MIND MAP A.

BASIC SCIENCE
1. PHYSIOLOGY
A. BASIC SCIENCE
THERMOREGULATION
1. PHYSIOLOGY
A. BODY TEMPERATURE
 Thermoregulation
Normal Body Temperature
2. PATHOLOGY
1. Body core temperature
 Fever
o Orally
3. ENTOMOLOGY Range of normal temperatures measured orally from less
 Aedes aegypti than 97°F (36°C) to over 99.5°F (37.5°C). The average
4. VIROLOGY normal core temperature is generally considered to be
 Dengue Virus between 98.0° and 98.6°F (36.6 - 37oC) when measured
orally.
B. CLINICAL SCIENCE o Rectally
1. DENGUE FEVER (DF) About 1°F higher (37.2 - 37.5oC) when measured rectally.
2. DENGUE HEMORRHAGIC FEVER (DHF) 2. Skin temperature
3. DENGUE SHOCK SYNDROME (DSS) Rises and falls with the temperature of the surroundings.
C. BHP & IIMC
Reference: Guyton and Hall: Textbook of Medical Physiology, 12 th
D. PATHOMECHANISM
edition.

B. CONTROLLING FACTORS OF BODY TEMPERATURE

Body temperature is controlled by balance of heat production and heat loss.

1. Heat Production

Factors that determine the rate of heat production, called the metabolic
rate of the body.
The most important of these factors are:
(1) Basal rate of metabolism of all the cells of the body;
(2) Extra rate of metabolism caused by muscle activity, including
muscle contractions caused by shivering;
 (3) Extra metabolism caused by the effect of thyroxine (and, to a less b. Conduction
extent, other hormones, such as growth hormone and testosterone) Only minute quantities of heat, about 3 percent, are normally lost from the
on the cells; body by direct conduction from the surface of the body to solid objects,
(4) Extra metabolism caused by the effect of epinephrine, such as a chair or a bed. Loss of heat by conduction to air, however,
norepinephrine, and sympathetic stimulation on the cells; represents a sizable proportion of the body's heat loss (about 15 percent)
(5) Extra metabolism caused by increased chemical activity in the cells even under normal conditions.
themselves, especially when the cell temperature increases; and Conduction of heat from the body to the air is self-limited unless the heated
(6) Extra metabolism needed for digestion, absorption, and storage of air moves away from the skin, so new, unheated air is continually brought in
food (thermogenic effect of food). contact with the skin, a phenomenon called air convection.
c. Convection
2. Heat Loss The removal of heat from the body by convection air currents is commonly
called heat loss by convection. Actually, the heat must first be conducted to
Most of the heat produced in the body is generated in the deep organs, the air and then carried away by the convection air currents.
especially in the liver, brain, and heart, and in the skeletal muscles during
d. Evaporation
exercise.
Then this heat is transferred from the deeper organs and tissues to the skin,
where it is lost to the air and other surroundings.
Therefore, the rate at which heat is lost is determined almost entirely by
two factors:
(1) How rapidly heat can be conducted from where it is produced in the
body core to the skin and
(2) How rapidly heat can then be transferred from the skin to the
surroundings.

