ACKNOWLEDGMENTS
We are greatly indebt
to the Almighty One for giving us blessing to finish this case report, “Dengue
Hemoragic Fevers”. This case report is
requirement to complete the clinical assistance program in Department of Child
Health in Haji Adam Malik General
Hospital, Medical Faculty of North Sumatera University.
We are also indebt to
our supervisor and adviser, dr. Rizky
Ardiansyah, M. Ked (Ped),
Sp. A
(K) for
much spent time to give us guidance, comments, and suggestions. We are grateful
because without Him,
this case report wouldn’t have taken its present shape.
This case
report has gone through series of developments and corrections. There were
critical but constructive and relevants suggestions from the reviewers.
Hopefully the content will be useful for everyone the future.
Writers
CONTENTS
ACKNOWLEDGMENTS.................................................................................................... i
CONTENTS.......................................................................................................................... ii
CHAPTER 1 INTRODUCTION.......................................................................................... 1
CHAPTER
2 LITERATURE REVIEW............................................................................... 3
CHAPTER 3 CASE REPORT.............................................................................................. 15
CHAPTER 4 DISCUSSION................................................................................................ 25
CHAPTER
5 SUMMARY.................................................................................................... 27
REFERENCES .................................................................................................................... 30
CHAPTER
1
INTRODUCTION
1.1
Background
Dengue is the most rapidly spreading mosquito-borne
viral disease of man kind, with a 30- fold increase in global incidence over
the last five decades. It is a major public health concern throughout the
tropical and subtropical regions of the world. Almost half the world's population
lives in countries where dengue is endemic. According to World Health
Organization (WHO), about 50–100 million new dengue infections are estimated to
occur annually in more than 100 endemic countries, with a steady increase in
the number of countries reporting the disease.(1) An estimated 500 000 people with DHF require
hospitalization each year. A very large proportion (approximately 90%) of them
are children aged less than five years, and about 2.5% of those affected die.
Epidemics of dengue are increasing in frequency. During epidemics, infection
rates among those who have not been previously exposed to the virus are often
40% to 50% but can also reach 80% to 90%.(3)
Approximately 1.8 billion (more than 70%) of the
population at risk for dengue worldwide live in Member States of the WHO
South-East Asia Region (SEAR) and Western Pacific Region, which bear nearly 75%
of the current global disease burden due to dengue. Of the 11 countries of
SEAR, 10 countries including Indonesia are endemic for dengue. The only
exception is the Democratic People's Republic of Korea. In 2012, SEAR countries
reported approximately 0.29 million cases, of which Thailand contributed almost
30%, Indonesia 29% and India 20%. (2)
Since 2000, epidemic dengue has spread to new areas
and has increased in the already affected areas of the region. In 2003, eight
countries -- Bangladesh, India, Indonesia, Maldives, Myanmar, Sri Lanka,
Thailand and Timor - Leste reported dengue cases. Epidemic dengue is a major
public health problem in Indonesia, Myanmar, Sri Lanka, Thailand and
Timor-Leste which are in the tropical monsoon and equatorial zone where Aedes
aegypti is widespread in both urban and rural areas, where multiple virus
serotypes are circulating, and where dengue is aleading cause of
hospitalization and death in children.(1)
The number of dengue cases has increased over the
last three to five years, with recurring epidemics. Moreover, there has been an
increase in the proportion of dengue cases with their severity, particularly in
Thailand, Indonesia and Myanmar. Reported case fatality rates for the region
are approximately 1%, but in India, Indonesia and Myanmar, focal outbreaks away
from the urban areas have reported case-fatality rates of 3--5%.(3)
In Indonesia, where more than 35% of the country’s
population lives in urban areas, 150 000 cases were reported in 2007 (the
highest on record) with over 25 000 cases reported from both Jakarta and West
Java. The case-fatality rate was approximately 1%.(1)
CHAPTER 2
LITERATURE REVIEW
2.1 Epidemiology
Dengue is one of the most important emerging viral
disease of humans in the world afflicting humanity in terms of morbidity and mortality.
Currently the disease is endemic in all continents except Europe. The
Epidemiology of dengue is a complex phenomenon that mainly depends upon an
intricate relationship between the 3 epidemiological factors: the host (man and
mosquito), the agent (virus) and the environment. The complexity of
relationship among these factors eventually determines the level of endemicity
in an area.(4)
2.1.1. Dengue Virus
The agent of dengue, i.e. dengue viruses, are
categorized under the genus Flavivirus. These viruses contain single stranded
RNA and are small in size (50 nm). There are four dengue virus serotypes which
are designated as DENV-1, DENV-2, DENV-3 and DENV- 4. These serotypes may be in
circulation either singly, or more than one can be in circulation in any area
at the same time. Although all four serotypes are antigenically similar, they
are different enough to elicit crossprotection only for a few months after
infection by any one of them. Infection with any one serotype confers lifelong
immunity to the virus serotype. (1)
The genome is cleaved by host and viral proteases in
three structural proteins (capsid, C, prM, the precursor of membrane, M,
protein and envelope, E) and seven nonstructural proteins (NS).(2)
2.1.2 Vector
Dengue viruses are transmitted by the bite of female
Aedes (Ae) mosquitoes. Ae.aegypti is the most potential vector
but other species such as Ae albopictus, Ae. polynesiensis and Ae.
niveus have also been incriminated as secondary vectors. Dengue is
transmitted by the bite of female Aedes mosquito. Female Aedes mosquito
deposits eggs singly on damp surfaces just above the water line. Under optimal
conditions the life cycle of aquatic stage of Ae. aegypti can be as
short as seven days. It is a day time feeder and can fly up to a
limited distance of 400 meters. To get one full blood mea the mosquito has to
feed on several persons, infecting all of them.(4)
2.1.3. Host
Dengue viruses, having evolved from mosquitoes,
adapted to non-human primates and later to humans in an evolutionary process.
