Dengue Management in

Children
Blok 27 – Agustus 2018

Outline

Epidemiology
Etiology and Pathogenesis

Clinical manifestation

Laboratory diagnosis confirmation

Case Classification

Management
2

Etiology – Dengue Virus

Virus DEN
• Arbovirus
• Vector: (A aegypti, A albopictus, A

polynesiensis, A niveus)
– nyamuk betina yg terinfeksi, menggigit di
siang hari
• Single-stranded RNA
• 4 serotypea (DEN-1, 2, 3, 4)
– Each serotype can cause fatal and severe
disease – Some genetic variants in each

serotype more virulent or have greater

epidemic potency

Pathogenesis of DHF/DSS

• The pathogenesis of DHF and DSS still needs to be

explored further
• Two basic theories, which are not mutual exclusive –
were frequently cited to explain the pathogenetic changes

– Secondary Heterologous Infection

or Antibody
Dependent Enhancement (ADE)
Theory – Virus Virulence Theory
• Both theories are supported by epidemiologic and
laboratory studies/evidence, and are most probably valid

Scott B. Halstead. WHO, SEARO, New Delhi, 1993. p80-103.

Duane J. Gubler. Clinical Microbiology Reviews, 1998:480-96

Secondary Heterologous Infection

or Antibody Dependent Enhancement

(ADE) theory
Secondary Heterologous Infection
Theory
• Patients experiencing a 2nd infection with heterologous
dengue virus (DenV) serotype ⇨ have significant higher
risk to have DHF/DSS

• Prior infection, through a process ⇨ antibody-dependent

enhancement (ADE), enhance the infection and
replication of DenV in mononuclear cells / macrophage
(more receptor uptake)

• This cells, produce and secrete vasoactive mediators

(particularly cytokines) ⇨ increase vascular permeability ⇨
hypovolemia and shock

Halstead SB. WHO, SEARO, New Delhi 1993

Gubler DJ. Clinical Microbiology Reviews 1998

• Homologous Antibodies Form Non-infectious Complexes

1
1
Dengue 1 virus Neutralizing antibody
to Dengue 1 virus
Non-neutralizing antibody 1

1 Complex formed by neutralizing antibody and virus

1
Pathogenesis of DHF - 1

• Heterologous Antibodies Form Infectious Complexes

2
2

2 Non-neutralizing antibody to Dengue

Dengue 2 virus 1 virus
2
Pathogenesis of
Complex formed by non-neutralizing
antibody and virusDHF - 2
Pathogenesis of DHF - 3
Heterologous Complexes Enter More Monocytes, Where Virus
Replicates
2
2
2
2
2
22
22

22
2
2 22
Dengue 2 virus Non-neutralizing antibody
2
Complex formed by non-neutralizing antibody and Dengue 2 virus

Dengue Clinical
Presentations

Dengue has a wide spectrum of

clinical presentations with often
unpredictable evolution:
• Self-limiting disease in most
patients
• Severe disease in a small
proportion of patients, characterized
by plasma leakage with/without
haemorrhage

10
DENGUE
EPIDEMIOLOGY

11
12

Figure Trends in incidence rate of DHF cases in

Indonesia from 1968 to 2013, measured in numbers of
cases per 100,000 person years.
13
Figure Case fatality ratios of DHF cases in Indonesia
from 1968 to 2013.

14

CLINICAL COURSE OF
DENGUE

15

Dengue mimics many clinical syndromes

Flu-like illness
Clues to diagnose dengue:
Viral exanthem
Understanding the dynamic and systemic Acute abdomen
nature of dengue
Infections
Knowing its various manifestations as the
Autoimmune
disease progresses from febrile phase to critical diseases
phase and evolves into recovery phase Haematological disorders
Dengue
16

