Case Report

DENGUE HEMORRHAGIC FEVER

COMPILED BY:

KARTHIKA RAJASEGARAN 120100469

SUPERVISOR:
dr. Nelly Rosdiana,M Ked (PED), SpA (K)

PEDIATRIC DEPARTMENT
FACULTY OF MEDICINE
UNIVERSITY OF NORTH SUMATERA
HAJI ADAM MALIK GENERAL HOSPITAL
MEDAN
2016
CHECKED ON :

RESULTS :

Supervisor

(dr.Nelly Rosdiana, M Ked (PED), SpA (K))

 ACKNOWLEDGEMENTS

We greatly indebt to the Almighty One for giving us blessing to complete this
case report tittle DENGUE HEMORRHAGIC FEVER. This case report is a
requirement to complete our clinical assesment programe in Pediatric Department
in Haji Adam Malik General Hospital of Medical Faculty in University of North
Sumatera.
We also indebt to honour our beloved supervisor dr.Nelly Rosdiana,M
Ked(Ped),SpA (K) for spending much time and to give us guidance,feedback and
suggestions. We are grateful because without her,this case report wouldnt have
taken its present shape.
This case report has gone through series of developments and
corrections.There were critical but constructive and relevant suggestions from the
reviewers.Hopefully the content will be useful for everyone in future.

Medan, June 2016

Writter
 CONTENT

ACKNOWLEDGMENT........................................................................................ i
CONTENT.. ii
CHAPTER 1 INTRODUCTION. 1
CHAPTER 2 LITERATURE REVIEW. 3
CHAPTER 3 CASE REPORT 14
CASE REPORT 4 DISCUSSION... 27
CASE REPORT 5 SUMMARY.. 31
REFERENCES 32
 1

CHAPTER I
INTRODUCTION

1.1 Background
Dengue virus infection is endemic in some tropical and subtropical regions,
and more than 100 countries in Africa, America, the Mediterranean, South Asia,
and West pacific. About 2.5 million residents in the area had been infected with
dengue virus. According to the World Health Organization there are
approximately 50-100 million cases of dengue virus infection each year, with
250000-500000 dengue hemorrhagic fever (DHF) and 24,000 of them died.1 In
Indonesia, dengue is a health problem, because almost all parts of Indonesia are at
risk for getting infected with dengue infection. Twelve of the 30 provinces in
Indonesia is endemic dengue, with a case fatality rate of 1.2% .2

Dengue hemorrhagic fever (DHF) is a disease caused by dengue virus

infection. Dengue is an acute disease with clinical manifestations of hemorrhage
leading to shock that lead to death. Dengue is caused by one of the four virus
serotypes of the genus Flavivirus, family Flaviviridae. Each serotype is
sufficiently different that there is no cross reaction and epidemics caused by
multiple serotypes (hyperendemicity) can occur. This virus can enter the human
body by the intermediary Aedes aegypti and Aedes albopictus. Both mosquito
species is found in almost every corner of Indonesia, except in places a height of
more than 1000 meters above sea level. All regions in Indonesia are at risk of
contracting dengue fever, because both the cause and the virus is already
widespread of vector mosquitoes in residential population as well as in public
places throughout Indonesia except for areas above an altitude of 100 meters
above sea level. Almost every year it occurs an Extraordinary Events (KLB) in
some area of rainy season. The disease is still a public health problem and is
endemic in most o thr districts / cities in Indonesia. Dengue Fever can affect all
age groups. Until now the disease Dengue fever is more common in children but
 2

in the last decade have seen the trend increase in the proportion of patients with
Dengue Hemorrhage Fever in adults.3

Dengue hemorrhagic fever (DHF) is an acute epidemic disease caused

by a virus transmitted by Aedes aegypti and Aedes albopictus. Patients who are
infected will have symptoms of mild to high fever, accompanied by headache,
preorbital pain, muscles and joints, until spontaneous bleeding (WHO, 2010).
There are about 2.5 billion people worldwide are at risk of dengue virus infection,
especially in tropical and subtropical regions, with an estimated 500,000 people
require hospitalization each year and 90% are being affected are children aged
less than 15 years4.

Total DHF case reported last year in 34 province of Indonesia was 71,668
people and 641 of them died. The total number of cases reported was less
compared to the year 2014 with the total number of cases reported was 112,511
and 871 of them died.5
 3

CHAPTER II
LITERATURE REVIEW

2.1 Definition
Dengue hemorrhagic fever (DHF): A syndrome due to the dengue virus
that tends to affect children under 10, causing abdominal pain, hemorrhage
(bleeding) and circulatory collapse (shock). DHF starts abruptly with high
continuous fever and headache plus respiratory and intestinal symptoms with sore
throat, cough, nausea, vomiting, and abdominal pain. Shock occurs after 2 to 6
days with sudden collapse, cool clammy extremities, weak pulse, and blueness
around the mouth (cyanosis). There is bleeding with easy bruising, blood spots in
the skin (petechiae), spitting up blood (hematemesis), blood in the stool (melena),
bleeding gums and nosebleeds (epistaxis).6

