1

CHAPTER 1
BACKGROUND

1.1 Background
Dengue virus infection is an acute fever caused by a virus of the genus
flavivirus, family Flaviviridae which has four serotypes are DEN-1, DEN-2,
DEN-3, and DEN-4, through the intermediary by Aedes aegypti or Aedes
albopictus. Fourth dengue serotypes are in Indonesia. DEN-3 is the
predominant serotype and is associated with severe cases, followed by DEN-2.1
At this time, the number of dengue cases is still high at around 10-25 per
100.000 population. The age at which most children affected by dengue are
aged 4-10 years. The death rate due to dengue fever from 2001 to 2007 is 1299
people.2 In Indonesia reported as many as 121.334 cases of dengue fever with a
mortality rate of 898 cases.3 The clinical spectrum of dengue can be divided
into silent dengue infection, dengue fever, dengue hemorrhagic fever and
dengue shock syndrome.1
1.2

Objective
This paper is one of the requirements to fullfil in the senior clinical

assistance programs in Pediatric Department of Haji Adam Malik General

Hospital, University of Sumatera Utara. In addition, this paper can be used as
reference to know and understanding a little about dengue infection.

CHAPTER 2
LITERATURE REVIEW
2.1.

Dengue Virus Infection

2.1.1

Definition

Dengue Virus Infection is a disease that caused by mosquitos bite, such

as Aedes Aegypty and Aedes Albopictus.1
Dengue hemorrhagic fever (Philippine, Thai, or Singapore hemorrhagic
fever; hemorrhagic dengue; acute infectious thrombocytopenic purpura) is an
acute and severe, often fatal, febrile disease caused by the dengue viruses, a group of
four antigenically related flaviviruses designated serotypes 1 through 4. 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.

2.1.2

Epidemiology
Dengue disease is endemic disease in many countries such as Indonesia,

Myamar, Thailand, Timor Leste, and others. In Indonesia, dengue disease is a

contagious disease and a frequent cause of outbreaks. This disease is second rank
disease of the top ten diseases that hospitalized patients in Indonesia in 2009.
Based on the data, the cases of dengue hemorrhagic fever as much as 121.334
with the death as many as 898 cases.3,4 Still high number of deaths due to dengue
fever can not be separated from risk factor of dengue shock syndrome. Based on
the results of research conducted Subahagio (2009) that 17% of patients with
dengue fever will develop into dengue shock syndrome.5 Meanwhile, according to
research conducted by Anders, et al., that children aged 6 to 10 years are at risk of
developing into dengue shock syndrome and girls are more likely to suffer from
dengue shock syndrome than boys.6

2.1.3 Etiology
Dengue fever is the cause of dengue virus has four serotypes (dengue-1,
dengue-2, dengue-3, dengue-4), which included in the Arbovirus group, genus
Flavivirus, family Flaviviridae. Arbovirus is a virus that is transmitted by
arthropods such as mosquitoes.1 Dengue virus entered to the human body through
the bite of aedes aegypti. In general, these mosquitoes bite during the day (9:00 to
10:00 pm) and afternoon (16:00 to 17:00). Aedes aegypty lives in tropical to
subtropical lowland. Adult mosquitoes are medium-sized, dark brown body, and
the body and legs are covered with scales and silvery white stripes.
Aedes aegypty likes the cool house, damp, dark, and alighted on clothing or
belongings hanging. A place to live in clear stagnant water such as a bath tub and
water reservoirs. Aedes aegypti mosquito lifespan of about 2 to 3 weeks, laying
about 200 to 400 grains, and flew a distance of about 100 meters.7
Aedes aegypti is a small, dark mosquito with white lyre shaped markings
and banded legs. They prefer to bite indoors and primarily bite humans. These
mosquitoes can use natural locations or habitats (for example treeholes and plant
axils) and artificial containers with water to lay their eggs. They lay eggs during
the day in water containing organic material (e.g., decaying leaves, algae, etc.) in
containers with wide openings and prefer dark-colored containers located in the
shade. About three days after feeding on blood, the mosquito lays her eggs inside
a container just above the water line. Eggs are laid over a period of several days,
are resistant to desiccation and can survive for periods of six or more months.
When rain floods the eggs with water, the larvae hatch. Generally larvae feed
upon small aquatic organisms, algae and particles of plant and animal material in
water-filled containers. The entire immature or aquatic cycle (i.e., from egg to
adult) can occur in as little as 7-8 days. The life span for adult mosquitoes is
around three weeks. Egg production sites are within or in close proximity to
households.
Aedes albopictus (Skuse), also called the Asian tiger mosquito, is a
vector for a series of human arboviruses among which flaviviruses (dengue virus,