The viraemia among humans builds up high titres two days before the onset of
the fever (non-febrile) and lasts 5–7 days after the onset of the fever
(febrile). It is only during these two periods that the vector species gets
infected. Thereafter, the humans become dead-ends for transmission. The spread
of infection occurs through the movement of the host (man) as the vectors’
movements are very restricted. The susceptibility of the human depends upon the
immune status and genetic predisposition. (3)
2.1.4.
Environmental Factors
The population of Ae. aegypti fluctuates with
rainfall and water storage. Its life span is influenced by temperature and
humidity, survives best between 16º-30º C and a relative humidity of 60-80%. Ae.
aegypti breeds in the containers, in and around the houses. Altitude is an
important factor in limiting the distribution of Ae. aegypti, it is
distributed between sea level and 1000 ft above sea level. Ae. aegypti is
highly anthropophilic and rests in cool shady places. The rural spread of Ae.
aegypti is a relatively recent occurrence associated with the development
of rural water supply schemes, improved transport systems, scarcity of water
and like style changes. Ae. aegypti breeds almost entirely in domestic
man-made water receptacles found in and around households, construction sites
and factories; natural larval habitats are tree holes, leaf axils and coconut
shells. In hot and dry regions, overhead tanks and ground water storage tanks
become primary habitats. Unused tyres, flower pots and desert coolers are among
the most common domestic breeding sites of Ae. Aegypti. (4)
2.1.5.
Transmission cycle
The
female usually becomes infected with the dengue virus when it takes a blood
meal from a person during the acute febrile (viremia) phase of dengue illness.
After an extrinsic incubation period of 8 to 10 days, the mosquito becomes
infected. The virus is transmitted when the infected female mosquito bites and
injects its saliva into the wound of the person bitten. The cycle of dengue
continues by this process. Dengue begins abruptly after an intrinsic incubation
period of 4 to 7 days (range 3–14 days). There is also evidence of vertical
transmission of dengue virus from infected female mosquitoes to the next
generation. Though transmission primarily occurs through the bite of a vector,
there are reports of dengue transmission through blood transfusion and organ
transplantation. There are also reports of congenital dengue infections
occurring in neonates born to mothers infected very late in pregnancy.(1)
2.2 Pathogenesis
Primary or first infection in non
immune persons usually causes Dengue fever. Subsequent dengue infection by
different serotype causes more severe illness like DHF/DSS. The key
manifestations of the DHF/DSS are sudden onset of shock, capillary leakage,
haemorrhagic diathesis/ thrombocytopenia occurring at the time of defervescence
of fever. Pathogenesis is not well defined but it is suggested that it
ismediated through soluble mediators, compliment activation and cytokines that
are responsible for various manifestations. (4)

2.3. Clinical Manifestation
Dengue virus infection may be asymptomatic or may
cause undifferentiated febrile illness (viral syndrome), dengue fever (DF), or
dengue haemorrhagic fever (DHF) including dengue shock syndrome (DSS).
Infection with one dengue serotype gives lifelong immunity to that particular
serotype, but there is only short-term cross-protection for the other
serotypes. The clinical manifestation depends on the virus strain and host
factors such as age, immune status, etc. (3)

Differentiation between dengue fever and dengue
hemorrhagic fever is difficult early in the course of illness. A relatively
mild 1st phase with abrupt onset of fever, malaise, vomiting, headache,
anorexia, and cough may be followed after 2-5 days by rapid clinical
deterioration and collapse. In this 2nd phase, the patient usually has cold,
clammy extremities, a warm trunk, flushed face, diaphoresis, restlessness,
irritability, mid epigastric pain, and decreased urinary output. Frequently,
there are scattered petechiae on the forehead and extremities; spontaneous
ecchymoses may appear, and easy bruising and bleeding at sites of venipuncture
are common. A macular or maculopapular rash may appear, and there may be
circumoral and peripheral cyanosis. Respirations are rapid and often labored.
The pulse is weak, rapid, and thready, and the heart sounds are faint. The
liver may enlarge to 4-6 cm below the costal margin and is usually firm and
somewhat tender. Approximately 20-30% of cases of dengue hemorrhagic fever are
complicated by shock (dengue shock syndrome). Dengue shock can be subtle,
arising in patients who are fully alert, and is accompanied by increased
peripheral vascular resistance and raised diastolic blood pressure. Shock is
not from congestive heart failure but from venous pooling. With increasing
cardiovascular compromise, diastolic pressure rises toward the systolic level
and the pulse pressure narrows. Fewer than 10% of patients have gross
ecchymosis or gastrointestinal bleeding, usually after a period of uncorrected
shock. After a 24-36 hr period of crisis, convalescence is fairly rapid in the
children who recover. The temperature may return to normal before or during the
stage of shock. Bradycardia and ventricular extrasystoles are common during convalescence.(5)

2.4
Laboratory Diagnosis
Unequivocal
diagnosis of dengue infection requires laboratory confirmation, either by
isolating the virus or detecting dengue-specific antibodies. For virus
isolation or detection of DENV RNA in serum specimens by serotype-specific,
real-time reverse transcriptase polymerase chain reaction (RT-PCR), an
acute-phase serum specimen should be collected within 5 days of symptom onset.
