CASE REPORT

DENGUE HEMORRHAGIC FEVER

By :
Angelin Putri Gozali (130100379)

Supervisor :
dr. Yazid Dimyati, M.ked(Ped), Sp.A (K)

PEDIATRIC DEPARTMENT
HAJI ADAM MALIK GENERAL HOSPITAL
FACULTY OF MEDICINE
UNIVERSITY OF SUMATERA UTARA
MEDAN
2017
 2

CONTENTS

CONTENTS ................................................................................... 2
CHAPTER I INTRODUCITON.................................................. 3
1.1. Background ............................................................................ 3
1.2. Objective ................................................................................ 4
CHAPTER II LITERATURE REVIEW .................................... 5
2.1. Definition ............................................................................... 5
2.2. Etiology .................................................................................. 5
2.3. Epidemiology ......................................................................... 5
2.4. Pathogenesis ........................................................................... 7
2.5. Pathophysiology ..................................................................... 8
2.6. Classification .......................................................................... 9
2.7 Clinical Manifestation ............................................................ 11
2.8. Diagnosis ................................................................................ 15
2.9. Differential Diagnose ............................................................. 17
2.10 Treatment ............................................................................... 17
2.10. Prognose ................................................................................. 13
CHAPTER III CASE REPORT .................................................. 20
CHAPTER IV DISCUSSION ...................................................... 27
CHAPTER V CONCLUSION ..................................................... 29
REFERENCE ................................................................................ 30
 3

CHAPTER I
INTRODUCTION

1.2 Background
Dengue fever (DF) and its severe form, the dengue hemorrhagic fever
(DHF) and dengue shock syndrome (DSS), is a re-emerging arboviral disease of
great public health importance, and it has spread to all tropical and sub-tropical
countries in the world.1 The actual numbers of dengue cases are underreported and
many cases are misclassified. One recent estimate indicates 390 million dengue
infections per year (95% credible interval 284–528 million), of which 96 million
(67–136 million) manifest clinically. Another study, of the prevalence of dengue,
estimates that 3.9 billion people, in 128 countries, are at risk of infection with
dengue viruses.2
In 2012, dengue was once again classified by the World Health
Organization (WHO) as the ‘most important mosquito-borne viral disease in the
world’ due to significant geographic spread of the virus and its vector into
previously unaffected areas and the subsequent costly burden of disease it brings.3
Before 1970, only 9 countries had experienced severe dengue epidemics. The
disease is now endemic in more than 100 countries in the WHO regions of Africa,
the Americas, the Eastern Mediterranean, South-East Asia and the Western
Pacific. The America, South-East Asia and Western Pacific regions are the most
seriously affected.1 A study of twelve countries in South East Asia (using
available data from 2001–2010) showed an aggregate annual economic burden of
US$950 million amongst the studied nations, with approximately 52% of these
costs coming from productivity loss.3
Indonesia is one of the largest countries in the dengue endemic region,
with a population of 251 million.4 The first time Dengue hemorrhagic fever
(DHF) was discovered in Indonesia was in 1968 in Surabaya with 58 cases
occurred in children, of which 24 children died.5 Based on Karyanti MR et al,
study using an on-going nationwide dengue surveillance program starting in 1968
 4

up to 2013, concluded that the incidence of DHF has increased substantially over
the past 45 year. The annual DHF incidence increased from 0.05/100,000 in 1968
to 35-40/100,000 in 2013, with the highest epidemic occurring in 2010
(85.70/100,000). In contrast, the case fatality ratio clearly decreased during the
same period and the age shifting towards older age groups (above 15 years of
age).4 Ministry of Health of Indonesia reported the number of DHF patients in
Indonesia within January through February 2016 were 8,487 patients, of which
108 patients died.6
Dengue is caused by viruses belonging to genus Flavivirus (family

Flaviviridae) with four known serotypes: DENV‑1 through DENV‑4. Infection

with one serotype confers life‑long immunity to that serotype and a few months

cross‑immunity to other serotypes. Sequential infection of two serotypes leads to

more severe type of disease (e.g. DHF). Aedes aegypti is the primary vector and
this mosquito lives in proximity to human habitations in urban areas and breeds

mostly in man‑made containers.1

Many experts hypothesize that dengue will increase in the future,

including geographic expansion and incidence.3 Based on longterm average vapor
pressure prediction, climate change and population projections, Hales et al,
predicted that approximately 50%–60% of the global population would be living
in areas at risk of dengue transmission by 2085.7
Due to poor disease surveillance, low level of reporting, low case fatality
rate, difficulties in diagnosis, and inconsistent comparative analyses, the true
incidence and impact of dengue is likely significantly higher than that which is
currently reported.3 Those reasons is why there still a need to understand more
about dengue hemorrhagic fever.
1.2 Objective
The purpose of this study is to understand the theory about dengue
hemorrhagic fever and applied it to DHF case in Haji Adam Malik General
Hospital.
 5

