1

CASE REPORT
Dengue Haemorrhagic Fever

Compiled by:
Fakhri Amin Nasution

110100298

Sabatini Manurung

110100310

Supervisor
dr. Wisman Dalimunthe, M.Ked(Ped), Sp.A(K)

Pediatric Departement
Medical Faculty of North Sumatera University
Central Public Hospital Haji Adam Malik Medan
2015

TABLE OF CONTENTS

COVER..........................................................................................

TABLE OF CONTENTS..............................................................

ii

CHAPTER I INTRODUCTION.................................................

CHAPTER II LITERATUR REVIEW.......................................

2.1.....................................................................................................................Dengue
....................................................................................................................
2.1.1 Definition............................................................................
2.1.2 Epidemiology......................................................................
2.1.3 Etiology and Pathophysiology............................................
2.1.4 Clinical Manifestation and Physical Examination..............
2.1.5 Laboratory Studies..............................................................
2.1.6 Differential Diagnosis.........................................................
2.1.7 Vector..................................................................................
2.1.8 Treatment............................................................................
2.1.9 Prognosis.............................................................................

3
3
3
5
8
9
10
11
12
21

CHAPTER III CASE REPORT..................................................

3.1 Objective............................................................................................
3.2 Case....................................................................................................
3.3 Follow Up..........................................................................................

22
22
22
33

CHAPTER IV DISCUSSION AND SUMMARY......................

33

4.1 Discussion..........................................................................................
4.2 Summary............................................................................................

33
34

REFERENCES.............................................................................

35

CHAPTER 1
INTRODUCTION

Fever

Dengue Fever (DF) is an acute epidemic disease caused by a virus that is

transmitted by the Aedes aegypti and Aedes albopictus. Infected sufferers will have
symptoms in the form of low-grade fever up high, accompanied by headache, pain
in the eyes, muscles and joints, to spontaneous bleeding.1
Dengue is a mosquito-borne viral infection. The infection causes flu-like
illness, and occasionally develops into a potentially lethal complication called
severe dengue. The global incidence of dengue has grown dramatically in recent
decades. About half of the world's population is now at risk. Dengue is found in
tropical and sub-tropical climates worldwide, mostly in urban and semi-urban areas.
Severe dengue is a leading cause of serious illness and death among children in
some Asian and Latin American countries.1
Endemic diseases were first recorded and reported in 1953-1954 in the
Philippines. Since then, the spread of DBD quickly occurred to most major
Southeast Asian countries, including Indonesia.1
Dengue fever cases in Indonesia first occurred in Surabaya in 1968. The
disease dengue fever discovered in 200 cities in 27 provinces and the outbreak has
occurred (Unusual) due to dengue fever. In 2014, until mid December noted sufferer
DBD in 34 provinces in Indonesia as many as 71.668 people, and 641 of them died.
The figure is lower than the previous year, i.e. the year 2013 by number of sufferers
as much as 112.511 people and the number of cases of death as much as 872
sufferers.2
The handling of patients spend a long time and cost a relatively large losses.
With standard management, dengue fever patients on average spent time in hospital
inpatient care for 4.2 1.5 days. 3 While the period of ill patients lived an average of
11 days, with the average duration of fever for 6 days. Costs or direct and indirect
losses incurred any inpatient at hospitals around USD 1,394.4
There is no specific treatment for dengue/severe dengue, but early detection
and access to proper medical care lowers fatality rates below 1%. Dengue
prevention and control depends on effective vector control measures.
Dengue is a mosquito-borne viral disease that has rapidly spread in all
regions of WHO in recent years. Dengue virus is transmitted by female mosquitoes

mainly of the species Aedes aegypti and to a lesser extent, A. albopictus. The
disease is widespread throughout the tropics, with local variations in risk influenced
by rainfall, temperature and unplanned rapid urbanization.1
Severe dengue (also known as Dengue Haemorrhagic Fever) was first
recognized in the 1950s during dengue epidemics in the Philippines and Thailand.
Today, severe dengue affects most Asian and Latin American countries and has
become a leading cause of hospitalization and death among children in these
regions.1
There are 4 distinct, but closely related, serotypes of the virus that cause
dengue (DEN-1, DEN-2, DEN-3 and DEN-4). Recovery from infection by one
provides lifelong immunity against that particular serotype. However, crossimmunity to the other serotypes after recovery is only partial and temporary.
Subsequent infections by other serotypes increase the risk of developing severe
dengue.1

CHAPTER II
LITERATURE REVIEW

2.1.

Dengue Fever
2.1.1

Definition

Dengue fever, a benign syndrome caused by several arthropodborne viruses,

is characterized by biphasic fever, myalgia or arthralgia, rash, leukopenia, and
lymphadenopathy. Dengue hemorrhagic fever is a severe, often fatal, febrile disease

caused by dengue viruses. It is characterized by capillary permeability,

abnormalities of hemostasis, and, in severe cases, a protein-losing shock syndrome
(dengue shock syndrome), which is thought to have an immunopathologic basis.5
2.1.2. Epidemiology
Dengue epidemics are known to have occurred regularly over the last three
centuries in tropical, subtropical, and temperate areas around the world. The first
epidemic of dengue was recorded in 1635 in the French West Indies. During the
18th, 19th and early 20th centuries, epidemics of dengue-like diseases were reported
and recorded globally, both in tropical as well as some temperate regions. Rush was
probably describing dengue when he wrote of break-bone fever occurring in
Philadelphia in 1780. Most of the cases during the epidemics of that time mimicked
clinical DF,although some displayed characteristics of the haemorrhagic form of the
disease.
In most Central and South American countries, effective disease prevention
was achieved by eliminating the principal epidemic mosquito vector, Aedes aegypti,
during the 1950s and 1960s. In Asia, however, effective mosquito control was never
achieved. A severe form of haemorrhagic fever, most likely akin to DHF, emerged in
some Asian countries following World War II. From the 1950s through 1970s, this
form of dengue was reported as epidemics periodically in a few Asian countries
such as India, Philippines and Thailand.
1. During the 1980s, incidence increased markedly and distribution of the virus expanded
tothe Pacific islands and tropical America (Halstead, S. C. Nelson Text Book of
Pediatric 19 th edition. 2011. chapter 261: 1147-1149). In the latter region, the species
re-infested most tropical countries in the 1980s on account of disbanding of the Ae.
aegypti eradication programme in the early 1970s. Increased disease transmission and
frequency of epidemics were also the result of circulation of multiple serotypes in Asia.
This brought about the emergence of DHF in the PacificIslands, the Caribbean, and
Central and South America. Thus, in less than 20 years by 1998, the American tropics
and the Pacific Islands went from being free of dengue to having a serious dengue/DHF
problem.