2.2 Epidemiology
The term hemorrhagic fever in Southeast Asia was first used in the
Philippines in 1953. In Indonesia Dengue was first suspected in Surabaya in 1968,
but the new virological confirmation was obtained in 1970 and in 1993 dengue
has spread to all provinces in Indonesia. In Indonesia, the disease was first
reported in 1968 in Surabaya with the number of people 58 people with the death
of 24 people (41.3%), but the virological confirmation was acquired in 1972.
Furthermore, since that time Dengue Hemorrhagic disease tends to spread
throughout the land Indonesian water, so that until 1980 all provinces in Indonesia
except East Timor have contracted the disease, and culminated in 1988 with the
incidence rate reached 13.45% per 100,000 population. This situation is closely
related to the increased mobility of the population. 1

In the past 50 years, recorded the incidence of dengue fever cases has
increased 30 times along with the development and population growth of the city
to the village in the last decade. Across the world, it is estimated there are at least
50 million of the 2.5 billion people living in endemic areas are infected with
 4

dengue virus each year. Dengue fever is the second highest cause after malaria.
Dengue infection is endemic in many countries of Southeast Asia, the Western
Pacific, the Americas and hiperendemis in Thailand. Dengue fever occurs mostly
in children aged less than 15 years of age.1

2.3 Etiology
Dengue fever (DD) and Dengue Hemorrhagic Fever (DHF) are caused by
dengue virus were included in group B Arthropod Borne Virus (Arboviroses)
which is now known as the genus flavivirus, family Flaviviridae, and has 4
serotype, namely; DEN-1, DEN2, DEN-3, DEN-4. Infection of one serotype
would cause antibodies to serotype concerned, whereas antibodies against other
serotypes is lacking, so it cannot provide adequate protection against the other
serotypes.3

Someone living in dengue endemic areas can be infected by 3 or 4 serotypes

during his lifetime. The fourth serotype of dengue virus can be found in various
regions in Indonesia. In Indonesia, dengue virus surveillance conducted since
1975 at several hospitals shows that the four serotypes found and circulate
throughout the year. Serotype DEN-3 is the predominant serotypes and assumed
many of which showed severe clinical manifestations.3

2.4 Pathogenesis
Two main pathophysiological changes occur in DHF/DSS. One is an
increased vascular permeability that gives rise to loss of plasma from the vascular
compartment. This results in haemoconcentration, low pulse pressure and other
signs of shock, if plasma loss becomes critical. The second change is a disorder in
haemostasis involving vascular changes, thrombocytopenia and coagulopathy. A
constant finding in DHF/DSS is activation of the complement system, with
profound depression of C3 and C5 levels. The mediators that increase vascular
permeability and the precise mechanism(s) of the bleeding phenomena seen in
dengue infections have not yet been identified; consequently, further studies are
 5

needed. Immune complexes have been described in DHF but their role is not yet
clear. Platelet defects may be both qualitative and quantitative, i.e. some
circulating platelets during the acute phase of DHF may be exhausted (incapable
of normal function).7
Therefore, even a patient with a platelet count greater than 100000 per
mm3 may still have a prolonged bleeding time. A mechanism that may contribute
to the development of DHF/DSS is enhancement of virus replication in
macrophages by heterotypic antibodies secondary infections with a virus of a
different serotype from that causing the primary infection, cross-reactive
antibodies that fail to neutralize virus may increase the number of infected
monocytes as dengue virusantibody complexes are taken into these cells. This in
turn may result in the activation of cross-reactive CD41 and CD81 cytotoxic
lymphocytes. The rapid release of cytokines caused by the activation of T cells
and by the lysis of infected monocytes mediated by cytotoxic lymphocytes may
result in the plasma leakage and haemorrhage that occur in DHF.7

2.5 CLINICAL MANIFESTATION

The incubation period of this disease is 3-15 days after a person stricken with
dengue virus . Subsequently, the patient will reveal a variety of signs and
symptoms of dengue fever, as follows :
a. A sudden high fever for 2-7 days with temperature of (38-40C)
b. Examination of tourniquet test, found (purpura) bleeding
c. The presence of bleeding in the eyelids (conjunctiva), nosebleed (epitacsis),
Faeces with wastes mixed with blood (melena), and others.
d. Liver enlargement (hepatomegaly)
e. Blood pressure decreases, causing shock.
f. In laboratory tests (blood) occurs 3-7 days to below 100,000 platelets per mm
(trombositopenia) and an increase in hematocrit values at ats 20% of the normal
value (hemoconcentration)
 6

g. The emergence of several clinical symptoms that accompany such as nausea,

vomiting, decreased appetite (anorexia), abdominal pain, diarrhea, chills,
convulsions, and headache.
h. Nose bleed and gums.
i. Fever causes soreness / pain in the joints.
j. The emergence of red spots on the skin due to rupture of blood vessels.
k.Other Clinical symptoms that can accompany the patient are epigastrium,
vomiting, diarrhea and epilepsi.8