CHAPTER II
LITERATURE REVIEW

2.1 Definition
Dengue hemorrhagic fever is an infectious disease resulting spectrum of
clinical manifestations that vary from the lightest, dengue fever, hemorrhagic
fever and dengue fever are accompanied by shock or dengue shock syndrome. Its
caused by dengue virus, transmitted by Aedes mosquitoes.8
2.2 Etiology
The dengue viruses are members of the Arthropod-Borne Virus group
(Arboviruses), genus Flavivirus and family Flaviviridae. These small (50 nm)
viruses contain single-strand RNA as genome. The dengue virus genome is
composed of three structural protein genes encoding the nucleocaprid or core
protein (C), a membrane-associated protein (M), an envelope protein (E), and
seven non-structural protein (NS) genes. Among non-structural proteins, envelope
glycoprotein, NS1, is of diagnostic and pathological importance. It is 45 kDa in
size and associated with viral haemagglutination and neutralization activity.9
There are four virus serotypes, which are designated as DENV-1, DENV-
2, DENV-3 and DENV-4. Infection with any one serotype confers lifelong
immunity to that virus serotype. Secondary infection with another serotype or
multiple infections with different serotypes leads to severe form of dengue
(DHF/DSS).9
2.3 Epidemiology
Dengue infection is the most rapidly spreading mosquitoborne viral
disease in the world. The World Health Organization (WHO) reported that the
incidence of increased dramatically over the last 50 years. Annually, about 50
million dengue infections occur, and approximately 500,000 patients are
hospitalized because of dengue hemorrhagic fever (DHF), of whom a very large
 6

proportion (approximately 90%) of them are children aged less than five years,
and about 2.5% of those affected die.9
Dengue viruses are transmitted by mosquitoes of the Stegomyia family
Aedes aegypti, a daytime biting mosquito, is the principal vector, and all 4 virus
types have been recovered from it. In most tropical areas, A. aegypti is highly
urbanized, breeding in water stored for drinking or bathing and in rainwater
collected in any container. Dengue viruses have also been transmitted by Aedes
albopictus mosquitoes.1,9,10

Figure 2.1 Geographical mapping of Indonesian provincial incidence rate of

DHF in 2010 – 2013.4
The annual DHF incidence increased significantly from 0.05/100,000 in
1968 to 35-40/100,000 in 2013. The highest epidemic peak was observed in 2010
with 86 DHF cases per 100,000 person-years. Bali and DKI Jakarta had the
highest incidence of DHF. In 2013, the five highest provincial incidences were
observed in Bali (168.5/100,000), DKI Jakarta (104.0/ 100,000), DI Yogyakarta
(96.0/100,000), East Kalimantan (92.7/100,000) and Sulawesi Tenggara
(66.8/100,000).
Increases in DHF incidence may be explained by increased vector density
or abundance because of lack of effective mosquito control, by viral
 7

genotypes/subtypes with increased virulence, by increased human mobility

(globalization and travel factors), by climate change factors, by socioeconomic
factors and by altered virus-host interaction leading to increased infectivity and
therefore more secondary infection.1,3,4
2.4 Pathogenesis
Several hypotheses for the pathogenesis of dengue hemorrhagic fever have
been proposed. Among them, Antibody-Dependent Enhancement (ADE) of
infection has long been thought to play a central role. The ADE hypothesis was
formulated to explain the finding that severe manifestations of DHF/DSS occur in
children experiencing a second dengue virus infection that has a different serotype
from previous one. This mechanism increases viral replication and causes higher
viremia due to an increased number of cells infected and the preexisting
antibodies to previous dengue virus that cannot neutralize but rather enhance
infection in vitro compared to individuals infected in the absence of enhancing
antibodies.11,12
When the concentrations of these antibodies, acquired actively or
passively (newborn babies less than 1 year old who acquire maternal anti-dengue
IgG antibody), fail to neutralize DENV, the residual antibodies complex with
DENV to facilitate infection of Fc receptorbearing cells. When dengue virus
immune complexes attach to macrophage Fc receptors, a signal is sent that
suppresses innate immunity, resulting in enhanced viral production. Early in the
acute stage of secondary dengue infections, there is rapid activation of the
complement system. Shortly before or during shock, blood levels of soluble tumor
necrosis factor receptor, interferon-γ, and interleukin-2 are elevated. C1q, C3, C4,
C5-C8, and C3 proactivators are depressed, and C3 catabolic rates are elevated.
The complement cascade is activated by a virus-antibody complex as well as by
several cytokines to release C3a and C5a which also have direct effects on
vascular permeability. The synergistic effects of IFN-g, TNFa and activated
complement proteins trigger plasma leakage of endothelial cells in secondary
dengue virus infection. Those factors, the virus itself, or viral nonstructural
 8

protein 1 (NS1) may interact with endothelial cells, blood clotting factors, and
platelets to produce increased vascular permeability.10-12