yellow fever virus, Japanese encephalitis virus, and West Nile virus) and
togaviruses (Ross River virus and Chikungunya virus). The species is known to be
an important vector of dengue, second only to Aedes aegypti, and is suspected to
be the only important vector of the Chikungunya outbreak on the Indian Islands
outbreak in 2006. The Asian tiger mosquito is a highly invasive mosquito species
and is difficult to control. It is an aggressive day biting mosquito whose bites can
cause dermatological and allergic reactions. It is considered a container breeder,
preferring to oviposit in small quantities of water such as drums, tyres, buckets,
flower saucers, tarpaulins, and manholes.
2.1.4

Classification
According to the WHO in 2011 that the dengue virus infections are

classified

as

follows:

Picture 1. Classification of Dengue Infection

2.1.5

Pathogenesis
Pathogenesis of dengue hemorrhagic fever is still debated. Based on

available data, there is strong evidence that the mechanism of imunopatologis role
occurrence of dengue hemorrhagic fever and dengue shock syndrome.
The immune response that is known to play a role in the pathogenesis of dengue
are:
a)

Humoral response in the form of antibodies that play a role in virus

neutralization process. Antibodies to dengue virus play a role in virus replication

accelerates in monocytes or macrophages. This hypothesis is called antibody
dependent enhancement.
b)
T lymphocytes both T-helper (CD4) and T cytotoxic (CD8) plays a role in
cellular immune response against dengue virus. TH1 differentiation of T helper
that will produce interferon gamma, IL-2 and lymphokine, while Th2 produces
IL-4, IL-5, IL-6 and IL-10;
c)
Monocytes and makrolag role in phagocytosis by opsonization virus
antibodies. However, this causes increased phagocytosis process of viral
replication and secretion of cytokines by macrophages;
d)
In addition, The activation of complement by immune complexes led to
the formation of C3a and C5a.
Halstead in 1973 filed a secondary heterologous infection hypothesis
which states that dengue fever occurs when a person is infected with the dengue
virus with different types. Re-infection causes anamnestic antibody reaction
resulting

in

high

concentrations

of

immune

complexes.

Less and Ennis in 1994 summarizes the opinion Halstead and other researchers;
states that dengue virus infection causes macrophage activation phagocyte virusantibody complex non neutralization so that the virus replicate in macrophages.
Macrophage infection by dengue virus causes the activation of T helper and
cytotoxic T thus produced lymphokines and interferon-gamma. Interferon gamma
activates monocyte thus secreted a variety of inflammatory mediators such as

TNF-, IL-1, PAF (platelet activating factor), IL-6 and histamine that causes
dysfunction of endothelial cells and plasma leakage. Increased C3a and C5a
occurs through activation of the virus-antibody complex that also resulted in the
leakage of plasma. Thrombocytopenia in dengue infections occur through the
mechanism of bone marrow suppression and destruction and shortening the life
span of platelets.8

