–50). The
time interval between infections and the particular viral sequence of infections
may also be of importance. For instance, a higher case fatality rate was observed
in Cuba when DEN- 2 infection followed a DEN-1 infection after an interval of
20 years compared to an interval of four years. Severe dengue is also regularly
observed during primary infection of infants born to dengue-immune mothers.
Antibody-dependent enhancement (ADE) of infection has been hypothesized
(51,52) as a mechanism to explain severe dengue in the course of a secondary
infection and in infants with primary infections. In this model, non-neutralizing,
cross-reactive antibodies raised during a primary infection, or acquired passively
at birth, bind to epitopes on the surface of a heterologous infecting virus and
facilitate virus entry into Fc-receptor-bearing cells. The increased number of
infected cells is predicted to result in a higher viral burden and induction of a
robust host immune response that includes inflammatory cytokines and mediators,
some of which may contribute to capillary leakage. During a secondary infection,
cross-reactive memory T cells are also rapidly activated, proliferate, express
cytokines and die by apoptosis in a manner that generally correlates with overall
disease severity. Host genetic determinants might influence the clinical outcome
of infection (53,54), though most studies have been unable to adequately address
this issue. Studies in the American region show the rates of severe dengue to be
lower in individuals of African ancestry than those in other ethnic groups. (54)

The dengue virus enters via the skin while an infected mosquito is taking a
bloodmeal. During the acute phase of illness the virus is present in the blood and
its clearance from this compartment generally coincides with defervescence.
Humoral and cellular immune responses are considered to contribute to virus

clearance via the generation of neutralizing antibodies and the activation of CD4+

and CD8+ T lymphocytes. In addition, innate host defence may limit infection by
the virus. After infection, serotype- specific and cross-reactive antibodies and

CD4+ and CD8+ T cells remain measurable for years.

Plasma leakage, haemoconcentration and abnormalities in homeostasis

characterize
 severe dengue. The mechanisms leading to severe illness are not
 well defined but the
 immune response, the genetic background of the individual

and the virus characteristics
 may all contribute to severe dengue.

Pathogenesis Dengue Fever

Major manifestations of DHF include (i) plasma leakage through elevated

vascular permeability, (ii) hemorrhage, and (iii) thrombocytopenia. Some of the
patients infected with dengue virus develop DHF, while most with symptomatic
infections end up as DF. The pathogenesis of DHF has been explained by two
theories. One theory is based on the virulence of infecting dengue viruses; virulent
dengue virus strains cause DHF, while avirulent dengue virus strains cause DF.
The other is based on immunopathogenesis. This theory suggests that DHF is
mediated by host immune responses including dengue virus-cross-reactive
antibodies that augment infections. These two theories have been considered as
opposing each other for a long period of time. However, it appears that they
represent different aspects of the pathogenesis of DHF.

Pathogenesis

The LVIP conducts basic and translational research into the biology of dengue
virus infection, host-virus interactions, and mechanisms of disease pathogenesis.
Dr. Rothman serves as Program Director for the Dengue Hemorrhagic Fever
Project, an international collaboration funded by the National Institute of Allergy
and Infectious Diseases, and also has ongoing collaborations with investigators in
South America. Studies performed in our laboratory examine dengue viral
replication, cellular responses to infection, and dengue virus-specific antibody and
T lymphocyte responses to natural infection and immunization.
Dengue is an acute febrile illness caused by any of four related flaviviruses
(dengue virus [DENV] serotypes 1-4), small enveloped viruses containing a non-
segmented positive-sense RNA genome. DENV infection is acquired through a
transmission cycle between humans and mosquitoes of the genus Aedes,
principally A. aegypti. (7)
In humans, there is a wide spectrum of clinical manifestations of dengue infection.
This ranges from an uncomplicated and self-limited febrile illness (dengue fever,
DF) to a plasma leakage syndrome accompanied by bleeding (dengue
hemorrhagic fever, DHF). Although DHF is observed in only a small percentage
of DENV infection, it plays a large role in the public health problem of dengue
because it can lead to shock and death. (7)