2.5 Pathophysiology
2.5.1 Plasma Leakage
The plasma leakage is due to the increased vascular permeability induced
by several mediators such as C3a, C5a during the acute febrile stage and
prominent during the toxic stage. The evidence of plasma leakage includes
hemoconcentration, hypoproteinemia/hypoalbuminemia, pleural effusion, ascites,
threatened shock and profound shock. The rising hematocrit may not be evidenced
because of either severe bleeding or early intravenous fluid replacement.13
2.5.2 Bleeding tendency
The bleeding diathesis is caused by vasculopathy, thrombocytopenia,
platelet dysfunction and coagulopathy.
 Vasculopathy
A positive tourniquet test indicating the increased capillary fragility is
found in the early febrile stage. It may be a direct effect of dengue virus as
it appears in the first few days of illness during the viremic phase.13
 Thrombocytopenia and platelet dysfunction
The mechanisms of thrombocytopenia include decreased platelet
production and increased peripheral destruction. Study of the bone marrow
of patients with DHF during the acute febrile stage and found marked
hypocellularity with a decrease in megakaryocytes, erythroblasts and
myeloid precursors. Additionally, the dengue virus can also bind to human
platelets in the presence of virus-specific antibodies, and an
immunemediated increased peripheral destruction of platelet,s markedly
prominent during 2 days before defervescence. Subsequently, the number
of platelets is rapidly increased in the convalescent stage and reaches the
normal level within 7–10 days after the defervescence.11,13
 Coagulopathy
 9

During the acute febrile stage, mild prolongation of the prothrombin time
and partial thromboplastin time, as well as reduced fibrinogen levels, have
been demonstrated in several studies. Variable reductions in the activities
of several coagulation factors, including prothrombin, factors V, VII, VIII,
IX and X, antithrombin and -antiplasmin, have been demonstrated. Fibrin
degradation product or D-dimer is slightly elevated. Most of the patients
have serum aspartate transaminase (AST) and alanine transaminase (ALT)
levels threeand twofold higher than normal, respectively. There is focal
necrosis of hepatic cells, swelling appearance of Councilman bodies and
hyaline necrosis of Kupffer cells. Proliferation of mononuclear leucocytes
and less frequently polymorphonuclear leucocytes occurs in the sinusoids
and occasionally in the portal areas.11,13

Figure 2.2 Pathophysiology change in DHF.14

2.6 Classification
Dengue virus infection may be asymptomatic or may cause
undifferentiated febrile illness (viral syndrome), dengue fever (DF), or dengue
 10

haemorrhagic fever (DHF) including dengue shock syndrome (DSS). The

classification can be seen in figure 2.3.14

Figure 2.3 Manifestation of dengue virus infection.14

2.6.1 Undifferentiated Fever

Infants, children and adults who have been infected with dengue virus,
especially for the first time (i.e. primary dengue infection), may develop a simple
fever indistinguishable from other viral infections. Maculopapular rashes may
accompany the fever or may appear during defervescence Upper respiratory and
gastrointestinal symptoms are common.14
2.6.2 Dengue fever
Dengue fever (DF) is most common in older children, adolescents and
adults. It is generally an acute febrile illness, and sometimes biphasic fever with
severe headache, myalgias, arthralgias, rashes, leucopenia and thrombocytopenia
may also be observed. Although DF may be benign, it could be an incapacitating
disease with severe headache, muscle and joint and bone pains (break-bone fever),
particularly in adults. Occasionally unusual haemorrhage such as gastrointestinal
bleeding, hypermenorrhea and massive epistaxis occur. In dengue endemic areas,
outbreaks of DF seldom occur among local people.14
2.6.3 Dengue hemorrhagic fever
Dengue hemorrhagic fever (DHF) is more common in children less than
15 years of age in hyperendemic areas, in association with repeated dengue
 11

infections. However, the incidence of DHF in adults is increasing. DHF is

characterized by the acute onset of high fever and is associated with signs and
symptoms similar to DF in the early febrile phase. There are common
haemorrhagic diatheses such as positive tourniquet test (TT), petechiae, easy
bruising and/or GI haemorrhage in severe cases. By the end of the febrile phase,
there is a tendency to develop hypovolemic shock (dengue shock syndrome) due
to plasma leakage. The presence of preceding warning signs such as persistent
vomiting, abdominal pain, lethargy or restlessness, or irritability and oliguria are
important for intervention to prevent shock. Abnormal haemostasis and plasma
leakage are the main pathophysiological hallmarks of DHF. Thrombocytopenia
and rising haematocrit/haemoconcentration are constant findings before the
subsidence of fever/ onset of shock. DHF occurs most commonly in children with
secondary dengue infection. It has also been documented in primary infections
with DENV-1 and DENV-3 as well as in infants.14
2.6.4 Expanded dengue syndrome
Unusual manifestations of patients with severe organ involvement such as
liver, kidneys, brain or heart associated with dengue infection have been
increasingly reported in DHF and also in dengue patients who do not have
evidence of plasma leakage. These unusual manifestations may be associated with
coinfections, comorbidities or complications of prolonged shock. Exhaustive
investigations should be done in these cases. Most DHF patients who have
unusual manifestations are the result of prolonged shock with organ failure or
patients with comorbidities or coinfections.14
2.7 Clinical Manifestation
Based on WHO Diagnosis, Treatment, Prevention and Control 2009, it
classified the clinical manifestation into three phase : febril phase, critical phase
and recovery phase.
 12

