DENGUE FEVER

/DENGUE
HEMORRHAGIC FEVER

Dr. Harun Hudari, SpPD FINASIM

CURRICULUM VITAE
Nama
: Dr. H. Harun Hudari, SpPD, FINASIM
TTL
: Palembang, 3 Mei 1970
Pendidikan :
- Dokter FK Universitas Sriwijaya 1996
- Spesialis Penyakit Dalam FK Universitas Sriwijaya 2008
Riwayat Pekerjaan :
1. Dokter PTT Puskesmas Muara Rupit 1997 2000
2. Dokter PNS RSUD Dr. MM Dunda Gorontalo 2001 2004
3. Dokter Spesialis Penyakit Dalam RSUD Banyuasin
2008 sekarang
4. Dokter Spesialis Penyakit Dalam FK UNSRI/RSMH
Palembang 2009 sekarang
HP : 081271621966 / 0711 7301744

About Dengue
Dengue is one of the most important mosquito-born
viral diseases affecting humans.
Viral life cycle involves humans and the mosquito
vector Aedes aegypti.
In the U.S. it has been found that the mosquito Aedes
albopictus also transmits the DEN virus.

The disease is caused by 4 serotypes of the Dengue

virus, a member of the genus Flavivirus: DEN-1, DEN2, DEN-3, DEN-4.
Infection with the DEN virus can result in Dengue
Fever (DF), Dengue Hemorrhagic Fever (DHF) and

Dengue is a tropical febrile disease

Dengue Fever has a long history

www.philadelphia-reflections.com/topic/17.htm

992- Chinese
Encyclopedia
1780- Philadelphia
break-bone
fever
Benjamin Rush

Isolated by Albert Sabin in 1944

Manifestations of the dengue

syndrome
Spectrum of illness:

Dengue virus
Infection
Asymptomatic

Symptomatic

Undifferentiated
fever

Dengue Fever

No
hemorrhage

Unusual
hemorrhage

Dengue Hemorrhagic Fever

(plasma leakage)

DHF 1& 2

DHF 3&4
DSS

Flaviviridae
(dengue, yellow fever,
TBE encephalitides)

Viral Haemorrhagic Fevers

Arenaviridae
(Lassa, Junin, Machupo, Guanarito)

Enveloped
RNA viruses

Filoviridae
(Ebola, Marburg)

Bunyaviridae
(CCHF, RVF,
Hantaviruses)

Geographic distribution:
Southeast Asia, the Caribbean,
the Western Pacific Regions.
Other epidemiological features:
High incidence in rainy season;
Spread rapidly;
High mobidity;

Distribution of dengue, Eastern Hemisphere

Distribution of Aedes aegypti (red shaded areas)

in the Americas in 1970,and in 1997

13

Dengue Virus
Family: Flaviviridae
ss +RNA
genome: 10
proteins
3 Structural
Coat, deliver
RNA to target
cells
7 Nonstructural
Enveloped
4 serotypes:
DEN-1, 2, 3, 4
Goodsell, David. "Dengue Virus." RCSB PDB-101. N.p., n.d.
Web. 23 Oct. 2012.

17

18

19

Immune Response

Ag/Ab level

Symptom
Antibody
NS1 Ag
Bite
DAY -7 -6 -5 -4 -3 -2 -1 1 2 3 4 5 6 7 8 9 10 11 12
ACUTE
PHASE

CRITICAL
PHASE

CONVALESENC
E PHASE

IgG

IgM
NS1
Ag

23

Day

Dengue Fever

Febrile Phase
Critical Phase
Recovery
Phase

Clinical course of dengue infection Febrile

Phase

Lasts for 2 7 days

Clinical features are indistinguishable between DF and DHF

Critical
Phase

Happens often after the 3rd day of fever

Clinical presentation depends on the presence and degree of
plasma leakage
Lasts for about 24-48 hours

Recovery
Phase

In DHF patients plasma leakage stops and is followed by

reabsorption of extravascular fluid

25

Febrile Phase
Usually lasts for 2 7 days
Fever is often accompanied by
Facial flushing, skin erythema, generalised body
ache, myalgia, arthalgia and headache
Anorexia, nausea and vomiting are common

Mild hemorrhagic manifestations may be

seen
This may include positive tourniquet test,
petechiae or mucosal bleeding

Earliest abnormality in FBC is a progressive

decrease in total WBC count
These features are indistinguishable
between DF and DHF
27

Critical Phase - 1
Occurs either
Towards the late febrile phase
Often after 3rd day of fever

or
Around defervescence
Usually between 3rd day to 5th day of fever;
but may go up to the 7th day of fever.