If the virus cannot be isolated or detected from this sample, a
convalescent-phase serum specimen is needed at least 6 days after the onset of
symptoms to make a serologic diagnosis by testing for IgM antibodies to dengue
with an IgM antibody-capture enzyme-linked immunosorbent assay (MAC-ELISA).(5)
Acute-phase
and convalescent-phase serum samples should be sent to the state health
department or tothe Centers for Disease Control and Prevention (CDC) for
testing. Acute-phase samples for virus diagnosis may be stored on dry ice
(-70°C) or, if delivery can be made within 1 week, stored unfrozen in a
refrigerator (4°C). Convalescent-phase samples should be sent in a rigid
container without ice, if next-day delivery is assured. Otherwise, they should
be shipped on ice in aninsulated container to avoid heat exposure during
transit.
Most tests for
anti-dengue antibodies yield nonspecificresults for flaviviruses, including
West Nile and St. Louis encephalitis viruses. Because commercial kits may vary
in sensitivity and specificity, test results may need to be confirmed by a
reference laboratory.(6)
2.5 Criteria for clinical diagnosis of DHF/DSS
Clinical
manifestations
•
Fever: acute onset, high and continuous, lasting two to seven days in most
cases.
•
Any of the following haemorrhagic manifestations including a positive
tourniquet test (the most common), petechiae, purpura (at venepuncture sites),
ecchymosis, epistaxis, gum bleeding, and haematemesis 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.
Laboratory
findings
•
Thrombocytopenia (100 000 cells per mm3 or less).
•
Haemoconcentration; haematocrit increase of ≥20%i 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.(3)
2.6. Management
Approach to clinical management of dengue Fever may
vary depending on severity of illness. The patients who have simple fever
without any danger signs or complications may be managed with symptomatic approach.
Those who have warning signs and symptoms should be closely monitored for
progression of disease. The patients of DHF without shock, significant bleeding
or involvement of various organs require aggressive management to reduce
morbidity and mortality. Patient may develop complications during later stage
of fever (defervescence) or a febrile phase, where clinician should be careful
to look for danger signs and signs of fluid overload.
2.6.1. Management of dengue fever
Management
of dengue fever is symptomatic and supportive
i. Bed rest is advisable during the acute phase.
ii. Use cold/tepid
sponging to keep temperature below 38.5 C.
iii. Antipyretics may
be used to lower the body temperature. Aspirin/NSAIDS like Ibuprofen, etc
should be avoided since it may cause gastritis, vomiting, acidosis, platelet
dysfunction and severe bleeding. Paracetamol is preferable in the doses given
below:
• 1-2 years: 60 -120
mg/dose
• 3-6 years: 120
mg/dose
• 7-12 years: 240 mg/dose
• Adult : 500 mg/dose
Note: In children the
dose of paracetamol is calculated as per 10 mg/Kg body weight per dose.
Paracetamol dose can be repeated at the intervals of 6 hrs depending upon fever
and body ache.
iv. Oral fluid and
electrolyte therapy is recommended for patients with excessive sweating or
vomiting.
v. Patients should be
monitored for 24 to 48 hours after they become afebrile for development of
complications.
Management
during febrile phase
Paracetamol is recommended to keep the temperature
below 39 C. Adequate fluid should be advised orally to the extent the patient
tolerates. Oral rehydration solution (ORS), such as those used for the
treatment of diarrhoeal diseases and / or fruit juices are preferable to plain
water. Intravenous fluid should be administered if the patient is vomiting
persistently or refusing to feed.
Patients should be closely monitored for the initial
signs of shock. The critical period is during the transition from the febrile
to the afebrile stage and usually occurs after the third day of illness. Sometimes
serial haematocrit determinations are essential to guide treatment plan, since
they reflect the degree of plasma leakage and need for intravenous
administration of fluids. Haematocrit should be determined daily specially from
the third day until the temperature remains normal for one or two days.
2.6.2
Management of DHF without Shock
Any person who has dengue fever with
thrombocytopenia, high haemoconcentration and presents with abdominal pain,
black tarry stools, epistaxis, bleeding from the gums etc. needs to be
hospitalized. All these patients should be observed for signs of shock. The critical
period for development of shock is during transition from febrile to abferile
phase of illness, which usually occurs after third day of illness. Rise of
haemoconcentration indicates plasma leakage and loss of volume for which proper
fluid management plays an important role.

Notes:
*Improvement:
Hct falls, pulse rate and blood pressure stable, urine output rises
**No
Improvement: Hct or pulse rate rises, pulse pressure falls below 20 mmHg, urine
output falls
2.6.3 Management of Shock
Immediately after hospitalization, the haematocrit,
platelet count and vital signs should be examined to assess the patient's
condition and intravenous fluid therapy should be started. The patient requires
regular and continuous monitoring. If the patient has already received about
1000 ml of intravenous fluid, it should be changed to colloidal solution
preferably Dextran 40 or if haematocrit further decreases fresh whole blood
transfusion 10-
20ml/kg/dose
should be given.