Picture 2. Pathogenesis of DHF

2.1.6. The Course of Disease

The course of disease in dengue hemorrhagic fever is divided into 3
phases. There are three phases of dengue hemorrhage fever such as:
1. Fever Phase
Phase fever lasts 2 to 7 days with a body temperature of about 39 C to 40
C. In the acute febrile phase usually accompanied by redness of the face,
erythema of the skin, pain in the whole body, and headache. Some patients

also complain of difficulty swallowing, pharyngeal pain, conjunctival pain,

loss of appetite, nausea, and vomiting. During the initial phase of fever is
difficult to distinguish between dengue fever and dengue hemorrhagic
fever. On dengue fever, once free of fever for 24 hours without fever,
patients will enter a period of healing. However, in patients with
hemorrhagic fever, after the febrile phase is completed it will go into a
critical phase.2
2. Critical Phase
Body temperature in the critical phase decreased by about 37.5 or down
below. This phase generally occurs in the third to fifth day of fever. In the
critical phase of increased capillary permeability causing leakage of
plasma. Critical phase lasts for 24 to 48 hours. If there is no leakage of
plasma, the patient's condition will improve but if there is leakage of
plasma, the patient's condition will deteriorate. Conditions of prolonged
plasma leakage and delays will cause shock.2
3. Recovery Phase
Patients who have passed the critical phase, there will be a process of reabsorption of fluids within 2 to 3 days and gradually the patient's condition
will improve. Healing phase lasts between 2 to 7 days. Generally dengue
fever patients who have successfully passed the critical phase will recover
without complications within 24 to 48 hours after the shock. The healing
phase is characterized by the condition of the patient began to improve,
appetite begins to increase, and vital signs were stable. In this phase of
intravenous fluids is usually discontinued, replaced with nutrition orally.2

Picture 3. Phase of DHF

2.1.7

Diagnosis
a. Dengue fever1
Is an acute febrile illness for 2-7 days, characterized by two or more of
the following clinical manifestations:
Headache.
Pain retro-oebital.
Myalgia / arthralgia.
Skin rash.
Bleeding manifestations (petechiae or positive bending test).
Torniquet test (+).

b. Dengue Hemorrhagic Fever1

Based on the 1997 WHO criteria for DHF diagnosis is made when all of
these things below filled :
Fever lasts 2-7 days, occasionally biphasic
Hemorrhagic tendencies
thrombocytopenia (<100,000 / mm3)
Evidence of plasma leakage, manifested
by: - Rise in hematocrit> 20%
- Drop in hematocrit following volume replacement
- Signs of plasma leakage

Picture 4. Grade of DHF

c. Dengue Shock Syndrome1

All four criteria of DHF must be present

Evidence of circulatory failure

Manifested by :
- Rapid and weak pulse
- Narrow pulse pressure (< 20 mmHg) or
- Hypotension for age, and
- Cold, clammy skin and restlessness

10

Picture 5. Diagnosis of DHF

2.1.8

Differential Diagnosis
- Measles
- ITP
- Chikungunya
- Scarlet Fever

2.1.9

Management

11

Picture 6. Management of Suspected Dengue Infection

12

Picture 7. Management of Suspected Dengue Fever (Inpatient) or Dengue

Fever

13

Picture 8. Management of DHF grade I and II.

14

Picture 9. Management of DHF grade III and IV.

15

CHAPTER III
CASE REPORT
3.1 Objective
The objective of this paper is to report a case of a 16 years old and 2
months old girl with a diagnosis of Dengue Hemorrhagic Fever.
3.2 Case
A 16 years and 2 months years old boy admitted to emergency room in
Haji Adam Malik General Hospital Medan on 26 th January 2016 at 12.40 p.m with
the main complain of fever since several days ago.
3.3 History of Disease
Patients present with fever experienced approximately 2 days before
entering Adam Malik hospital. Fever with high temperature and goes down with
the consumption of fever medicine. The patient also complain about headache and
vomiting for the last 3 days. History of spontaneous bleeding was not found.
History of nausea and vomiting was found since three days ago. Headache
encountered since 2 days ago. Abdominal pain and joint pain was found. Coughs
and colds was not found. Black colour stool was found. Urination was within
normal range. History of traveling out of town and to the malaria endemic area
was denied.