Many factors contribute to the risk for DHF, but one of the most important factors
is pre-existing immunity from an earlier DENV infection. Infection with one
DENV only provides long-lasting protection against that serotype; sequential
infection with multiple different DENV serotypes is therefore possible, and,
because of the increasing global circulation of DENV, this has been occurring
with increasing frequency in tropical areas of the world. The basis for the
association of DHF with secondary DENV infection is a major subject of research
in the LVIP. We hypothesize that both the quality and timing of DENV-specific
antibody and T lymphocyte responses influence whether their overall effect is
beneficial (controlling DENV replication and reducing the severity of illness) or
harmful (creating a ‘cytokine storm’ leading to plasma leakage). The results of
our research will be applied to evaluation and management of patients with
dengue and to development and testing of vaccines and therapeutics against
dengue.(7)
Clinical
infection with any of the four dengue serotypes can produce the full spectrum of
illness and severity. The spectrum of illness can range from a mild, non-specific
febrile syndrome to classic dengue fever (DF), to the severe forms of the disease,
dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS). Severe
forms typically manifest after a two to seven day febrile phase and are often
heralded by clinical and laboratory warning signs. Early clinical recognition of
dengue infection and anticipatory treatment for those who develop DHF or DSS
can save lives. While no therapeutic agents exist for dengue infections, the key to
the successful management is timely and judicious use of supportive care,
including administration of isotonic intravenous fluids or colloids, and close
monitoring of vital signs and hemodynamic status, fluid balance, and hematologic
parameters.

As the early presentations of DF and DHF/DSS are similar and the course of
infection is short, timely identification of persons that will develop severe
manifestations can be challenging. There is a long-standing debate as to whether
DHF/DSS represents a separate pathophysiological process or is merely the
opposite end of a continuum of the same illness. DF follows an uncomfortable but
relatively benign self-limited course. DHF may appear as a relatively benign
infection at first but can quickly develop into life-threatening illness as fever
abates. DHF can usually be distinguished from DF as it progresses through its
three predictable pathophysiological phases:
  Febrile phase: Viremia-driven high fevers
 Critical/plasma leak phase: Sudden onset of varying degrees of plasma
leak into the pleural and abdominal cavities
 Convalescence or reabsorption phase: Sudden arrest of plasma leak with
concomitant reabsorption of extravasated plasma and fluids

For optimal management of the patient with dengue infection, it is important to

understand these phases and to be able to distinguish DHF from DF. Early
recognition of a patient’s clinical phase is important in order to tailor clinical
management, monitor effectiveness of the treatment, and to anticipate when
changes in their management are needed.

Laboratory Diagnosis

In endemic areas, early symptoms of dengue fever mimic many other prevalent
diseases such as chikungunya, malaria, viral infection, urinary tract infection,
typhoid,leptospirosis,etc.For proper management exclusion of these conditions is
hence very crucial.

Laboratory diagnosis tests Laboratory diagnosis can be carried out by one or more
of the following tests.

1. ELISA-based NS1 antigen tests

Dengue NS1 antigen, a highly conserved glycoprotein which is produced in both

membrane-associated and secretion forms, is abundant in the serum of patients
during the early stages of DENV infection. It has been found to be useful as a tool
for the diagnosis of acute dengue infections. It is a simple test that is more specific
and shows high sensitivity. (6)

NS1 enables detection of the cases early, i.e. in the viremic stage, which has
epidemiological significance for containing the transmission.The NS1 ELISA-
based antigen assay is commercially available for DENV and many investigators
have evaluated this assay for sensitivity and specificity. The NS1 assay may also
be useful for differential diagnostics between flaviviruses because of the
specificity of the assay. (6)

2. IgM-capture enzyme-linked immunosorbent assay (MAC-ELISA)

MAC-ELISA has been widely used in the past few years. It is a simple test that
requires very little sophisticated equipment. MAC-ELISA is based on detecting
the dengue-specific IgM antibodies in the test serum by capturing them using anti-
human IgM that was previously bound to the solid phase. This is followed by
addition of dengue antigen if the IgM antibody from the patient's serum is anti-
dengue, it will bind to the dengue antigen. An enzyme- substrate is added to give
a colour reaction for easy detection. (6)

The anti-dengue IgM antibody develops a little faster than IgG and is usually
detectable by day 5 of the illness. However, the rapidity with which IgM develops
varies considerably among patients. Some patients have detectable IgM on days 2
to 4 after the onset of illness, while others may not develop IgM for seven to eight
days after the onset. In some primary infections, detectable IgM may persist for
more than 90 days, but in most patients it wanes to an undetectable level by 60
days. It is reasonably certain, however, that the person had a dengue infection
sometime in the past two to three months. MAC-ELISA has become an invaluable
tool for surveillance of DF/DHF. In areas where dengue is not endemic, it can be
used in clinical surveillance for viral illness or for random, population-based
serosurveys, with the certainty that any positives detected are recent infections. It
is especially useful for hospitalized patients, who are generally admitted late in
the illness after detectable IgM is already present in the blood. (6)