This phase lasts for 24- 48 hours

28

Critical Phase - 2
During this phase if,

Minimal or no plasma
leakage occurs
Patient feels better as
the temperature
subsides
Dengue fever

Critical volume of plasma

leakage occurs
Patient develops DHF
Varying degrees of
circulatory disturbances
occur depending on the
degree of plasma leakage

29

Critical Phase -3
In more severe form of plasma
leakage
Patients may sweat, become restless,
have cool extremities and prolonged
capillary filling time
The pulse rate increases, diastolic BP
increases and the pulse pressure
narrows

30

Blood pressure, pulse pressure, heart rate in

hypovolemic shock
120
110
100
90
80
70
60
Compensated shock Decompensated shock

Time

Critical Phase - 3
Clinical warning signs of severe dengue or
high possibility of rapid progression to shock

32

Critical phase - 4
Thrombocytopenia and
hemoconcentration are usually
detectable before the onset of shock
HCT level correlates well with plasma
volume loss and disease severity.
However HCT values may be equivocal
and hence unhelpful when there is
frank hemorrhage or with untimely
HCT determinations
33

Recovery Phase
Plasma leakage stops after 24-48 hours of
defervescence
This followed by reabsorption of
extravascular fluid
Patients general well being improves,
appetite returns, gastrointestinal
symptoms abate, hemodynamic status
stabilises and diuresis ensues.
Recovery of platelet count is typically
preceded by the recovery of WCC count
34

WHO classification - DHF

Grade 1
In the presence of haemoconcentration, fever and
symptoms, a positive TT and/or easy bruising

Grade 2
spontaneous bleeding in addition to the manifestation from
Grade 1

Grade 3*
circulatory failure rapid, week pulse and narrowing of pulse
pressure or hypotension with the presence of cold,
clammy skin and restlessness.

Grade 4*
profound shock with undetectable blood pressure or pulse.
35

 Grade 1 & 2 Non-shock DHF

Grade 3 & 4 DSS

36

Pathophysiology of DHF - 1
Primary pathophysiological abnormality
in DHF and DSS is an acute increase in
vascular permeability
Plasma leakage results in
hemoconcentration and hypovolemia
or shock
Hypovolemia leads to reflex
tachycardia and generalised
vasoconstriction
37

Pathophysiology of DHF - 2
Clinical manifestations of
vasoconstriction in various systems
are;
Skin
coolness, pallor and delayed capillary refill time

Cardiovascular system
raised diastolic blood pressure and a narrowing pulse
pressure

Renal system
reducing urine output

Gastrointestinal system
vomiting and abdominal pain

Central nervous system

lethargy, restlessness, apprehension, reduced level of
consciousness

Respiratory system
tachypnoea (respiratory rate >20/min)

38

Kasus DBD
1.Demam akut 2-7 hari, bersifat bifasik.
2. Manifestasi perdarahan
uji tourniquet positif
petekia, ekimosis, atau purpura
Perdarahan mukosa, saluran cerna, dan tempat bekas
suntikan
Hematemesis atau melena
3. Trombositopenia < 100.00/pl
4. Kebocoran plasma yang ditandai dengan
Peningkatan nilai hematrokrit >_ 20 % dari nilai baku sesuai
umur dan jenis kelamin.
Penurunan nilai hematokrit >_ 20 % setelah pemberian cairan
yang adekuat
39
Efusi pleura, asites, hipoproteinemi

40

41

42

TATALAKSANA
1. Demam dengue
Pasien DD dapat berobat jalan, tidak perlu dirawat.
Pada fase demam pasien dianjurkan
Tirah baring, selama demam.
Obat antipiretik atau kompres hangat
Asetosal tidak dianjurkan gastritis, perdarahan,
/asidosis.
cairan dan elektrolit per oral, jus buah, sirop, susu,
disamping air putih, paling sedikit diberikan selama 2 hari.
Monitor suhu, jumlah trombosit dan hematokrit sampai fase
konvalesen.

43

 2. DBD
Jenis Cairan (rekomendasi WHO)
Kristaloid.
Larutan ringer laktat (RL) ,
Larutan ringer asetat (RA), Larutan garam faali (GF)
Dekstrosa 5% dalam larutan ringer laktat (D5/RL)
Dekstrosa 5% dalam larutan ringer asetat (D5/RA)
Dekstrosa 5% dalam 1/2 larutan garam faali (D5/1/2LGF)
(Catatan:Untuk resusitasi syok dipergunakan larutan RL atau
RA tidak boleh larutan yang mengandung dekstran)

Koloid.
Dekstran 40
Plasma
Albumin
44

Monitoring tanda vital

Koreksi Gangguan Metabolik dan Elektrolit
Pemberian Oksigen
Transfusi Darah

45

Volume Therapy

Fluid replacement : renal, enteral or dermal loss (interstitial

space)
Crystalloids distributes in the intravasuclar and interstitial
space filling thereby the extravascular space up
Volume replacement : acute or subacute loss from the
intravasuclar
- Colloids contain oncotic substances
- Ideally the volume stays intravasal
General Fluid Replacement
Crystalloids : Compensation extracellular fluid losses
Plasma Volume Replacement
Colloids : Compensation of acute or subacute intravascular
fluid losses

Perbedaan Terapi berdasarkan

kompartemen cairan
Terapi kasus
dehidrasi
penggantian kehilangan
cairan di semua ruang
extracellular

fluid replacement
Kristaloid
49

Terapi kasus
hypovolemia
penggantian kehilangan
cairan di ruang intravascular

(= kehilangan darah)

volume replacement
Koloid

Effects of Osmolarity on Cell Volume

Efek osmolarity cairan pada sel

KENAPA SAAT DBD PERLU CAIRAN?

