CASE REPORT

Dengue Haemorrhagic Fever

Presenter: Thaneswaran .M
Sumita .M
Day/Date: Tuesday/30th November 2010
Supervisor : dr.Hj.Tiangsa br.Sembiring,SpA(K)

INTRODUCTION
Dengue fever (DF) or Dengue haemorrhagic fever (DHF) is a growing public
health problem in the subtropics. In South-East Asia, with a total population of 1.5
billion, approximately 1.3 billion people live at risk of acquiring DF or DHF.
Currently, DHF is the leading cause of hospital admissions and death among
children in this region.1
Dengue, the most common arboviral illness transmitted worldwide, is caused
by infection with 1 of the 4 serotypes of dengue virus, family Flaviviridae, genus
Flavivirus ,single-stranded nonsegmented RNA viruses. Dengue is transmitted by
mosquitoes of the genus Aedes, which are widely distributed in subtropical and
tropical areas of the world, and is classified as a major global health threat by the
World Health Organization (WHO).9 Most patients with dengue infection have
only mild disease or classic dengue fever, with influenza-like symptoms, severe
headache, and aching joints and muscles. However, in a small percentage of
patients maybe half a million people every year potentially lethal forms of
dengue called dengue hemorrhagic fever and dengue shock syndrome develop.2

Dengue virus transmission follows two general patterns which is epidemic dengue
and hyperendemic dengue. Epidemic dengue transmission occurs when dengue
virus is introduced into a region as an isolated event that involves a single viral
strain. If the number of vectors and susceptible pediatric and adult hosts is

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sufficient, explosive transmission can occur, with an infection incidence of 25%-
50%. Mosquito-control efforts, changes in weather, and herd immunity contribute
to the control of these epidemics. Transmission appears to begin in urban centers
and then spreads to the rest of a country. This is the current pattern of transmission
in parts of Africa and South America, areas of Asia where the virus has
reemerged, and small island nations. Travelers to these areas are at increased risk
of acquiring dengue during these periods of epidemic transmission.2
At present, the only method of controlling or preventing dengue and DHF
is to combat the vector mosquitoes. Aedes aegypti breeds primarily in man-made
containers like earthenware jars, metal drums and concrete cisterns used for
domestic water storage, as well as discarded plastic food containers, used
automobile tyres and other items that collect rainwater. It can also breed
extensively in natural habitats such as tree holes and leaf axils. In recent years,
Aedes albopictus, a secondary dengue vector in Asia, has become established in
the United States, several Latin American and Caribbean countries, in parts of
Europe and in one African country. The rapid geographic spread of this species
has been largely attributed to the international trade in used tyres. Dengue
continues to be a global challenge because the pathogenesis of DHF is not fully
understood, there is no immediate prospect of a vaccine and the mosquito control
measures are inadequate. The wide spread DHF epidemics during 2003 reinforces
the belief that DHF has come to stay in this country and will continue to spread to
newer areas unless vector control measures are taken up on war footing.3

EPIDEMIOLOGY
Dengue haemorrhagic fever is now endemic in more than 100 countries in
Africa, the Americas, the Eastern Mediterranean, Southeast Asia and the Western
Pacific, Southeast Asia and the Western Pacific are most seriously affected. Some
2500 million people two fifths of the world.’s population are now at risk from

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dengue. WHO currently estimated 50 million cases of dengue infection worldwide
every year and during epidemics of dengue, attack rates among susceptibles are
40 to 90%. An estimated 500,000 cases of DHF require hospitalization each year,
of whom a very large proportion are children.3
Figure 1: Dengue, countries or areas at risk, 2008

Indonesia is the largest country in the region with a population of 245

million. Almost sixty per cent of the people live on the island of Java, which is
most severely afflicted by periodic outbreaks of dengue disease. However, the
disease is endemic in many large cities and small towns throughout the country
and has also spread to certain smaller villages, where population movement and
density are high.Epidemic DF has been reported in all 27 Indonesian provinces,
whereas in 1968 only two provinces had reported dengue cases.1

Figure 2: The incidence rate and case-fatality rate of DHF in Indonesia in

2005.

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 An increase in commercial air travel has subsequently aided the
transmission of the virus between populations so that dengue is now endemic in
over 100 countries throughout tropical and sub-tropical areas of the world. The
main vector Aedes aegypti is found worldwide between latitudes 35ºN and 35ºS
.The principle areas affected include the Caribbean, South and Central America,
Mexico, Africa, the Pacific Islands, South East (SE) Asia, Indian sub-continent,
Hawaii, and Australia (see Figure 1). By 2002, more than 2.5 billion people were
at risk of infection (roughly 40% of the world’s population). An estimated 50-100
million illnesses occur annually, 250,000-500,000 of which are dengue
haemorrhagic fever, many of these in children. The estimated global mortality rate
is 25,000 per annually.4

VIROLOGY
The genome of Dengue virus consists of a single stranded, non
segmented, positive sense ribonucleic acid (RNA) of about 11 kb in length . The
genome is translated into a single polypeptide which is co- and post-
translationally processed by host signalases as well as the virus encoded serine
protease into the three structural and seven non structural proteins (NS) in the
order C-prM-E-NS1-NS2A-NS2B-NS3-NS4A-NS4B-NS5 that traverse the
Endoplasmic Reticulum (ER) membrane .Dengue and other flaviviruses are
thought to replicate in the cytoplasm, mature on intracellular membranes and
egress by exocytosis and in some cases by budding at the plasma membrane . The
host ER is the primary site of envelope glycoprotein biogenesis, genomic

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replication, and particle assembly of flaviviruses. In the course of productive
infection, flaviviruses induce proliferation and hypertrophy of the ER membranes
Moreover, a large amount of flaviviral proteins are synthesized in infected cells,
thus overwhelming the ER folding capacity. As a natural consequence, we
hypothesize that these events will lead to the activation of the ER stress response
which in turn will modulate various signaling pathways resulting in cell survival
or death decisions.5
TRANSMISSION
Transmission occurs following a bite from an infected Aedes mosquito. It
is most widely transmitted by Ae. aegypti and Ae. albopictus (Asia, Philippines
and Japan), other Aedes species also transmit disease in specific areas; Ae.
polynesiensis, Ae. scutellaris and Ae. pseudoscutallaris (Pacific Islands and New
Guinea), Ae. polynesiensis (Society Islands) and Ae. niveus (Philippines).4
The cycle of transmission typically involves humans and mosquitoes. The
virus is spread from an infected human to a mosquito and then to another human,
often in areas where there are dense human populations. The mosquito can
transmit dengue if it immediately bites another host. Humans are the main
reservoir for the dengue virus, although nonhuman primates in Asia and Africa
may also be infected.2,4