Of the 2.5 billion people around the world living in dengue endemic
countries and at risk of contracting DF/DHF, 1.3 billion live in 10 countries of the
WHO South-East Asia (SEA) Region which are dengue endemic areas. Till 2003,
only eight countries in the Region had reported dengue cases.By 2009, all Member
countries reported dengue outbreaks. Timor-Leste reported an outbreak in 2004 for
the first time. Bhutan also reportedits first dengue outbreak in 2004. Similarly,
Nepal too reported its first indigenous case of dengue in November 2004.
The reported dengue cases and deaths between 1985 and 2009 in 10
countries of the WHO SEA Region underscore the public health importance of this
disease in the Region.6
Dengue fever cases in Indonesia first occurred in Surabaya in 1968. The
disease dengue fever discovered in 200 cities in 27 provinces and the outbreak has
occurred (unusual) due to dengue fever. In 2014, until mid December noted sufferer
DBD in 34 provinces in Indonesia as many as 71.668 people, and 641 of them died.
The figure is lower than the previous year, i.e. the year 2013 by number of sufferers
as much as 112.511 people and the number of cases of death as much as 872
sufferers.2

2.1.3. Etiology and Pathophysiology

DF/DHF is caused by dengue virus which is members of the genus
Flavivirus and family Flaviviridae. These small (50 nm) viruses contain singlestrand RNA as genome. The virion consist of a nucleocapsid with cubic symmetry
enclosed in a lipoprotein envelope. The dengue virus is composed of three structural
protein genes encoding the nucleocapsid or core protein (C), a membrane-associated
protein (M), an envelope protein (E), and seven non-structural protein (NS) genes.6
Lifelong immunity against the infecting serotype (so-called homotypic
immunity) is conferred by virus-neutralizing antibodies. Antibodies induced by one
serotype can cross-react with the other serotypes (heterotypic immunity), but
heterotypic neutralizing titers wane over time. Below a certain threshold and
depending on antibody specificity, antibodies fail to neutralize and instead opsonize;
this helps the virus to infect cells bearing IgG receptors. This phenomenon, termed
antibody-dependent enhancement, increases the number of infected cells and is
thought to lead to higher virus titers and a more pronounced inflammatory
response.7
Antibody-dependent enhancement is linked to the presence of nonneutralizing or subneutralizing levels of dengue virusreactive IgG induced by a
primary infection, or acquired passively in newborns. A large infected cell mass
results in elevated concentrations of acute-phase response proteins, cytokines, and
chemokines; generation of immune complexes; and consumption of complement
and release of split products. The activation, proliferation, and secretion of
cytokines in tissues by memory T lymphocytes recognizing conserved and altered
peptide ligands are postulated to add to the inflammatory milieu during secondary
infections. Collectively, the host immunologic response is thought to create a
physiological environment in tissues that promotes capillary permeability when the
viral burden is in rapid decline. However, the exact mechanisms are unclear.
Interactions between dengue nonstructural protein 1 (NS1) and the surface
glycocalyx layer may result in release of heparan sulfate into the circulation, thereby
altering the filtration characteristics of the layer and resulting in leakage of proteins.
Loss of essential coagulation proteins probably plays a major role in the

development of the typical coagulopathy, which is usually manifested as an increase

in the partial-thromboplastin time accompanied by low fibrinogen levels but with
little evidence of procoagulant activation. Heparan sulfate may also function as an
anticoagulant and contribute to the coagulopathy.8

10

Figure 1. Antibody-Dependent Enhancement of Dengue Infection7

Antibody-dependent enhancement has been thought to contribute to DHF
which, in children and adults, is typically associated with secondary infection with a
heterotypic serotype. Also at risk for enhanced disease are infants who are born to
dengue-immunemothers and who therefore have maternally derived dengueneutralizing IgGs. These IgGs protect for several months, but titers wane and infants
enter a period of increased risk of dengue hemorrhagic fever after primary
infection.7
The hallmark of DHF is the increased vascular permeability resulting in
plasma leakage, contracted intravascular volume, and shock in severe cases. The
leakage is unique in that there is selective leakage of plasma in the pleural and
peritoneal cavities and the period of leakage is short (2448 hours). Rapid recovery
of shock without sequelae and the absence of inflammation in the pleura and
peritoneum indicate functional changes in vascular integrity rather than structural
damage of the endothelium as the underlying mechanism.
Higher levels of viral load in DHF patients in comparison with DF patients
have been demonstrated in many studies. The levels of viral protein, NS1, were also
higher in DHF patients. The degrees of viral load correlate with measurements of
disease severity such as the amount of pleural effusions and thrombocytopenia,
suggesting that viral burden may be a key determinant of disease severity.9

2.1.4

Clinical Manifestation and Physical Examination1

Dengue fever presents in a nonspecific manner and may not be

distinguishable from other viral or bacterial illness. Clinical description of dengue

fever is an acute febrile illness of 2-7 days duration associated 2 or more of the
following:
Fever: acute onset, high and continuous, lasting two to seven days in most cases.