However, in case of persistent shock even after
initial fluid replacement and resuscitation with plasma or plasma expanders,
the haematocrit continues to decline, internal bleeding should be suspected. It
may be difficult to recognize and estimate the degree of internal blood loss in
the presence of haemoconcentration. It is thus recommended to give whole blood
in small volumes of 10ml/kg/hour for all patients in shock as a routine
precaution. Oxygen should be given to all patients in shock. Treatment
algorithm for patients with DHF with shock:

Crystalloid:
Normal Saline, ringer lactate
Colloid:
Dextran 40/degraded gelatine polymer (polygeline)
#ABCS=
Acidosis, Bleeding, Calcium (Na++ &K+), Sugar
Notes:
*Improvement:
Hct falls, pulse rate and blood pressure stable, urine output rises
**No
improvement: Hct or pulse rate rises, pulse pressure falls below 20 mmHg, urine
output
falls
Unstable
vital signs: urine output falls, signs of shock

-Crystalloid:
Normal Saline, ringer lactate
-Colloid:
Dextran 40/degraded gelatine polymer (polygeline)
-
ABCS= Acidosis, Bleeding, Calcium (Na++ &K+), Sugar
Notes:
*Improvement:
Hct falls, pulse rate and blood pressure stable, urine output rises
**No
Improvement: Hct or pulse rate rises, pulse pressure falls below 20 mmHg, urine
output falls
·
Unstable vital signs: Urine output
falls, signs of shock
·
In cases of acidosis, hyperosmolar or
Ringer's lactate solution should not be used
·
Serial platelet and Hct determinations:
drop in platelets and rise in Hct are essential for early diagnosis of DHF
·
Cases of DHF should be observed every
hour for vital signs and urine output
2.6.4. Management of severe bleeding
In case of severe bleeding, patient should be
admitted in the hospital and investigated to look for the cause and site of
bleeding and immediately attempt should be made to stop the bleeding. Internal
bleeding like GI bleeding may be sometime severe and difficult to locate.
Patients may also have severe epistaxis and haemoptysis and may present with
profound shock. Urgent blood transfusion is life saving in this condition.
However, if blood is not available shock may be managed with proper IV fluid or
plasma expander.. If the patient has thrombocytopenia with active bleeding, it
should be treated with blood transfusion and then if required platelet
transfusion. In case of massive haemorrhage blood should be tested to rule out
coagulopathy by testing for prothrombin time (PT) and aPTT. Patients of severe bleeding
may have liver dysfunction and in such case, liver function test should also be
performed. In rare circumstances, intracranial bleed may also occur in some
patients who have severe thrombocytopenia and abnormality in coagulation
profile.
2.7.
Criteria for admission of a patient
If a DF patient presents with significant bleeding
from any site, signs of hypotension,
persistent
high grade fever, rapid fall of platelet count, sudden drop in temperature should
be
admitted in hospital. However, those patients who have evidence of organ
involvement
should
also be admitted for proper monitoring and management. Dengue patients with
warning signs and symptoms should be admitted and closely monitored.
2.8. Criteria for discharge of patients
The admitted patients who have recovered from acute
dengue infection having no fever for atleast 24 hours, normal blood pressure,
adequate urine output, no respiratory distress, persistent platelet count
>50,000/cu.mm should be discharged from hospital.
2.9.
Indication of Platelet transfusion
1. Platelet count less than 10000/cu.mm in absence
of bleeding manifestations (Prophylactic platelet transfusion).
2. Haemorrhage with or without thrombocytopenia.
Packed cell transfusion/FFP along with platelets may
be required in cases of severe bleeding with coagulopathy. Whole fresh blood
transfusion doesn't have any role in managing thrombocytopenia.
Platelets can be classified as random donor
platelets (prepared by buffy coat removal method or by platelet rich plasma
method), BCPP (buffy coat pooled platelet) and single donor platelets (SDP) or
aphaeretic platelets (AP).
2.10.
Vaccine for dengue infection
Till now there is no licensed vaccine available
against dengue viral infection. Several
rials are ongoing in the world for the development of tetravalent dengue
vaccine. So far phase III trials of a recombinant, live attenuated tetravalent
dengue vaccine (CYD-TDV) has completed in Five Asian countries in children
which may be promising in preventing dengue infection in near future.
CHAPTER
3
CASE
REPORT
3.1. Case
KA, a five years 7 months old boy with 15 kg of body weight nd 109
cm of body height came to Unit Gawat Darurat RS Haji Adam Malik on 6th mei 2016
at 20.10 p.m. His chief complaint was a fever since 3 days ago.
3.2. History Of Disease
KA, a five year 7 months years old boy
with 15 kg of body weight and 109 cm of body height. KA is the eldest child in
the family (from2 siblings) came to Unit Gawat Darurat RS with a fever as a
main complaint , and the fever is reduce
with antipyretic drugs. The highest temperature measure was 39
. It was taken by
his mother. No history of shivering.

Diarhhea was experienced within
these 6 days before being admitted to the hospital. The frequency of diarrhea
experienced more than 3 times a day. The
consistensy of stool was more liquid than a waste. The patient also
felt nauseated since 6 days before came to the hospital. Patient vomited once
before coming to the hospital. The vomit contents is the food and the drinks he
consumed.
Patient also experienced headache
and joint pain since 3 days ago. Abdominal pain
also found during history taking. There is no history of epixtasis,
hematemesis and melena. There was no problem found with his urinary system.
Defecation frequency is more then 3 times a day. His mother also complaint
there was a reddish skin (rash) at the upper and lower extrimities. There was
no history of seizure.
3.3. History of Medication
Patient previously treated by a general practitioner prior to
referral to RS Haji Adam Malik, Medan.he was givem Chloramphenicol,
Parasetamol, pseudoefedrin HCL, metoclopramide and diazepam.
3.4. History of Family’s Disease
Patient’s family does not have the same
history of disease as patient but the symptoms showed by patient’s friend is
the same with patient.