Figure 3: Mechanism of transmission

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Humans serve as the primary reservoir for dengue; however, certain non human
primates in Africa and Asia also serve as hosts but do not develop dengue
hemorrhagic fever. Mosquitoes acquire the virus when they feed on a carrier of
the virus. The mosquito can transmit dengue if it immediately bites another host.2

VECTORS
A. aegypti, found worldwide in the tropics and subtropics, is the principal
vector. The Aedes mosquito prefers to breed in water-filled receptacles, usually
close to human habitation. They often rest in dark rooms (e.g. in bathrooms and
under beds) and breed in clean, stagnant water in containers that collect rainwater,
such as tires, tin cans, pots, and buckets.4
Figure 4: Vector

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 Female Aedes are highly susceptible to dengue virus, feeds preferentially
on human blood, is a daytime feeder, has an almost imperceptible bite, and is
capable of biting several people in a short period for one blood meal. 6 They inflict
an innocuous bite and are easily disturbed during a blood meal, causing them to
move on to finish a meal on another individual, making them efficient vectors.3
In addition, transmission occurs after 8-12 days of viral replication in the
mosquito's salivary glands (extrinsic incubation period). The mosquito remains
infected for the remainder of its 15- to 65-day lifespan. Vertical transmission of
dengue virus in mosquitoes has been documented. The eggs of Aedes mosquitoes
withstand long periods of desiccation, reportedly as long as 1 year, but are killed
by temperatures of less than 10°C.2

PATHOGENESIS
After an infected mosquito has bitten a person, the virus replicates in
regional lymph nodes and is disseminated through the lymphatic system and
blood to other tissues. Replication in the reticuloendothelial system and skin
results in viremia. The incubation period ranges from 3 to 14 days, but it is
usually 4 to 7 days. Infection with dengue virus of any of the four serotypes
causes a spectrum of illness, ranging from no symptoms or mild fever to severe
and fatal hemorrhage, depending largely on the patient’s age and immunologic
condition.6
Viral virulence and immune responses have been considered as two major
factors responsible for the pathogenesis of DHF. Virological studies areattempting
to define the molecular basis of viral virulence. The immunopathological
mechanisms appear to include a complex series of immune responses. A rapid
increase in the levels of cytokines and chemical mediators apparently plays a key
role in inducing plasma leakage, shock and haemorrhagic manifestations. It is
likely that the entire process is initiated by infection with a socalled virulent
dengue virus, often with the help of enhancing antibodies in secondary infection,
and then triggered by rapidly elevated cytokines and chemical mediators produced
by intense immune activation.3

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The pathogenesis of DHF is poorly understood. DHF caused by primary or secondary
dengue infection is due to the occurrence of abnormal immune response involv ing
production of cytokines or chemokines, activation of T-lymphocytes and disturbance
of the hemostatic system. The elevated mediators include C3a, C5a, tumor necrosis
factor-α, interleukin (IL)-2, IL-6, IL-10, interferon-α and histamine.9–14 Halstead
described the antibody-dependent enhancement whereby, upon the second infection
with a heterotypic dengue virus,15 the subneutralizing concentration of the cross-
reacting antibody from the previous infection may opsonize the virus and enhance its
uptake and replication in the macrophage or mononuclear cells. Secondary infection
with a heterotypic dengue virus is associated with increased risk of developing DHF in
individuals who have recovered from a primary dengue virus with a first serotype. The
level of T-cell activation in a secondary dengue infection is also enhanced, occurring
as a phe- nomenon known as original antigenic sin,16,17 and is undergoing
programmed cell death. Many dengue- specific T-cells are of low affinity for the
infected virus and show higher affinity for other, probably previously encountered
serotypes. Profound T-cell activation and death during acute dengue infection may
suppress or delay viral elimination, leading to the higher viral loads and increased
immunopathology found in patients with DHF. 7
Most patients who develop dengue hemorrhagic fever or dengue shock
syndrome have had prior infection with one or more dengue serotypes. In

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individuals with low levels of neutralizing antibodies, nonneutralizing antibodies
to one dengue serotype, when bound by macrophage and monocyte Fc receptors,
have been proposed to result in increased viral entry and replication and increased
cytokine production and complement activation. This phenomenon is called
antibody-dependent enhancement.2

PATHOPHYSIOLOGY
Two main pathophysiological changes occur in DHF/DSS are increase in
vascular permeability that gives rise to loss of plasma from vascular compartment
and disorder in haemostasis.6

a. Evidence of plasma leakage

The plasma leakage is due to the increased vascular permeability induced
by several mediators such as C3a, C5a during the acute febrile stage and
prominent during the toxic stage. Capillary damage allows fluid, electrolytes,
small proteins, and, in some instances, red cells to leak into extravascular spaces.3
The evidence of plasma leakage includes hemoconcentration, hypoproteinemia/
hypoalbuminemia, pleural effusion, ascites, threatened shock and profound shock.
The rising hematocrit may not be evidenced because of either severe bleeding or
early intravenous fluid replacement.7

b. Bleeding tendency
The bleeding diathesis is caused by vasculopathy, thrombocytopenia,
platelet dysfunction and coagulopathy.2
Vasculopathy
A positive tourniquet test indicating the increased capillary fragility is
found in the early febrile stage. It may be a direct effect of dengue virus as it
appears in the first few days of illness during the viremic phase.7

Thrombocytopenia and platelet dysfunction

Patients with DHF usually have platelet counts less than 100 × 10 9/L.
Thrombocytopenia is most prominent during the toxic stage. The mechanisms of

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thrombocytopenia include decreased platelet production and increased peripheral
destruction. 3
Additionally, the increased peripheral destruction is markedly prominent
during 2 days before defervescence. The bone marrow then revealed
hypercellularity with an increase in the megakaryocyte, erythroblast and myeloid
precursors. Hemophagocytosis of young and mature erythroid and myeloid cells,
lymphocytes and platelets was observed.Survival of patients and transfused
platelets was markedly decreased because of immune-mediated injury of platelets.
Platelet dysfunction as evidenced by the absence of adenosine diphosphate (ADP)
release was initially demonstrated in patients with DHF during the convalescent
stage by Mitrakul et al. in 1977. The subsequent study during the febrile and early
convalescent stages by Srichaikul et al. in 1989 also demonstrated the impaired
platelet aggregation response to ADP that returned to a normal response 2–3
weeks later. An increase in plasma β-thromboglobulin and platelet factor 4,
indicating increased platelet secretory activity, was observed. The platelet
dysfunction might be the result of exhaustion from platelet activation triggered by
immune complexes containing dengue antigen.7