Figure 2.4 Course of dengue illness

2.7.1 Febrile phase

After an average intrinsic incubation period of 4–6 days (range 3–14
days). Patients typically develop a high-grade fever suddenly. This acute febrile
phase usually lasts 2-7 days and is often accompanied by facial flushing, skin
erythema, generalized body ache, myalgia, arthralgia, retro-orbital eye pain,
photophobia, rubeliform exanthema and headache. Some patients may have a sore
throat, an injected pharynx, and conjunctival injection. Anorexia, nausea and
vomiting are common. It can be difficult to distinguish dengue clinically from
non-dengue febrile diseases in the early febrile phase. A positive tourniquet test in
this phase indicates an increased probability of dengue. Mild haemorrhagic
manifestations such as petechiae and mucosal membrane bleeding (e.g. of the
nose and gums) may be seen. Easy bruising and bleeding at venepuncture sites is
present in some cases. Massive vaginal bleeding (in women of childbearing age)
and gastrointestinal bleeding may occur during this phase although this is not
common. The liver may be enlarged and tender after a few days of fever. The
earliest abnormality in the full blood count is a progressive decrease in total white
cell count, which should alert the physician to a high probability of dengue.
 13

2.7.2 Critical phase

The period of plasma leakage, begins around the transition from the febrile
to the afebrile phase usually on days 3–8 of illness. Evidence of plasma leakage,
pleural effusion and ascites may, however, not be detectable by physical
examination in the early phase of plasma leakage or mild cases of DHF. A rising
haematocrit, e.g. 10% to 15% above baseline, is the earliest evidence. Progressive
leukopenia followed by a rapid decrease in platelet count usually precedes plasma
leakage. The period of clinically significant plasma leakage usually lasts 24-48
hours.
The degree of haemoconcentration above the baseline haematocrit reflects
the severity of plasma leakage; however, this may be reduced by early intravenous
fluid therapy. Hence, frequent haematocrit determinations are essential because
they signal the need for possible adjustments to intravenous fluid therapy. Pleural
effusion and ascites are usually only clinically detectable after intravenous fluid
therapy, unless plasma leakage is significant. A right lateral decubitus chest
radiograph, ultrasound detection of free fluid in the chest or abdomen, or gall
bladder wall oedema may precede clinical detection. In addition to the plasma
leakage, haemorrhagic manifestations such as easy bruising and bleeding at
venepuncture sites occur frequently. A significantly decreased serum albumin
>0.5 gm/dl from baseline or <3.5 gm% is indirect evidence of plasma leakage
Warning signs usually precede the manifestations of shock and appear
towards the end of the febrile phase. The shock is characterized by a rapid and
weak pulse with narrowing of the pulse pressure ≤20 mmHg with an increased
diastolic pressure, e.g. 100/90 mmHg, or hypotension. Signs of reduced tissue
perfusion are: delayed capillary refill (>3 seconds), cold clammy skin and
restlessness. Patients in shock are in danger of dying if no prompt and appropriate
treatment is given. Patients may pass into a stage of profound shock with blood
pressure and/or pulse becoming imperceptible (Grade 4 DHF). It is noteworthy
that most patients remain conscious almost to the terminal stage. Shock is
reversible and of short duration if timely and adequate treatment with volume-
replacement is given.
 14

Figure 2.5 Warning Signs

2.7.3 Recovery phase

As the patient survives the 24-48 hour critical phase, a gradual
reabsorption of extravascular compartment fluid takes place in the following 48-
72 hours. General wellbeing improves, appetite returns, gastrointestinal symptoms
abate, haemodynamic status stabilizes, and diuresis ensues. Some patients have a
confluent erythematous or petechial rash with small areas of normal skin,
described as “isles of white in the sea of red”. Some may experience generalized
pruritus. Bradycardia and electrocardiographic changes are common during this
stage. The haematocrit stabilizes or may be lower due to the dilutional effect of
reabsorbed fluid. The white blood cell count usually starts to rise soon after
defervescence but the recovery of the platelet count is typically later than that of
the white blood cell count. Respiratory distress from massive pleural effusion and
ascites, pulmonary oedema or congestive heart failure will occur during the
critical and/or recovery phases if excessive intravenous fluids have been
administered
 15

2.8 Diagnosis
Table 2.1 WHO classification of dengue infections and grading of severity of
DHF

Diagnostic Test test :

Dengue viraemia in a patient is short, typically occurs 2–3 days prior to
the onset of fever and lasts for four to seven days of illness. During this period the
dengue virus, its nucleic acid and circulating viral antigen can be detected
Antibody response to infection comprises the appearance of different types
of immunoglobulins; and IgM and IgG immunoglobulin isotypes are of diagnostic
value in dengue. IgM antibodies are detectable by days 3–5 after the onset of
illness, rise quickly by about two weeks and decline to undetectable levels after 2–
3 months. IgG antibodies are detectable at low level by the end of the first week,
increase subsequently and remain for a longer period (for many years). Because of
the late appearance of IgM antibody, i.e. after five days of onset of fever,
serological tests based on this antibody done during the first five days of clinical
 16

illness are usually negative. During the secondary dengue infection (when the host
has previously been infected by dengue virus), antibody titres rise rapidly. IgG
antibodies are detectable at high levels, even in the initial phase, and persist from
several months to a lifelong period. IgM antibody levels are significantly lower in
secondary infection cases.