The various methods by which heat is lost from the skin to the surroundings.
They include radiation, conduction, convection, and evaporation.
a. Radiation
Loss of heat by radiation means loss in the form of infrared heat rays, a type
of electromagnetic wave. The human body radiates heat rays in all
directions. Heat rays are also being radiated from the walls of rooms and
other objects toward the body. If the temperature of the body is greater Reference: Guyton and Hall: Textbook of Medical Physiology, 12th
than the temperature of the surroundings, a greater quantity of heat is edition.
radiated from the body than is radiated to the body.
 Primary motor center for shivering terdapat di dorsomedial portion dari
C. RESPONSE TO CHANGE IN BODY TEMPERATURE posterior hypothalamus dekat dinding the third ventricle. Area ini
1. Temperature-Decreasing Mechanisms When the Body Is Too Hot
normalnya diinhibisi oleh sinyal dari heat center di anterior hypothalamus-
The temperature control system uses three important mechanisms to preoptic area.
reduce body heat when the body temperature becomes too great:
Rangsangan sinyal dingin dari kulit dan spinal cord
a. Vasodilation of skin blood vessels. ↓
 This is caused by inhibition of the sympathetic centers in the Area teraktivasi saat temperature menurun
posterior hypothalamus that cause vasoconstriction. Full ↓
vasodilation can increase the rate of heat transfer to the Turun melalui bilateral tract ke brainstem
skin as much as eightfold. ↓
b. Sweating. Lateral column of the spinal cord
c. Decrease in heat production. ↓
 The mechanisms that cause excess heat production, such as Anterior motor neuron
shivering and chemical thermogenesis, are strongly ↓
inhibited. Meningkatkan tonus skeletal muscle
↓
2. Temperature-Increasing Mechanisms When the Body Is Too Cold Shivering

When the body is too cold, the temperature control system institutes o Sympathetic "Chemical" Excitation of Heat Production
exactly opposite procedures. They are: Stimulasi simpatis, epinephrine, dan norepinephrine
↓
a. Skin vasoconstriction throughout the body. Meningkatkan metabolisme sel (chemical thermogenesis)
 This is caused by stimulation of the posterior hypothalamic ↓
sympathetic centers. Kemampuan untuk uncouple fosforilasi oksidative
b. Piloerection. ↓
 Piloerection means hairs "standing on end." Sympathetic Kelebihan makan di oksidasi
stimulation causes the arrector pili muscles attached to the ↓
hair follicles to contract, which brings the hairs to an upright Produksi panas
stance. o Increased Thyroxine Output as a Long-Term Cause of Increased Heat
c. Increase in thermogenesis (heat production).
 Heat production by the metabolic systems is increased by Production
promoting shivering, sympathetic excitation of heat
production, and thyroxine secretion.
o Hypothalamic stimulation of shivering
 Pendinginan dari anterior hypothalamic-preoptic area - Contoh: demam yang disebabkan oleh
↓ o Gram-negative (pneumonia)
Meningkatkan produksi hormone neurosecretory
Thyrotropin-Releasing Hormone oleh hypothalamus
o Rickettsial diseases
↓ o Typhoid fever
Hypothalamic portal vein o Central nervous system disorders
↓ o Falciparum (malignant tertian) malaria.
Stimulasi anterior pituitary gland sekresi TSH
↓
Simulasi kelenjar thyroid sekresi Thyroxine
↓
Meningkatkan kecepatan metabolisme sel

Reference: Guyton and Hall: Textbook of Medical Physiology, 12 th

edition.

2. PATHOLOGY
FEVER 2. Intermittent
A. DEFINITION

Fever represents an increase in body temperature due to resetting of the

hypothalamic thermoregulatory set point as the result of endogenous
pyrogens released from host macrophages or endothelial cells.
Reference: Porth’s Pathophysiology, 9th edition

Fever is is an elevation of body temperature that exceeds the normal daily

variation and occurs in conjunction with an increase in the hypothalamic set
point [e.g., from 37°C to 39°C (98.6°F to 102.2°F)].
th
- Demam dengan fluktuasi yang lebar (lebih dari 1oC)
Reference: Harrison’s Principle of Internal Medicine, 18 edition
- Suhu badan turun ke tingkat yang normal selama beberapa jam
B. TYPE OF FEVER dalam satu hari. Biasanya normal atau rendah pada pagi hari dan
mencapai puncaknya pada jam 4-8 sore.
The type of febrile patterns:
- Contoh penyakit:
1. Continuous (sustained)
o Localized pyogenic infection dengan bacteremia
- Demam terus menerus diatas suhu normal
- Suhu bervariasi sepanjang hari tapi tidak lebih dari 2.0oF/ 10C o Bacterial endocarditis
(fluktuasi).
 o Malaria 3. Remittent

o Salmonellosis - Fluktuasi lebih dari 10C

- Suhu tubuh turun tidak pernah mencapai normal.
o Milliary tuberculosis
- Contohnya: first week of typhoid fever.
Pada malaria bisa terdapat pola quotidian, tertian ataupun quartan.