Coagulopathy
During the acute febrile stage, mild prolongation of the prothrombin time
and partial thromboplastin time, as well as reduced fibrinogen levels, have been
demonstrated in several studies. Variable reductions in the activities of several
coagulation factors, including prothrombin, factors V, VII, VIII, IX and X,
antithrombin and α-antiplasmin, have been demonstrated. Fibrin degradation
product or D-dimer is slightly elevated.9
Low levels of anticoagulant proteins C and S and antithrombin III were
found to be associated with increasing severity of shock, presumably due to
plasma leakage. Elevated levels of tissue factor, thrombomodulin and
plasminogen activator inhibitor-1 reflect endothelial, platelet and/or monocyte
activation and may be a secondary response to direct activation of fibrinolysis by
the dengue virus. The coagulation abnormality is well compensated for in the

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majority of patients without circulatory collapse. Most of the patients have serum
aspartate transaminase (AST) and alanine transaminase (ALT) levels threeand
twofold higher than normal, respectively. There is focal necrosis of hepatic cells,
swelling appearance of Councilman bodies and hyaline necrosis of Kupffer cells.
Proliferation of mononuclear leucocytes and less frequently polymorphonuclear
leucocytes occurs in the sinusoids and occasionally in the portal areas.2,9

CLINICAL FEATURES
Classic dengue or “breakbone fever” is characterized by a sudden onset of
high-grade fever, accompanied by a severe headache, pain behind the eyes (retro-
orbital pain), and fatigue, and it is often associated with severe myalgias,
particularly of the lower back, arms, and legs, and arthralgias, especially of the
knees and shoulders.The fever usually lasts five to seven days. A rash, typically
macular or maculopapular and often confluent with the sparing of small islands of
normal skin has been reported in about half of infected persons. It usually appears
near the time of defervescence, often lasts for two to four days, and may be
accompanied by scaling and pruritus. Other signs and symptoms include flushed
facies (usually during the first 24 to 48 hours), lymphadenopathy, injected
conjunctivae, an inflamed pharynx, and mild respiratory and gastrointestinal
symptoms. 6
Fever in persons with symptomatic dengue fever may be as high as 39,4 –
41,1°C (103 - 106°F).3 The fever typically begins on the third day and lasts 5-7
days, abating with the cessation of viremia. Fever is often preceded by chills,
erythematous mottling of the skin, and facial flushing (a sensitive and specific
indicator of dengue fever). Occasionally, and more commonly in children, the
fever abates for a day and then returns, a pattern that has been called saddleback
fever. Patients are at risk for development of dengue hemorrhagic fever or dengue
shock syndrome at approximately the time of defervescence.2

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Gum bleeding, epistaxis,cmenorrhagia, and gastrointestinal hemorrhage are
only occasionally seen. Very rare complications of dengue fever include
myocarditis, hepatitis, and neurologic abnormalities, such as encephalopathy and
neuropathies. Laboratory findings commonly associated with dengue fever
include thrombocytopenia, leukopenia with lymphopenia, mild-to-moderate
elevations of hepatic aminotransferases and lactate dehydrogenase, and
hyponatremia.6

DIAGNOSIS
The WHO guidelines propose the following classification for
symptomatic dengue infection :

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 Figure 1 Manifestation of dengue virus infection

To fulfil the WHO case definition for DHF, the following must all be
present.9,10
1. Fever or history of acute fever, lasting 2-7 days, occasionally biphasic.
2. Bleeding (haemorrhagic tendencies), evidenced by at least one of the
following:
a. a positive tourniquet test (TT)
b. petechiae, ecchymosis, or purpura
c. bleeding from the mucosa, gastrointestinal tract, injection sites or
other locations
d. haematemesis or melena
3. Thrombocytopaenia (100,000 cells per mm3 or less)
4. Evidence of plasma leakage due to increased vascular permeability,
manifested by at least one of the following:
a. a rise in the haematocrit equal or greater than 20% above average
for age, sex and population
b. a drop in the haematocrit following volume-replacement treatment
equal to or greater than 20% of baseline
c. signs of plasma leakage such as pleural effusion, ascites, and
hypoproteinaemia.
The onset of shock may be subtle, indicated by raised diastolic pressure
and increased PVR in an alert patient.2 To fulfil the case definition for Dengue
Shock Syndrome (DSS), the four criteria above for DHF (fever, haemorrhagic

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tendencies, thrombocytopaenia, and plasma leakage) must all be present plus
evidence of circulatory failure manifested as: 10
a. Rapid and weak pulse
b. Narrow pulse pressure (<20 mmHg)
c. Hypotension for age (this is defined as systolic pressure < 80
mmHg for those less than five years of age, or <90 mmHg for those five
years of age and older.)
d. Cold clammy skin and restlessness.
The diagnosis of dengue infection is confirmed by testing positive for
either virus isolation using culture, polymerase chain reaction (PCR) from the
clinical specimens such as serum in the early febrile stage, or serological studies.6
In both primary and secondary dengue infections, there is a relatively transient
appearance of antidengue immunoglobulin M (IgM) antibodies. These disappear
after 6-12 wk, which can be used to time a dengue infection.10

In 2nd primary dengue infections, most antibody is of the IgG class. The
positive serological studies define as a fourfold or more increase in the
hemagglutination inhibition test, complement fixation, enzyme immunoassay, or
neutralization test, between acute and convalescent sera or positive test for
dengue-specific IgM/IgG performed by enzyme-linked immunosorbent assay
(ELISA).6 The secondary dengue infection is defined when the hemagglutination
inhibition titer was 1:2560 or more, or the ratio of IgG and IgM was >1.8.
Crossreactions with other flaviviruses interfere with serologic testing,
particularly the ELISA for IgG, and this affects the interpretation of test results in
travelers exposed to other flavivirus infections, including those previously
vaccinated against flavivirus infections, such as yellow fever and Japanese
encephalitis.6
The most commonly used test for the diagnosis of dengue is the IgM
capture ELISA, but this test is negative early in the course of the disease, should
be performed only four to five days after the onset of symptoms, and gives only a
probable diagnosis. Usually such samples should be collected not earlier than 5

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days nor later than 6 wk after onset. Rheumatoid factor may lead to an IgM
capture assay that is false positive for dengue.6,10
Primary infections are characterized by an increase in dengue-specific IgM
antibodies 4 to 5 days after the onset of fever and by an increase in IgG antibodies
only after 7 to 10 days. IgM antibodies are detectable for three to six months,
whereas IgG antibodies remain detectable for life. In secondary infections, the
level of IgM antibodies is lower than in primary infections and the antibodies are
sometimes even absent, whereas levels of IgG antibodies rise rapidly in secondary
infections, even during the acute phase. Thus, the presence of high titers of IgG
early in the course of the disease is a criterion for secondary infection.6

CLASSIFICATION
DHF is lassified into four grade of severity, where grades III and IV are
considered to de DSS. The presence of thrombocytopenia with concurrent
haemoconcentration differentiates grades I and II DHF from DF: 9
1. Grade I is defined as fever and non-specific constitutional signs
and symptoms; the only haemorrhagic manifestation is a positive TT
and/or easy bruising.
2. Grade II is the same as grade I but includes spontaneous bleeding,
usually in the form of skin or other haemorrhages.
3. Grade III is circulatory failure manifested by a rapid, weak pulse
and narrowing of the pulse pressure or hypotension, with the presence of
cold, clammy skin and restlessness.
4. Grade IV is profound shock with undetectable blood pressure or
pulse.
Grades III and IV are define are as DSS.