History of medication: History of family: Family history of the same disease was found.
History of parents medication: Unclear

Physical Examination:

16

Present Status:

Level of consciousness: Compos mentis. Body

temperature: 37,9 C, BW: 35 kg, BH: 160 cm. anemic (-/-), ikteric (-/-),
dyspnea (-), cyanosis(-), edema (-).

Eye
: light reflex +/+, isochoric pupil, conjunctiva palpebra
inferior pale (-/-)
Ear : within normal range
Nose : within normal range
Mouth
: within normal range

Localized Status
- Head: Eye: eye light reflect +/+, conjunctiva palpebral inferior pale -/-,
Ear/Nose/Mouth: within normal range.
- Neck:
Jugular Vein Pressure: R+2 cm H2o
- Thorax:
Symetrical fusiformis, Retractions (-), RR: 20x/i/regular,
respiratory sound: vesicular, additional sound (-), HR: 90 x/i,
regular, murmur (-).
- Abdomen:
Soepel, Peristaltic (+) N, Hepar and Lien: unpalpable, Epigastric
pain (+).
- Extremities:
Petechial rash is found on the lower of left arm, pulse: 90x/i,
regular, weak, cold acral, CRT < 3, edema pretibial (-), blood
pressure: 110/80 mmHg.

Laboratory Findings:
26rd Jan 2015
Complete Blood Count:
Test

Result

Unit

Referal

17

Hemoglobin

15.20

g%

13.2-17.3

Erythrocyte

5.13

106/mm3

4.20-4.87

Leucocyte

2.19

103/mm3

4.5-11.0

Thrombocyte

113

103/mm3

150-450

Hematocrite

42,80

43-49

Eosinophil

0.00

1-6

Basophil

0.200

0-1

Neutrophil

66.00

37-80

Lymphocyte

21.70

20-40

Monocyte

12.10

2-8

Neutrophil

3.98

103/L

2.7-6.5

absolute
Lymphocyte

1.31

103/L

1.5-3.7

absolute
Monocyte absolute

0.73

103/L

0.2-0.4

Basophyl absolute

0.01

103/L

0-0.1

MCV

71.50

fL

85-95

MCH

25.50

Pg

28-32

MCHC

35.70

g%

33-35

Blood Glucose

93.00

mg/dL

<200

Sodium

129

mEq/L

135-155

Kalium

5.0

mEq/L

3.6-5.5

Chloride

101

mEq/L

96-106

Diagnosis: Dengue hemorrhagic fever without shock

Therapy:
-

IVFD D5% NaCl 0.45% 40 drops/minute macro

Inj. Paracetamol 500mg/IV
MB Diet 2000kkal + 90gr protein

18

Prognosa:
Dubia ad bonam

Follow Up:
26th Jan 2016
S
Fever (+)

07.00
O

P
IVFD

D5%

Mentis , T: 37,8 oC, BW: 45

NaCl

0.45%

kg, BH: 160 cm.

120 drops/min

Sensorium:

Head:

Eye

Isochoric

A
Compos DHF

Reflect
Pupil,

+/+,
Conj.

micro
-

Inj.

19

Palpebral Inferior Pale -/-,

paracetamol

Mouth/Nose/Ear: Normal.

500

Neck: JVP R+2 H2O

hours/

Thorax:

intravenous.

