INFECTIONS OF DENGUE

VIRUSES

Dr.Nuchin MD,MBA.

District Surveillance Officer, Belgaum

Venue of presentation- DHO Office Belgaum

Audience-Medical Officers of Belgaum District
Date-14-07-2009
Dengue fever
 An acute febrile disease.

 Dengue is the fastest emerging and most

common Arboviral infection in the world

 Most rapidly spreading vector borne disease

 Dengue is found in tropical and sub-tropical

climates worldwide, mostly in urban and semi-
urban areas.(WHO)
 Problem statement- World
 At present 100 countries are affected
 2.5billion people are at risk(2/5)
 The maximum burden is borne by countries
of the Asia Pacific Region.
 Mortality is highest during the initial period
of the outbreak or epidemic.
 (The geographical spread includes northern Australia and northern Argentina, and the entire Singapore, Malaysia,
Taiwan, Thailand, Vietnam, Indonesia, Honduras, Costa Rica, Philippines, Pakistan, India, Sri Lanka, Bangladesh,
Mexico, Suriname, Puerto Rico, Jamaica, Bolivia, Brazil, Guyana, Venezuela, Barbados, Trinidad and Samoa)
Contnd…
 New infections annually: 50-100 million
 Deaths: 30,000 annually
 People at risk: 2.5-3 billion
 Hospitalized (DHF) cases: 500 000/year
(90% of those affected are children)
 Disease burden: 465,000 Disability
Adjusted Life Years (DALY)
Global burden

Prevalent from Highly

 Burden in SEAR (SEA- HF)
All the countries are
reporting the
disease
A leading cause of
hospitalization and
death among
children next only to
ADDs and ARIs (First
in I,M,T)
 30 million DF cases and 2 lakh DHF
cases with 15000 deaths occur
annually
BURDEN OF DISEASE IN S.E.ASIA

A. CATEGORY-A - INDONESIA,MYANMAR,AND THAILAND

- Major PHP, leading cause of hospitalization and deaths among
children, multiple virus serotype circulating and Aedes aegypty
is the main epdemic vector and role of Aedes albopictus
uncertain, disease spreading to rural environment
A. CATEGORY-B - INDIA,BANGALADESH,MALDIVES,AND SRILANKA-
DHF an emerging disease, cyclical epidemics becoming more
frequent, multiple virus serotype circulating ,expanding
geographically within the country Aedes aegypty is the main
epdemic vector and role of Aedes albopictus uncertain,
A.CATEGORY-C -BHUTAN, NEPAL-
No reported cases and
endemicity uncertain
B.CTEGORY-D - DPR KOREA- non-
endemic
 Problem statement- India
 In India first outbreak of dengue was recorded
in 1780

 Virus was first isolated in Calcutta in1945

 A dengue hemorrhagic fever epidemic

occurred in India for the first time in Calcutta
between July 1963 & March 1964

 A major outbreak in New Delhi, occurred in

1996 with 10252 cases and 423 deaths.
Major outbreaks In India
1963 Kolkata
1964 Vishakapattanam &
Chennai
1968 Pondicherry
1998 Various places in North
India
1996 Delhi
 State wise distribution of
cases
12
Dengue in India since 1996
Year Cases Deaths
1996 10500 440
1997 1177 36
1998 707 18
1999 944 17
2000 650 7
2001 3306 53
2002 1926 33
2003 12754 215
2004 4153 45
2005 11928 156
Problem statement- India
Karnataka
 Dengue incidence is on rise
Belgaum district
Year Cases Deaths

2005 3 __________

2006 5 __________

2007 9 __________

2008 5 ___________

2009 52
 History
The exact origins of the disease are not clear
It is said that it originated in Africa and was spread
worldwide with the slave trade.
The name dengue is derived from the Swahili "Ka-
Dinga pepo" that describes the disease as a sudden
cramp like disease caused by an evil spirit.
 In the wild- The virus has a life cycle very similar to
that of yellow fever involving passing between
primates living in the jungle canopy and mosquitoes
that feed on them.
 It is believed that the virus was transferred to
man by the bite of the tiger-striped mosquito
(Aedes albopticus) as man began clearing the
jungle and building settlements.
 The commonest vector is now the closely-
related mosquito Aedes aegypti which is
African in origin but has spread throughout the
tropics in the Old and New Worlds.
Contnd..
 The earliest reports of a dengue-like disease are
from Chin Dynasty China (265-420 AD).