2.6 Diagnosis
Diagnosis of DHF is made when there are 2 clinical criteria and two
laboratory criteria. The diagnosis of dengue fever is made based on criteria which
consists of clinical and laboratory criteria. It is intended to reduce the excessive
diagnosis (overdiagnosed). Clinical criteria dengue fever is an acute fever for 2-7
days is marked by two or more clinical manifestations such as headache, retro-
orbital pain, myalgia / arthralgia, rash, hemorrhagic manifestations (petechiae or
tourniquet test), leukopenia and dengue serology positive or found patients with
dengue fever or dengue hemorrhagic fever has been confirmed in the same
location and time.
Clinical criteria:
1. Sudden Acute Fever 2-7 days, is biphasic
2. There hemorrhagic manifestations characterized by:
- Rumple lead test (+)
- Petechiae, ecchymosis, purpura
- Mucosal bleeding, epistaxis, bleeding gums
- Haematemesis and melena

Laboratory criteria:
1. Thrombocytopenia (100,000 / mm3 or less)
2. There is at least one sign of plasma leakage as follows:
- Increased hematocrit> 20% compared to standard according to age and gender.
 7

- Decrease hemtokrit> 20% after receiving fluid therapy, compared with the
previous hematocrit values.
- Signs of plasma leakage such as pleural effusion, ascites or hipoproteinemia.

The first two clinical criteria with thrombocytopenia or increased

hematocrit , sufficient for clinical diagnosis of dengue fever . And pleural effusion
or hipoalbumin , can confirm the diagnosis , especially in patients with anemia or
bleeding . In case of shock, increased hematocrit and their thrombocytopenia,
supporting the diagnosis of dengue dengue.3
Dengue hemorrhagic fever is divided into four degrees based on the
severity:

Table 1: The grade classification of Dengue Hemorrhagic Fever3

 8

2.7 Differential Diagnosis

The differential diagnosis should be considered where there is clinical with
typhoid fever, measles, influenza, chikungunya and leptospirosis. In the early
course of the disease, differential diagnoses include bacterial, viral, or parasitic
infections such as typhoid fever, measles, influenza, fever, chikungunya,
leptospirosis. The existence of a clear thrombocytopenia accompanied
hemoconcentrate can differentiate between dengue and other diseases.9
Dengue hemorrhagic fevers have to be differientiated by chikungunya
fever (DC). Chikungunya fever is infected by all family members and
transmission are similar to influenza. When compared with the DBD, DC show
sudden fever, febrile period is shorter, the temperature is higher, mostly
accompanied by a maculopapular rash, conjunctival injection and joint pain are
more common. The proportion of positive tourniquet test, petechiae and epistaxis
is similar to dengue. In the DC was not found gastrointestinal bleeding and
shock.9
Bleeding such as petechiae and ecchymosis was found in some infectious
diseases eg: sepsis, meningococcal meningitis. At the outset sepsis patient with
fever and found a sign of infection. Besides, it is clear that there leukocytosis
with predominance of polymorphonuclear cells (a leftward shift in counts),
examination of erythrocyte sedimentation rate (ESR) can be used to distinguish a
bacterial infection with a virus. In clear and the symptoms of meningococcal
menigitis meningeal stimulation and abnormalities in fluid examination
serebrospinalis.9
Idiopathic thrombocytopenia purpura (ITP) is difficult to distinguish the
degree of dengue fever II thus obtained accompanied by bleeding under the skin.
On the day - the first day, the diagnosis of ITP is difficult to distinguish with
DHF, but at ITP fever quickly disappeared or accompanied fever. Not found
leukopenia, may not find hemoconcentrate. In the healing phase dengue platelet
counts returned to normal faster than ITP.9
Bleeding can also occur in leukemia or aplastic anemia. In leukemia
irregular fever, lymph nodes may be palpable and very anemic. Examination of
 9

peripheral blood and bone marrow will clarify the diagnosis of leukemia. In
aplastic, fever arising from secondary infection, examination of blood were found
pancytopenia (leukocytes, hemoglobin and platelets decreases). In patients with
severe bleeding, chest X-ray examination and protein content can help with the
diagnosis. In DHF found hipoproteinemia as pleural effusion and plasma leakage.9

2.8 Medication
Loss of plasma volume
The major pathophysiological abnormality seen in DHF/DSS is an acute
increase in vascular permeability leading to loss of plasma from the vascular
compartment. Studies reveal a reduction in plasma volume of more than 20% in
severe cases. The evidence that supports the existence of plasma leakage includes
findings of pleural effusion and ascites by examination or radiography,
haemoconcentration, hypoproteinaemia and serous effusion (at post mortem). 7
The fact that no destructive or inflammatory vascular lesions are observed
suggests that transient, functional vascular changes due to short-acting mediators
occur. Plasma leakage can lead to shock, which, if uncorrected, leads to tissue
anoxia, metabolic acidosis and death. The haemostatic changes in DHF include
three elements: vascular changes, thrombocytopenia and disorders of coagulation.
All patients demonstrate an increase in capillary fragility, reflected by positive
tourniquet tests and easy bruising. Most patients with DSS and some non-shock
patients exhibit disseminated intravascular coagulation, as evidenced by
concomitant thrombocytopenia, prolonged partial thromboplastin time, a
decreased fibrinogen level and increased levels of fibrinogen degradation
products.7
In cases of prolonged uncontrolled shock, disseminated intravascular
coagulation can cause bleeding and may play an important role in the
development of lethal shock. About one third of patients who experience shock,
mostly those in whom shock is refractory, manifest bleeding, mainly from the
gastrointestinal tract. In the majority of patients who die, gastrointestinal
haemorrhage is observed. Early and effective replacement of plasma losses with
 10