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 Figure 2 The spectrum of dengue illness

In addition, the guidelines list indicators that may be used to guide the
diagnosis of DHF/DSS. These indicators may help clinicians to establish an early
diagnosis, ideally before the onset of shock but are not intended to be substitutes
for the case definitions. The listed indicators of DHF/DSS are: high fever of acute
onset, hemorrhagic manifestations (at least a positive TT), hepatomegaly, shock,
thrombocytopaenia, and hemoconcentration. The first two clinical observations,
plus one of the laboratory findings establishes a provisional diagnosis of DHF.
The of shock in a patient with a provisional diagnosis of DHF supports the
diagnosis of DSS.8

DIFFERENTIAL DIAGNOSIS
Early in the febrile phase, the differential diagnose for DHF/DSS includes
a wide spectrum of viral, bacterial and parasitic infections. Chikungunya fever
may be difficult to differentiate clinically from DF and mild or early cases of
DHF.8 In addition, DHF can also mimic Kawasaki disease, yellow fever,
hantavirus infections, meningococcemia and other viral hemorrhagic fevers.8
By the third or fourth day, laboratory findings may establish a diagnosis
before shock occurs. Shock virtually rules out a diagnosis of chikungunya fever.

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Marked thrombocytopenia with concurrent haemoconcentration differentiates
DHF/DSS from diseases such as endotoxin shock from bacterial infection or
meningococcaemia.9
The differential diagnosis of dengue fever includes viral respiratory and
influenza-like diseases, the early stages of malaria, mild yellow fever, scrub
typhus, viral hepatitis, and leptospirosis. Four arboviral diseases have dengue-like
courses but without rash: Colorado tick fever, sandfly fever, Rift Valley fever, and
Ross River fever.10
In dengue fever, pancytopenia may occur after the 3-4 days of illness. A
recent systematic review found that patients with dengue had significantly lower
total WBC, neutrophil, and platelet counts than patients with other febrile
illnesses in dengue-endemic populations. Leukopenia, often with lymphopenia, is
observed near the end of the febrile phase of illness.2 Neutropenia may persist or
reappear during the latter stage of the disease and may continue into
convalescence with white blood cell counts of <2,000/mm3.10
Other abnormalities include moderate elevations of the serum
transaminase levels, consumption of complement, mild metabolic acidosis with
hyponatremia, occasionally hypochloremia, slight elevation of serum urea
nitrogen, and hypoalbuminemia.10
The most common hematologic abnormalities during dengue hemorrhagic
fever and dengue shock syndrome are hemoconcentration with an increase of
>20% in hematocrit, thrombocytopenia, prolonged bleeding time, and moderately
decreased prothrombin level that is seldom <40% of control. Fibrinogen levels
may be subnormal and fibrin split products elevated.3
Thrombocytopenia has been demonstrated in up to 50% of dengue fever
cases. Platelet counts of less than 100,000 cells/μL are seen before defervescence
and the onset of shock. The platelet count and hematocrit level should be
monitored at least every 24 hours to facilitate early recognition of dengue
hemorrhagic fever and every 3-4 hours in severe cases of dengue hemorrhagic
fever or dengue shock syndrome.2

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 Cultures of blood, urine, CSF, and other body fluids should be performed
as necessary to exclude or confirm other potential causes of the patient's
condition. Arterial blood gas should be assessed in patients with severe cases to
assess pH, oxygenation, and ventilation. Typing and crossmatching of blood
should be performed in cases of severe dengue hemorrhagic fever or dengue
shock syndrome because blood products may be required.2
Serum specimens should be sent to the laboratory for serodiagnosis, PCR,
and viral isolation. Serodiagnosis is made based on a rise in antibody titer in
paired IgG or IgM specimens. Results vary depending on whether the infection is
primary or secondary. The IgM capture enzyme-linked immunosorbent assay
(MAC-ELISA) has become the most widely used assay, although other tests,
including complement fixation (CF), neutralization test (NT), hemagglutination
inhibition (HI), and IgG ELISA are also used.10

Imaging Studies
Chest radiography of the chest reveal pleural effusions (left > right) in
nearly all patients with dengue shock syndrome. Bilateral pleural effusions are
common in patients with dengue shock syndrome.2
Positive and reliable ultrasonographic findings include fluid in the chest
and abdominal cavities, pericardial effusion, and a thickened gallbladder wall.
Thickening of the gallbladder wall may presage clinically significant vascular
permeability. The electrocardiogram may show sinus bradycardia, ectopic
ventricular foci, flattened T waves, and prolongation of the P-R interval.2,10

MANAGEMENT
There is no specific treatment for DHF. Dengue fever is usually a self-
limited illness, as there are no specific antiviral medications for dengue infections,
and only supportive care is required. Therapy for DHF is wholly symptomatic and
aims at controlling the clinical manifestations of shock and hemorrhage.7

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 No specific diet is necessary for patients with dengue fever. Patients may
become dehydrated from fever, lack of oral intake, or vomiting. Patients who are
able to tolerate oral fluids should be encouraged to drink oral rehydration solution,
fruit juice, or water to prevent dehydration. Return of appetite after dengue
hemorrhagic fever or dengue shock syndrome is a sign of recovery. Bedrest is
recommended for patients with symptomatic dengue fever, dengue hemorrhagic
fever, or dengue shock syndrome. Table 1 shows high risk patients and some
indication for admission to hospital.9

Table 1 - High-risk dengue patients and indication for admission to hospital/ICU

High-risk dengue patients that need special attention

Infants under 1 year of age
Overweight/obese patients
Massive bleeding
Change of consciousness, especially restlessness and irritability or coma
Presence of underlying diseases e.g. thalassemia, G-6-PD deficiency, heart
disease

Indication for admission

Excessive family concern or cannot be followed up
Very weak, cannot eat or drink, not drinking/feeding poorly
Spontaneous bleeding
Platelet counts ≤ 100,000 cells/mm3 and/or rising Hct 10-20%
Clinical deterioration in defervescence
Severe abdominal pain/vomiting
Significant dehydration requiring intravenous fluids

Admit immediately if there are signs of shock. These signs are as follows:
Rapid pulse with no fever
Prolonged capillary refill time
Cold clammy skin, mottling