Saat menderita DBD, cairan tubuh banyak hilang
karena:

KEBOCORA
N SEL

DEMAM

PERDARAHA
N

MUAL &
MUNTAH

BAHAYA DEHIDRASI PADA PASIEN DBD :

Demam lambat turunnya
Pematangan trombosit terhambat perdarahan sulit
dihentikan
Kekentalan darah meningkat supply oksigen dan
nutrisi ke seluruh tubuh melambat
Tekanan darah tidak stabil
Kekuatan otot berkurang

Cairan tubuh
(air + ION)
berkurang.

POTENSI
DEHIDRASI

Approach to the Management

Management Decisions

Groups A
may be sent
home
tolerate
adequate
volumes of
oral fluids
and pass
urine at
least once
every 6
hours

Groups B
referred for

in-hospital
managemen
t
with
warning
signs, coexisting
conditions,
with certain
social

Groups C
require
emergency
treatment
and urgent
referral
severe
dengue (in
critical
phase)

Group A Action Plan

Encourage intake of ORS, fruit juice and other fluids

Paracetamol and tepid sponge for fever
Advise to come back if with
no clinical improvement
severe abdominal pain
persistent vomiting
cold and clammy extremities,
lethargy or irritability or restlessness,
bleeding
not passing urine for more than 46 hours.
monitor:
temperature pattern, volume of fluid intake and losses, urine output, warning
signs, signs of plasma leakage and bleeding, haematocrit, and white blood cell
and platelet counts

Group B (with warning signs)

Action Plan
reference hematocrit before fluid therapy
isotonic solutions

57 ml/kg/hour for 12 hours, then

reduce to 35 ml/kg/hr for 24 hours,
and then reduce to 23 ml/kg/hr or less
according to the clinical response
reassess:

haematocrit remains the same or rises only minimally 23

ml/kg/hr for another 24 hours
worsening vital signs and rising haematocrit rising 510
ml/kg/hour for 12 hours

Group B (with warning signs)

Action Plan
Give minimum intravenous fluid volume:
maintain good perfusion and urine
output of about 0.5 ml/kg/hr

Intravenous fluids are usually needed for only

2448 hours.
Reduce intravenous fluids gradually when the
rate of plasma leakage decreases towards the
end of the critical phase.

monitor:

vital signs and peripheral perfusion (14 hourly until the

patient is out of the critical phase)
urine output (46 hourly)
hematocrit (before and after fluid replacement, then 6
12 hourly)
blood glucose
organ functions (renal profile, liver profile, coagulation
profile)

Group B (without warning signs)

Action Plan
Encourage oral fluids
If not tolerated, start intravenous fluid
therapy of 0.9% saline or Ringers lactate
with or without dextrose at maintenance rate
Patients may be able to take oral fluids after a few
hours of intravenous fluid therapy.

Give the minimum volume required to

maintain good perfusion and urine output.
Intravenous fluids are usually needed only for
2448 hours.
Close monitoring

Group C Action Plan

admit to a hospital with access to intensive
care facilities and blood transfusion
plasma losses should be replaced
immediately and rapidly with isotonic
crystalloid solution or, in the case of
hypotensive shock, colloid solutions
blood transfusion: with suspected/severe
bleeding

judicious intravenous fluid

resuscitation: sole
intervention required

Group C Action Plan

Goals of fluid resuscitation:

improving central and peripheral circulation

(decreasing tachycardia, improving BP,
warm and pink
extremities, and capillary refill time <2
seconds)

improving end-organ perfusion

i.e. stable conscious level (more alert or
less restless), urine output 0.5 ml/kg/hour,
decreasing metabolic acidosis.

60

61

TATALAKSANA ENSEFALOPATI DENGUE

udem otak dan alkalosis,
syok teratasi ganti cairan dengan tidak
mengandung HC03dan cairan dikurangi.
Edem otak dexametason 0,5 mg/kg BB/kali / 8
jam,
Perdarahan saluran cerna , kortikosteroid (-)
Disfungsi hati, vitamin K intravena 3-10 mg selama
3 hari,
BSS > 80 mg. Mencegah peningkatan tekanan
intrakrani kurangi jumlah cairan ( diuretik), koreksi
asidosis dan elektrolit.
Mengurangi produksi amoniak neomisin dan
laktulosa.
Transfusi darah
62

Kriteria Memulangkan Pasien

memenuhi semua keadaan dibawah ini
1.Tampak perbaikan secara klinis
2.Tidak demam selaina 24 jam tanpa antipiretik
3.Tidak dijumpai distres pernafasan (disebabkan oleh efusi
pleura atau asidosis)
4. Hematokrit stabil
5. Jumlah trombosit cenderung naik > 50.000/pl
6. Tiga hari setelah syok teratasi
7. Nafsu makan membaik

63

Thank
you
Arigatou

64

Terima
kasih
65

66