4. Saddleback (biphasic)

Pola quotidian : Demam terjadi setiap hari Demam beberapa hari, lalu terdapat gap selama satu hari dilanjutkan
dengan beberapa hari tambahan demam.
Contoh penyakit:
o Dengue fever
o Yellow fever
o Colorado tick fever
Pola tertian : Demam terjadi setiap dua hari sekali ( hari ke 1 dan 3 ) o Influenza
o Poliomyelitis
o Limfositik choriomeningitis

Pola quartan : Demam terjadi setiap 3 hari sekali ( hari ke 1 dan 4 )

 C. PATHOGENESIS

Infection ( Exogenous
Infection pyrogens
( Exogenous – ex :–microbial
pyrogens ex :
microbial products,
products, microbial
microbial toxinstoxins / whole
/ whole
microorganism)
microorganism)
Monocytes/macrophages,
Monocytes/macrophages,
endothelial cells, others
endothelial others
Pyrogenic cytokines
IL-1,
IL-1,IL-6, TNF,INF
IL-6, TNF, INF
Hypothalamic
Hypothalamic endothelium
endothelium

5. Pel-Ebstein Fever Asam

Asam arachidonat
arachidonat→→ PGE
PGE22
Demam selama beberapa minggu sekali diikuti dengan masa afebrile Cyclic AMP
Cyclic AMP
Circulation
yang sama dan pengulangan siklus. Elevated
Elevated thermoregulatory
thermoregulatory set set
point
Contoh penyakit: point
Heat
Heat conservation,
conservation, heat production
heat production
(Autonomik
(Autonomik :: vasokontriksi,
vasokontriksi, Endokrin :: menggigil,
menggigil,
 Hodgkin’s disease (Pola Pel-Ebstein)
Behavioral :: menggunakan
Behavioral menggunakan selimut)
selimut)

Fever

3. ENTOMOLOGY

Vektor DBD adalah nyamuk. Di Indonesia ada 3 jenis nyamuk yang bisa
menularkan virus dengue yaitu : Aedes aegypti, Aedes albopictus dan Aedes
scutellaris.

Aedes aegypti
A. MORPHOLOGY
Morfologi tahapan Aedes aegypti sebagai berikut:
a. Telur

Telur berwarna hitam dengan ukuran ± 0,80 mm, berbentuk oval yang
mengapung satu persatu pada permukaan air yang jernih, atau menempel
pada dinding tempat penampung air. Telur dapat bertahan sampai ± 6 bulan
di tempat kering.

b. Jentik (larva)

Ada 4 tingkat (instar) jentik/larva sesuai dengan pertumbuhan larva

tersebut, yaitu: 1) Instar I : berukuran paling kecil, yaitu 1-2 mm 2) Instar II :
2,5-3,8 mm 3) Instar III : lebih besar sedikit dari larva instar II 4) Instar IV :
berukuran paling besar 5 mm.