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 Narrowing of pulse pressure ≤ 20 mmHg, e.g. 100/80
Hypotension
Oliguria, no urine for 4-6 hours
Change of consciousness: drowsiness to stupor, restlessness, irritability
(encephalopathy)

World Health Orgnization, Dengue Haemorrhagic Fever: 1997

The treatment of dengue fever in the febrile phase is symptomatic (Table

2). Fever is treated with paracetamol. Salicylates and other nonsteroidal anti-
inflammatory drugs should be avoided as these may predispose a child to mucosal
bleeding.6 Patients who do not receive a proper treatment usually die within 12–24
hours after shock ensues. The most important aspect in managing patients with
DHF is close observation by the attending physicians and nurses with frequent
clinical and laboratory monitoring.8

Table 2 - Steps to the management of the febrile phase

Resting, oral fluids

Reduction of fever: Tepid sponge after a dose of paracetamol 10-15 mg/kg/day for
high fever ≥ 39oC, every 4 to 6 hours

Nutritional support: Soft, balanced, nutritious diet, juice and electrolyte solution -
plainwater is not adequate.Avoid black- or red-colored food or drinks (may be
mistaken for bleeding)

Other supportive and symptomatic treatment

• Domperidone -1 mg/kg/day in three divided doses in case of severe
vomiting for 1-2 days. One single dose may be adequate
• H2-blockers (ranitidine) - recommended in case of gastrointestinal
bleeding

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 • Antibiotic - not necessary; it may lead to complications
• Steroid is ineffective in preventing shock DHF. It may cause harm
Intravenous fluids: In case of doubt, provide intravenous fluids, guided by serial
hematocrit, blood pressure, and urine output levels. The volume of fluid should be
targeted at treating mild to moderate isotonic dehydration (5-8% deficit); just
correct dehydration, and discontinue it as soon as possible
If sent home- Advise about warning signs and symptoms of shock and ask to
report immediately if any of the following symptoms occur
• Clinical deterioration in defervescence (no fever or low-grade fever)
• Any type of bleeding
• Severe vomiting/abdominal pain
• Intense thirst
• Drowsiness, desire for sleeping all the time
• Refusal to eat or drink
• Cold, clammy skin and extremities, restlessness, irritability, decreased
urine output or no urine for 4-6 hours
• Behavioral changes e.g. confusion, use of foul language
Follow up preferably everyday - from the 3rd day until afebrile for 24-48 hours.
Important points to evaluate are :
• History of bleeding, abdominal pain, vomiting, appetite, fluid intake,
and urine output
• Physical examination: vital signs, liver size and tenderness
• Blood counts: WBC ≤ 5,000 cells/mm3 with lymphocytosis and
increase in atypical lymphocytes – and platelet counts ≤ 100,000
cells/cumm – indicates progression to critical phase. Rising Hct of 10-
20% - indicates that the patient has progressed to the critical phase
• Liver function tests in every patient who shows a change in
consciousness, restlessness, confusion and irritability

World Health Orgnization, Dengue Haemorrhagic Fever: 1997

Patients who develop signs of dehydration, such as tachycardia, prolonged
capillary refill time, cool or mottled skin, restlessness, acute abdominal pain,
diminished pulse amplitude, altered mental status, decreased urine output, rise in

21 | P a g e
hematocrit levels, narrowed pulse pressure, or hypotension, should be hospitalized
as require admission for intravenous fluid administration.9
Ringer’s lactate is infused at a rate of 7 mL/kg over 1 hour. After 1 hour, if
hematocrit level decreases and vital parameters improve, the fluid infusion rate
should be decreased to 5 mL/kg over the next hour and to 3 mL/kg/hour for 24-48
hours. When the patient is stable, as indicated by normal blood pressure,
satisfactory oral intake and urine output, the child can be discharged.8
If at 1 hour the hematocrit level rises and vital parameters do not show
improvement, the fluid infusion rate should be increased to 10 mL/kg over the
next hour. In case of no improvement, the fluid infusion rate should be further
increased to 15 mL/kg over the third hour. If no improvement is observed in vital
parameters and hematocrit level at the end of 3 hours, colloids or plasma infusion
(10 mL/kg) should be administered (Figure 3). Once the hematocrit level and vital
parameters are stable the infusion rate should be gradually reduced and
discontinued over 24-48 hours.8,9

22 | P a g e
 Figure 3 Management for DHF grade I and II

Intravenous fluids should be stopped when the hematocrit level falls below
40% and adequate intravascular volume is present. At this time, patients reabsorb
extravasated fluid and are at risk for volume overload if intravenous fluids are
continued. Do not interpret a falling hematocrit value in a clinically improving
patient as a sign of internal bleeding.2
The most important element of treatment in a critically ill patient or in a
patient with DSS is providing intensive care with close monitoring of blood
pressure, hematocrit levels, platelet count, urinary output, hemorrhagic
manifestations, and level of consciousness (Table 3). With adequate and
appropriate fluid replacement, DSS is rapidly reversible.8,9

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 Table 3
Steps to the management of the critical phase/DHF and dengue shock
syndrome

General measures
• Give oxygen via face mask/nasal cannula in case of shock/impending
shock. NCPAP should be preferred if there is acute respiratory failure
associated with DSS
• Frequent monitoring
• Stop bleeding with proper techniques e.g. anterior nasal packing for
massive epistaxis
• Avoid blind invasive procedures e.g. no nasogastric tube insertion, no
gastric lavage
• Essential nursing care
• Sedation is needed in some cases to restrain an agitated child. Chloral
hydrate(12.5-50 mg/kg), orally or rectally, is recommended.
• Long-acting sedatives should be avoided

Monitoring of children with DHF/DSS

• Vital signs should be checked every 15-30 minutes until the patient is
stable, and every 1-2 hours thereafter
• Hematocrit levels must be checked every 2 hours for 6 hours, then
every 4 hours until the patient is stable. Monitoring at every 12 hours
during recovery
• Fluid balance sheet: type of fluid, amount, rate etc
• Accurate measurement of urine output
• Serum electrolytes and blood gases should be checked every 12 hours
• DIC profile and liver function tests as and when indicated
• Weight should be measured every 12 hours

Obtain laboratory tests

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 • In uncomplicated DHF cases, Hematocrit and platelet counts are the
only necessary tests
• In those at high risk of complicated DHF
Blood grouping/cross matching
Blood glucose
Blood electrolyte (Na, Ca, K, CO2)
Liver function test
Renal function test (BUN, creatinine, uric acid)
Blood gas
Coagulogram (PTT, PT, TT)

IV fluid
IV fluids should be given only when the patient enters the critical phase:
thrombocytopenia ≤ 100,000, rising Hct of 10-20%. IV fluid before critical phase
cannot prevent shock, but may cause fluid overload