Clinical Course of
Dengue
17

Vignette of febrile phase

• Usually lasts 2 to 7 days

• High temperature; may be modified by antipyretics

• Common symptoms: myalgia, headache, retro-orbital pain, aches,

rash

• Difficult to differentiate dengue from viral febrile illness

• Normal CBC in first 1 to 2 days of fever

Quality of life may be affected1

• Changes in behaviour and mood

• Inability to focus and concentrate on work and self-care

Children
Nausea and vomiting may be prominent

1 Lum et al. Quality of Life of Dengue Patients. Am J Trop Med Hyg, 2008.

18
Headache, Bleeding gums retroorbita and nose
pain
Exanthema
Vomiting
Diarrhoea
Muscle pain
Joint pain
19

Febrile phase
Sudden-onset fever
Dehydration
Progressive leucopenia
Progressive thrombocytopenia
Conditions that mimic the febrile phase of dengue
Viral infections
Influenza, measles, rubella Chikungunya, West Nile virus Enterovirus Other viral
haemorrhagic fever Infectious mononucleosis Acute HIV seroconversion illness
Leptospirosis Bacterial infections
Typhoid Rickettsia infections (typhus, scrub typhus, etc.)
Parasitic infections
Malaria
Measles, rubella Infectious mononucleosis, enterovirus
Febrile illness with
Chikungunya, West Nile virus, Scarlet fever, meningococcal infection a rash
Leptospirosis, typhoid Rickettsia infections (typhus, scrub typhus, etc.) Syphilis, acute
HIV seroconversion illness Autoimmune diseases (e.g. SLE) Adverse drug reaction
Rotavirus Diarrhoeal diseases
Salmonellosis Other enteric infections
20

Laboratory
* WHO 2009 Dengue guideline
21
WHO 2011 Dengue guideline
Clinically
Acute febrile phase
Increase in haematocrit concurrent with rapid dcrease in
platelet count, folllowed by blood pressure and pulse
changes
No clinical improvement or worsening in afebrile phase –
abdominal pain or tenderness – persistent vomiting –
refusal of oral intake - clinical fluid accumulation –
mucosal bleed – lethargy or restlessness or irritability –
liver enlargement > 2 cm – postural hypotension – oliguria

Dengue phase
Some patients
Critical phase
Warning signs*
Recovery phase

Pleural effusion Ascites

22
Signs of shock
Severe dengue Severe
plasma leakage Severe
bleeding Severe organ Progressive leucopenia
impairment

Critical phase

Fever defervescene

Increase in haematocrit
Signs of plasma leakage

Progressive thrombocytopenia
Conditions that mimic the critical phase of dengue
Acidotic breathing/ respiratory distress
Acute appendicitis Acute abdomen
Acute cholecystitis Perforated viscus Diabetic ketoacidosis
Diabetic ketoacidosis Lactic acidosis Renal failure Acute respiratory distress syndrome
(ARDS)
Sepsis, septic shock Acute gastroenteritis Infections
Leptospirosis, typhoid, typhus, malaria Viral hepatitis Acute HIV seroconversion illness
Systemic lupus erythematosus Autoimmune diseases
Idiopathic Thrombotic thrombocytopenic thrombocytopenic purpura
purpura Systemic vascultis
Malignancies
Acute leukaemia Lymphoma Other malignancies
Others
Liver cirrhosis with portal hypertension Adverse drug reaction
23

Transition from febrile phase to critical phase

• Usually day 4 to day 7 of illness
• Could be as early as day 3 or as late as day 7 or 8
• Coincides with defervescence
Development of warning signs:
Identify dengue patients already in shock or at risk of
developing shock
Clinical Warning Signs
Laboratory Warning Signs 1. Severe abdominal pain
1. Leukopenia 2. Persistent vomiting
2. Rapid decrease platelet count 3. Mucosal bleed
3. Rising haematocrit 4. Lethargy; restlessness 5. Liver
enlargement >2cm 6. Clinical fluid accumulation
24
9

Pearls: laboratory warning signs

Leucopenia

• Occurs 24 hours before rapid decrease in platelet count

• Not predictive of plasma leakage

• Good indicator that patient could have dengue

Rapid decrease in platelet count + rising trend in haematocrit

• Occur shortly before or at defervescence

• May precede changes in blood pressure and pulse pressure

• Indicate an increase in vascular permeability

NOTE: Changes in haematocrit may be masked by IV fluid therapy

25

What happens during the critical phase?

Increased vascular permeability Deterioration in patient’s condition

How long does plasma leakage
last?
Significant plasma leakage
24 – 48 hours

Development of warning signs

Death
What could happen without treatment?

Shock occurs when critical volume of plasma is lost through leakage.

Shock is often preceded by warning signs.

Body temperature may be sub-normal when shock occurs.

The total white cell count may increase (instead of leukopenia) in patients
with severe bleeding at this stage.

26

Do all dengue patients enter critical phase?

NOT all patients will experience the critical phase

Clinical course of patient without significantly increased vascular

permeability:

• Fever subsides → general condition improves and appetite recovers

• May have leukopenia

• Mild to moderate thrombocytopenia

27

Vignette of recovery phase

What happens in recovery phase?