c. Pupa

Pupa berbentuk seperti ‘koma’. Bentuknya lebih besar namun lebih ramping
dibanding larva (jentik)nya. Pupa Aedes aegypti berukuran lebih kecil jika
dibandingkan dengan rata-rata pupa nyamuk lain. Aktivitas menggigit nyamuk Aedes aegypti biasanya mulai pagi dan petang
hari, dengan 2 puncak aktifitas antara pukul 09.00 -10.00 dan 16.00 - 17.00.
d. Nyamuk dewasa
Aedes aegypti mempunyai kebiasaan mengisap darah berulang kali dalam
Nyamuk dewasa berukuran lebih kecil jika dibandingkan dengan ratarata satu siklus gonotropik, untuk memenuhi lambungnya dengan darah.
nyamuk lain dan mempunyai warna dasar hitam dengan bintik-bintik putih
C. CONTROL
pada bagian badan dan kaki.
Pengendalian spesies nyamuk ini dilakukan dengan berbagai cara:
Reference: Depkes
1. Kimiawi
B. LIFE CYCLE
Dengan pemberian Larvasida (abate) ke dalam tempat penampungan
Nyamuk Aedes aegypti seperti juga jenis nyamuk lainnya mengalami
air/penyimpanan air bersih atau penggunaan insektisida seperti
metamorfosis sempurna, yaitu: telur - jentik (larva) -pupa - nyamuk.
Organophospat (Malathion, methyl pirimiphos), Pyrethroid (Cypermethrine,
Stadium telur, jentik dan pupa hidup di dalam air. Pada umumnya telur akan
lamda-cyhalotrine, cyflutrine, Permethrine & S-Bioalethrine) dengan cara
menetas menjadi jentik/larva dalam waktu ± 2 hari setelah telur terendam
fogging (pengasapan).
air. Stadium jentik/larva biasanya berlangsung 6-8 hari, dan stadium
kepompong (Pupa) berlangsung antara 2-4 hari. Pertumbuhan dari telur 2. Biology
menjadi nyamuk dewasa selama 9-10 hari. Umur nyamuk betina dapat
mencapai 2-3 bulan. Pengendalian vektor biologi menggunakan agent biologi seperti
predator/pemangsa, parasite (Romanomermes iyengeri), bakteri (Baccilus
Reference: Depkes thuringiensis israelensis), sebagai musuh alami stadium pra dewasa vektor
DBD. Jenis predator yang digunakan adalah Ikan pemakan jentik (cupang, 4. VIROLOGY
tampalo, gabus, guppy, dll). DENGUE VIRUS
A. TAXONOMY
3. Management Lingkungan
- Merupakan Arbovirus
Manajemen lingkungan adalah upaya pengelolaan lingkungan sehingga - Termasuk kedalam RNA virus
tidak kondusif sebagai habitat perkembangbiakan atau dikenal sebagai - Family flaviviridae
source reduction seperti 3M plus (menguras, menutup dan memanfaatkan - Genus flavivirus
barang bekas, dan plus: menyemprot, memelihara ikan predator, menabur
larvasida dll); dan menghambat pertumbuhan vektor (menjaga kebersihan B. CLASSIFICATION
lingkungan rumah, mengurangi tempat-tempat yang gelap dan lembab di Terdiri dari 4 type yaitu DEN-1, DEN-2, DEN-3, DEN-4.
lingkungan rumah dll).
C. CHARACTERISTIC
4. Pemberantasan Sarang Nyamuk(PSN) - positive-sense
- single-stranded RNA
Pengendalian Vektor DBD yang paling efisien dan efektif adalah dengan
- icosahedral capsid
memutus rantai penularan melalui pemberantasan jentik. Pelaksanaannya
- enveloped viruses
di masyarakat dilakukan melalui upaya Pemberantasan Sarang Nyamuk
- have 3 group antigen (E,C,M)
Demam Berdarah Dengue (PSN-DBD) dalam bentuk kegiatan 3 M plus.
The RNA genome is surrounded by multiple copies of small basic
Untuk mendapatkan hasil yang diharapkan, kegiatan 3 M Plus ini harus
proteins; the capsid (C) protein and the matrix (M) proteins cover
dilakukan secara luas/serempak dan terus menerus/berkesinambungan.
the core. The lipid bilayer envelope membrane contains envelope
Tingkat pengetahuan, sikap dan perilaku yang sangat beragam sering
(E) protein, which is glycosylated in many flaviviruses.
menghambat suksesnya gerakan ini. Untuk itu sosialisasi kepada
masyarakat/ individu untuk melakukan kegiatan ini secara rutin serta Reference: Sherris Medical Microbiology, 5th edition
penguatan peran tokoh masyarakat untuk mau secara terus menerus
menggerakkan masyarakat harus dilakukan melalui kegiatan promosi
kesehatan, penyuluhan di media masa, serta reward bagi yang berhasil Surface antigen
FLAVIVIRIDAE
melaksanakannya.