11

Any of the following haemorrhagic manifestations including a positive tourniquet

test (the most common), petechiae, purpura (at venapuncture sites), ecchymosis,
epistaxis, gum bleeding, and hematemesis and/or melena.
Enlargement of the liver (hepatomegaly) is observed at some stage of the illness in
90%98% of children. The frequency varies with time and/or the observer.
Shock, manifested by tachycardia, poor tissue perfusion with weak pulse and
narrowed pulse pressure (20 mmHg or less) or hypotension with the presence of
cold, clammy skin and/or restlessness.7

2.1.5

Laboratory studies

Thrombocytopenia (100.000 cells per mm3 or less).

Haemoconcentration; haematocrit increase of 20% from the baseline of patient or
population of the same age.
The

first

two

clinical

criteria,

plus

thrombocytopenia

and

haemoconcentration or a rising haematocrit, are sufficient to establish a clinical

diagnosis of DHF. The presence of liver enlargement in addition to the first two
clinical criteria is suggestive of DHF before the onset of plasma leakage. The
presence of pleural effusion (chest X-ray or ultrasound) is the most objective
evidence of plasma leakage while hypoalbuminaemia provides supporting evidence.
This is particularly useful for diagnosis of DHF in the following patients:
anaemia.
severe haemorrhage.
where there is no baseline haematocrit.
rise in haematocrit to <20% because of early intravenous therapy.
In cases with shock, a high haematocrit and marked thrombocytopenia support the
diagnosis of DSS. A low ESR (<10 mm/first hour) during shock differentiates DSS
from septic shock.

12

Figure 2. WHO classification of dengue infections and grading of severity of

DHF

2.1.6

Differential Diagnosis
The differential diagnosis of dengue fever includes dengue-like diseases,

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. Colorado tick fever
occurs sporadically among campers and hunters in the western USA; sandfly fever
in the Mediterranean region, the Middle East, southern Russia, and parts of the
Indian subcontinent; and Rift Valley fever in North, East, Central, and South Africa.
Ross River fever is endemic in much of eastern Australia, with epidemic extension
to Fiji. In adults, Ross River fever often produces protracted and crippling arthralgia
involving weight-bearing joints.

13

Because meningococcemia, yellow fever, other viral hemorrhagic fevers,

many rickettsial diseases, and other severe illnesses caused by a variety of agents
may produce a clinical picture similar to dengue hemorrhagic fever, the etiologic
diagnosis should be made only when epidemiologic or serologic evidence suggests
the possibility of a dengue infection.5
Early in the febrile phase, the differential diagnoses include a wide spectrum
of viral, bacterial, and protozoal infections similar to that of DF. Haemorrhagic
manifestations, e.g. positive tourniquet test and leucopenia (5000 cells/mm3)
suggest dengue illness. The presence of thrombocytopenia with concurrent
haemoconcentration differentiates DHF/DSS from other diseases. In patients with
no significant rise in haematocrit as a result of severe bleeding and/or early
intravenous fluid therapy, demonstration of pleural effusion/ascites indicates plasma
leakage. Hypoproteinaemia/albuminaemia supports the presence of plasma leakage.
A normal erythrocyte sedimentation rate (ESR) helps differentiate dengue from
bacterial infection and septic shock. It should be noted that during the period of
shock, the ESR is <10 mm/hour.10

2.1.7 Vector
Environmental management
Environmental management involves planning, organization, execution and
monitoring of activities for the modification and/or manipulation of environmental
factors or their interplay with human beings with a view to prevent or minimize
vector breeding and reduce human-vector-virus contact.
Environmental management methods

Environmental

modification:

This

includes

any

long-lasting

physical

transformation of land, water, and vegetation aimed at reducing vector habitats

without causing unduly adverse effects on the quality of the human environment.
Environmental manipulation: This incorporates planned recurrent activities aimed
at producing temporary changes in vector habitats that involve the management of

14

essential and non-essential containers, and the management or removal of

natural breeding sites.
Changes to human habitation or behaviour: These feature the efforts made to
reduce man-vector-virus contact and/or manipulation of environmental factors or
their interplay with human beings with a view to prevent or minimize vector
breeding and reduce human-vector-virus contact. The control of Ae.aegypti in Cuba
and Panama in the early part of the 20th century was based mainly on environmental
management such measures remain applicable wherever dengue is endemic. In 1982
the World Health Organization defined three kinds of environmental management.

2.1.8. Treatment
Monitoring

of

dengue/DHF

patients

during

the

critical

period

(thrombocytopenia around 100 000 cells/mm3). The critical period of DHF refers to
the period of plasma leakage which starts around the time of defervescence or the
transition from febrile to afebrile phase. Thrombocytopenia is a sensitive indicator
of plasma leakage but may also be observed in patients with DF. A rising
haematocrit of 10% above baseline is an early objective indicator of plasma leakage.
Intravenous fluid therapy should be started in patients with poor oral intake or
further increase in haematocrit and those with warning signs.

The following parameters should be monitored:

General condition, appetite, vomiting, bleeding and other signs and symptoms.
Peripheral perfusion can be performed as frequently as is indicated because it is an
early indicator of shock and is easy and fast to perform.
Vital signs such as temperature, pulse rate, respiratory rate and blood pressure
should be checked at least every 24 hours in non-shock patients and 12 hours in
shock patients.