Vascular permeability reverts to normal → Gradual reabsorption of
extravascular fluid in next 48 to 72 hours

Clues to progression from critical phase to recovery phase

Clinical clues: 1. Improvement in general well-being and stable

haemodynamic status 2. Diuresis 3. Biphasic fever 4. May have
bradycardia 5. Isles of white in the a sea of red

Laboratory clues:

1. HCT stabilizes.
HCT may lower due to dilutional effect of reabsorbed fluid
(haemodilution). 2. WBC usually starts to rise soon after
defervescence. 3. Thrombocytopenia persists longer than leucopenia.
28
Summary of clinical problems during each phase
Febrile Phase
Dehydration
Critical Phase
Recovery Phase
High fever → Neurological disturbances
Contributing factors:
1. Hallucination 1. Poor oral intake from anorexia and nausea
2. Febrile seizures 2. Insensible fluid loss from high fever
Plasma leakage → hypovolaemia and shock
Severe haemorrhage
Organ impairment to liver, kidneys and other organs
Hypervolaemia with fluid overload because of inappropriate fluid management
29
Compensated shock in the early stage (normal or elevated blood pressure)
Decompensated shock in the late stages (hypotension & unrecordable blood pressure)
Warning
Stable Hours
signs
Hours Compensated

shock
Hours Hypotensive

shock
Min

Cardiac arrest
Identification and treatment of early shock will improve clinical outcome.
Delayed treatment leads to a clinical course complicated by severe bleeding and
organ impairment. Severe bleeding will exacerbate the shock state and if
unrecognized will cause refractory and irreversible shock with a very poor
outcome.
Pitfall: Why is it easy to miss dengue shock?
Even in the severe shock state, the patient appears deceptively normal or
“stable” with a lucid conscious level.
A careful physical examination is critical to recognizing a patient in shock before
the stage of cardiovascular collapse.
30

Pearls and pitfalls: dengue shock

Dengue shock presents as a physiologic-time continuum
22

LABORATORY
DIAGNOSIS
CONFIRMATION

31

Laboratory Diagnostic Options

in a Patient with Suspected
Dengue Infection 32
Simmons CP et al. N Engl J Med 2012;366:1423-1432

Interpretation of dengue

diagnostic test

• Handbook mangement of dengue, TRD-WHO,2012

33
CASE CLASSIFICATION

34

1997 WHO Dengue

WHO Classificatio
 35
n 2011 WHO-SEARO
2011 WHO-SEARO
2009 WHO
2009 WHO
2009 WHO
WHO has proposed several
guidelines
WHO SEARO 1997 Guidelines
36

WHO 1997 Dengue

Classification
DF DHF
1. Fever 2-7 days + +
2. Haemorrhagic tendencies
❑ Positive tourniquet test or ❑ Spontaneous bleeding

+/- +
3. Thrombocytopenia
+/- +
❑ ≤ 100,000/mm3 4. Plasma leakage
❑ a rise or a drop in the haematocrit ≥ 20% ❑ pleural
effusion, ascites and
hypoproteinaemia
-+
37

WHO 1997 Dengue

Classification
Grade Sign and Symptomps Laboratory
DF ~ DHF without plasma leakage
DHF
I Fever with non-specific constitutional symptoms; the
only hemorrhagic manifestation is a positive
tourniquet test &/or easy bruising evidence of plasma
Thrombocytopenia
leakage
(platelet count II DHF grade I plus spontaneous
bleeding ≤100,000/μL) III Circulatory failure
manifested by a rapid, weak pulse,
narrowing of pulse pressure, or hypotension, cold &
clammy skin, restlessness
IV Profound shock with undetectable pulse and blood
pressure
38

• Changes in the epidemiology

– became endemic disease (expansions
into other regions) – increasing adult cases
• Clinical manifestation are more
varied
• The incidence of severe cases
increase
– The development of mild cases into

severe cases is difficult to detect

• Difficulties in applying the criteria for

DHF in the clinical situation, together

with the increase in clinically severe

dengue cases which did not fulfil the

strict criteria of DHF

39
1997 2009

WHO TDR 2009 Dengue

Classification
WHO proposed a dengue case classification
system in 2009:
• Supported by set of clinical and/or laboratory
parameters
• Emphasize the importance of detecting

clinically significant plasma leakage early as a

feature that distinguishes severe from non severe

dengue cases
• Classification levels would help clinicians in

decision making about intensity of treatment and

observation
40

WHO TDR 2009 Dengue

Classification

41
• Some cases of DF and DHF
came with unusual manifestation
• Triage system was needed for
early detection of shock and
prompt management