plasma expander or fluid and electrolyte solution results in a favourable outcome

in most cases. 7
With adequate and appropriate fluid administration, DSS is rapidly
reversible. Early and rapid resuscitation from shock and the correction of
metabolic and electrolytic disturbances will prevent disseminated intravascular
coagulation. The prognosis depends mainly on the early recognition and treatment
of shock, which depend on careful monitoring and prompt action. It is not
necessary to hospitalize all patients with suspected DHF, since shock develops in
only about one-third. The finding of a continuing drop in the platelet count
concurrent with a rise in the haematocrit is an important indicator of the onset of
shock. So that early signs of shock can be recognized patients should have
repeated platelet and haematocrit determinations. Parents and other persons caring
for patients should be advised to watch for signs of deterioration or warning signs
of shock such as restlessness or lethargy, acute abdominal pain, cold extremities,
skin congestion or oliguria. The critical period is usually on the day of
defervescence, typically after the third day of illness.7
Dengue haemorrhagic fever
Thirst and dehydration result from high fever, anorexia and vomiting; thus
fluid intake by mouth should be ample. An electrolyte replacement solution or
fruit juice is preferable to plain water. Oral rehydration solution, as for the
treatment of diarrhea disease, is recommended.7
During the acute febrile phase there is some risk of convulsions.
Antipyretics may be indicated in patients with hyperpyrexia, particularly those
with a history of febrile convulsions. Salicylates should be avoided since they
may cause bleeding and acidosis, or precipitate Reye or Reye-like syndrome.
Paracetamol is preferable to reduce fever but should be used with caution, in the
following doses:
10-15mg/kgBW/once
A dose should be administered when body temperature is greater than 38.5 C, but
no more than 6 doses should be administered in a 24-hour period.7
 11

Patients should be closely observed for signs of shock. The critical period
is the transition from the febrile to the afebrile phase of illness, which usually
occurs after the third day. Hematocrit determinations are an essential guide to
therapy at that stage, since they indirectly indicate the degree of plasma leakage
and the corresponding need for intravenous fluid. A rising hematocrit usually
precedes changes in blood pressure and pulse. The hematocrit should be
determined daily from the third day of illness until the patients fever has subsided
for 1 or 2 days. If determination of the hematocrit is not possible, hemoglobin
determination may be used, although it is less sensitive.7
Parenteral fluid therapy can be given in an outpatient rehydration unit for
patients in whom fever, vomiting or anorexia produce dehydration. The fluid used
to correct dehydration is chosen according to the nature of the fluid loss. In cases
of isotonic dehydration, 5% glucose (50g/l) diluted 1:2 or 1:1 in physiological
(normal) saline should be used. Bicarbonate-containing solutions should not be
used for the initial intravenous management of dehydration in DHF, and should be
reserved for cases where there are persistent fluid losses from diarrhea. The
necessary volume of replacement fluid is equivalent to the amount of fluid and
electrolyte lost: thus, 10ml/kg should be administered for each 1% of normal body
weight lost.7
Maintenance fluid requirements, calculated according to the Halliday &
Segar formula should be added to the replacement fluid volume. Since the rate of
plasma leakage is not constant (it is more rapid when body temperature drops) the
volume and rate of intravenous fluid therapy should be adjusted according to the
volume and rate of plasma loss. Plasma loss can be monitored by changes in the
hematocrit, vital signs or volume of urine output. However, even where there is
massive plasma loss, judicious fluid replacement is necessary to avoid
overhydration.7

Indications for hospitalization

 12

Hospitalization for bolus intravenous fluid therapy may be necessary

where significant dehydration (10% of normal body weight) has occurred and
rapid volume expansion is needed. 7
Signs of significant dehydration include:
Tachycardia
Increased capillary refill time
Cool, mottled or pale skin
Diminished peripheral pulses
Changes in mental status
Oliguria
Sudden rise in haematocrit or continuously elevated haematocrit despite
administration of fluids
Narrowing of pulse pressure (20mmHg (2.7kPa))
Hypotension (a late finding representing uncorrected shock).7

Criteria for discharging in patients

The following criteria should be met before patients recovering from DHF/ DSS
are discharged:
Absence of fever for at least 24 hours without the use of antifever therapy
(cryotherapy or antipyretics)
Return of appetite
Visible clinical improvement
Good urine output
Stable haematocrit
Passing of at least 2 days after recovery from shock
No respiratory distress from pleural effusion or ascites
Platelet count of more than 50000 per mm3.7
 13