Type of IV fluid used: isotonic salt solution (normal saline or Ringer 's lactate)

In young infants without shock-N/2 saline in 5% dextrose; colloid solutions in

patients who already have volume overload, i.e., massive pleural effusion
Fluid replacement rate – minimum necessary to maintain effective circulatory
volume, excess amount will leak into the pleural and peritoneal spaces

Initial rate of administration

• DSS grade III – 10 mL/kg/hour for 1-2 hours
• Grade IV – Free flow or 20 mL/kg/dose IV bolus until BP can be
measured (usually within 5-15 minutes), then reduce the rate to 10
mL/kg/hour for 1-2 hours
• Non-shock patients: normal maintenance or + 5%deficit and then
reduce the rate to minimum after 2-4 hours, if possible. Body weight <
15 kg: 4-7 mL/kg/hour. Body weight 15-40 kg: 3-5 mL/kg/hour
• Colloids: The initial rate is 10 mL/kg/hour; this will reduce Hct by
about 10 percentage points e.g. from 53 to 43%. After that, reduce to 5,

25 | P a g e
 then to 3 mL/kg/hour

Increase or decrease the rate of IV fluid depending on: clinical signs of shock,
hematocrit level, urine output

In case of no response to IV fluids: consider and correct

• Massive plasma leakage
• Concealed internal bleeding – decrease in Hct
• Hypoglycemia – Blood sugar < 60 mg%
• Hyponatremia, hypocalcemia – electrolytes
• Acidosis – indicates metabolic acidosis in blood gas analysis

Duration of IV fluid infusion: between 24-48 hours as plasma loss may continue
for 24-48 hours. It should be discontinued when the hematocrit level falls to
approximately 40%, with stable vital signs. A good urine flow indicates sufficient
circulating volume. Reabsorption of extravasated plasma occurs 48 hours after the
termination of shock (manifested by a further drop in hematocrit levels after
intravenous fluid administration has been stopped), and hypervolemia, pulmonary
edema or heart failure may occur if more fluid is given. It is extremely important
that a drop in hematocrit levels at this later stage is not interpreted as a sign of
internal bleeding.Strong pulse and blood pressure and adequate dieresis are good
signs at this stage. The return of the patient’s appetite is also a sign of recovery.

Blood and platelet transfusion

• The indications for fresh whole blood or packed red cell transfusion are
significant blood loss > 10% (6-8 mL/kg), hemolysis, concealed
internal bleeding
• Dose: Fresh whole blood 10 mL/kg/dose, packed red cells 5
mL/kg/dose
• Indication for platelet transfusion: significant bleeding with
thrombocytopenia or if platelet count is less than 10,000/mm3 (10-20
mL/kg of platelets). Mild reductions in platelet counts are usually not
associated with significant bleeding. Platelets return to normal within 7-

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 9 days. Only 0.4% of DHF patients need platelet transfusion

World Health Orgnization, Dengue Haemorrhagic Fever: 1997

In children with hypotension (DSS grade III), Ringer’s lactate solution,

10-20 mL/kg, should be infused over 1 hour or given as bolus 20 mL/kg if blood
pressure is unrecordable (DSS grade IV). The bolus may be repeated twice if there
is no improvement. If there is no improvement in vital parameters and hematocrit
level rises, colloids 10 mL/kg should be rapidly infused. If the hematocrit level is
falling without improvement in vital parameters, blood transfusion is necessary,
presuming that lack of improvement is due to occult blood loss (Figure 4). Once
improvement starts, the fluid infusion rate should be gradually decreased.9
Patients who are unresponsive to fluids may have myocardial dysfunction
and decreased left ventricular performance, which may be easily detected by
echocardiography. Low platelet count may not be predictive of bleeding. Platelets
or blood should not be transfused based upon platelet count alone. In children
with severe thrombocytopenia in absence of significant bleeding, platelet infusion
does not alter the outcome. Infusion of fresh frozen plasma and platelet
concentrates may be beneficial in patients with disseminated intravascular
coagulation.8,9

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 Figure 4 Management for DSS

COMPLICATIONS
The complications can occur from DHF include 2,9
1. Electrolyte imbalance : Hyponatremia, Hypocalcemia
2. Fluid overload (overhydration) : avoid the common causes of fluid
overload, which are:
a. Early IV fluid therapy- in the febrile phase
b. Excessive use of hypotonic solutions
c. Non-reduction in the rate of IV fluid after initial resuscitation
d. Blood loss replaced with fluids in cases with occult bleeding
e. Judicious fluid removal using colloids with controlled diuresis
(furosemide 1 mg/kg infusion over 4 hours) or dialysis

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 3. Large pleural effusions, ascites
4. Disseminated intravascular coagulation

CRITERIA FOR DISCHARGING IN PATIENTS

Patients who are resuscitated from shock rapidly recover. Patients with
dengue hemorrhagic fever or dengue shock syndrome may be discharged from the
hospital when they meet the following criteria:2,9
1. Afebrile for at lease 24 hours without antipyretics
2. Good appetite, clinically improved condition
3. Adequate urine output
4. Stable hematocrit level
5. At least 48 hours since recovery from shock: stable pulse, blood
pressure and breathing rate
6. Absence of respiratory distress from pleural effusion and no ascites
7. Platelet count greater than 50,000 cells/μL
8. No evidence of external or internal bleeding
9. Convalescent confluent petechial rash

PROGNOSIS
Significant morbidity and mortality can result if early recognition and
monitoring of severe forms are not done. If left untreated, the mortality of DHF or
DSS patients may be as high as 40-50%. Early recognition of illness, careful
monitoring and appropriate fluid therapy alone have decreased mortality to 1%. If
shock is identified when pulse pressure starts to drop and intravenous fluids are
administered, the outcome will be excellent. Infrequently, there is residual brain
damage caused by prolonged shock or occasionally by intracranial hemorrhage.10
Recovery is fast and most patients recover in 24-48 hours without any
sequelae. The outcome may not be so good if the patient develops cold
extremities. Most deaths from DHF/DSS are caused by prolonged shock, massive
bleeding, fluid overload and acute liver failure with encephalopathy. Severe
refractory shock, DIC, ARDS, liver failure and neurological manifestations singly

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or in combination were the commonest causes of death in a recent series. The case
fatality rate is high with shortage of experienced medical teams.9

PREVENTION AND CONTROL

At present, no specific drug or vaccine is available against the dengue
virus. The control is primarily dependent on vector control.1,8,9
1) Environmental changes: improved water supply, mosquito proofing of
overhead tanks, cisterns and underground reservoirs.
2) Personal protection: protective clothing, mats, aerosol coils (pyrethrum),
repellents e.g., DEET, permethrin impregnated in cloth, insecticide-treated
mosquito nets and curtains.
3) Biological control: by larvivorous fish: Gambria affinis and Peorilia
reticulate. Bacteria – Bacillus thuringiensis H-14, Bacillus sphaericus – in
polluted water.
4) Chemical control: 1% temephos sand granules. Space sprays – malathion,
fenitrothion, pirimiphos (only in major DHF epidemics). Insect growth
regulators – interfere with development of the immature stages of the
mosquito in larvae or disruption of pupal stage.