15

Serial haematocrit should be performed at least every four to six hours in stable
cases and should be more frequent in unstable patients or those with suspected
bleeding. It should be noted that haematocrit should be done before fluid
resuscitation. If this is not possible, then it should be done after the fluid bolus but
not during the infusion of the bolus.
Urine output (amount of urine) should be recorded at least every 8 to 12 hours in
uncomplicated cases and on an hourly basis in patients with profound/prolonged
shock or those with fluid overload. During this period the amount of urine output
should be about 0.5 ml/kg/h (this should be based on the ideal body weight).
Additional laboratory tests
Adult patients and those with obesity or suffering from diabetes mellitus should
have a blood glucose test conducted. Patients with prolonged/profound shock and/or
those with complications should undergo the laboratory investigations. Correction
of the abnormal laboratory results should be done: hypoglycemia, hypocalcemia and
metabolic acidosis that do not respond to fluid resuscitation. Intravenous (IV)
vitamin K1 may be administered during prolonged prothrombin time. It should be
noted that in places where laboratory facilities are not available, calcium gluconate
and vitamin K1 should be given in addition to intravenous therapy. In cases with
profound shock and those not responding to IV fluid resuscitation, acidosis should
be corrected with NaHCO3 if pH is <7.35 and serum bicarbonate is <15 mEq/L.
Intravenous fluid therapy in DHF during the critical period
Indications for IV fluid:
when the patient cannot have adequate oral fluid intake or is vomiting.
when HCT continues to rise 10%20% despite oral rehydration.
impending shock/shock.
The general principles of fluid therapy in DHF include the following:
Isotonic crystalloid solutions should be used throughout the critical period except
in the very young infants <6 months of age in whom 0.45% sodium chloride may be
used.

16

Hyper-oncotic colloid solutions (osmolarity of >300 Osm/l) such as dextran 40 or

starch solutions may be used in patients with massive plasma leakage, and those not
responding to the minimum volume of crystalloid (as recommended below).
Isooncotic colloid solutions such as plasma and hemaccel may not be as effective.
A volume of about maintenance +5% dehydration should be given to maintain a
just adequate intravascular volume and circulation.
The duration of intravenous fluid therapy should not exceed 24 to 48 hours for
those with shock. However, for those patients who do not have shock, the duration
of intravenous fluid therapy may have to be longer but not more than 60 to 72 hours.
This is because the latter group of patients has just entered the plasma leakage
period while shock patients have experienced a longer duration of plasma leakage
before intravenous therapy is begun.
In obese patients, the ideal body weight should be used as a guide to calculate the
fluid volume.

Figure 3. Requirement of fluid based on ideal body weight

Rate of intravenous fluids should be adjusted to the clinical situation. The rate of IV
fluid differs in adults and children. Table 10 shows the comparable/equivalent rates
of IV infusion in children and adults with respect to the maintenance.

17

Figure 4. Rate of IV fluid in adults and children

Warning signs:
- No clinical improvement or worsening of the situation just before or during the
transition to afebrile phase or as the disease progresses
- Persistent vomiting, not drinking
- Severe abdominal pain
- Lethargy and/or restlessness, sudden behavioural changes
- Bleeding: Epistaxis, black stool, haematemesis, excessive menstrual bleeding, dark
coloured urine (haemoglobinuria) or haematuria.
- Giddiness
- Pale, cold, and clammy hands and feet
- Less/no urine output for 4-6 hours

Management of patients with warning signs1

It is important to verify if the warning signs are due to dengue shock
syndrome or other causes such as acute gastroenteritis, vasovagal reflex,
hypoglycemia, etc. The presence of thrombocytopenia with evidence of plasma
leakage such as rising haemotocrit and pleural effusion differentiates DHF/ DSS
from other causes. Blood glucose level and other laboratory tests may be indicated
to find the causes. Management of DHF/DSS is detailed below. For other causes, IV
fluids and supportive and symptomatic treatment should be given while these
patients are under observation in hospital. They can be sent home within 8 to 24
hours if they show rapid recovery and are not in the critical period (i.e. when their
platelet count is >100 000 cells/mm3).
Management of DHF grade I, II (non-shock cases)1

18

In general, the fluid allowance (oral + IV) is about maintenance (for one
day) + 5% deficit (oral and IV fluid together), to be administered over 48 hours. For
example, in a child weighing 20 kg, the deficit of 5% is 50 ml/kg x 20 = 1000 ml.
The maintenance is 1500 ml for one day. Hence, the total of M + 5% is 2500 ml
(Figure 8). This volume is to be administered over 48 hours in nonshock patients.
Management of shock: DHF Grade 31
DSS is hypovolemic shock caused by plasma leakage and characterized by
increased systemic vascular resistance, manifested by narrowed pulse pressure
(systolic pressure is maintained with increased diastolic pressure, e.g. 100/90
mmHg). When hypotension is present, one should suspect that severe bleeding, and
often concealed gastrointestinal bleeding, may have occurred in addition to the
plasma leakage. It should be noted that the fluid resuscitation of DSS is different
from other types of shock such as septic shock. Most cases of DSS will respond to
10 ml/kg in children or 300500 ml in adults over one hour or by bolus, if
necessary. However, before reducing the rate of IV replacement, the clinical
condition, vital signs, urine output and haematocrit levels should be checked to
ensure clinical improvement.
Management of prolonged/profound shock: DHF Grade 41
The initial fluid resuscitation in Grade 4 DHF is more vigorous in order to
quickly restore the blood pressure and laboratory investigations should be done as
soon as possible for ABCS as well as organ involvement. Even mild hypotension
should be treated aggressively. Ten ml/kg of bolus fluid should be given as fast as
possible, ideally within 10 to 15 minutes. When the blood pressure is restored,
further intravenous fluid may be given as in Grade 3. If shock is not reversible after
the first 10 ml/kg, a repeat bolus of 10 ml/kg and laboratory results should be
pursued and corrected as soon as possible. Urgent blood transfusion should be
considered as the next step (after reviewing the preresuscitation HCT) and followed
up by closer monitoring, e.g. continuous bladder catheterization, central venous
catheterization or arterial lines. It should be noted that restoring the blood pressure
is critical for survival and if this cannot be achieved quickly then the prognosis is
extremely grave. Inotropes may be used to support the blood pressure, if volume