2.9 Prevention
Prevention of dengue disease is highly dependent on vector control, the
mosquito Aedes aegypti. Mosquito control can be done by using some appropriate
method, namely:
A. Environment
Environmental methods to control mosquitoes, among others with mosquito
nets eradication (PSN), solid waste management, modification of mosquito
breeding by-product of human activity, and improved design of the house. As an
example: - The bathtub drain / water-reservoir at least once a week. - Replace /
drain vase and place- birdbath once a week. - Closes with a tightly water tap. -
Burying cans, used batteries and tires around the house.9
B. Biological
Biological control among others, by using larvae-eating fish, and bacteria
(Bt.H-14).
C. Chemical
Fumigation / fogging (using malathion and fenthion), useful to reduce the
possibility of transmission to a certain time limit. - Giving abate powder
(temephos) in areas such as water reservoirs, water jar, a vase of flowers, ponds,
and others. The most effective way to prevent this disease is to combine the ways
above, called "3M Plus", namely closing, draining, hoard. It also did some pluses,
such as maintaining larvae-eating fish, sow larvicides, use mosquito nets at
bedtime, put gauze, spraying with insecticides, using repellent, installing
mosquito coils, mosquito checked periodically and adjusted to the conditions.9

2.10 Prognosis
The prognosis of dengue fever associated with antibodies obtained or initial
infection with the virus that causes dengue. Severity look of age , and the initial
infection against dengue virus serotypes of the other so can result in severe
complications hemorrhagic . Prognosis is determined also by the length of
treatment for shock in dengue shock syndrome ( SSD ) . The prognosis is good if
coped maximum of 90 minutes . Prognosis will look bad if it exceeds 90 minutes.
 14

CHAPTER 3
CASE REPORT

3.1 Objective
The objective of this paper is to report a case of a 17 years old boy with
diagnosis of Dengue Haemorrhagic Fever.

3.2 Case
PI, a 17 years old boy, with 50 kg of body weight and 160 cm of body height,
came to RSUP Haji Adam Malik on 9 Mei 2016 at 3 .00pm. His main complaint
was fever.

History of disease:
PI, a 17 years old boy, with 50 kg of body weight and 160 cm of body height,
came to RSUP Haji Adam Malik Medan on 9th Mei 2016 at 03.00pm with high
fever as his chief complaint. It has been experienced by patient for the past 5 days
before being admitted to the RSUP Haji Adam Malik hospital. Fever has been
reduced by paracetamol. Spontaneous bleeding was found. There was bleeding in
his gums for the past 5 day. Body rash was found around the patients body. He
also had 5 days history of malaise and generalised epigastric pain. He also
complained of having Blackish colour faeces. There was no cough, sore throat, or
diarrhea . Patient complained of having headache and vomiting. Patients parent
also told that many Dengue cases reported around their housing area lately.
Patient has been to a clinic and referred to Adam Malik Hospital.

History of medication :IVFD Ringer Laktat, Inj.Ranitidin,

Inj Metoclopramide, Paracetamol
History of family : None
History of parents medication : None
 15

History of pregnancy : The age of the patients mother was 24

during pregnancy. The gestation age was 9
months.

History of birth : The patient was born with normal delivery

and cried immediately after birth. Body
weight at birth was 3000 gram, body length
at birth was unclear and head circumference
was unclear. Cyanosis (-), Jaundice (-).

History of feeding : Exclusive breast feeding was given for about

6 months, formula feeding , porridge milk
(8-11months), porridge rice (8months-1
years), family food (2-3 years old).

History of immunization : Not clear. Patients mom doesnt have good

knowledge about immunization.

History of growth and development : Ppatients mother reported that

patients growth is normal. The patient
had developed talking, crawling, and
walking skills on time.
Physical Examination:
Present status:
Sensorium : Compos Mentis Body temperature: 38.9C
HR: 78 bpm RR: 30times/min
BW: 50 kg BH: 160 cm
BP : 110/70
anemic (-), icteric (-), dyspnoea (-), cyanosis (-), edema (-).

Localized status:
 16

Head :
Face : edema (-)
Eye : llight reflex (+/+), isochoric pupil, pale palpebral
conjunctiva(-/-)
Ears : both ear lobes are normal morphologically
Nose : septum deviation (-), nasal canule (-)
Mouth : dysphagia (-)
Neck :
Lymph node enlargement (-),
Thorax :
Ssymmetrical fusiform, retraction (-)
HR: 78 bpm, regular, murmur (-/-)
RR: 30 x/i, regular, ronchi (-/-)
Abdomen :
Soepel, normal peristaltic, liver and spleen unpalpable
Extremities :
pulse 78 bpm, regular, adequate p/v, felt warm, CRT < 3,
pitting edema (-/-), muscular rigidity (-), Rumple lead test
(+)
Genital : Male

Differential diagnosis : 1. Dengue Hemorrhagic Fever

2. Dengue Fever
Working diagnosis : Dengue Haemorrhagic Fever without Shock

Medications : IVFD Ringer Laktat 5cc/kgbw/hr

Paracetamol 3 x 500mg
Ranitidin inj/8hour/iv
Monitor vital sign
 17

(Complete blood analysis from the reffered clinic on 8th May)