 The illness was called “water poison” and

known to be associated with flying insects near
water

 The first recognized Dengue epidemics

occurred almost simultaneously in Asia, Africa,
and North America in the 1780s (when the
disease was first described), shortly after the
identification and naming of the disease in
1779.
Epidemics occurred in
• Cairo and Alexandria (Egypt, 1799);

• Jakarta (then called Batavia, Indonesia, 1799);

• Philadelphia (United States, 1780);

• Madras (India, 1780).

• Outbreaks have occurred throughout the

temperate and tropical climes since then.
 Population movements during World War
II spread the disease globally.
 A pandemic of dengue began in
Southeast Asia after World War II and
has spread around the globe since then
(1950)
 The DHF was first recognized in
Philippines in 1953
Chronology
1950s A pandemic began in
Southeast Asia
by 1975 DHF had become a
leading cause of death
among children in the
SEAR.
By 1980s Dengue epidemics-
became more common

By the late 1990s dengue became the

most important
mosquito-borne
disease affecting
humans after malaria
Epidemiolo


gy
Inter play of three factors

Host

Interaction

The Virus Environment

Mosquito
The Virus
Dengue Virus
Dengue Virus
Electron
Micrograms
 Virology
 An Arbovirus

Family Flaviviridae
Genus Flavivirus
Serotypes Den1,2,3 &4
 Single stranded positive sense enveloped
RNA viruses
 50-60 nm
 Four serotypes are there (DEN-1, 2, 3, 4)
 The virus was isolated by Sabin in 1944

By 1956, all the four serotypes of the

virus were identified

Each serotype provides specific lifetime

immunity, and short-term cross-immunity

All serotypes can cause severe and fatal

disease

Second, third and possibly four infections are

possible.
Reservoir- Both Man and Mosquito.
The transmission cycle is “Man-
Mosquito-Man”

Incubation period- Intrinsic IP- 3-14

days average 5-8 days
Extrinsic IP- 8-12 days

Period of communicability- Few hours

to one day prior to the onset of
symptoms to 5 days
Immunity
 Infection with one serotype confers lifelong
immunity to that serotype and only temporary
and transient protection to other three
 Sequential infection increases the risk of
DHF/DSS
 Significant outbreaks of dengue fever tend to
occur every five or six months.
 The cyclical rise and fall in numbers of dengue
cases is thought to be the result of seasonal
cycles interacting with a short-lived cross-
immunity for all four strains in people who have
had dengue
Immunity-Contnd…
 When the cross-immunity wears off the
population is more susceptible to transmission
whenever the next seasonal peak occurs.
 Thus over time there remain large numbers of
susceptible people in affected populations
despite previous outbreaks due to the four
different serotypes of dengue virus and the
presence of unexposed individuals from
childbirth or immigration.
Mode of transmission
 Dengue is transmitted by bite of
infected Aedes mosquitoes,
particularly A. aegypti and
A.albopictus.
 Dengue may also be transmitted
via infected blood products
(blood transfusions, plasma, and
platelets), but the scale of this
problem is unknown.
 Transovarian transmission of
viruses-
 HOW DENGUE SPREADS
Mosquitoes transmit
engue to human dendritic 1
ells

Dengue targets areas 2

ith high WBC counts 4
iver, spleen, lymph
odes, bone marrow, and 33
ands)

3. Dengue enters
WBCs & lymphatic
tissue
4. Dengue enters blood
circulation http://phil.cdc.gov/PHIL_Images/08051999/00004/dengue_phf/sld0
Then, within the mosquito, the virus replicates
during an extrinsic incubation period of 8-12 days.

 After which it becomes infective to man during its

whole life time
Pathogenesis
Pathogenesis of DHF- decides the
course of disease
 Not clearly understood

 Many theories have been put forward

 A new hypothesis of immunopathogenesis

(ADE) is proposed for the development of the
DHF/DSS.

 According to it , in order to clear the virus in

the body, there occurs

An aberrant over activation of immune system

Overproduction of cytokines (that affect
monocytes, endothelial cells, and
hepatocytes)

The abnormal production of

autoantibodies to platelet and endothelial
cells.