Mother
|
|
Father
|
|
Name
|
: Vivin Sofyana
|
Name
|
: Ilhamsyah
|
Age
|
: 29 tahun
|
Age
|
: 36 tahun
|
Religion
|
: Islam
|
Religion
|
: Islam
|
Race
|
: Jawa
|
Race
|
: Jawa
|
Occupation
|
: Ibu Rumah Tangga
|
Occupation
|
: Staf pengajar / Dosen
|
Education
|
: SMA
|
Education
|
: S2
|
Revenue
|
: -
|
Revenue
|
: Rp. 3 juta/ bulan
|
First son
|
: Khairul Azman
|
Second daughter
|
: Khanza Alia Fitri
|
Age
|
: 5 years 7 months
|
Usia
|
: 1 years 9 monts
|
Gender
|
: Boy
|
Gender
|
: Girl
|
Occupation
|
: siswa TK
|
Occupation
|
: -
|
3.5. Family Medical History
No history of disease in patient’s
family
3.6. History of Birth
The patient was born spontaneously
pervaginam, assisted by a midwife. Gestation weeks were approximately 36
months. Body weight at birth was 2800 gram. Cyanosis and Jaudice were not found
at bitrh. Patient’s mother was 22 years old when she gave birth and there was
no history of disease. Medication
consumed during pregnancy (-) Herbal medication (+)
3.7. History of feeding
0 - 3 month : Breast feeding
3 – 6 month : Breast feeding and Formula feeding
> 6 month :
Formula feeding and porridge
3.8. History of Immunization
Patient had a complete
immunization.
Hepatitis B :
3x
BCG :
1x at 2 month
Polio :
4x at 0,2,4,6 months
DTP :
3x at 2,4,6 months
Measles :
1x at 9 month
3.9. History of Growth and Development
According to patient’s mother
growth and development went normal. Patient lifted up his head at 3 month,
patient could stand up and walk at 1 year 2 months.
3.10. Physical Examination :
Present Status:
Sensorium :
Compos mentis, GCS : 15
Temperatur : 36,4

Body Weight: 15
kg Body Height:
109 cm.
dyspnea (-),
cyanosis (-), edema (-)
Localized Status :
Head
· Face : edema (-)
·
Eye : light reflex (+/+), isochoric pupil, pale inferior palpebral conjunctiva(-/-)
·
Ears : both ear lobe in normal morphologic
·
Hidung : septum deviation (-), nasal flares
(-), normal morphologic
·
Mouth : Normal morphologic
Neck
·
Lymph node enlargement (-)
Thorax
·
Simetris fusiformis, retraction (-/-), RR: 25 bpm, regular, ronchi (-/-) Respiratory sound : vesiculer,
additional sound (-), HR: 90 bpm, regular, murmur (-).
·
Abdomen: Soepel, peristaltik sound (+) normal, epigastric pain (+). Hepar and Lien: unpalpable.
·
Extremity:
TD : 90/70 mmHg, HR: 90 kali/min,
regular, warm
exterimity, CRT < 3”, pretibial oedem (-), ptechie (+) at upper and lower extrimity.
Laboratory Finding: 07 May 2016 07:02:46
Complete Blood Analysis:
Test
|
Result
|
Unit
|
References
|
Hemoglobin
|
13.2
|
g%
|
10.8 – 15.6
|
Erythrocyte
|
4.97
|
106/mm3
|
4.50 – 6.50
|
Leucocyte
|
3.03
|
103/mm3
|
4.5 - 13.5
|
Thrombocyte
|
84
|
103/mm3
|
150-450
|
Hematocrite
|
39
|
%
|
33 – 45
|
Eosinophil
|
0
|
%
|
1-5
|
Basophil
|
0.3
|
%
|
0-1
|
Neutrophil
|
56.50
|
%
|
25 – 60
|
Lymphocyte
|
35.30
|
%
|
25 – 50
|
Monocyte
|
7.90
|
%
|
1 – 6
|
Neutrophil Absolute
|
1.71
|
103/µL
|
2.4-7.3
|
Lymphocyte Absolute
|
1.07
|
103/µL
|
1.7-5.1
|
Monocyte absolute
|
0.24
|
103/µL
|
0.2-0.6
|
Basophil absolute
|
0.01
|
103/µL
|
0-0.1
|
Eusinophil absolute
|
0
|
103/µL
|
0.1 – 0.3
|
MCV
|
79
|
fL
|
69 – 93
|
MCH
|
26.6
|
Pg
|
22 – 34
|
MCHC
|
33.5
|
g%
|
32 – 36
|
RDW
|
12.4
|
%
|
11 – 15
|
PCT
|
0.110
|
%
|
0.1 – 0.5
|
ELECTROLYTE
|
|
|
|
Calsium
|
7.9
|
Mg/dl
|
8.4 – 10.2
|
Sodium
|
131
|
Mg/dl
|
135 – 155
|
Pottasium
|
3.6
|
Mg/dl
|