Test Result Unit References

Hemoglobin 15.9 g% 13-18
Erythrocyte 5.61 106/mm3 4.50- 6.50
Leucocyte 3,210 103/mm3 4000-11000
Thrombocyte 66,000 103/mm3 150000-450000
Hematocrite 44 % 39-54
Eosinophil 1,20 % 1.00-3.00
Basophil 1.10 % 0-1
Neutrophil 19,40 % 50.00-70.00
Lymphocyte 23.00 % 20.00-40.00
Monocyte 6,10 % 2.00-8.00
Neutrophil absolute 3.2 103/L 2.7-6.5
Lymphocyte 2.5 103/L 1.5-3.7
absolute
Monocyte absolute 0.35 103/L 0.2-0.4
Eosinophil absolute 0.07 103/L 0-0.10
Basophil absolute 0.06 103/L 0-0.1
MCV 82 Fl 81-99
MCH 28,3 Pg 27.0-31.0
MCHC 34,5 g% 31.0-37.0
 18

Carbohydrate Metabolism
Blood Glucose 89 mg/dL < 200

Electrolite
Natrium 138 mEq/L 135-155
Potassium 4.6 mEq/L 3.6-5.5
Chloride 103 mEq/L 96106
 19

Complete blood analysis (9th May 2016 ) (1st day in RSUP HAM)
Test Result Unit References
Hemoglobin 12.6 g% 13-18
Erythrocyte 4.42 106/mm3 4.50- 6.50
Leucocyte 3.570 103/mm3 4000-11000
Thrombocyte 69,500 103/mm3 150000-450000
Hematocrite 37 % 39-54
Eosinophil 0.95 % 1.00-3.00
Basophil 0.50 % 0-1
Neutrophil 30.20 % 50.00-70.00
Lymphocyte 28,20 % 20.00-40.00
Monocyte 7.80 % 2.00-8.00
Neutrophil absolute 2.8 103/L 2.7-6.5
Lymphocyte 2.92 103/L 1.5-3.7
absolute
Monocyte absolute 0.32 103/L 0.2-0.4
Eosinophil absolute 0.04 103/L 0-0.10
Basophil absolute 0.02 103/L 0-0.1
MCV 80 Fl 81-99
MCH 28,5 Pg 27.0-31.0
MCHC 34,5 g% 31.0-37.0

Imnoserologi
Test Result Unit References
Ati DHF IgM Negatif - Negatif
Anti DHF IgG Positif - Positif

Carbohydrate Metabolism
Blood Glucose 93 mg/dL < 200
 20

Liver Function Test

Bilirubin Total 1.20 mg/dL 0.2-1.2
Bilirubin Direct 0.40 mg/dL < 0.5
AST/SGOT 33 U/L 5-34
ALT/SGPT 51 U/L 0-51
 21

FOLLOW UP

9th May 2016 (1st day in RSUP HAM)

S Fever (+), Cough (-),Epigastrium Pain(+), Vomiting (+),Gums bleeding
(+),Body rash (+) Blackish feases (+)
O Sens: CM ,Temperature: 39.0o C BW: 50KG
Head :
Eye : light reflex (+/+); isochoric pupil (-/-), pale conjungtiva
palpebra (-/-)
Ear: within normal range
Nose : within normal range
Mouth: gums bleeding (+)
Neck: limph node enlargement (-)
Thorax : symmetric fusiform, refraction (-)
HR: 88bpm, reguler, murmur(-)
RR: 20 bpm, reguler, ronchi (-)
Abdomen: soepel, peristaltic (+) normal, ; liver/ spleen
not palpable
Extremities: pulse: 88 bpm, regular, adequate p/v, warm, CRT < 3,
BP : 110/70 mmHg, Rumple lead test (+)

A Dengue Hemorragic Fever without Shock

P Bed Rest
IVFD Ringer Laktat 5cc/kgbw/hr = 250cc/kgbw/hr
Paracetamol 3 x 500mg
Ranitidin inj / 8 hours/iv
Close Monitoring of Vital Sign
Complete blood test/6hr
 22

10th May 2016 (2nd day in RSUP HAM)

S Fever (+) , Cough (-),Epigastrium (-),Vomitting (-),Gums bleeding (-),
Body Rash (-), Blackish feases (-)
O Sens:CM ,Temperature: 38.5C BW: 50KG
Head :
Eye : light reflex (+/+); isochoric pupil (-/-), pale conjungtiva
palpebra (-/-)
Ear: within normal range
Nose : within normal range
Mouth: gums bleeding (-)
Neck: limph node enlargement (-)
Thorax : symmetric fusiform, retraction (-)
HR: 90 bpm, reguler, murmur(-)
RR: 22 bpm, reguler, ronchi (-)
Abdomen: soepel, peristaltic (+) normal, ; liver/ spleen
not palpable
Extremities: pulse: 90 bpm, regular, adequate p/v, warm, CRT < 3,
BP : 120/60 mmHg,