5. Pengendalian Vektor Terpadu (integrated Vector

Management/IVM)

Reference: Depkes
 B. CLINICAL SCIENCE
1. DENGUE VIRUS INFECTION

Reference: Comprehensive Guideline for Prevention and Control of Reference: Dengue Guideline for Diagnosis, Treatment, Prevention
Dengue Hemorrhagic Fever, WHO 2011 and Cotrol, WHO 2009

2. DENGUE FEVER (DF)

A. DEFINITION

Dengue fever is dengue infection caused by dengue virus of family

flaviviridae.

Reference: Manson’s Tropical Infectious Disease, 23rd Edition

B. EPIDEMIOLOGY
- Dengue is endemic throughout the tropical and subtropical zone
- In endemic area dengue occur most frequently in children aged
between 2 and 15 years
- Severe dengue is usually associated with secondary dengue
infection and during primary infection in infant less than 1 year.
Reference: Manson’s Tropical Infectious Disease, 23rd Edition - Retro-orbital pain
- Myalgia
C. ETIOLOGY - Arthralgia/bone pain
- Dengue virus - Rash
Serotype:
- Hemorrhagic manifestation
o DENV 1 - Leukopenia (WBC ≤5000 cell/mm3)
o DENV 2 - Thrombocytopenia (platelet count <150.000 cell/mm3)
o DENV 3
- Rising hematocrit (5-10%)
o DENV 4
- Dengue virus transmitted by Aedes mosquitoes. And at least one of following:

Reference: Manson’s Tropical Infectious Disease, 23rd Edition - Supportive serology on single serum sample:
o Titer ≥ 1280 with hemagglutination inhibition test,
D. CLASSIFICATION Comparable IgG titer with ELIS, or
*see above o Tasting positive in IgM antibody test, and
- Occurrence at the same location and time as confirmed case of
E. CLINICAL MANIFESTATION dengue fever
- Fever
o Body temperature 39-40oC Confirmed Diagnosis
o Biphasic
- Headache Probable case with at least one of the following:
- Myalgia - Isolation of dengue virus from serum, CSF, or autopsy sample
- Arthralgia - Fourfold or greater increase in serum IgG (by HI test) or increase in
- Rash IgM antibody specific to dengue fever
- Retro-orbital eye pain - Detection of dengue virus or antigen in tissue, serum or CSF by
Reference: Comprehensive Guideline for Prevention and Control of Dengue immunohistochemistry, immunofluorescence or ELISA
Hemorrhagic Fever, WHO 2011 - Detection of dengue virus genomic sequence by reverse
transcription polymerase chain reaction (RT-PCR).
F. DIAGNOSIS
Reference: Comprehensive Guideline for Prevention and Control of
Probable Diagnosis Dengue Hemorrhagic Fever, WHO 2011
Acute febrile illness with 2 or more of the following:

- Headache
 G. DD

Reference: Comprehensive Guideline for Prevention and Control of

Dengue Hemorrhagic Fever, WHO 2011 - Adequate fluid intake
o Adequate oral fluid intake may reduce the number of
hospitalizations
H. MANAGEMENT o The choice of fluids should be based on the local culture:
coconut water in some countries, in others rice water or
barley water.
o Oral rehydration solution or soup and fruit juices may be
given to prevent electrolyte imbalance
o Commercial carbonated drinks that exceed the isotonic
level (5% sugar) should be avoided

- Paracetamol
o The recommended dose is 10 mg/kg/dose, not more than
3−4 times in 24 hours in children and not more than 3 g/day
in adults).
o Sponge with tepid water if the patient still has a high fever
o Do not give acetylsalicylic acid (aspirin), ibuprofen or other
non-steroidal anti-inflammatory agents (NSAIDs) or
intramuscular injections, as these aggravate gastritis or
bleeding.
Reference: Handbook for Clinical Management of Dengue, WHO 2012
 3. DENGUE HERROHAGIC FEVER (DHF)
A. DEFINITION

Dengue Hemorrhagic Fever is dengue infection caused by dengue virus

manifest as fever, hemorrhagic manifestation and plasma leakage.