19

replacement has been considered to be adequate such as in high central venous

pressure (CVP), or cardiomegaly, or in documented poor cardiac contractility.
Management of severe haemorrhage1
If the source of bleeding is identified, attempts should be made to stop the
bleeding if possible. Severe epistaxis, for example, may be controlled by nasal
packing. Urgent blood transfusion is life-saving and should not be delayed till the
HCT drops to low levels. If blood loss can be quantified, this should be replaced.
However, if this cannot be quantified, aliquots of 10 ml/kg of fresh whole blood or 5
ml/kg of freshly packed red cells should be transfused and response evaluated. The
patient may require one or more aliquot.
In gastrointestinal bleeding, H-2 antagonists and proton pump inhibitors have been
used, but there has been no proper study to show its efficacy.
There is no evidence to support the use of blood components such as platelet
concentrates, fresh frozen plasma or cryoprecipitate. Its use could contribute to fluid
overload.
Recombinant Factor 7 might be helpful in some patients without organ failure, but
it is very expensive and generally not available.
Signs of recovery
Stable pulse, blood pressure and breathing rate.
Normal temperature.
No evidence of external or internal bleeding.
Return of appetite.
No vomiting, no abdominal pain.
Good urinary output.
Stable haematocrit at baseline level.
Convalescent confluent petechiae rash or itching, especially on the extremities.

20

Criteria for discharging patients

Absence of fever for at least 24 hours without the use of anti-fever therapy.
Return of appetite.
Visible clinical improvement.
Satisfactory urine output.
A minimum of 23 days have elapsed after recovery from shock.
No respiratory distress from pleural effusion and no ascites.
Platelet count of more than 50 000/mm3. If not, patients can be recommended to
avoid traumatic activities for at least 12 weeks for platelet count to become normal.
In most uncomplicated cases, platelet rises to normal within 35 days.
Management of complications
The most common complication is fluid overload.
Detection of fluid overload in patients
Early signs and symptoms include puffy eyelids, distended abdomen (ascites),
tachypnoea, mild dyspnoea.
Late signs and symptoms include all of the above, along with moderate to severe
respiratory distress, shortness of breath and wheezing (not due to asthma) which are
also an early sign of interstitial pulmonary oedema and crepitations.
Restlessness/agitation and confusion are signs of hypoxia and impending respiratory
failure.
Management of fluid overload
All hypotonic solutions should be stopped. In the early stage of fluid overload,
switch from crystalloid to colloid solutions as bolus fluids. Dextran 40 is effective
as 10 ml/kg bolus infusions, but the dose is restricted to 30 ml/kg/day because of its
renal effects. Dextran 40 is excreted in the urine and will affect urine osmolarity.
Patients may experience sticky urine because of the hyperoncotic nature of
Dextran 40 molecules (osmolarity about twice that of plasma). Voluven may be

21

effective (osmolarity = 308 mosmole) and the upper limit is 50 ml/kg/day. However,
no studies have been done to prove its effectiveness in cases of DHF/DSS. In the
late stage of fluid overload or those with frank pulmonary oedema, furosemide may
be administered if the patient has stable vital signs. If they are in shock, together
with fluid overload 10 ml/kg/h of colloid (dextran) should be given. When the blood
pressure is stable, usually within 10 to 30 minutes of infusion, administer IV 1
mg/kg/dose of furosemide and continue with dextran infusion until completion.
Intravenous fluid should be reduced to as low as 1 ml/kg/h until discontinuation
when haematocrit decreases to baseline or below (with clinical improvement). The
following points should be noted:
These patients should have a urinary bladder catheter to monitor hourly urine
output.
Furosemide should be administered during dextran infusion because the
hyperoncotic nature of dextran will maintain the intravascular volume while
furosemide depletes in the intravascular compartment.
After administration of furosemide, the vital signs should be monitored every 15
minutes for one hour to note its effects.
If there is no urine output in response to furosemide, check the intravascular
volume status (CVP or lactate). If this is adequate, pre-renal failure is excluded,
implying that the patient is in an acute renal failure state. These patients may require
ventilatory support soon. If the intravascular volume is inadequate or the blood
pressure is unstable, check electrolyte imbalances.
In cases with no response to furosemide (no urine obtained), repeated doses of
furosemide and doubling of the dose are recommended. If oliguric renal failure is
established, renal replacement therapy is to be done as soon as possible. These cases
have poor prognosis.
Pleural and/or abdominal tapping may be indicated and can be life-saving in cases
with severe respiratory distress and failure of the above management. This has to be
done with extreme caution because traumatic bleeding is the most serious
complication and leads to death. Discussions and explanations about the

22

complications and the prognosis with families are mandatory before performing this
procedure.1
2.1.9. Prognosis
The prognosis of dengue fever may be adversely affected by passively
acquired antibody or by prior infection with a closely related virus that predisposes
to development of dengue hemorrhagic fever.5

23

CHAPTER III
CASE REPORT
3.1 Objective
The objective of this paper is to report a case of 9 years old boy with a
diagnosis of Dengue Haemorrhagic Fever.
3.2 Case
MW, a 9 years old boy, with 38 kg of weight and 138 cm of stature, is a
patient of infection unit in Pediatric Department in Central Public Hospital Haji
Adam Malik Medan on August2nd 2015 at 03.00. His chief complaint was fever.
History of disease :
MW, a boy, 9 years old, brought by his parents to the Emergency Room on
Sunday, 2nd August 2015 complaining on fever since 6 days before admitted to the
hospital. It occurred with high temperature suddenly, continuously, and responded
with anti-pyretic drugs. There are no history of seizure and shivering.
Patient also complained about headache since 6 days ago.
Abdominal pain has been experienced by patient 1 day ago, especially at epigastric.
Nausea and vomiting has been experienced for 6 days, frequency 2-3 times a day,
amount 3-4 table spoon each vomiting, contained ingested food. Vomited was also
contained blood for once, two days before admitted to the hospital.
History of pale and nose or gum bleeding were not found. History of black stool
was not found. Red spots found on the chest, abdomen, and arms. Red spots
showed up three days ago. Urination and defecation within normal limit.
History of previous illness :
The patient was referred from RS. Abd. Manan Simatupang Kisaran with the
diagnosis DHF grade III.