Figure 2.6 Approximate timeline of primary and secondary dengue virus

infections and the diagnostic methods that can be used to detect infection

Hence, a ratio of IgM/IgG is commonly used to differentiate between primary and

secondary dengue infections. The IgM/IgG ratio is used to distinguish primary
infection from secondary dengue infection . A dengue virus infection is defined as
primary if the capture IgM/IgG ratio is greater than 1.2, or as secondary if the
ratio is less than 1.2.14
Table 2.2 Interpretation of Immunoserology Test.16
 17

2.9 Differential Diagnosis

 Arboviruses: Chikungunya virus (this has often been mistaken for dengue
in South-East Asia).
 Other viral diseases: Measles; rubella and other viral exanthems; Epstein-
Barr Virus (EBV); enteroviruses; influenza; hepatitis A; Hantavirus.
 Bacterial diseases: Meningococcaemia, leptospirosis, typhoid, melioidosis,
rickettsial diseases, scarlet fever.
 Parasitic diseases: Malaria.
2.10 Treatment
Indications for IV fluid:
 when the patient cannot have adequate oral fluid intake or is vomiting.
 when HCT continues to rise 10%–20% despite oral rehydration.
 Impending shock/shock.
The general principles of fluid therapy in DHF include the following:14
 Isotonic crystalloid solutions should be used throughout the critical
period except in the very young infants <6 months of age in whom 0.45%
sodium chloride may be used.
 Hyper-oncotic colloid solutions (osmolarity of >300 mOsm/l) such as
dextran 40 or starch solutions may be used in patients with massive
plasma leakage, and those not responding to the minimum volume of
crystalloid (as recommended below). Iso-oncotic colloid solutions such as
plasma and hemaccel may not be as effective.
 A volume of about maintenance +5% dehydration should be given to
maintain a “just adequate” intravascular volume and circulation.
 The duration of intravenous fluid therapy should not exceed 24 to 48
hours for those with shock. However, for those patients who do not have
shock, the duration of intravenous fluid therapy may have to be longer but
not more than 60 to 72 hours. This is because the latter group of patients
has just entered the plasma leakage period while shock patients have
 18

experienced a longer duration of plasma leakage before intravenous

therapy is begun.
 In obese patients, the ideal body weight should be used as a guide to
calculate the fluid volume
Table 2.4 Rate of IV Fluids.14

 Management of non-shock dengue

Figure 2.7 Rate of Infusion in non-shock cases.14

 19

 Management of dengue shock

Figure 2.8 Infus Rate in DSS.14

Laboratory investigations (ABCS) should be carried out in both shock and non-
shock cases when no improvement is registered in spite of adequate volume
replacement (Table 2.4)

Table 2.4 Laboratory investigation in both shock and non shock.14

 20

CHAPTER III
CASE REPORT

Case
Name : Nadila
Age :10 years old 4 months 6 days
Gender : Girls
Address : Swadaya Road Number 8
No. MR : 00.65.30.14
Entry date : 23/8/2017
Main complaint : fever

History of disease :
 It has been experienced by the patient since four days ago, The fever
characteristic was continuous, and the fever was decreased with fever
medications. Shivering and seizures didn’t found
 Vomiting was found one day before entering the hospital, the frequency
was 20 times a day, the vomit consist of what the patients eat and drink.
The volume of vomit ± half of aqua cup. Gastrointestinal pain in lower
right quadrant (+), Nausea (+)
 Myalgia and arthralgia (-). Retro-orbtal pain was found.
 History of spontaneous bleeding like nose bleed was found two days ago,
it only happened once, the volume of blood ± 3 cc. Gum bleeding melena
and bruising didn’t found
 Sore throat was found two days before entering the hospital. Cough was
found, the sputum color is white, blood didn’t found. Pain when
swallowing food (+)
 21

 Hard to breath has been experienced by the patient since one day ago. It
was not related with the weather. The patient felt better when she sleep
tilted to the right and it felt so much worst with activities.
 History of the same disease has not been found. The patient live in a place
where flood often happened. History of traveling to endemic place didn’t
found.
Physical Examination :
 Preset Status : level of consciousness : Compos mentis. Temperature :
38°C. BW : 29 Kg. BH : 131 cm.
 Localized Status :
 Head :
Eye : light reflex (+/+), ishocoric pupil diameter 2mm/2mm, pale palpebra
conjungtiva (-/-), ikteric sclera (-/-)
Ears : within normal range
Nose : nostril breathing (-)
Mouth : cyanosis (-),Tonsil hyperemic, T3 – T3, crypta (+)
 Neck : lymph node enlargement (-)
 Thorax : simetris fusiform, retraction (-)
HR : 122 bpm, regular, murmur (-)
RR : 24 bpm, regular, ronchi (-/-), wheezing (-/-)
 Abdomen : soepel, normal peristaltic, hepar was palpable at 4 cm below
arcus costae, line was not palpable.
 Extremities : pulse 122 bpm, regular, p/v adequate, warm acral, CRT < 3”,
BP : 100/60 mmHg
Laboratory finding from Emergency Unit Adam Malik Hospital :
Hb/Ht 15,3 /42%
White blood cells 6110
Platelet 237000
Blood Glucose 111 mg/dl
Na/Kalium/Clorida 129/4,5/00
Working Diagnosis : Dengue fever + Tonsilofaringitis
Differential Diagnosis : Dengue Hemorrhagic fever, typhoid
 22