B. EPIDEMIOLOGY

Di Indonesia (berdasarkan DepKes 2014) sekitar 71.668 mengidap DHF

dan sekitar 641 orang meninggal dunia, dengan angka kejadian
terbanyak pada Provinsi Jawa Barat.

C. RISK FACTOR

Following host factor contribute to more severe disease:

Reference: Comprehensive Guideline for Prevention and Control of
- Infant and elderly
Dengue Hemorrhagic Fever, WHO 2011
- Obesity
- Pregnant woman E. PATHOGENESIS
- Peptic ulcer disease F. PATHOPHYSIOLOGY
- Woman who have menstruation or abnormal vaginal bleeding
- Hemolytic disease
- Chronic disease (DM, hypertension, asthma)
- Patient on steroid or NSAID treatment

Reference: Comprehensive Guideline for Prevention and Control of

Dengue Hemorrhagic Fever, WHO 2011

D. CLASSIFICATION
 PATHOPHYSIOLOGY DENGUE HEMORRHAGIC FEVER

Subsequent infection with Exogenous pyrogens

different virus serotype

Stimulate mononuclear cells

Heterologous antibodies do not
neutralize new serotype
Production endogenous pyrogens (IL-1, IL-6, TNF)

Form infectious complexes

Enter systemic circulation

Antibody dependent enhacement (ADE)

To peripheral tissue
Virus uptake by Fc receptor on
mononuclear cells
↑ PGE2 in peripheral tissue

Can enter greater proportion of

mononuclear cells Activate peripheral
nociceptive pathway

↑ virus replication& production

Myalgia Arthralgias

Secondary heterologous dengue infection

Viraemia

To hypothalamic endothelium

Induce synthesis PGE2

Activation & sensitization of Trigger PGE2 receptor on glial cells Heat over production
cranial perivascular sensory
afferent
Stimulate release cyclic AMP Pengeluaran panas via
vasodilatasi perifer
Headache ↑ thermoregulator set point
erythema
Heat conservation & production
Flushing rash
Fever
 Viraemia

Virus antibody complex

Antibody dependent enhacement (ADE)

Infected mononuclear cells Release NS1 protein Complement activation

Antigen presenting cells ↑ Cross reactivity NS1 Anafilatoxin C3a, C5a

antibody on surface
endothelium
↑ T cells activation & proliferation

↑ produce cytokines (TNF alfa, IL-

16, IL-13, IL-18)

↑ vascular permeability

Plasma leakage

hemoconcentration Shock hypovolemia Move albumin to

extravascular
↑ hematocrite ↓ intravascular volume
Hypoproteinemia

↓ cardiac ouput
↓intravascular oncotic pressure

↓ tissue perfusion hypotension

Loss fluid to interstitial potential space

Capillary refill > 2s Impaired cell

metabolism Pleural effusion ascites
Lethargy, restlessnes

Impaired O2 use

Anaerobic metabolism

↑ lactic acid
 Virus antibody complex

Antibody dependent enhacement (ADE) Direct destructive IgM type of antiplatelet

on bone marrow antibody binding comlement
Liver: replicating in Bone marrow: precursor cells
hepatocyte & replicating in Lysis of platelet
kuppfer cells stromal cells

Hepatocyte injury Suppression of hemopoesis Thrombocytopenia

Impaired metabolism Leukopenia Coagulopathy

↓ ATP ↑ tendency to hemorrhage

Na pump ↓ GI bleeding, + tourniquet test, skin

petechiae, purpura, ecchymoses,
↑ influx Ca2+, H2o, Na epistaxis, gum bleeding.