History of medication :
Cefotaxime inj. 1gr/12 hour, Ranitidine inj. 1amp/12 hour, Novalgin inj. 1amp/8
hour, Tranexamic acid 1amp/12 hour IM.

24

History of Mothers pregnancy :

Pregnant on the age of 27, aterm pregnancy, 36 weeks. There was no history
of fever, hypertension, diabetic mellitus and consumption of
herbal medicine during the pregnancy.
History of birth :
Spontaneous, attendend by doctor, BW 3000 gram, BL unknown.
Immediately cried after birth and no bluish history was found.
History of feeding :
From birth to 2 months

: Breast milk only

From 2 months to 4 months

: Breast milk only

From 4 months to 6 months

: Breast milk and rice porridge

From 6 months to 1 year 3 months

: Family menu

From 1 year 3 months until now

: Family menu

History of Growth and Development :

Sitting

: 4 months

Crawling : 7 months
Standing : 12 months
Walking : 12 months
History of immunization :
Hepatitis B, Measles, DPT, BCG and Polio vaksin were all complete.
History of Family Disease
There is no relative with thyphoid fever or dengue fever.
Physical Examination:

Present status: Level of consciousness: compos mentis.

Body temperature: 38.8C, BP: 110/70 mmHg, HR: 115 bpm, RR: 28 bpm, Weight:
38 kg, Stature: 138 cm, Weight for Age: 126,6%, Stature for Age: 101,5%, Weight
for Stature: 122,5%
Anemia (-), icteric (-), dyspnea (-), cyanosis (-), edema (-).

25

Localized status:
Head:
Light reflexes (+/+), pupile were isochoric, conjunctiva palpebra inferior pale (-/-)
Ear,nose, and mouth are within normal limit.
Thorax:
Symmetrical fusiformis, Chest retraction (-), ptechiae (+)
Breath sounds are absent in right lower lung.
HR 115x/i, regular, murmur (-)
RR 28x/i, regular, ronchi (-/-)
Abdomen:
Soepel. Peristaltic (+).Liver palpable 2cm below the right costal. Spleen unpalpable.
Shifting dullness (+). Fluid wave (+). Ptechiae (+).
Extremities:
Pulse 115x/i, regular, adequate pressure and volume, warm acrals, CRT < 3, blood
pressure 110/80mmHg, Tourniquet test (+).

Laboratory Findings (August2th, 2015) 04.34

Test
Complete Blood Count
Hemoglobin
Erythrocite
Hematocrit
Leucocyte
Thrombocyte
MCV
MCH
MCHC
RDW
Eosinophil
Basophil
Neutrophil
Lymphocyte
Monocyte

Result

Unit

Referral

14.20
4.74
37.80
8.27
52.0
79.70
30.00
37.60
12.40
0.00
2.70
47.40
41.70
8.20

g%
106/mm3
%
103/mm3
103/mm3
fL
Pg
g%
%
%
%
%
%
%

12,0 14,4
4.40-4.48
37 41
4.5 13,5
150-450
81-95
25-29
29-31
11.6-14.8
1-6
01
37 80
20 40
28

26

Laboratory Findings (August2th, 2015) 21.29

Test
Result
Unit
Complete Blood Count
Hemoglobin
12.50
g%
Erythrocite
4.24
106/mm3
Hematocrit
33.90
%
Leucocyte
8.30
103/mm3
Thrombocyte
93.0
103/mm3
MCV
80.0
fL
MCH
29.50
Pg
MCHC
36.90
g%
RDW
12.40
%
Eosinophil
0.10
%
Basophil
1.00
%
Neutrophil
44.20
%
Lymphocyte
44.10
%
Monocyte
10.60
%
th
Laboratory Findings (August3 , 2015)
Test
Result
Complete Blood Count
Hemoglobin
11.60
Erythrocite
3.99
Hematocrit
32.10
Leucocyte
6.53
Thrombocyte
138.0
MCV
80.50
MCH
29.10
MCHC
36.10
RDW
12.40
Eosinophil
0.30
Basophil
0.600
Neutrophil
39.10
Lymphocyte
45.30
Monocyte
14.70
Liver Function Test
Alkaline Phosphatase (ALP)
AST / SGOT
ALT / SGPT

Referral
12,0 14,4
4.40-4.48
37 41
4.5 13,5
150-450
81-95
25-29
29-31
11.6-14.8
1-6
01
37 80
20 40
28

Unit

Referral

g%
106/mm3
%
103/mm3
103/mm3
fL
Pg
g%
%
%
%
%
%
%

12,0 14,4
4.40-4.48
37 41
4.5 13,5
150-450
81-95
25-29
29-31
11.6-14.8
1-6
01
37 80
20 40
28

75
315
200

Conclusion : Trombositopenia

Working Diagnosis:
DHF grade II + Pleural effusion + Overweight

Management:

U/L
U/L
U/L

< 300
< 38
< 41

27

- Semi fowler position

- IVFD D5%, NaCl 0,45% 7cc/kgBW
- Ranitidine Inj. 20mg/8 hours IV
- Paracetamol 3x500 mg (if necessary)
Diet MII 1890 kkal + 60 gr protein