Therapy : IVFD RL 10 cc and then maintenance 70 cc/minute micro

Further investigation plan : Check complete blood analysis, blood glucose,
Electrolyte, Immunoserology (Ig M and Ig G anti Dengue), urine analysis

FOLLOW UP
24th August – 29th August 207

24th August 2017

S Fever (-), Nausea (+), gastrointestinal pain (+), vomiting (+),
decreased in appetite (+)
O level of consciousness : Compos mentis. Temperature : 37,4°C. BW :
29 Kg.
 Head :
Eye : light reflex (+/+), ishocoric pupil diameter 2mm/2mm,
pale palpebra conjungtiva (-/-), ikteric sclera (-/-)
Ears : within normal range
Nose : nostril breathing (-)
Mouth : cyanosis (-) Tonsil hyperemic, T3 – T3, crypta (+)
 Neck : lymph node enlargement (-)
 Thorax : simetris fusiform, retraction (-)
HR : 97 bpm, regular, murmur (-)
RR : 22 bpm, regular, ronchi (-/-), wheezing (-/-)
 Abdomen : soepel, normal peristaltic, hepar was palpable at 4
cm below arcus costae, lien not palpable.
 Extremities : pulse 97 bpm, regular, p/v adequate, warm acral,
CRT < 3”, BP : 90/60 mmHg

A  Dengue Fever + Tonsilofaringitis

 Dengue Hemorrhagic fever
 Typhoid
P  IVFD D5% Nacl o,45%70 gtt/i micro
 Paracetamol Tab 3 x 500 mg
 Diet MB 680 kkal with 58 gr protein
 Check Ig G and Ig M anti dengue, complete blood analysis,
USG upper and lower abdomen, Th, urine analysis

Laboratory Results on 24th August 2017

Complete blood analysis
Hb 14,2 mg/dl
 23

White Blood Count 10030 /mL

Ht 39%
Platelet 148.000
MCV/MCH/MCHC 68 fl/ 24,7 pg/ 36, g/dl
N/L/M/E/B 17,2/62,6/9,5/0/0,7

Immunoserology
Ig M anti dengue Negative
Ig G anti dengue Positive
Urine analysis
Color Bright yellow
Glucose Negative
Billirubin Negative
Keton Negative

pH 6,0
Protein Negative
Nitrit Negative
White blood cells Negative
Blood Negative

25th August 2017

S: Fever (-), Nausea (+), gastrointestinal pain (+) vomiting (-),
O: level of consciousness : Compos mentis. Temperature : 36,7°C. BW : 29
Kg.
 Head :
Eye : light reflex (+/+), ishocoric pupil diameter 2mm/2mm, pale
palpebra conjungtiva (-/-), ikteric sclera (-/-)
Ears : within normal range
Nose : nostril breathing (-)
Mouth : cyanosis (-) Tonsil hyperemic, T3 – T3
 Neck : lymph node enlargement (-)
 Thorax : simetris fusiform, retraction (-)
HR : 90 bpm, regular, murmur (-)
RR : 20 bpm, regular, ronchi (-/-), wheezing (-/-)
 Abdomen : soepel, normal peristaltic, hepar was palpable at 4 cm
below arcus costae, lien not palpable.
 Extremities : pulse 90 bpm, regular, p/v adequate, warm acral,
CRT < 3”, BP : 90/60 mmHg

A  Dengue Fever + Tonsilofaringitis

 Dengue Hemorrhagic fever
 24

 Typhoid
P  IVFD D5% Nacl o,45%70 gtt/i micro
 Paracetamol Tab 3 x 500 mg
 Diet MB 680 kkal with 58 gr protein

Thorax X-Ray 25th August 2017

Interpretation
Right sinus costophrenicus blunting. Infiltrate(-). CTR <50%. Trachea in the
middle
Conclusion : right pleural effusion

26th – 27th August 2017

S Fever (-), Gastrointestinal pain (+)
O level of consciousness : Compos mentis. Temperature : 36,8°C.
 Head :
Eye : light reflex (+/+), ishocoric pupil diameter 2mm/2mm,
pale palpebra conjungtiva (-/-), ikteric sclera (-/-)
Ears : within normal range
Nose : nostril breathing (-)
Mouth : cyanosis (-) Tonsil hyperemic (-), T2 – T2
 Neck : lymph node enlargement (-)
 Thorax : simetris fusiform, retraction (-)
HR : 87 bpm, regular, murmur (-)
RR : 18 bpm, regular, ronchi (-/-), wheezing (-/-)
 25

 Abdomen : soepel, normal peristaltic, hepar was palpable at 4

cm below arcus costae, lien not palpable.
 Extremities : pulse 87 bpm, regular, p/v adequate, warm acral,
CRT < 3”, BP : 100/60 mmHg

A  Dengue Hemorrhagic fever + Tonsilofaringitis

 Typhoid
P  IVFD D5% Nacl 0,45% 70 gtt/menit mikro
 Paracetamol tab 3x500mg
 Diet MB 1680 kkal with 58 gr protein.