3.6 – 5.5
|
Chloride
|
96
|
Mg/dl
|
96 – 106
|
Laboratorium findings: 07 may 2016 21:17:18
Complete Blood Analysis:
Test
|
Result
|
Unit
|
References
|
Hemoglobin
|
14.2
|
g%
|
10.8 – 15.6
|
Erithrocyte
|
5.28
|
106/mm3
|
4.50 – 6.50
|
Leukocyte
|
2.94
|
103/mm3
|
4.5 - 13.5
|
Trombocyte
|
32
|
103/mm3
|
150-450
|
Hematocrite
|
42
|
%
|
33 – 45
|
Eosinophil
|
0
|
%
|
1-5
|
Basophil
|
1
|
%
|
0-1
|
Neutrophill
|
38.8
|
%
|
25 – 60
|
Lymphocyte
|
53.70
|
%
|
25 – 50
|
Monocyte
|
6.50
|
%
|
1 – 6
|
Neutrophil Absolute
|
1.14
|
103/µL
|
2.4-7.3
|
Lymphocyte Absolute
|
1.58
|
103/µL
|
1.7-5.1
|
Monocyte absolute
|
0.19
|
103/µL
|
0.2-0.6
|
Basophil absolute
|
0.03
|
103/µL
|
0-0.1
|
Eusinophil absolute
|
0
|
103/µL
|
0.1 – 0.3
|
MCV
|
80
|
fL
|
69 – 93
|
MCH
|
26.9
|
Pg
|
22 – 34
|
MCHC
|
33.5
|
g%
|
32 – 36
|
PCT
|
0.04
|
Mg/dl
|
0.1 – 0.5
|
Laboratorium Findings: 08 may 2016 09:41:42
Complete Blood Analysis:
Tes
|
Hasil
|
Unit
|
Rujukan
|
Hemoglobin
|
14.3
|
g%
|
10.8 – 15.6
|
Eritrocyte
|
5.37
|
106/mm3
|
4.50 – 6.50
|
Leukocyte
|
4.1
|
103/mm3
|
4.5 - 13.5
|
Trombocyte
|
18
|
103/mm3
|
150-450
|
Hematocrite
|
43
|
%
|
33 – 45
|
Eosinophil
|
0.2
|
%
|
1-5
|
Basophil
|
1
|
%
|
0-1
|
Neutrophil
|
29
|
%
|
25 – 60
|
Lymphocyte
|
59.8
|
%
|
25 – 50
|
Monocyte
|
10
|
%
|
1 – 6
|
Neutrophil Absolute
|
1.19
|
103/µL
|
2.4-7.3
|
Lymphocyte Absolute
|
2.45
|
103/µL
|
1.7-5.1
|
Monocyte absolute
|
0.41
|
103/µL
|
0.2-0.6
|
Basophil absolute
|
0.03
|
103/µL
|
0-0.1
|
Eosinophil absolute
|
0.01
|
103/µL
|
0.1 – 0.3
|
MCV
|
79
|
fL
|
69 – 93
|
MCH
|
26.6
|
Pg
|
22 – 34
|
MCHC
|
33.6
|
g%
|
32 – 36
|
PCT
|
0.02
|
%
|
0.1 – 0.5
|
RDW
|
12.3
|
%
|
11- 15
|
|
|
|
|
Laboratorium Findings: 08 may 2016 21:45:43
Complete Blood Analysis:
Tes
|
Hasil
|
Unit
|
Rujukan
|
Hemoglobin
|
12.8
|
g%
|
10.8 – 15.6
|
Eritrocyte
|
4.77
|
106/mm3
|
4.50 – 6.50
|
Leukocyte
|
4.9
|
103/mm3
|
4.5 - 13.5
|
Trombocyte
|
26
|
103/mm3
|
150-450
|
Hematocrite
|
38
|
%
|
33 – 45
|
Eosinophil
|
0.4
|
%
|
1-5
|
Basophil
|
0.4
|
%
|
0-1
|
Neutrophil
|
29
|
%
|
25 – 60
|
Lymphocyte
|
62.7
|
%
|
25 – 50
|
Monocyte
|
7.5
|
%
|
1 – 6
|
Neutrophil Absolute
|
1.44
|
103/µL
|
2.4-7.3
|
Lymphocyte Absolute
|
3.11
|
103/µL
|
1.7-5.1
|
Monocyte absolute
|
0.37
|
103/µL
|
0.2-0.6
|
Basophil absolute
|
0.02
|
103/µL
|
0-0.1
|
Eosinophil absolute
|
0.02
|
103/µL
|
0.1 – 0.3
|
MCV
|
79
|
fL
|
69 – 93
|
MCH
|
26.8
|
Pg
|
22 – 34
|
MCHC
|
34
|
g%
|
32 – 36
|
PCT
|
0.03
|
%
|
0.1 – 0.5
|
RDW
|
12.3
|
%
|
11- 15
|
|
|
|
|
Laboratory findings: 09 may 2016 01:40:30
Complete Blood Analysis:
Test
|
Result
|
Unit
|
References
|
Hemoglobin
|
12.7
|
g%
|
10.8 – 15.6
|
Eritrhocyte
|
4.78
|
106/mm3
|
4.50 – 6.50
|
Leucoyte
|
6.34
|
103/mm3
|
4.5 - 13.5
|
Trombocyte
|
36
|
103/mm3
|
150-450
|
Hematocrite
|
38
|
%
|
33 – 45
|
Eosinophill
|
0.3
|
%
|
1-5
|
Basophil
|
0.5
|
%
|
0-1
|
Neutrophil
|
36.9
|
%
|
25 – 60
|
Limphocyte
|
56.6
|
%
|
25 – 50
|
Monocyte
|
5.7
|
%
|
1 – 6
|
Neutrophil Absolute
|
2.34
|
103/µL
|
2.4-7.3
|
Lymphocyte Absolute
|
3.59
|
103/µL
|
1.7-5.1
|
Monocyte absolute
|
0.36
|
103/µL
|
0.2-0.6
|
Basophil absolute
|
0.03
|
103/µL
|
0-0.1
|
Eosinophil absolute
|
0.02
|
103/µL
|
0.1 – 0.3
|
MCV
|
79
|
fL
|
69 – 93
|
MCH
|
26.6
|
Pg
|
22 – 34
|
MCHC
|
33.8
|
g%
|
32 – 36
|
PCT
|
0.04
|
%
|
0.1 – 0.5
|
RDW
|
12.2
|
%
|
11- 15
|
3.11. Differential diagnose
1.