Release Ca2+ from store RE Cells swelling

Aktif protease, phospholipase hepatomegaly

necrosis

AST, ALT ↑ in serum

 G. CLINICAL MANIFESTATION - Increase capillary permeability  plasma leakage  pleural
1. Febrile Phase effusion & ascites
- High grade fever suddenly - Shock occur when critical volume of plasma is lost through leakage
- Usually last 2-7 days - Warning signs
- Facial flushing
- Skin erythema 3. Recovery Phase
- Generalized body ache As patient survive 24-48 hours critical phase.
- Myalgia - General well-being improve
- Arthralgia - Appetite return
- Headache - GI symptoms abate
- Retro-orbital eye pain - Hemodynamic status stabilizes
- Diuresis ensues
GI Symptoms
Reference:
- Anorexia
- Nausea - Handbook for Clinical Management of Dengue, WHO 2012
- Vomiting - Guideline for Diagnosis, Treatment, Prevention and Control of
Dengue, WHO 2009
Mild Hemorrhagic Manifestation

- Petechiae H. DIAGNOSIS
- mucosal membrane bleeding All of following:
o nose
o gum 1. Acute onset of fever of 2-7 days duration (high and continuous)
- vaginal bleeding & GI bleeding (not common) 2. Hemorrhagic manifestation
Shown by:
Liver  is often enlarged and tender after few days of fever o Positive tourniquet test
2. Critical Phase o Petechiae
- Around time defervescence, when temperature drop to 37,5-38oC o Eccymoses or purpura
or less and remain below this level usually on days 3-7 of illness. o Bleeding from mucosa, GI tract, injection site
- Increase in capillary permeability in parallel with increasing 3. Platelet count ≤100.000 cell/mm3
hematocrit level may occur 4. Objective evidence of plasma leakage due to increased vascular
- Progressive leukopenia followed by rapid decrease in platelet count permeability. Shown by:
usually precedes plasma leakage
 o Rising hematocrit/hemoconcentration ≥20% from baseline I. MANAGEMENT
or decrease in convalescence, or Group B
o Evidence plasma leakage such as pleura effusion, ascites, or (Referred for in-hospital care)
hypoproteinemia/albuminemia.

Reference: Comprehensive Guideline for Prevention and Control of Dengue

Hemorrhagic Fever, WHO 2011

Reference: Handbook for Clinical Management of Dengue, WHO 2012

J. COMPLICATION
- DSS
- DIC
- Multiple organ failure

K. PROGNOSIS

Prognosis jika tanpa komplikasi umumnya dubia ad bonam, karena hal ini
tergantung dari derajat beratnya penyakit.
 - Rapid and weak pulse with narrowing of the pulse pressure ≤ 20
4. DENGUE SHOCK SYNDROME (DSS) mmHg with increase diastolic pressure (e.g., 100/90), or
A. DEFINITION hypotension,
- Signs of reduced tissue perfusion are:
DSS is hypovolemic shock caused by plasma leakage and characterized by o Delayed capillary refill (>3 second)
increased systemic vascular resistance, manifested by narrow pulse o Cold clammy skin
pressure. o Restlessness
Reference: Comprehensive Guideline for Prevention and Control of Dengue Reference: Comprehensive Guideline for Prevention and Control of Dengue
Hemorrhagic Fever, WHO 2011 Hemorrhagic Fever, WHO 2011
B. RISK INITIAL STAGE OF SHOCK
- Compensatory mechanism that maintained normal systolic blood
Induction of vascular permeability and shock depend on multiple factor,
pressure produce tachycardia
including:
- Peripheral vasoconstriction with reduced skin perfusion manifested
- Presence of enhancing and non-neutralizing antibodies as cold extremities, delayed capillary refill time (>2 second, weak
- Age volume peripheral pulse
 Susceptibility to DHF/DSS drops considerable after 12 year of age - As peripheral vascular resistance increase, diastolic pressure rise
- Sex toward the systolic pressure and pulse pressure narrow (≤ 20
 Female are more often affected than male mmHg).
- Race
WORSENING HYPOVOLEMIC SHOCK
 Caucasian are more often affected than black
- Manifest as increase tachycardia and peripheral vasoconstriction
- Nutritional status
o Extremities cold and cyanosed
- Sequence of infection
o Limb become mottled, cold and clammy
e.g., serotype 1 followed by serotype 2 seem to be more dangerous
- By this stage
than serotype 4 followed by serotype 2.
o Breathing become more rapid and increase in depth
- Infecting serotype
(kussmaul’s breathing)  compensation for metabolic
Type 2 is more dangerous than other serotype.
acidosis
Reference: Harrison’s Infectious Disease, 1st edition 2010 - Finally, there is decompensation
o Both systolic and diastolic disappear suddenly and
C. PATHOGENESIS & PATHOPHYSIOLOGY dramatically
D. CLINICAL MANIFESTATION o And patient is said to hypotensive or decompensated shock
Shock is characterized by: - At this time
 o Peripheral pulse disappear while central pulse (femoral) will
be weak
- One key clinical sign of this deterioration is change in mental state
as brain perfusion declines
o Restlessness
o Confused
o Extremely lethargic
o Seizure may be occur