A molecular mimicry occurs between

platelets/endothelial cells and dengue virus
antigens

viral entry , viral replication , rate of

cell infection - increased
Manifestation Of Dengue Virus
Infections
 Infection with any serotype can be asymptomatic or lead to one
of the four clinical scenarios of increasing severity:
undifferentiated fever, dengue fever, DHF, and DSS
Synonym/Breakbone fever
Synonyms
Dandy fever
Duengero fever
Saddle back fever
Seven day fever
 MECHANISM OF
THROMBOCYTOPENIA
40

Central Peripheral

Bone marrow ↑Utilization ↑ Platelet

suppression -Excessive destruction
used for
platelet
aggravation
-
Consumptive
coagulopathy
A) ASYMPTOMATIC

Undifferentiated
Fever

Without haemorrhage

B) SYMPTOMATIC Dengue Fever

With unusual
haemorrhage

Dengue No shock (Grade I & II)

Haemorrhagic
Fever
DSS (Grade III & IV)
Asymptomatic (Subclinical
infections)
 About 30% of the total infections

 They sensitize the immune system

Symptomatic
 1) Undifferentiated Fever
 Definition- a group of
illnesses resulting from
infection by any of the
arboviruses pathogenic to
humans, in which the only
constant manifestation is fever
 May be the most common
manifestation of dengue
 It was found in a prospective study
that 87% of students infected
were either asymptomatic or only
mildly symptomatic
 Other prospective studies
including
DS Burke, et al. A all age-
prospective groups
study also
of dengue infections
demonstrate
in Bangkok. Am J Trop Medsilent transmission
Hyg 1988; 38:172-80.
2) Dengue Fever without haemorrhage

( Classical dengue fever)

 is an acute febrile illness of 2-7 days duration (Fever is in
most of the cases is followed by a remission of
2hours- 2days-biphasic curve - with two peaks) with two
or more of the following manifestations:

1.Headache
2.Muscle and joint pain (severe-break-bone
fever)- >78%
3.Nausea/vomiting
4. Retro orbital pain

5. Rash (Day 2-5)-Rashes appear in remission

period or in second febrile period which lasts
for 1-2 days. The rash is accompanied by
similar but milder symptoms

(Rash- During the first half of the febrile period- diffuse flushing, mottling or fleeting pin-point
eruptions on the face, neck and chest
It becomes maculopapular or scarletiniform on 3rd -4th day- It starts on the chest and trunk and
spreads to extremities and rarely spreads to face. It may be accompanied by itching and
hyperaesthesia. The rash lasts for 2 hours to several days and may be followed by
desquamation.)

4. Hemorrhagic manifestations (petichiae and

positive tourniquet test) and, leucopenia.
 Tourniquet Test
Inflate blood pressure cuff to a
point midway between systolic
and diastolic pressure for 5
minutes
Positive test: 20 or more
petechiae per 1 inch2 (6.25
cm2)
Pan American Health Organization: Dengue and Dengue Hemorrhagic
Fever: Guidelines for Prevention and Control. PAHO: Washington, D.C.,
1994: 12.
Positive Tourniquet Test

2.5
cm
 Hepatomegaly

 Low blood pressure

 All the primary infections result in this

type of dengue fever

 In children, DF is usually mild

 “Dengue triad”: fever, rash, and headache

(Carson-DeWitt 2004).
DENGUE -MACULO-
PAPULAR RASH.
fever.
Petechiae
 PETECHIAE

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Subconjunctival
haemorrhage
 Other common symptoms include-
Extreme weakness
Anorexia
Constipation
Altered taste sensation
Colicky pain and abdominal tenderness
Dragging pain in inguinal region
Sore throat
General depression
What is the end result?

 Complete recovery is the rule

 Severe weakness many persist for
many days after the fever leaves us
 Death occurs very rarely
 4) Dengue Fever with unusual
haemorrhage
 Occasionally variable degrees of
thrombocytopenia and cutaneous
hemorrhage are observed.