Laboratory Results on 27th August 2017

Complete blood analysis
Hb 12 mg/dl
White Blood Count 5460 /mL
Ht 34%
Platelet 215.000
MCV/MCH/MCHC 70 fl/ 24,9 pg/ 35,7 g/dl
N/L/M/E/B 26/55,10/15,4/3,10/0,4

USG upper and lower abdomen result

visible free fluid in the pelvic cavity
appears right pleural effusion
liver is normal, flat surface size, homogeneous parenchyma, no focal mass.
Gall bladder size is normal. the wall do not thicken, there is no stone in it
Spleen and pancreas normal
Both kidneys size are normal, neither stone nor pelvic system widening
There is no enlarged lymph paraaorta gland
Vesica urinaria wall is clean, no mass or stone in it
Normal-sized uterus, homogeneous parenchyma and invisible focal mass
Conclusion : Right pleura effusion and free fluid in the pelvic cavity
 26

28th August – 29 August 2017

S Fever (-), Gastrointestinal pain (-)
O level of consciousness : Compos mentis. Temperature : 36,8°C.
 Head :
Eye : light reflex (+/+), ishocoric pupil diameter 2mm/2mm,
pale palpebra conjungtiva (-/-), ikteric sclera (-/-)
Ears : within normal range
Nose : nostril breathing (-)
Mouth : cyanosis (-) Tonsil T2-T1 hyperemic (-)
 Neck : lymph node enlargement (-)
 Thorax : simetris fusiform, retraction (-)
HR : 82 bpm, regular, murmur (-)
RR : 20 bpm, regular, ronchi (-/-), wheezing (-/-)
 Abdomen : soepel, normal peristaltic, hepar and lien not
palpable.
 Extremities : pulse 82 bpm, regular, p/v adequate, warm acral,
CRT < 3”, BP : 100/60 mmHg

A  Dengue Hemorrhagic Fever + Tonsilofaringitis

 Dengue Fever
P  IVFD D5% Nacl 0,45% 70 gtt/menit mikro
 Paracetamol tab 3x500mg
 Diet MB 1680 kkal with 58 gr protein.

CHAPTER IV
DISCUSSION
Theory
Clinical Manifestation :
Dengue fever
acute febrile illness, and sometimes
biphasic fever with severe headache,
myalgias, arthralgias, rashes, leucopenia
and thrombocytopenia may also be
observed. Although DF may be benign,
it could be an incapacitating disease
with severe headache, muscle and joint
and bone pains (break-bone fever),
particularly in adults. Occasionally
unusual haemorrhage such as
gastrointestinal bleeding,
hypermenorrhea and massive epistaxis
occur.
Dengue Hemorrhagic Fever
DHF is characterized by the acute onset
of high fever and is associated with
signs and symptoms similar to DF in the
early febrile phase. There are common
haemorrhagic diatheses such as positive
tourniquet test (TT), petechiae, easy
bruising and/or GI haemorrhage in
severe cases. By the end of the febrile
phase, there is a tendency to develop
hypovolemic shock (dengue shock
syndrome) due to plasma leakage. The
presence of preceding warning signs
such as persistent vomiting, abdominal
pain, lethargy or restlessness, or
irritability and oliguria are important for
intervention to prevent shock. .
Evidence of plasma leakage, pleural
effusion and ascites may, however, not
be detectable by physical examination
in the early phase of plasma leakage or
mild cases of DHF. A rising
haematocrit, e.g. 10% to 15% above
baseline, is the earliest evidence.
Progressive leukopenia followed by a
27
Case
Fever has been experienced by the
patient since four days ago, The fever
characteristic was continuous, and the
fever was decreased with fever
medications.
Vomiting was found one day before
entering the hospital, the frequency
was 20 times a day, the vomit consist
of what the patients eat and drink. The
volume of vomit ± half of aqua cup.
Gastrointestinal pain in lower right
quadrant (+), Nausea (+) Retro-orbtal
pain was found.
History of spontaneous bleeding like
nose bleed was found two days ago, it
only happened once, the volume of
blood ± 3 cc.
Hard to breath has been experienced by
the patient since one day ago. It was
not related with the weather. The
patient felt better when she sleep tilted
to the right and it felt so much worst
with activities.
The patient live in a place where flood
often happened.
 28

rapid decrease in platelet count usually

precedes plasma leakage.
Diagnosis : Ig M : negative ; Ig G : positive ->
Clinical manifestation + laboratory secondary infection
(Thrombocytopenia < 100.000, Ht > X-Ray shows : right pleural effusion
20%, serology test) USG shows : right pleural effusion
Treatment : Treatment :
A volume of about maintenance +5% IVFD D5% Nacl o,45%70 gtt/i micro
dehydration should be given to maintain Paracetamol Tab 3 x 500 mg
a “just adequate” intravascular volume Diet MB 680 kkal with 58 gr protein
and circulation.
The duration of intravenous fluid
therapy should not exceed 24 to 48
hours for those with shock. However,
for those patients who do not have
shock, the duration of intravenous fluid
therapy may have to be longer but not
more than 60 to 72 hours.
 29