Symetris

Fusiformis, Retraction (-)

HR: 86x/i, Systolic Murmur

-

Abdomen: Soepel, Normal

Hepar

unpalpable,

Lien:

Check for IgG

anti dengue

(-), RR: 24x/i, Ronchi -/-.

peristaltic,

mg/

Complete
Blood test

unpalpable, Epigastric Pain

(+).
Extremities: Pulse: 86x/i,
Regular,

Weak,

Warm

Acral, CRT < 3, Edema

Pretibial (-), BP : 110/70
mmHg.
Rumple leed Test (+)

Follow Up:
26th Jan 2016
S
Fever (+)

17.00
O
Sensorium:

A
Compos DHF

P
- IVFD D5% NaCl

Mentis , T: 37,8 oC, BW: 45

0.45%

kg, BH: 160 cm.

drops/min micro

Head: Eye Reflect +/+,

Isochoric

Pupil,

Conj.

Palpebral Inferior Pale -/-,

Mouth/Nose/Ear: Normal.

- Inj.

120
paracetamol

500 mg/ 8 hours/

intravenous.
- Check for IgG anti

20

Neck: JVP R+2 H2O

Thorax:

dengue

Symetris

- Complete

Fusiformis, Retraction (-)

HR:

90x/i,

Murmur(-),

blood

test

Systolic

RR:

22x/i,

Ronchi -/-.
Abdomen: Soepel, Normal
peristaltic,

Hepar

unpalpable,

Lien:

unpalpable, Epigastric Pain

(+).
Extremities: Pulse: 90x/i,
Regular, Adequate, Warm
acral, CRT < 3, Edema
Pretibial (-), BP : 110/70
mmHg.
Rumple leed Test (+)

Follow Up:
27th Jan 2016
S
Fever (+)

06.00
O
Sensorium: Alert, T: 39.1 oC, DHF
BW: 45 kg, BH: 160 cm.
Head:

Eye

isochoric

Reflect
pupil,

P
- IVFD
NaCl

+/+,
Conj.

Palpebral Inferior Pale -/-,

D5%
0.45%

120 drops/min
micro
- Inj.

Nouth/nose/Ear: Normal.

paracetamol

Neck: JVP R+2 H2O

500

Thorax: Symetris Fusiformis,

hours/

mg/

21

Retraction (-) HR: 110x/i,

intravenous.

Systolic Murmur (-), RR:

24x/i, Ronchi -/-.
Abdomen: Soepel, Normal
Peristaltic, Hepar unpalpable,
Lien: unpalpable. Epigastric
pain (-).
Extremities:
regular,

Pulse: 110x/i,

Adequate, Warm

Acral, CRT < 3, Edema

Pretibial (-), BP : 110/60
mmHg.
Rumple leed Test (+)
IgM : IgG : +

Follow Up:
28th Jan 2016
S
Fever (-)

16.30
O
Sensorium: CM, T: 37,2 oC, DHF
BW: 45 kg, BH: 160 cm.
Head:

Eye

Isochoric

Reflect
Pupil,

P
- IVFD
NaCl

+/+,
Conj.

Palpebral Inferior Pale -/-,

D5%
0.45%

120 drops/min
micro
- Inj.

Mouth/Nose/Ear: Normal.

paracetamol

Neck: JVP R+2 H2O

500

Thorax: Symetris Fusiformis,

hours/

Retraction (-) HR: 96x/i,

intravenous.

mg/

22

Systolic Murmur (-), RR:

- Murolax supp

28x/i, Ronchi -/-.

Abdomen: Soepel, Normal
Peristaltic, Hepar unpalpable,
Lien: unpalpable. Epigastric
pain (-).
Extremities:
regular,

Pulse: 118x/i,

Adequate, Warm

Acral, CRT < 3, Edema

Pretibial (-), BP : 110/70
mmHg.

CHAPTER IV
DISCUSSION

Case

Theory

23

A 16 years and 2 months years old boy - According to research that children
admitted to emergency room in Haji aged 6 to 10 years are at risk of
Adam Malik General Hospital Medan on developing into dengue hemorrhagic
26th January 2016 at 12.40 p.m with the fever and girls are more likely to suffer
main complain of fever since several from dengue hemorrhagic fever than
days ago and was diagnosed with boys.
Dengeu hemorrhagic fever..