 Infrequently, DF may be accompanied by

unusual bleeding complications that may
cause death .
Unusual Presentations of
Dengue Fever
1)Encephalopathy :(Den2 and den3 are
neurovirulent, 2-3% of total cases)-
Decreased level of consciousness-lethargy,
confusion and coma
Seizures
Nuchal rigidity
Paresis
2)Hepatic damage
3) Cardiomyopathy
4)Severe gastrointestinal hemorrhage
Dengue Hemorrhagic Fever-
 A severe form of the disease
 Occurs in persons already sensitized
( secondary)
The first infection sensitizes the patient,
while second produces an immunological
catastrophe
Begins abruptly with high fever accompanied by
facial flushing and headache

Anorexia, vomiting, epigastric discomfort, tenderness

at the right costal margin and generalised abdominal
pain are common

During the first few days the illness usually

resembles classical DF, but after a few days the
patient becomes irritable, restless, and sweaty. These
symptoms are followed by a shock -like state

Rash may appear early or late in the course of illness

 Febrile convulsions may occur in infants
There may be bleeding under the skin
(purpura), from the gums and from the
gastrointestinal tract.
Hemorrhagic Manifestations
of DHF
 Skin hemorrhages: petechiae,
purpura, ecchymoses
 Gingival bleeding

 Nasal bleeding

 Gastro-intestinal bleeding:

haematemesis, melena,
haematochezia
 Hematuria

 Increased menstrual flow

4 Necessary Criteria:
1. Fever, or recent history of acute fever

2. Hemorrhagic manifestations

3. Low platelet count (100,000/mm3 or less)

4. Objective evidence of “leaky capillaries:”

elevated hematocrit (20% or more over
baseline)
low albumin
pleural or other effusions
Four Grades of DHF
 Grade 1
Fever and nonspecific constitutional symptoms
Positive tourniquet test is only hemorrhagic
manifestation

 Grade 2
Grade 1 manifestations + spontaneous bleeding

 Grade 3
Signs of circulatory failure (rapid/weak pulse,
narrow pulse pressure, hypotension, cold/clammy skin)

 Grade 4
Profound shock (undetectable pulse and BP)
DENGUE GRADATION

http://w3.whosea.org/en/Section10/Section332/Section554_25
 DISEASE SPECTRUM
MILD SEVERE

DF DHF
+ Thrombocytopenia +++
Thrombocytopenia
Hidden Vasc. Perm1?
Overt Vasc. Perm.
 DF DENGUE PATHOGENESIS
DHF
DSS
Ag-Ab-complement complex

Serous
-Fever
effusion
-Flushed face Hepatomegaly Dead
(pleural, ascite)
-Headache
-Retro-orbital Hypoprotidemia Acidosi
pain s
-Myalgia ↑ capillary Hypovolemia
Shock Anoxia
-Arthralgia permeability (haemoconcentratio
n)
-Rash
Thrombocytopenia* DIC

- Intestinal
Haemorrhagi
c haemorrhag
e
manifestation
*Trombocytopenia is not constant in 68
-Leucopenia DF
Danger Signs in DHF that
predict progression to DSS
Abdominal pain - intense
and sustained
Persistent vomiting
Abrupt change from fever
to hypothermia, with
sweating and prostration
Restlessness or somnolence
This thermometer illustrates the developments in the
illness that are progressive warning signs that DSS may
occur.
The initial evaluation is made by determining how many
days have passed since the onset of symptoms.
Most patients who develop DSS do so 3-6 days after onset
of symptoms. Therefore, if a patient is seven days into the
illness, it is likely that the worst is over.
If the fever goes between three and six days after the
symptoms began, this is a warning signal that the patient
must be closely observed, as shock often occurs at or
around the disappearance of fever.
Other early warning signs to be alert for include a drop in
platelets, an increase in hematocrit, or other signs of plasma
leakage.
If you document hemoconcentration and thrombocytopenia
and other signs of DHF and the patient meets the criteria for
DHF, the prognosis and the patient's risk category have
changed. Though dengue fever does not often cause
fatalities, a greater proportion of DHF cases are fatal.
The next concern would be observation of the danger signs—
severe abdominal pain, change in mental status, vomiting
and abrupt change from fever to hypothermia. These often
herald the onset of DSS.
The goal of treatment is to prevent shock. The plasma
leakage syndrome is self-limited. If you can support the
patient through the plasma leakage phase and provide
sufficient fluids to prevent shock, the illness will resolve
itself.
 PURPURA

http://www.pediatrics.wisc.edu/education/derm/tutb/85m.jpg
ECCHYMOSIS

http://www-medlib.med.utah.edu/WebPath/ATHHTML/ATH036.html
NASAL HEMORRHAGING

http://www.cgste.mq/brainstorm/dengue/image/hemo.gif
 Criteria for clinical diagnosis
of Dengue Shock Syndrome
1. 4 criteria for DHF