Dengue hemorrhagic fever without shock
2. Typhoid fever
3.
Leptospirosis
3.12. Confirm Diagnosis
Dengue Hemorrhagic fever without
shock
3.13. Therapy
-
IVFD RL 3cc / KgBB , 45 cc/ hour
-
Zinc
1x 20 mg
-
Paracetamol
3 x 150 mg
3.14. Planning
-
Complete
blood analysis / 6 jam, IgG dan IgM anti
dengue, Foto Thorax
3.15. Prognosis
Dubia ad Bonam
FOLLOW UP
Date : 7 may 2016
S
|
Fever (+), Spontaneous bleeding
(-), diarrhea (+)
|
O
|
Sens: CM T: 37,9 oC BW: 15 kg BH: 109 cm
Head : Eye : LR (+/+),isochoric pupil ,
pale inferior palpebral
conjunctiva (-/-), E/N/M: normal morphologic
Thorax:
Simetris fusiformis, retraction,
HR: 100 x/min,
regular, murmur (-)
RR: 22 x/min,
regular, ronchi (-/-)
Abdomen:
soepel, peristaltik (+) N, H/L : unpalpable
Upper extrimity: HR 94
x/min, regular, P/V adequate, warm extrimity, CRT <3”, BP: 110/70
mmHg, ptechie (+)
Lower extrimity : pretibial
oedem (-)
|
A
|
1. DHF without shock
|
P
|
IVFD RL 3 cc / kgBB / jam
Zinc 1x20 mg
Paracetamol 150 mg / day
Planning :complete blood
analysis, IgG dan IgM anti dengue, chest radiography
|
Date : 8 may 2016
S
|
Fever (+), Spontaneous bleeding
(-), mencret (+)
|
O
|
Sensorium:
CM T: 38,1 oC BW: 15 kg BH: 109 cm
Head: Mata
RC (+/+), Isochoric
pupil,pale konj. palpebral inferior (-/-), E/N/M: normal morphologic
Thorax:
Simetris fusiformis, retraction (-).
HR: 100 x/min,
regular, murmur (-)
RR: 20 x/min,
regular, ronchi (-/-)
Abdomen:
soepel, peristaltik (+) N, H/L : unpalpable, shifting dullness (+)
Upper extrimity: HR 95 x/min,
regular, P/V adequate, warm extrimity, CRT
<3”, BP: 100/70 mmHg, ptechie (+) at upper and lower extrimity
|
A
|
1. DHF without shock
|
P
|
IVFD RL 3 cc / kgBB / jam
Zinc 1x20 mg
Paracetamol 150 mg / day
Planning : complete blood
analysis every 6 hour
|
Date : 9 may 2016
S
|
Fever (+), Spontaneous
bleeding (-),
|
O
|
Sens:
CM T: 37,9 oC BW: 15 kg BH: 109 cm
Head : Eye LR(+/+),Isochor pupil, pale inferior palpebra
conjunctiva (-/-), E/N/M: normal morphologic
Thorax:
Simetris fusiformis, Retraction (-),
HR: 104 x/min,
regular, murmur (-)
RR: 22 x/min,
regular,
Respiratory sound : weaker at right lungs, ronchi (-/-)
Abdomen:
soepel, peristaltik (+) N,shifting dullness (+) H/L : unpalpable
Upper extrimity: HR 94
x/min, regular, P/V cukup, warm extrimity, CRT <3”, BP: 110/70
mmHg, ptekie (+) pada ekstrimitas
atas dan bawah
|
A
|
1. DHF without shock
|
P
|
IVFD RL 3 cc / kgBB
Zinc 1x20 mg
Paracetamol 150 mg / day
Planning : Complete blood
analysis , IgG dan IgM anti dengue,
|
Date : 10 may 2016
S
|
Fever (-), Spontaneous
bleeding (-),
|
O
|
Sens:
CM T: 36,9 oC BW: 15 kg BH: 109 cm
Head : Eye LR(+/+),Isochor pupil, pale inferior palpebra
conjunctiva (-/-), E/N/M: normal morphologic
Thorax:
Simetris fusiformis, Retraction (-),
HR: 120 x/min,
regular, murmur (-)
RR: 18 x/min,
regular,
Respiratory sound : weaker at right lungs, ronchi (-/-)
Abdomen :
soepel, peristaltik (+) N,shifting dullness (-) H/L : unpalpable
Upper extrimity: HR 94
x/min, regular, P/V cukup, warm extrimity, CRT <3”, BP: 100/70 mmHg
|
A
|
1. DHF without shock
|
P
|
IVFD RL 3 cc / kgBB
Zinc 1x20 mg
Planning : Complete blood
analysis , IgG dan IgM anti dengue,
|
Date : 11 may 2016
S
|
Fever (-), Spontaneous
bleeding (-),
|
O
|
Sens:
CM T: 36,9 oC BW: 15 kg BH: 109 cm
Head : Eye LR(+/+),Isochor pupil, pale inferior palpebra
conjunctiva (-/-), E/N/M: normal morphologic
Thorax:
Simetris fusiformis, Retraction (-),
HR: 120 x/min,
regular, murmur (-)
RR: 18 x/min,
regular,
Respiratory sound : weaker at right lungs, ronchi (-/-)
Abdomen:
soepel, peristaltik (+) N,shifting dullness (-) H/L : unpalpable
Upper extrimity: HR 94
x/min, regular, P/V cukup, warm extrimity, CRT <3”, BP: 100/70 mmHg
|
A
|
1. DHF without shock
|
P
|
Patient discharge after fever
was diminished but the respiratory sound still weaker at right lungs with
improvement.