42
2011 2009

Manifestation of dengue virus

infection
43

WHO Classification of Dengue Infection

and Grading of Severity WHO-SEARO

2011
DF/D HF Grade Signs & Symptoms Laboratory DF

Fever • • • • • • • 44

Headache Retro-orbital Myalgia Arthralgia/bone Rash

Hemorrhage No with 2 following signs pain pain

evidence manifestations of plasma leakage

Leucopenia cells/mmThrombocytopenia (≤150.000 Rising

10%) No 3) (WBC ≤5000 hematocrit cells/mm(5%- 3)

evidence of plasma loss

DHF DHF I II Fever tourniquete & hemorrhagic test)

and manifestation evidence of plasma (positive

leakage As grade I plus spontaneous bleeding

Thrombocytopenia <100.000 Hematocrit

cells/mmrising 3 ≥20% DHF* III As pulse, hypotensive,

grade narrow I or restless pulse II plus pressure

circulatory (≤20 failure mmHg), (weak DHF* IV As

undetectable grade III plus BP & profound pulse

shock with

Dengue Diagnosis
Classification
1997 2009 2011
• Dengue fever • Dengue without
warning signs
• Dengue fever
• DHF grade I
• Dengue with warning signs
• DHF grade I
• DHF grade II • DHF grade II
• DHF grade III/DSS (dengue shock syndrome) • Severe
dengue (severe plasma leakage, hemorrhage,
organ involvement)
• DHF grade III /DSS (dengue shock syndrome)
• DHF grade IV (DSS with profound shock)
• DHF grade IV
• Expanded dengue syndrome (unusual
manifestation, organ involvement, co-morbidity
45

46
2011 WHO-SEARO
2009 WHO
2011 WHO-SEARO
IPS - Pediatric Tropical
2011 WHO-SEARO
Infectious Disease
Working Group

HARMONIZED
2014 IPS Guidelines for Diagnosis
and Management of Dengue
Infection in Children

✚✚

What is new in IPS 2014

dengue guidelines?
• Warning signs
• Triage system in PHC/ hospital
• Determination of compensated shock
and decompensated shock as a guide for
early and targeted treatment
• Concern to A-B-C-S (Acidosis, bleeding,
calcium, sugar)
• Expanded dengue syndrome
• The diagnosis of dengue infection in the
hospital should be accompanied by dengue
Ag detection or serological Ab tests
• High risk group

47

Unusual Dengue
manifestations complication
• Electrolytes • Dengue
disturbance encephalopathy
• Fluid overload • Massive bleeding
• Dual infection
• Renal abnormality
• Miocarditis
48

Expanded Dengue Syndrome

High risk group

The following host factors contribute to more severe

disease and its complications:
• infants and the elderly,
• obesity,
• pregnant women,
• peptic ulcer disease,
• women who have menstruation or abnormal vaginal bleeding,
• haemolytic diseases such as glucose-6-phosphatase
dehydrogenase (G-6PD) deficiency,
• thalassemia and other haemoglobinopathies,
• congenital heart disease,
• chronic diseases such as diabetes mellitus, hypertension,
asthma, ischaemic heart disease, chronic renal failure, liver
cirrhosis,
• patients on steroid or NSAID treatment, and
• others.

49

PATIENT ASSESSMENT
AND EVALUATION
50

Patient assessment: four important steps

Step 1: History taking

Step 2: Clinical examination

Step 3: Investigations

Step 4: Diagnosis, phase of disease and severity

51

Step 1: History taking

What are important histories in dengue patients?

1. Date of onset of fever or illness

2. Symptoms and severity

3. The 3 golden questions:

• How much oral fluid intake: quantity and quality?

• How much urine output: frequency, volume and time of most recent
voiding?
• What activities could the patient do during the febrile illness?

4. Other fluid losses: diarrhoea, vomiting

5. Presence of warning signs

52

Step 1: History taking

What are other relevant histories?

6. Family or neighbour with dengue, or travel to dengue-endemic

areas

7. Medications (including non-prescription or traditional medicine) in

use?

List of medications and last time they were taken.

8. Risk Factors: infancy, pregnancy, obesity, diabetes mellitus,

hypertension, etc.
Why do we ask?