PROLONGED HYPOTENSIVE SHOCK

- Prolonged hypotensive shock and hypoxia lead to
o Metabolic acidosis
o Multiple organ failure Reference: Comprehensive Guideline for Prevention and Control of Dengue
o Extremely difficult clinical course Hemorrhagic Fever, WHO 2011
- It may take few hours for patient to progress from warning sign to
- Criteria for severe dengue
compensated shock, and few hours for compensated shock to
hypotensive shock. But only minutes for hypotensive shock to
cardiorespiratory collapse and cardiac arrest.

Reference: Handbook for Clinical Management of Dengue, WHO 2012

E. DIAGNOSIS

Reference: Handbook for Clinical Management of Dengue, WHO 2012

- Laboratory test
o Full Blood Count (FBC)
 Leukopenia
  Rapid decrease in platelet count
o Hematocrit (HCT)
o Other organ function test as indicated
 Liver function
 Serum electrolyte
 Urea and creatinin
 ECG
 Etc

Reference: Handbook for Clinical Management of Dengue, WHO 2012

F. MANAGEMENT

Reference: Handbook for Clinical Management of Dengue, WHO 2012

 G. ADMISSION CRITERIA

Reference: Guideline for Diagnosis, Treatment, Prevention and Control of

Dengue, WHO 2009

H. DISCHARGE CRITERIA

Reference: Guideline for Diagnosis, Treatment, Prevention and Control of

Dengue, WHO 2009
 I. COMPLICATION Nabi Muhammad SAW bersabda:
- Metabolic acidosis
- Electrolyte imbalance “jika kamu mendengar tentang tha’un di suatu tempat, mka janganlah kamu
memasukinya (tempat itu). Apabila kamu (terlanjur) berada di tempat yang
- Multiple organ failure: hepatic, renal, encephalopathy etc
terkena wabah itu, maka janganlah kamu keluar darinya (tempat itu)”.
Reference: Comprehensive Guideline for Prevention and Control of Dengue
Hemorrhagic Fever, WHO 2011 D. PATHOMECHANISM
J. PROGNOSIS
- Prolonged or uncorrected shock have poor prognosis and high
mortality
- Without treatment, patient may die within 12-24 hours

Reference: Comprehensive Guideline for Prevention and Control of Dengue

Hemorrhagic Fever, WHO 2011

C. BHP & IIMC

Konseling dan Edukasi
1. Pinsip konseling pada demam berdarah dengue adalah
memberikan pengertian kepada pasien dan keluarganya tentang
perjalanan penyakit dan tata laksananya, sehingga pasien dapat
mengerti bahwa tidak ada obat/medikamentosa untuk
penanganan DBD, terapi hanya bersifat suportif dan mencegah
perburukan penyakit. Penyakit akan sembuh sesuai dengan
perjalanan alamiah penyakit.
2. Modifikasi gaya hidup
a. Melakukan kegiatan 3M: menguras, mengubur, menutup.
b. Meningkatkan daya tahan tubuh dengan mengkonsumsi
makanan bergizi dan melakukan olahraga secara rutin.
Reference: Panduan Praktik Dokter di Fasilitas Pelayanan Kesehatan
Primer, IDI, 2014