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 The aim of doing this paper is to report a case of grade II dengue
hemorrhagic fever of an 6 year-old girl that was admitted at the Infection Unit of
Pediatric Ward Haji Adam Malik General Hospital.

CASE
EN, a 6 year-old girl, 19 kg, 116 cm, was admitted to the Infection Unit of
Pediatric Ward Haji Adam Malik General Hospital on October 29th, 2010 at 02.00
am with chief complaint was fever. The fever occured suddenly since 3 days ago
with a characteristic of high fever which relieved with fever relieving medication.
Shivers and seizures were not found. .
Pain behind the eyes was not found. Patient experienced epistaxis 1 day
ago. Small red patches were found on hands and legs since a day ago. Neither
gingival bleeding and black stool.Patient complained of fatigue since 3 days ago.
Nausea and vomiting were found since 3 days ago with a frequency of 3x/day.
Volume: ¼ Aqua cup. Micturition and defecation were normal.

History of previous illness: This patient was referred from RSU Dr.Hadrianus
Sinaga for the diagnosis of the Dengue Haemorrhagic
Fever.
History of drugs usage : Ringer Lactat,Cefadroxil,Parasetamol,Ranitidine

PHYSICAL EXAMINATION
Generalized Status:
Body weight (BW) : 19 kg Body length (BL) : 120 cm
BW/ BL : 90,4% (normoweight)
Consciousness: Was Clear Body Temperature : 38,6 ۫C
Anemic (-), icteric (-), cyanosis (-), oedema (-), dyspnea (-)

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 Localized Status:
Head : Eye: light reflexes (+/+), isochoric pupil (right=left), pale inferior
conjunctival palpebral (-/-), palpebra edema (-/-)
Mouth/Ears /Nose: Within normal limit
Neck : Lymph node enlargement (-), JVP: R-2cmH₂O
Chest : Symmetrical fusiformic, retraction of epigastric (-)
HR: 123 bpm, regular, no murmur
RR: 20 rpm, regular, no rales
Abdominal : Soepel, peristaltic was normal,
Liver : Not palpable
Spleen: Not palpable
Extremities : Pulse: 123 bpm, regular, pressure/volume: adequate
BP: 90/50 mmHg, CRT < 3’’ cold acral, ptechiae (+) o/t superior-
inferior dextra-sinistra extremities
Rumple leed : (+)
Urogenital : Female, within normal limit
Laboratorium Findings (October 29th 2010) from
Emergency Unit of Adam Malik
Test Result Normal Value
Complete Blood Count
Hemoglobin (Hb) 12.20 g% 11-15g%
Erytrocyes (RBC) 5.2 x 106/mm3 3.0-5.3x106mm3
Leucocytes (WBC) 2,5 x 103/ mm3 5.000-10.000x103/mm3
Hematocrit 45,90 % 36-46%
Thrombocyte 55x 103/ mm3 150-400x103mm3
MCV 80.70 fL 83-103fL
MCH 26.80pg 28-34pg
MCHC 33.20g% 32-36g%
RDW 13.30 % 39-46%
Cell Count
Neutrophil 52% 37- 80%
Lymphocyte 35,20% 20-40%
Monocyte 11,60% 2-8%
Eosinophil 0,00% 1-6%
Basophil 1,200% 0-1%

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Differential diagnosis :- DHF grade II
- Chikugunya
Working diagnosis : DHF grade II

Management :
• IVFD RL 5 cc/BW  95gtt/i micro
• Paracetamol 3x250 mg
• Diet porridge 1450kkal with 38 grams of protein.

Investigation Plan : Routine Blood Count/6 hour

Follow Up
Follow Up October 29th 2010 06.00 am
th
S Fever (+) 4 day, epistaxis (+), red spots in body (+)
O Consciousness: Was Clear T: 38,0 ۫C BW: 19,0 kg BL: 116cm
BW/BL: 90,4 % (normoweight)
Head : Eyes: Light reflexes (+/+), isochoric pupil, pale inferior
palpebral conjunctiva (-), Ears/Nose/Mouth: Within normal
limits,
Neck : Lymph nodes enlargement (-), JVP: R-2cmH₂O
Chest : Symmetrical fusiformic, retraction of epigastrial (-),
HR : 100 bpm, regular, no murmur
RR : 30 rpm, regular, no rales
Abdomen : Soepel, normal peristaltic, epigastrial pain (-),
Liver / Spleen: Not palpable
Extremities: Pols 100 bpm, regular, Pressure/Volume:adequate,
CRT < 3” warm acral, BP :90/60mmHg, ptechiae (+) o/t superior-inferior
dextra-sinistra extremities
A DHF Grade II

P • IVFD RL 5 cc/BW/hour  95 gtt/i micro

• Paracetamol 3x250 mg

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 • Diet porridge 1450 kkal with 38 grams of protein

Investigation plan :
- Routine Blood Count / 6 hours
- consult to Infection Division
- Lab examination IgG and IgM anti dengue

Laboratory findings at 12.00 pm:

Hb : 12,7 g%
Ht : 44,80 %
L : 3,17 x 103/ mm3
Plt : 51 x 103/ mm3
Laboratory findings at 06.00 pm:
Hb : 13,00 g%
Ht : 45,40 %
L : 3,84 x 103/ mm3
Plt : 47 x 103/ mm3

Follow Up October 30th 2010 06.00 am

th
S Fever (-) 5 day, epistaxis (-), red spots in body (+)
O Consciousness : Was Clear T: 37,1 ۫C BW: 19 kg BL: 116cm
BW/BL: 90,4 %
Head : Eyes: Light reflexes (+/+), isochoric pupil, pale inferior
palpebral conjunctiva (-), Ears/Nose/Mouth: Within
normal limits,

Neck : Lymph nodes enlargement (-), JVP: R-2cmH₂O

Chest : Symmetrical fusiformic, retraction of epigastrial (-),
HR : 100 bpm, regular, no murmur
RR : 26 rpm, regular, no rales

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 Abdomen : Soepel, normal peristaltic, epigastrial pain (-),
Liver / Spleen: Not palpable
Extremities : Pols 98 bpm, regular, Pressure/Volume:adequate,
CRT < 3” warm acral, BP :90/60mmHg, ptechiae (+) o/t superior-inferior
dextra-sinistra extremities
Investigation plan : Waiting for IgG and IgM anti dengue lab result