9. Jungle trekking or swimming in waterfall

Consider leptospirosis, typhus, malaria

10. Recent unprotected sexual or drug use behaviour

Consider acute HIV seroconversion illness

53

Step 2: Clinical examination

General assessment:

Mental state

Hydration state

Haemodynamic state

Clinical evidence of warning signs:

Bleeding manifestations: mucosal bleeding

Abdominal tenderness

Liver enlargement

Fluid accumulation: pleural effusion, ascites

Other important signs:

Rash
Tachypnoea/acidotic breathing: indicates shock

Tourniquet test: repeat if negative or if there is no bleeding

manifestation

54

Hemodynamic
Assessment
Hemodynamic Parameters Hypotensive Shock
Stable Circulation Hypotensive Shock
Compensated Shock
Conscious level
Compensated Shock
Clear and lucid Clear and lucid
Hypotensive Shock
Restless, combative

Capillary refill Brisk (≤2 sec) Prolonged (>2 sec) Very prolonged, mottled
skin

Extremities Warm and pink Cool peripheries Cold, clammy

Peripheral pulse volume

▶ Normal blood
Good volume Weak and thready
Feeble or absent pressure for age ▶ Normal pulse
pressure for age
Heart rate Normal heart rate ▶ Normal systolic
for age
Tachycardia for age Severe ▶ Normal systolic
tachycardia or pressure, but rising diastolic
bradycardia in late shock
pressure ▶ Narrowing pulse
Blood pressure
 pressure, but rising diastolic
(≤ 20 mmHg) ▶ Hypotension ▶
pressure ▶ Narrowing pulse
Unrecordable blood
pressure ▶ Postural hypotension
(≤ 20 mmHg) ▶ Hypotension ▶
▶ Narrow pulse pressure
Unrecordable blood
▶ Narrow pulse pressure pressure

▶ Narrow pulse pressure

(≤ 20 mmHg) ▶ Hypotension ▶
Unrecordable blood
(≤ 20 mmHg) ▶ Hypotension ▶
Unrecordable blood
Respiratory rate
Normal respiratory rate for age
Tachypnea Hyperpnea or
Kussmaul’s
Tachypnea Hyperpnea or
Kussmaul’s
breathing (metabolic acidosis)
breathing (metabolic acidosis)

Urine output Normal Reducing trend Oliguria or anuria

55

Pitfalls in clinical examination of dengue patients

A patient with high fever (39oC) has tachycardia, cold

extremities and delayed capillary refill time.

• Is he or she in shock?

• What other features do you need to consider?

* Reminder: Haemodynamic assessment is the foundation of dengue
clinical management.

A wrong interpretation could lead to a wrong decision in fluid

management.

56

Pitfalls in clinical examination of dengue patients

Always look at the BIG picture before “zooming in”.
History: When was fever onset? In which phase of disease is the
patient?
Remember: Clinical features come as a “package”, not in isolation.
Intake/output: What was the patient’s fluid intake and urine output?

Big Picture
Any warning signs? What was the patient’s pulse
volume?
57

Step 3: Investigations

Dengue investigation basics

• Complete blood count (CBC) with haematocrit (HCT) are usually all
that are necessary for monitoring

• Of special importance are:

• HCT;
• white blood cell count (WBC) and;
• platelet count

• An HCT in the first 3 days of illness suffices for the baseline HCT; in
acute cases, age-specific population HCT levels can substitute for a
patient’s baseline

•A steep drop in platelet count with a rising HCT compared to

baseline suggests progression to the plasma leakage/critical phase of
dengue

•A falling WBC followed by falling platelet count by Day 3 or 4 of

illness is almost surely dengue

58

Step 3: Investigations

Who should get a complete blood count (CBC)?

• All patients with fever ≥3 days

• All patients with warning signs (urgently)
• All patients with shock (CBC and glucose check urgently)

o If resources are available, all febrile patients should get baseline CBC
at
first visit. A normal CBC in the febrile phase does not exclude dengue. o
If resources are limited, CBC for febrile patients with poor oral intake
and/or poor urine output.
When should a patient be referred for immediate medical treatment?

• Rising HCT or high HCT

• Leucopenia and/or thrombocytopenia
• Presence of warning signs, shock
• Poor oral intake/not passing urine

59

Step 3: Investigations

Dengue-specific diagnostic tests *

• For confirmation, e.g. NS1/IgM rapid tests or nucleic acid detection

(depending on resources of health facility)

• Not necessary for the acute management of patients but valuable in

unusual manifestations, suspected dengue deaths in the area, or for
patients who progress rapidly from mild to severe dengue or death

Other tests? *

• Blood chemistry tests (liver function, glucose, serum electrolytes,

urea, creatinine
• Should be considered in patients with risk factors and severe
disease
60

Step 4: Diagnosis, phase of disease and severity

1. Does the patient have dengue or other

illnesses?