A Dengue Hemorragic Fever without Shock

P Bed Rest
IVFD Ringer Laktat 3cc/kgbw/hr = 150cc/kgbw/hr
Paracetamol 5oomg (if needed)
Close Monitoring of Vital sign
Complete blood test
11th May 2016 (3rd day in RSUP HAM)
S Fever (-) , Cough (-),Epigastrium (-),Vomitting (-),Gums bleeding (-),Body
Rash (-) Blackish Feases (-)
 23

O Sens:CM ,Temperature: 37.4 C BW: 50KG

Head :
Eye : light reflex (+/+); isochoric pupil (-/-), pale conjungtiva
palpebra (-/-)
Ear: within normal range
Nose : within normal range
Mouth: within normal range
Neck: limph node enlargement (-)
Thorax : symmetric fusiform, retraction (-)
HR: 88bpm, reguler, murmur(-)
RR: 22 bpm, reguler, ronchi (-)
Abdomen: soepel, peristaltic (+) normal, ; liver/ spleen
not palpable
Extremities: pulse: 88 bpm, regular, adequate p/v, warm, CRT < 3,
BP : 120/70 mmHg

A Dengue Hemorragic Fever without Shock

P Bed Rest
IVFD Ringer Laktat 3cc/kgbw/hr = 150cc/kgbw/hr
Close Monitoring of Vital Sign
Complete blood test
 24

12th May 2016 (4th day in RSUP HAM)

S Fever (-) , Cough (-),Epigastrium (-), Vomiting (-),Gums bleeding (-),Body
Rash (-)
O Sens:CM ,Temperature: 36.8 C BW: 50KG
Head :
Eye : light reflex (+/+); isochoric pupil (-/-), pale conjungtiva
palpebra (-/-)
Ear: within normal range
Nose : within normal range
Mouth: within normal range
Neck: limph node enlargement (-), neck stiffness (-)
Thorax : symmetric fusiform, retraction (-)
HR: 90bpm, reguler, murmur(-)
RR: 24 bpm, reguler, ronchi (-)
Abdomen: soepel, peristaltic (+) normal, ; liver/ spleen
not palpable
Extremities: pulse: 90 bpm, regular, adequate p/v, warm, CRT < 3,
BP : 120/70 mmHg, Rashes (-)

A Dengue Hemorragic Fever without Shock

P Bed Rest
Discharged
 25

Complete blood analysis (10th May 2016 ) (3rd day in RSUP HAM)
Test Result Unit References
Hemoglobin 14.6 g% 13-18
Erythrocyte 5.33 106/mm3 4.50- 6.50
Leucocyte 5,140 103/mm3 4000-11000
Thrombocyte 88,000 103/mm3 150000-450000
Hematocrite 43 % 39-54
Eosinophil 4,70 % 1.00-3.00
Basophil 0,50 % 0-1
Neutrophil 25,30 % 50.00-70.00
Lymphocyte 32,30 % 20.00-40.00
Monocyte 5,68 % 2.00-8.00
Neutrophil absolute 2,70 103/L 2.7-6.5
Lymphocyte 3,28 103/L 1.5-3.7
absolute
Monocyte absolute 0.29 103/L 0.2-0.4
Eosinophil absolute 0.24 103/L 0-0.10
Basophil absolute 0.03 103/L 0-0.1
MCV 81 Fl 81-99
MCH 27,4 Pg 27.0-31.0
MCHC 33,8 g% 31.0-37.0
 26

Complete blood analysis (11th May 2016 ) (4th day in RSUP HAM)
Test Result Unit References
Hemoglobin 14,2 g% 13-18
Erythrocyte 5.28 106/mm3 4.50- 6.50
Leucocyte 5,410 103/mm3 4000-11000
Thrombocyte 139,400 103/mm3 150000-450000
Hematocrite 43 % 39-54
Eosinophil 10,50 % 1.00-3.00
Basophil 0,50 % 0-1
Neutrophil 24,10 % 50.00-70.00
Lymphocyte 33,70 % 20.00-40.00
Monocyte 10,90 % 2.00-8.00
Neutrophil absolute 2,28 103/L 2.7-6.5
Lymphocyte 2,85 103/L 1.5-3.7
absolute
Monocyte absolute 0.58 103/L 0.2-0.4
Eosinophil absolute 0.56 103/L 0-0.10
Basophil absolute 0.04 103/L 0-0.1
MCV 82 Fl 81-99
MCH 27,0 Pg 27.0-31.0
MCHC 33,0 g% 31.0-37.0
 27