2. Evidence of circulatory failure manifested indirectly

by all of the following:
Rapid and weak pulse
Narrow pulse pressure (≤ 20 mm Hg) OR hypotension for age
Cold, clammy skin and altered mental status

It is sometimes not easy to categorize the disease,

mixed presentations can also be seen
Adequate treatment and prompt referral saves the
patient's life
Early signs of shock include restlessness, cold
clammy skin, rapid weak pulse, narrowing of
pulse pressure, and hypotension.
DHF patients may rapidly progress into dengue
shock syndrome (DSS), which, if not treated
correctly, can lead to profound shock and death.
Most patients who develop DSS do so 3-6days
after onset of symptoms.
If a patient is 7 days into the illness, it is likely
that the worst is over
 Risk Factors Reported for

DHF
Virus strain- strain 2 is more virulent followed by
3,1 and 4

 Pre-existing anti-dengue antibody

previous infection

maternal antibodies in infants ( dengue

infection in pregnant mother may result
in passive transfer of anti-dengue IgG to
the foetus (or congenital infection)
 Risk Factors for DHF

(continued)
Higher risk in secondary infections
( Hyperendemic regions)
 Higher risk in locations with two or more serotypes circulating
simultaneously at high levels (hyper endemic regions)

Host genetics—for example, race seems to

be a factor: data from Cuba suggest that
whites may be at greater risk, and blacks at
lower risk. And
Age—in Southeast Asia, children are most
affected, though in the Americas, all age-
groups are affected.
Dengue Infection in
Pregnancy
 Limited information
 Vertical transmission
 Dengue infection may be associated
with:
 Spontaneous abortion and fetal death
Premature births

1. Chye, 1997; 2. Boussemart, 2001; 3. Carles, 1999; 4. 2000

Infection and Pregnancy

 10-25% of fetal loss caused by

maternal or fetal infection
 Due to:
High maternal fever
Reduced blood flow from infected
placenta
Fetal infection and damage of vital
organs
 Clinical Evaluation in
Dengue Fever
Blood pressure
Evidence of bleeding in skin or
other sites
Hydration status
Evidence of increased vascular
permeability-- pleural effusions,
ascites
Tourniquet test
 Population 5%

Infection 24%
76%
Asymptomatic Clinical Cases 6%
Infection 94%
DF DHF/DSS
(non-DHF) 0.8%
99.2%
survive Death

Rates in dengue model

by Shepard et al. Vaccine. 2004, 22:1275-1280.
Dengue + bleeding = DHF
Need 4 WHO criteria, capillary permeability
DHF kills only by hemorrhage
Patient dies as a result of shock
Poor management turns dengue into DHF
Poorly managed dengue can be more
severe, but DHF is a distinct condition, which
even well-treated patients may develop
Positive tourniquet test = DHF
Tourniquet test is a nonspecific indicator of
capillary fragility
Differential diagnosis
Influenza
Measles
Rubella
Malaria
Typhoid fever
Leptospirosis
Meningococcemia
Rickettsial infections
Bacterial sepsis
Other viral hemorrhagic fevers
Pleural Effusion Index

PEI = A/B x 100

B
A
Vaughn DW, Green S, Kalayanarooj S, et al. Dengue in the early febrile
phase: viremia and antibody responses. J Infect Dis 1997; 176:322-30.
Laboratory diagnosis
Laboratory diagnosis is essential for confirmation of
dengue virus infections.
Routine lab tests
1)CBC- WBC, Platelets, Haematocrit
(Adults: Females 0.36 - 0.44 Males 0.39 - 0.50)
2)Albumin
3)Liver function test
4)Urine- for microscopic hematuria
 Dengue specific tests