3. Isolation Of dengue virus

Isolation of most strains of dengue virus from clinical specimens can be

accomplished in the majority of cases, provided that the sample is taken in the
first five days of illness and processed without delay. Specimens that may be
suitable for virus isolation include acute phase serum, plasma or washed buffy
coat from the patient, autopsy tissues from fatal cases, especially liver, spleen,
lymph nodes and thymus and mosquitoes collected in nature. Isolation of the virus
takes 7–10 days, hence it may not be very useful for starting the management of
patients with DF/DHF. (6)

4. PCR

Molecular diagnosis based on reverse transcription polymerase chain reaction

(RT-PCR), such as one-step or nested RT-PCR, nucleic acid sequence-based
amplification (NASBA) or real-time RT-PCR has gradually replaced the virus
isolation method as the new standard for the detection of dengue virus in acute-
phase serum samples. (6)

5. NVBDCP-recommended tests for laboratory diagnosis

– For confirmation of dengue infection, Government of India (GoI) recommends

use of ELISA-based antigen detection test (NS1) for diagnosing the cases from
the first day onwards and antibody detection test IgM capture ELISA (MAC-
ELISA) for diagnosing the cases after the fifth day of onset of disease. (6)

– Directorate of National Vector Borne Disease Control Programme (NVBDCP),

GoI has identified a network of laboratories (sentinel surveillance hospitals and
apex referral laboratories) for surveillance of dengue fever cases across the
country since 2007. These laboratories are also meant to augment the diagnostic
facilities in all endemic areas. They are linked with Apex Referral Laboratories
(ARLs) with advanced diagnostic facilities for backup support and serotyping of
dengue samples.(5)

– These laboratories receive the samples, diagnose and send the report (line list)
regularly to districts/municipal health authorities for implementation of preventive
measures to interrupt the transmission. .(5)

– NS1 antigen tests – GoI introduced ELISA-based NS1 antigen test in 2010 in
addition to MAC-ELISA tests which can detect the case during day 1 to day 5 of
illness. .(5)
 6. Supply of kits

– IgM ELISA test kits (1 kit = 96 tests) are being provided to the identified
laboratories through the National Institute of Virology (NIV), Pune since 2007.
The cost is borne by GoI. Buffer stock is also maintained at NIV, Pune. .(5)

– For procurement of dengue NS1 antigen test kits, fund has been provided to the
states. States are suppose to procure it as per GoI guidelines and provide the same
to sentinel surveillance hospitals (SSHs) every year as per their technical
requirement. .(5)

Management

 Bed rest is advisable during the acute phase.

 Use cold/tepid sponging to keep temperature below 38.50 C.
 Antipyretics may be used to lower the body temperature. Aspirin/NSAIDS
like
 Ibuprofen, etc should be avoided since it may cause gastritis, vomiting,
acidosis, platelet dysfunction and severe bleeding. Paracetamol is
preferable in the doses given : Adult : 500 mg/dose
 Oral fluid and electrolyte therapy is recommended for patients with
excessive sweating or vomiting.
 Patients should be monitored for 24 to 48 hours after they become afebrile
for development of complications.

Preventiv

At present, the main method to control or prevent the transmission of dengue virus
is to combat vector mosquitoes through:

 preventing mosquitoes from accessing egg-laying habitats by

environmental management and modification;
 disposing of solid waste properly and removing artificial man-made
habitats;
  covering, emptying and cleaning of domestic water storage containers on a
weekly basis;
 applying appropriate insecticides to water storage outdoor containers;
 using of personal household protection measures, such as window screens,
long-sleeved clothes, repellents, insecticide treated materials, coils and
vaporizers (These measures have to be observed during the day both at
home and place of work since the mosquito bites during the day);
 improving community participation and mobilization for sustained vector
control;
 applying insecticides as space spraying during outbreaks as one of the
emergency vector-control measures;
 active monitoring and surveillance of vectors should be carried out to
determine effectiveness of control interventions.

Careful clinical detection and management of dengue patients can significantly

reduce mortality rates from severe dengue.(5)
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5. https://www.cdc.gov/dengue/clinicallab/clinical.html
6. National Guidelines for Clinical Management of Dengue Fever
7. https://web.uri.edu/lvip/research/