CHAPTER V
CONCLUSION

Patient N, ages 4 yo, weight 29 kg and height 131 cm came to the

Emergency Unit of Haji Adam Malik General Hospital on 23th August 2017 with
fever. It has been experienced by the patient since four days ago, The fever
characteristic was continuous, and the fever was decreased with fever
medications. Vomiting was found one day before entering the hospital, the
frequency was 20 times a day, the vomit consist of what the patients eat and drink.
The volume of vomit ± half of aqua cup. Gastrointestinal pain in lower right
quadrant (+), Nausea (+). Retro-orbtal pain was found. History of spontaneous
bleeding like nose bleed was found two days ago, it only happened once, the
volume of blood ± 3 cc. Sore throat was found two days before entering the
hospital. Cough was found, the sputum color is white, blood didn’t found. Pain
when swallowing food (+). Hard to breath has been experienced by the patient
since one day ago. It was not related with the weather. The patient felt better when
she sleep tilted to the right and it felt so much worst with activities.
Based on anamnesis, physical examination and investigation the patient
was finally diagnose with Dengue Hemorrhagic Fever with Tonsilofaringitis. And
treated with :
 IVFD D5% Nacl o,45%70 gtt/i micro
 Paracetamol Tab 3 x 500 mg
 Diet MB 680 kkal with 58 gr protein
 30

REFERENCE

1. Bhatia R, Dash AP, Sunyoto T.Changing Epidemiology of Dengue in

South-East Asia. WHO South-East Asia J Public Health. 2013;2:23-7.
2. WHO | Dengue and Severe Dengue [Internet]. Citied in : 4 September 2017.
From : http://www.who.int/mediacentre/factsheets/fs117/en/
3. Murray NEA, Quam MB, Smith AN. Epidemiology of dengue: past, present
and future prospects. Clinical Epidemiology. 2013:5. 299-309
4. Karyanti, et al. The Changing Incidence of Dengue Haemorrhagic Fever I
Indonesia: a 45-year registry based analysis. BMC Infectious Disease. 2014,
14:412.1-7
5. Departemen Kesehatan Republik Indonesia. Buletin Jendela Epidemiologi
Demam Berdarah Dengue, Jakarta. Badan Litbang dan Pengembangan
Kesehatan. 2010.
6. Departemen Kesehatan Republik Indonesia. Wilayah KLB DBD Ada di 11
Provinsi. 2016. From :
http://www.depkes.go.id/article/view/16030700001/wilayah-klb-dbd-ada-di-
11-provinsi.html
7. Hales S, de Wet N, Maindonald J, Woodward A. Potential effect of
population and climate changes on global distribution of dengue fever: an
empirical model. Lancet. 2002;360(9336):830–834
8. Candra, A. Demam Berdarah Dengue 2010: Epidemiologi, Patogenesis dan
Faktor Risko Penularan. Ikatan Dokter Anak Indonesia. 2012.
9. Comprehensive and treatment who
10. Kliegman R, Stanton B, St. Geme JW, Schor N.F, Behrman RE. Nelson
textbook of pediatrics. 20th edition. Phialdelphia, PA: Elsevier;2016.
11. Lei HY, Huang KJ, Lin YS, Yeh TM, Liu HS, Liu CC.
Immunopathogenesis of Dengue Hemorrhagic Fever. Am J Infect Dis.
2008;4(1):1 – 9.
12. Guzman MG, Alvarez M, Halstead SB. Secondary infection as a risk factor
for dengue hemorrhagic fever/dengue shock syndrome : an historical
perspective and role on antibody-dependent enhacement of infection.
Archuves of Virology. 2013; 158(7): 1445 – 59.
13. Chuansumrit A, Tanganararatchakit K. Pathiphysiology and management of
dengue hemorrhagic fever. Transfusion alternatives in transfusion medicine.
2006;8(1) : 3-11.
14. World Health Organization. Comprehensive Guidelines for Prevention and
Control of Dengue and Dengue Hemorrhagic Fever. WHO South-East
Asia.2011.
15. World Health Organization. Dengue Guidelines for Diagnosis, Treatment,
Prevention and Control, New edition. WHO Geneva. 2009.
16. Pedoman Diagnosis dan Tatalaksana Infeksi Virus Dengue pada Anak.
UKK Infeksi dan Penyakit Tropis IDAI.2012