Virus isolation
PCR

Serology ( IgM or
rising IgG titre)-
MAC ELISA IgM
capture test is done
at DSU- Belgaum
 Temperature, Virus Positivity and
Anti-Dengue IgM , by Fever Day
Temperature (degrees Celsius)

100

Dengue IgM (EIA units)

300
39.5
Percent Virus Positive

80
39.0 225
38.5 60
150
38.0 40
37.5 20 75

37.0
0 0
-4 -3 -2 -1 0 1 2 3 4 5 6
Fever Day
Mean Max. Temperature Virus Dengue IgM
Adapted from Figure 1 in Vaughn et al.,
J Infect Dis, 1997; 176:322-30.
Primary Infection

IgM antibodies appear approximately 5 days after

onset of symptoms and rise for the next 1-3
weeks 

IgM antibodies detectable for up to 6 months

IgG are detectable at approximately 14 days after

onset of symptoms and are maintained for life
Secondary Infection
Approximately 5% patients do not produce
detectable levels of specific IgM

IgM titre can be slower to rise in secondary

infection

IgG appears approximately 2 days after

symptoms appear

IgG titre significantly higher in secondary

infection
 Management
No specific treatment for
dengue fever.

With appropriate intensive

supportive therapy, mortality
may be reduced to less than
1%.

Maintenance of the circulating

fluid volume is the mainstay
of managing patients with
DHF
Outpatient triage
No hemorrhagic manifestations and the
patient is well hydrated- Home treatment
Hemorrhagic manifestations or hydration
is borderline (Grade I & Grade II) –
Outpatient observation or hospitalization
With warning signs (even without profound
shock) Grade III & Grade IV- Hospitalize
Management of dengue fever is
symptomatic and supportive
Bed rest – during the acute febrile
phase
A rise in hematocrit value- significant
plasma loss-indicates the parenteral
therapy- hospitalization
Volume replacement therapy
 Lost plasma should be replaced early
with an electrolyte solution, plasma, or
plasma expanders to prevent or treat
reduced blood volume (hypovolemic)
shock. Patients with mild dengue
hemorrhagic fever can usually be
rehydrated orally.
 Fluids
 Rest
 Antipyretics (avoid aspirin and non-
steroidal
anti-inflammatory drugs)
 Monitor blood pressure, hematocrit,
platelet
count, level of consciousness
 Signs of recovery
 Absence of fever for 24 hours (without
anti-fever therapy) and return of appetite
 Visible improvement in clinical picture
 Stable hematocrit
 3 days after recovery from shock
 Platelets 50,000/mm
 No respiratory distress from pleural
effusions/ascites
99

MANAGEMENT OF DF
100

MANAGEMENT OF
DHF
 MANAGEMENT OF DHF
101

 The manifestations and management of

DHF during the febrile phase are the
same as DF.
102

MENAGEMENT OF
DHF
GRADE I & II
 Type of IV fluids
103
 Crystalloid solutions
- 5%D/NSS
- 5%D/N/2* (only for < 1 year of age)
- 5%DLR
- 5%DAR

 Colloid solutions
- 10% Dextran 40
- 10% Haes-Sterile

D= Dextrose, NSS= Normal Saline Solution,

AR= Acetate Ringer, LR= Lactate Ringer
 IV fluid therapy for DHF grade I & II
Start IV fluid 3ml/kg/h
104
crystalloid solutions
over 1 – 3h
No improvement, stationary (2)
Improvement (1)
Continue with the same IV
fluid for another 1 – 3h
IV fluid 3 ml/kg/h another 3h
Reevaluation VS hourly
Reevaluation Ht, VS hourly
Improvement aggravation (3)
Further Improvement
↑ IV fluid to 6 ml/kg/h
1 – 3h
↓IV fluid to 1.5 ml/kg/h over 3h
More aggravation (4)
Still improvement

IV fluid 1.5 ml/kg/h over 24 – See DHF grade III or IV

48h and stop
 1. Improvement:
105 ↓ Ht, stable pulse & Blood Pressure, ↑ urine
diuresis

2. No improvement, stationary:
Pulse and BP not changed and still having
oliguria

3. Aggravation: pulse faster and oliguria

4. More aggravation:
weak and rapid pulse or not detectable,
narrow pulse pressure, hypotension or not
measurable blood pressure
106