Patients has a history of fever, nausea

and vomiting, headache, abdominal and
joint pain, black colour stool,

and

petechie rash.

The clinical manifestation of DHF are:

Fever lasts 2-7 days with 2 of the
following such as headache, retroorbital
pain, myalgia, athralgia, and rash.
Hemorrhagic manifestation.

Laboratory criteria of DHF are :

Based on laboratory result, trombosit was Thrombocytopenia (<100,000 / mm3)
Evidence of plasma leakage,
113.000/mm3
manifested by :
- Rise in hematocrit> 20%
- Drop in hematocrit following
volume replacement
- Signs of plasma leakage
Patient

was

classified

into

dengue - DHF is classified into grade I, II, III

hemorrhagic fever as manifested :

-

Rumple leed test +

and IV. DHF is diagnosed with the help

of rumple leed test

Patient was treated with :

-

IVFD D5% NaCl 0.45% 120

drops/min micro

Inj. paracetamol 500 mg/ 8 hours/

The management of dengue

hemorrhagic fever grade I is :
IVFD D5% NaCl 0,45% 6-7
ml/kgbw/hour within 3-4 hours,

24

intravenous.

and then evaluation. (if the vital

Monitoring for shock sign

sign still abnormally, higher the

fluid to 10-15 ml/kgbw/hour. If
the vital sign turn normally,
lower the fluid to 5 to 3
ml/kgbw/hour and then weve to
evalution again). In this case the
patient also diagnose with mildmoderate gastroenteritis, so we
give this patient initial therapy
with IVFD D5% NaCl 0,45%
120gtt/min micro

CHAPTER V
SUMMARY
A 16 years and 2 months years old boy admitted to emergency room in
Haji Adam Malik General Hospital Medan on 26 th January 2016 at 12.40 p.m with
the main complain of fever since several days ago.
Patients present with fever experienced approximately 2 days before
entering Adam Malik hospital. Fever with high temperature and goes down with

25

the consumption of fever medicine. The patient also complain about headache and
vomiting for the last 3 days. History of spontaneous bleeding was not found.
History of nausea and vomiting was found since three days ago. Headache
encountered since 2 days ago. Abdominal pain and joint pain was found. Coughs
and colds was not found. Black colour stool was found. Urination was within
normal range. History of traveling out of town and to the malaria endemic area
was denied.
Patients was treated with IVFD D5% NaCl0,45% 120gtt/min(mikro) for
rehydration and was give paracetamol 500mg/8hours/oral for the fever.

REFERENCES

1. Antonius H, Eva Devita, Setio H, Ellen P. 2009. Pedoman Pelayanan Klinis

IDAI : Infeksi Virus Dengue. Ikatan Dokter Anak Indonesia.

26

2. WHO. 2009. Dengue guidelines for diagnosis, treatment, prevention, and

control. World Health Organization.
3. Depkes RI. 2009. Profil Kesehatan Indonesia 2009. Diunduh :
www.depkes.go.id.
4. Depkes RI. 2005. Pencegahan dan Pemberantasan Demam Berdarah di
Indonesia. Jakarta : Direktorat Jenderal Pengendalian Penyakit dan Kesehatan
Lingkungan.
5. Subahagio. 2009. Menentukan Faktor Resiko Dominan Kejadian Dengue Syok
Sindrome pada Penderita DBD. Diunduh : digilib.bmf.litbang.depkes.go.id.
6. Anders, K.L, et al. 2011. Epidemiological factor associated with dengue shock
syndrome and mortality in hospitalized dengue patients.
AM.J.Trop.Med.Hyg,84(1).127-134.
7. Saleha Sungkar. 2011. Buku Ajar Parasitologi Kedokteran. Jakarta : FKUI.
8. Wichman, O, et al., 2012. Pathogenesis of Dengue Hemmorhagic Fever. J.
Tropical Medicine and International Health. 102-108.