Planning:
- Complete blood count test per 12 hours
- IgM and IgG anti-dengue test
- Fluid balance per 6 hours
- Abdominal USG
- Urinalysis and fecal analysis
- Septic work up

28

3.3 FOLLOW UP
August, 2nd 2015 (03.30)
S: Fever (+), Dyspnoe (-), Seizure (-)
O: Sens: CM, T: 38.8C, HR: 115 bpm, RR: 28 bpm
Weight: 38 kg, Stature: 138 cm, Weight for Age: 126,6%,
Stature for Age: 101,5%, Weight for Stature: 122,5%
Head : Light reflexes (+/+), pupile were isochoric, conjunctiva palpebra inferior
pale (-/-). Ear, nose, and mouth are within normal limit.
Neck : Lymph node enlargement (-)
Thorax : Simetris fusiformis, retraction (-). Heart rate 115 bpm, regular, murmur
(-), Respiratory rate 28 bpm, regular, ronchi (-/-), Breath sounds are absent in right
lower lung.
Abdomen : Soepel. Peristaltic (+) normal. Liver palpable 2cm below the right costal
arches. Spleen unpalpable. Shifting dullness (+). Fluid wave (+). Ptechiae (+).
Extremities : Pulse 115 bpm, regular, adequate volume and pressure, warm acrals,
CRT < 3, blood pressure 110/80mmHg, Tourniquet test (+).
A: DHF grade II + Pleural effusion + Overweight
P:
-

Semi fowler position

IVFD D5%, NaCl 0,45% 7cc/kgBW
Ranitidine Inj. 20mg/8 hours IV
Paracetamol 3x500 mg

Planning:
-

Complete blood count test per 12 hours

August, 2nd2015 (08.00)

S: Fever (-), Dyspnoe (-), Seizure (-)
O: Sens: CM, T: 36.5C, HR: 100 bpm, RR: 24 bpm
Weight: 38 kg, Stature: 138 cm, Weight for Age: 126,6%,

29

Stature for Age: 101,5%, Weight for Stature: 122,5%

Head : Light reflexes (+/+), pupile were isochoric, conjunctiva palpebra inferior
pale (-/-). Ear, nose, and mouth are within normal limit.
Neck : Lymph node enlargement (-)
Thorax : Simetris fusiformis, retraction (-). Heart rate 100 bpm, regular, murmur
(-), Respiratory rate 26 bpm, regular, ronchi (-/-), Breath sounds are absent in right
lower lung.
Abdomen : Soepel. Peristaltic (+) normal. Liver palpable 2cm below the right costal
arches. Spleen unpalpable. Shifting dullness (+). Fluid wave (+). Ptechiae (+).
Extremities : Pulse 100 bpm, regular, adequate volume and pressure, warm acrals,
CRT < 3, blood pressure 100/80mmHg, Tourniquet test (+).
A: DHF grade II + Pleural effusion + Overweight
P:

- Semi fowler position

- IVFD D5%, NaCl 0,45% 7cc/kgBW
- Ranitidine Inj. 20mg/8 hours IV
- Paracetamol 3x500 mg (if necessary)
Diet MII 1890 kkal + 60 gr protein
Planning:
-

Complete blood count test per 12 hours

IgM and IgG anti dengue test
Fluid balance per 6 hours
Abdominal USG
Urinalysis and fecal analysis
Septic work up

August, 3rd2015
S: Fever (-), Dyspnoe (-), Seizure (-)
O: Sens: CM, T: 36.8C, HR: 102 bpm, RR: 24 bpm
Weight: 38 kg, Stature: 138 cm, Weight for Age : 126,6%, Stature for Age : 101,5%,
Weight for Stature : 122,5%
Head : Light reflexes (+/+), pupile were isochoric, conjunctiva palpebra inferior
pale (-/-). Ear, nose, and mouth are within normal limit.
Neck : Lymph node enlargement (-)

30

Thorax :Simetris fusiformis, retraction (-). Heart rate 102 bpm, regular, murmur (-),
Respiratory rate 24 bpm, regular, ronchi (-/-), Breath sounds are absent in right
lower lung.
Abdomen : Soepel. Peristaltic (+) normal. Liver palpable 2cm below the right costal
arches. Spleen unpalpable. Shifting dullness (+). Fluid wave (+). Ptechiae (+).
Extremities : Pulse 102 bpm, regular, adequate volume and pressure, warm acrals,
CRT < 3, blood pressure 100/70mmHg, Tourniquet test (+).
A: DHF grade II + Pleural effusion + Overweight
P:

- Semi fowler position

- IVFD D5%, NaCl 0,45% 3cc/kgBW
- Ranitidine Inj. 20mg/8 hours IV
- Paracetamol 3x500 mg (if necessary)
Diet MII 1890 kkal + 60 gr protein
Planning:
-

Fluid balance per 6 hours

Observation hemodynamic status
Complete blood count test per 12 hours
Abdominal USG

August, 4th2015
S:

Fever (-), Dyspnoe (-), Seizure (-)

O:

Sens: CM, T: 37C, HR: 112 bpm, RR: 24 bpm

Weight: 38 kg, Stature: 138 cm, Weight for Age : 126,6%,
Stature for Age : 101,5%, Weight for Stature : 122,5%
Head : Light reflexes (+/+), pupile were isochoric, conjunctiva palpebra inferior
pale (-/-). Ear, nose, and mouth are within normal limit.
Neck : Lymph node enlargement (-)
Thorax : Simetris fusiformis, retraction (-). Heart rate 112 bpm, regular, murmur
(-), Respiratory rate 24 bpm, regular, ronchi (-/-)
Abdomen : Soepel. Peristaltic (+) normal. Liver palpable 1cm below the right
costal arches. Spleen unpalpable. Shifting dullness (+). Fluid wave (+). Ptechiae
(+).