MANAGEMENT OF DHF
GRADE III
 Type of solutions
107
 Crystalloid solutions:
- 5%D/NSS
- 5%DLR*
- 5%D/AR
 Colloid solution:
- Dextran 40
- Fresh whole blood
(FWB)
* Lactate Ringer solutions are contra-indicated
in case of acidosis.
NSS or Acetate Ringer should be used instead of LR
in case of shock
 IV fluid therapy for DHF grade III
Ht immediately, IV fluid 10ml/kg/h
crystalloid solutions over 1 – 2h +
108
oxygen
Improvement No improvement
Control Ht
↓ IV to 6 ml/kg/h
over 3h Ht ↑ Ht ↓
Further Improvement Dextran 40 10ml/kg/h FWB 10ml/kg/h
↓IV to 3 ml/kg/h and repeated if
over 6h necessary (not exceed
30ml/kg/day)
Always
improvement
No improvement Improvement
↓IV to 1.5 ml/kg/h ↓ IV fluid of crystalloid
ASCB* see
over 24 – from 10 → 6 →
complications
48h and 3 → 1.5 ml/kg/h
guideline
stop
109  A – Acidosis (Bicarbonate Na 8.4%
1ml/kg/dose)
 S – Blood sugar (<60mg%) →
D10% 5ml/kg/dose.
 C – Calcemia ( Ca gluconate 10%
1ml/kg/dose Max: 1 ampoule
 B- Bleeding → Blood Transfusion,
Platelet Transfusion
 OXYGEN USED IN SHOCK
110
CASES
 If shock: oxygen (nasal
prongs)
- Infant < 1 year = 1L/min
- Children > 1 year = 2L/min
111
MANAGEMENT OF DHF
GRADE IV
(PROFOUND SHOCK)
112
Type of solutions
 Crystalloid solutions:
- NSS
- AR
 Colloid solution:
- Dextran 40
- Fresh Whole Blood
 IV fluid therapy for DHF grade IV
NSS or AR 10ml/kg bolus
113

Improvement No improvement

5%NSS/DAR NSS/AR 10ml/kg bolus

10ml/kg 1 – 2h

Improvement No improvement Improvement No improvement

Lab: Hct, blood gas, ionogram, Ca,

↓ IV 10 → 6 → 3 → 1.5 ml/kg/h LFT, BUN, creatinin, glucose
discontinue IV after 24 – 48h
Hct ↑ Hct ↓
Dextran 40 10ml/kg/h and FWB 10ml/kg/h
repeated if necessary
Improvement No improvement Improvement

ASCB and see complications

guideline
 Fluid Overload
 The common causes:
114
 Early IV fluid therapy in the early febrile phase
 Use of hypotonic solution

 Do not reduce the rate of IV fluid and do not

discontinue IV fluid when entering convalescence
period
 Do not use colloidal solution when indicates

 Do not give blood transfusion when there is

concealed bleeding and continue giving crystaloid
and colloidal solutions
 Do not calculate the amount of IV fluid according to
ideal body weight in obese/overweight patients
 Note for Overweight
115 Patients
 Use ideal body weight (weight for age)
to calculate the IV fluid in
overweight/obese patients

 Maximum weight for IV calculation is

50 kg (for adult and overweight
patients)

Weight (kg) = 2 (Age + 4)

(Child aged between 1-10
years)
 Management of Patient
116
with Fluid Overload
 Change IV fluid to Dextran 40
 Insert urinary catheter with special precaution
 Furosemide 1mg/kg/dose IV. Vital signs should be
monitored every 15 min for at least 1 hour after
furosemide and observe clinical signs of shock
 Shock: Colloidal solution: Dextran 40 10ml/kg/h IV
over 10-15 minutes or until the patient has stable vital
signs, usually not more than 30 min and then switch to
crystalloid solution.
Prevention and
Control
 IVCM-Integrated
Vector control
Management
 Vaccines
 No licensed vaccine at present

 Effective vaccine must be tetravalent, otherwise

protection against only one or two dengue viruses
could increase the risk of more serious disease.

 Field testing of an attenuated tetravalent vaccine

currently underway

 Effective, safe and affordable vaccine will not be

available in the immediate future
Thank You !