A DHF Grade II
P • IVFD RL 3cc/BW  57 gtt/i micro
• Diet porridge 1450 kkal with 38 grams of protein
Laboratory findings at 06.00 am :
Hb : 12,10 g%
Ht : 44.80%
L : 7,35 x 103/ mm3
Plt : 41 x 103/ mm3

Laboratory findings at 12.00 pm:

Hb : 12,40 g%
Ht : 45,10 %
L : 9,19 x 103/ mm3
Plt : 57 x 103/ mm3
Laboratory findings at 06.00 pm :
Hb : 13,30 g%
Ht : 42.80 %
L : 5,11 x 103/ mm3
Plt : 66 x 103/ mm3

Laboratory findings at 00.00 am :

Hb : 12,60 g%
Ht : 42.50%
L : 6,54 x 103/ mm3

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 Plt : 72 x 103/ mm3
Imunoserologi : Virus
Anti DHF IgM : Positif
Anti DHF IgG : Positif

Follow Up October 31st 2010 06.00 am

th
S Fever (-) 6 day, red spots in body (+)
O Consciousness : Was Clear T: 36,7C BW: 19 kg BL: 116cm
BW/BL: 90,4%,
Head : Eyes: Light reflexes (+/+), isochoric pupil, pale inferior
palpebral conjunctiva (-), Ears/Nose/Mouth: Within normal
limits,
Neck : Lymph nodes enlargement (-), JVP: R-2cmH₂O
Chest : Symmetrical fusiformic, retraction of epigastrial (-),
HR : 86 bpm, regular, no murmur
RR : 24 rpm, regular, no rales
Abdomen : Soepel, normal peristaltic, epigastrial pain (-),
Liver / Spleen: Not palpable
Extremities: Pols 86 bpm, regular, Pressure/Volume:adequate,
CRT < 3” warm acral, BP :90/60mmHg, ptechiae (+) o/t superior-inferior
dextra-sinistra extremities

A DHF Grade II

P • IVFD RL 3 cc/BW/hour  57 gtt/i micro

• Diet porridge 1450 kkal with 38 grams of protein

- Investigation : - Routine Blood Count at 06.00pm

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 Laboratory findings at 12.00 pm :
Hb : 11,50 g%
Ht : 39.60 %
L : 7,22 x 103/ mm3
Plt : 64 x 103/ mm3

Laboratory findings at 06.00 pm :

Hb : 11,4 g%
Ht : 38.50 %
L : 7,39 x 103/ mm3
Plt : 65 x 103/ mm3

Follow Up October 1st 2010 06.00 am

S Fever (-)
O Consciousness : Was Clear T: 36,8C BW: 19 kg BL: 116cm
BW/BL: 90,4%
Head : Eyes: Light reflexes (+/+), isochoric pupil, pale inferior
palpebral conjunctiva (-), Ears/Nose/Mouth: Within normal
limits,

Neck : Lymph nodes enlargement (-), JVP: R-2cmH₂O

Chest : Symmetrical fusiformic, retraction of epigastrial (-),
HR : 88 bpm, regular, no murmur
RR : 24 rpm, regular, no rales
Abdomen : Soepel, normal peristaltic, epigastrial pain (-),
Liver / Spleen: Not palpable
Extremities: Pols 88 bpm, regular, Pressure/Volume:adequate,
CRT < 3” warm acral, BP :90/60mmHg
A DHF Grade II

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P • IVFD RL 3 cc/BW/ hour  57 gtt/i micro
• Diet porridge 1450 kkal with 38 grams of protein

Laboratory findings at 06.00 am :

Hb : 11,40 g%
Ht : 37.40 %
L : 6,96 x 103/ mm3
Plt : 93 x 103/ mm3

Patient is discharged from the hospital.

DISCUSSION

According to WHO, all 4 criteria must be fulfilled to make the diagnosis

of DHF, which are: 1) fever or history of acute fever lasting 2-7 days; 2) bleeding
(haemorrhagic tendencies); 3) thrombocytopaenia (100.000 cells per mm3 or
less); and 4) evidence of plasma leakage due to increased vascular permeability.
In this patient all of the criteria were found, which were 1) sudden of high-grade
fever since 3 days ago; 2) small red patches (petechies) on hands and legs and
history of bleeding nose as haemorrhagic tendencies; and from the laboratory

38 | P a g e
results were 3) thrombocytopaenia (platelet 55.000/mm3) and 4) raised of
hematocrit (44,9%) as the evidence of plasma leakage.
Laboratory examinations of IgM and IgG are important to find out
whether its primary or secondary infections. Primary infections are characterized
by an increase in dengue-specific IgM antibodies 4 to 5 days after the onset of
fever and by an increase in IgG antibodies only after 7 to 10 days. IgM antibodies
are detectable for three to six months, whereas IgG antibodies remain detectable
for life.In this patient,IgM and IgG were checked on day 5th .Both IgM and Ig G
were positive and this concludes that this patient has been exposed with one of the
dengue serotypes earlier and currently suffering the secondary infection. Isolation
of most strains of dengue virus from clinical specimens can be accomplished in
which the sample is taken in the first few days of illness and processed without
delay to know the serotype of the dengue virus .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. In this patient,serotype of the
denque virus could not been found as isolation of virus were not done.

The severity of DHF are classified into 4 gradings according to WHO

guidelines which are:
1. Grade I is defined as fever and non-specific constitutional signs and
symptoms; the only haemorrhagic manifestation is a positive TT and/or
easy bruising.
2. Grade II is the same as grade I but includes spontaneous bleeding, usually
in the form of skin or other haemorrhages.
3. Grade III is circulatory failure manifested by a rapid, weak pulse and
narrowing of the pulse pressure or hypotension, with the presence of cold,
clammy skin and restlessness.

39 | P a g e
 4. Grade IV is profound shock with undetectable blood pressure or pulse.
Grades III and IV are define are as DSS.
Spontaneous bleeding (petechiaes and history of epistaxis) was found
because the girl had petechiaes on her extremities. Thus, the patient was
diagnosed as DHF grade II.
There is no specific treatment for DHF, only supportive care is required.
Therapy for DHF is wholly symptomatic and aims at controlling the clinical
manifestations of shock and hemorrhage. This patient was given intravenous fluid
(RL) and paracetamol. This patient was discharged from hospital after the routine
blood count showed that platelet and hematocrit level were in normal value
(93000/mm3 and 37.40%).

SUMMARY
It has been reported a case of a 6-year-old girl with dengue haemorrhagic
fever grade II. The diagnosis was established based on history taking, clinical
manifestation, and laboratory findings. Treatment for this patient was only
supportive and symptomatic. This patient was discharged from hospital after the
condition the routine blood count of platelet and hematocrit level were in normal
value.

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