31

Extremities : Pulse 112 bpm, regular, adequate volume and pressure, warm acrals,
CRT < 3, blood pressure 100/80mmHg, Tourniquet test (+).
A: DHF grade II + Pleural effusion + Overweight
P:

- Semi fowler position

- IVFD D5%, NaCl 0,45% 3cc/kgBW
- Ranitidine Inj. 20mg/8 hours IV
- Paracetamol 3x500 mg (if necessary)
Diet MII 1890 kkal + 60 gr protein
Planning:
-

Fluid balance per 6 hours

Observation hemodynamic status
Complete peripheral blood test per 12 hours

August, 5th2015
S: Fever (-), Dyspnoe (-), Seizure (-)
O: Sens: CM, T: 36C, HR: 96 bpm, RR: 20 bpm
Weight: 38 kg, Stature: 138 cm, Weight for Age: 126,6%,
Stature for Age: 101,5%, Weight for Stature: 122,5%
Head : Light reflexes (+/+), pupile were isochoric, conjunctiva palpebra inferior
pale (-/-). Ear, nose, and mouth are within normal limit.
Neck : Lymph node enlargement (-)
Thorax : Simetris fusiformis, retraction (-). Heart rate 96 bpm, regular,

murmur

(-), Respiratory rate 20 bpm, regular, ronchi (-/-)

Abdomen : Soepel. Peristaltic (+) normal. Liver palpable 1cm below the right costal
arches. Spleen unpalpable. Shifting dullness (+). Fluid wave (+). Ptechiae (+).
Extremities : Pulse 96 bpm, regular, adequate volume and pressure, warm acrals,
CRT < 3, blood pressure 110/80mmHg, Tourniquet test (+).
A: DHF grade II + Pleural effusion + Overweight
P:
-

Semi fowler position

32

- IVFD D5%, NaCl 0,45% 3cc/kgBW

- Ranitidine Inj. 20mg/8 hours IV
Diet MII 1890 kkal + 60 gr protein
Planning:
-

CHAPTER IV
DISCUSSION AND SUMMARY
4.1.

Discussion
This case reporting a 9 year 4 months old boy brought to emergency departement of

Haji Adam Malik General Hospital due to fever for 6 days with high temperature. There is
history of vomited blood. There is no history of maternal illness, the baby was born aterm
via normal delivery with no abnormalities. Vital sign is within normal range, except the
temperature. Physical examination revealed petechiae and hepatomegaly. Breath sounds
are absent in right lower lung via thorax auscultation. Laboratory examination showed a
slight anemia with thrombocytopenia.
Clinical description of dengue fever is an acute febrile illness of 2-7 days duration
associated 2 or more of the following:
Fever: acute onset, high and continuous, lasting two to seven days in most cases.
Any of the following haemorrhagic manifestations including a positive tourniquet testg
(the most common), petechiae, purpura (at venepuncture sites), ecchymosis, epistaxis, gum
bleeding, and haematemesis and/or melena.

33

Enlargement of the liver (hepatomegaly) is observed at some stage of the illness in 90%
98% of children. The frequency varies with time and/or the observer.
Shock, manifested by tachycardia, poor tissue perfusion with weak pulse and narrowed
pulse pressure (20 mmHg or less) or hypotension with the presence of cold, clammy skin
and/or restlessness.7

4.2.

Summary
MW, a 9 years 4 months old boy with weight of 38 kg and stature of 138 cm, is a

new patient of Infection Unit in Pediatric Department of Haji Adam Malik General
Hospital on 2ndAugust 2015. His main complaint was fever with history of vomiting
contained blood. Based on the anamnesis, physical examination, and laboratory findings,
patient has been diagnosed with Dengue Hemorrhagic Fever grade II.

34

REFERENCES

World Health Organization, 2015. Comprehensive Guidelines For Prevention and Control Of
Dengue
and
Dengue
HemorrhagicFever.
Available
from
:http://www.who.int/mediacentre/factsheets/fs117/en/&ei=k0E22PxL&lc=idID&s=1&m=16
5&ts=1440464943&sig=APONPFmpVBNzkBkYEwYFMIjC2pJ1zDjBQ

Demam Berdarah Biasanya Mulai Meningkat di Januari, 2015. Kementrian Kesehatan Republik
Indonesia. Available from :http://www.depkes.go.id/article/view/15011700003/demamberdarah-biasanya-mulai meningkat-di-januari.html).

Tai DY, Chee YC, Chan KW. The natural history of dengue illness based on a study of hospitalised
patients in Singapore. Singapore Medical Journal. 1999;40:238242.

Siregar, F.A., 2004. Epidemiologi dan Pemberantasan Demam Berdarah Dengue di Indonesia.
Digitized by USU Digital Library.

Halstead, S. C. Nelson Text Book of Pediatric 19 th edition. 2011. chapter 261: 1147-1149.

World Health Organization. Comprehensive guidelines for prevention and control of dengue and
dengue hemorragic fever. Revised and expanded edition. New Delhi: WHO, Regional Office
for South East Asia; 2011

Schmidt, A. C. Response to Dengue Fever The Good, The Bad and The Ugly ?N Engl J Med
2010, Vol 363(5):484-487.

Simmons, C. P. et al. Dengue. N Engl J Med 2012, Vol 366:1423-1432

Libraty DH, Endy TP, Houng HS. et al. Differing influences of virus burden and immune activation
on disease severity in secondary dengue-3 virus infections. Journal of Infectious Diseases.
2002 May 1; 185(9): 121321.

10

Srikiatkhachorn A., 2009.Plasma leakage in dengue haemorrhagicfever.Thromb Haemost.

102(6):10429.)

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Holiday M.A., Segar W.E. Maintenance need for water in parenteral fluid therapy. Pediatrics 1957;
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