CHAPTER IV
DISCUSSION

Theory Case
Definition PI is a child with main complaint
Dengue hemorrhagic fever (DHF) : A continuous fever, spontaneous bleeding
syndrome due to the dengue virus that gums and body rash for 5 days.
tends to affect children,
causing abdominal pain, hemorrhage
(bleeding) and circulatory collapse
(shock). DHF starts abruptly with high
continuous fever and headache plus
respiratory and intestinal symptoms
with sore throat, cough, nausea,
vomiting, and abdominal pain. Shock
occurs after 2 to 6 days with sudden
collapse, cool clammy extremities,
weak thready pulse, and blueness
around the mouth (circumoral
cyanosis). There is bleeding with easy
bruising, blood spots in the skin
(petechiae), spitting up blood
(hematemesis), blood in the stool
(melena), bleeding gums and
nosebleeds (epistaxis)
Clinical Manifestation PIs main complaint was high
a. A sudden high fever for 2-7 days fever as chief complaint.It has
with temperature of (38-40C) been experienced by patient for
 28

b. Examination of tourniquet test, found the past 5 days before being

(purpura) bleeding admitted to the RSUP Haji
c. The presence of bleeding in the Adam Malik hospital. Fever
eyelids (conjunctiva), nosebleed has been reduced by
(epitacsis), Faeces with wastes mixed paracetamol.
with blood (melena), and others. There was bleeding in his gums
d. Liver enlargement (hepatomegaly) for the past 5 day.During the
e. Blood pressure decreases, causing night of the admitted body rash
shock. was found around the body.
f. In laboratory tests (blood) occurs 3-7 Rumple lead test (+)
days to below 100,000 platelets per mm Blackish colour faeces found
(trombositopent) and an increase in (+)
hematocrit value 20% of the normal He also had 5 days history of
value (hemoconcentration) malaise,generalised epigastric
g. The emergence of several clinical pain. There was no cough,sore
symptoms that accompany such as throat, or diarrhea . Patient
nausea, vomiting, decreased appetite complained of having headache
(anorexia), abdominal pain, diarrhea, and vomiting.
chills, convulsions, and headache. Lab results shows that patient
h. Nose bleed and gums. had thrombocytopenia.
i. Fever causes soreness / pain in the Normal blood pressure found.
joints. Hematocrit value is in normal
j. The emergence of red spots on the range.
skin due to rupture of blood vessels. Thus, patient doesnt have
k. Other Clinical symptoms that can shock.
accompany the patient are epigastrium,
vomiting, diarrhea and epilepsi.
 29

Diagnosis
Clinical criteria: Based on the theory, this patient
1. Sudden Acute Fever 2-7 days also fulfilled some of the
2. There hemorrhagic manifestations clinical and laboratory criteria
characterized by: to be diagnosed as dengue
- Rumple lead test (+) hemorrhagic fever such as:
- Petechiae, ecchymosis, purpura Fever past 5 days
- Mucosal bleeding, epistaxis, bleeding Rumple lead test (+)
gums Petechiae was found
- Haematemesis and melena Thrombositopenia was found in
lab results.
Laboratory criteria: Gums bleeding was found
1. Thrombocytopenia (100,000 / mm3 No sign of plasma leakage
or less) found because there is normal
2. There is at least one sign of plasma hematocrit value, no pleural
leakage as follows: effusion, ascites or
- Increased hematocrit> 20% compared hipoprotenemia.
to standard according to age and
gender. Thus, with all this criteria found
- Decrease hemtokrit> 20% after patient is diagnosed with dengue
receiving fluid therapy, compared with hemorrhagic fever without shock.
the previous hematocrit values.
- Signs of plasma leakage such as
pleural effusion, ascites or
hipoproteinemia.

Theraphy PI was given total bed rest.

Bed Rest
 30

Oksigen Oxygen was not given to the

IVD NaCl /IVFD Ringer Laktat patient because patient doesnt
Addition of colloid/plasma have any difficulties in
Dekstran/FPP 10-20 (max 30) breathing and his saturation of
ml/kg/bb/jam oxygen was good.
Whole blood transfusion if IVFD Ringer Laktat
needed 5cc/kgbw/hour was given on the
Anti Emetics first day. Once the patient was
Paracetamol stable and doesnt look weak the
ivfd Ringer Laktat was reduced
to 3cc/kgbw/hour.
Paracetamol 500mg tab was
given whenever the patient had
body temperature more than
38.5c. Same as the theory it
states paracetamol is given
when the patient has body
temperature more than 38.5c.
10-15mg/kgbw
 31

CHAPTER V
SUMMARY

PI, a boy, 17 years old, with 50kg of Body Weight and 160 cm of
Body Height, came to RSUP Haji Adam Malik Medan on 9th Mei 2016 at
03.00pm with high fever as chief complaint. It has been experienced by
patient for the past 5 days before being admitted to the RSUP Haji Adam
Malik hospital. Fever has been reduced by paracetamol. Spontaneous
bleeding was found. . There was bleeding in his gums for the past 5 day. Body
rash was found around the body. He also had 5 days history of malaise,
generalised epigastric pain. There was no cough, sore throat, or diarrhea .
Patient complained of having headache and vomiting. Patient had blackish
feases for 2 days. DHF cases were reported around patients housing area for
the past few months. Patient has been diagnosed with Dengue Hemorrhagic
Fever without shock in a clinic and reffered to Haji Adam Malik General.
Patient was diagnosed with Dengue Hemorrhagic Fever without shock and
treated with IVFD Ringer Laktat 5cc/kgbw/hr then reduced to 3cc/kgbw/hr,
Paracetamol 500mg whenever patient had fever, Ranitidin inj and total bed
rest from 9st Mei until 11th Mei. Patient was discharged on 12th Mei 2016 with
no sign and symptoms of DHF.
 32

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