Patient’s education:
Patient needs a rest
Drink enough water
Parasetamol is given if fever is
found
|
CHAPTER
4
DISCUSSION
Dengue
viral infected person may be asymptomatic or symptomatic and clinical
manifestations vary from undifferentiated fever to florid haemorrhage and
shock. Clinical Features of DF: An
acute febrile illness of 2-7 days duration with two or more of the following
manifestations: Headache, retro-orbital pain, myalgia, arthralgia, rash,
haemorrhagic manifestations. In this case was found fever
as a main complaint. The fever was reduce with antipyretic drugs. The highest
temperature measure was 39
. It was taken by his mother. No history of shivering. Patient
experienced headache and joint pain since 3 days ago. His
mother also complaint there was a reddish skin (rash) at the upper and lower
extrimities. The patient also felt nauseated since 6 days before came to the
hospital. Patient vomited once before coming to the hospital. The vomit
contents is the food and the drinks he consumed.

Diagnosis of Dengue Hemoragic Fever is a
case of clinical criteria of dengue Fever, plus
Haemorrhagic tendencies evidenced by one or more of the following: Positive
tourniquet test, petechiae, ecchymoses or purpura, bleeding from mucosa,
gastrointestinal tract, injection sites or other sites, plus thrombocytopenia
(<100 000 cells per cumm), plus evidence of plasma leakage due to increased
vascular permeability, manifested by one or more of the following: Arise in
average haematocrit for age and sex > 20%, a more than 20% drop in
haematocrit following volume replacement treatment compared to baseline, and
Signs of plasma leakage (pleural effusion, ascites, hypoproteinemia). In this
case there was petechiae, Abdominal pain also found during history taking. Based on
the laboratorium result show that there was thrombocytopenia (84.000/mm3). There was shifting dullness and
when auskultasi in the respiratory sound found weaker at right lungs. This auskultation
was supported by chest radiography that found pleural effusion in the right
lung. In this case there was no rapid and weak pulse and narrow pulse pressure ( mmHg) or hypotension
for age, cold and clammy skin and restlessness.
Any person who has
dengue fever with thrombocytopenia, high haemoconcentration and presents with
abdominal pain, black tarry stools, epistaxis, bleeding from the gums etc. needs
to be hospitalized. All these patients should be observed for signs of shock.
The critical period for development of shock is during transition from febrile
to abferile phase of illness, which usually occurs after third day of illness.
Rise of haemoconcentration indicates plasma leakage and loss of volume for
which proper fluid management plays an important role. Despite the treatment,
if the patient develops fall in BP, decrease in urine output or other features
of shock, the management for DHF without shock should be instituted. Oral
rehydration should be given along with antipyretics like Paracetamol, sponging,
etc. So, for this patient was given IVFD RL 3 cc / kgBB
for rehydration, Zinc 1x20 mg, and Paracetamol 3x 150 mg if the
patient got fever.
Criteria for discharge of patients, the admitted patients
who have recovered from acute dengue infection having no fever for atleast 24
hours, normal blood pressure, adequate urine output, no respiratory distress,
persistent platelet count >50,000/cu.mm should be discharged from hospital.
(3)
Vaccine for dengue infection till now there is no
licensed vaccine available against dengue viral infection. Several trials are ongoing
in the world for the development of tetravalent dengue vaccine. So far phase
III trials of a recombinant, live attenuated tetravalent dengue vaccine
(CYD-TDV) has completed in Five Asian countries in children which may be
promising in preventing dengue infection in near future.(3)
CHAPTER
5
SUMMARY
KA, a boy, a five years 7 months old boy with 15 kg of body weight nd 109 cm
of body height came to Unit Gawat Darurat RS Haji Adam Malik on 6th mei 2016 at
20.10 PM with fever asa a chief complaint. Diarrhea, joint pain, headache,
stomach pain were found during history taking. Ptekie was also found during
physical examination. Patient diagnosed with Dengue Hemorrhagic Fever and
treated with supportive and symptomatic therapy. Patient treated with Fluid
therapy, Zinc and Paracetamol for the symptomatic complaint. Therapy were given
onward for 4 days with an improvement in clinical manifestation on day 4. On
11th may 2016, patient returned home after clinical improvement found during examination.
REFERENCE
1.
World Health Organization.
National Guidelines for Clinical Management of Dengeu Fever; 2015.
2. World
Health Organization and Tropical Diseases Research. Handbook for clinical
management of dengue. Geneva: World Health Organization; 2012.
3. World
Health Organization Guidelines for Clinical
Management of Dengue Fever, Dengue Hemorragic Fever, and Dengue Shock Sindrome;CDC.
4. World
Health Organization Dengue Guidelines for
Diagnosis, Treatment, Prevention, and Controls; 2009.
5. World
Health Organization. Comprehensive guidelines for prevention and control of
dengue and dengue hemorrhagic fever. New Delhi:WHO,SEARO; Revised and expanded
edition.2008.
6. Elsevier. Nelson Textbook of Pediatrics. 2015
7. World
Health Organization. Dengue and Dengue Hemoragic
Fever; 2008
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