2. Which phase of dengue

(febrile/critical/recovery)?

3. What is the hydration state?

4. Are dengue warning signs present?

5. What is the haemodynamic state?

6. What is the best medical plan for the patient?

61
Step 1: History taking

Step 2: Clinical examination: 5-in-1 magic touch

Step 3: Investigations

Step 4: Diagnosis with dengue phase and severity

Step 5: Management decision

Management of dengue

62

Step 1: History taking

Step 2: Clinical examination: 5-in-1 magic touch

Step 3: Investigations

Step 4: Diagnosis with dengue phase and severity

Step 5: Management decision

• Send home • Require emergency

Group A
treatment and urgent referral
• Require emergency
• Refer for in- hospital
treatment and urgent referral
management
Group C
Group B Group C
Management of dengue
63
Outpatient management: Group A
Group A – Send home if
patient meets all of the
following Intake: Getting
adequate volume of oral
fluids
Output: Passing urine at
least once every 4 to 6 hours
Does not have any warning
signs
Has stable haematocrit and
hemodynamic status
Patients who are able to “drink enough to pee enough”
Does not have co-existing
conditions
1. Give anticipatory guidance
before sending home
(see patient handout)
1. Follow up daily
2. Do serial CBCs
3. Identify warning signs
early
64

Keys to good home care

1. Bed rest

2. Encourage oral intake

What is adequate oral intake?

6 to 8 glasses of fluid for adults and accordingly in children

What types of fluid? Milk, coconut water, fruit juice (caution with diabetes
patient), oral rehydration solution, barley water, rice water, clear soup
Water alone may cause electrolyte imbalance.

3. Manage fever

Give paracetamol if fever is higher than 38°C Adult - not more than 4 g per day Child
- 10 mg/kg/dose, not more than 4 times a day Tepid (lukewarm water) sponging Do
not give ibuprofen or aspirin (or other non-steroidal anti-inflammatory drugs)

65

Keys to good home care (cont.)

4. Reduce breeding habitats around the home and kill adult

mosquitoes

5. Return to hospital IMMEDIATELY if no improvement or warning

signs
appear

Frequent vomiting, unable to drink or scanty urine

Severe abdominal pain

Severe tiredness, drowsiness, mental confusion or seizures

Bleeding:

Red spots or patches on the skin

Bleeding from nose or gums

Vomiting blood

Black coloured stools

Heavy menstruation or vaginal bleeding

Pale, cold or clammy hands and feet

Breathing difficulty

66

Outpatient Management: Group B

Group B (any of following)

Has warning signs Has co- without a reliable means of

existing condition: Diabetes transport
mellitus Renal failure 1. Admit for inpatient care
Pregnancy Infant Elderly
Has social circumstances: 2. Monitor hemodynamic
Living alone Living far away status
frequently 5. Correct metabolic
acidosis,
3. Use HCT to guide electrolytes as needed
interventions

4. Use isotonic IV fluids

judiciously 67

Haematocrit should not be interpreted on its own

Haematocrit should always be interpreted in the context of

and “in phase” with:

1. Haemodynamic evaluation at time of sampling

2. Before or after IV fluid therapy?

3. Before or after transfusion with whole blood or packed cells?

4. Phase of disease, where in the clinical course is the patient: day 2

vs day 5

IMPORTANT REMINDER:

Haemodynamic state should be the principal driver of IV fluid

therapy

Haematocrit level should only be a guide

NOT the other way around!

68
Interpretation of rising or persistently high haematocrit
A rising or persistently high haematocrit
Active
Unstable vital signs plasma
leakage
A rising or persistently high haematocrit
Need for further fluid replacement
Stable haemodynamic status
Does not require extra intravenous fluid
Continue to monitor closely. HCT should start to fall within next 24 hours
as plasma leakage stops.
69

Emergency management: Group C

Group C (any of following)

Severe plasma leakage treatment and urgent

with shock and/or fluid referral
accumulation with
respiratory distress

Severe bleeding

Severe organ impairment:

AST or ALT ≥1000 and/or

impaired consciousness
Requires emergency
70
When to start and stop intravenous fluid therapy

Febrile phase

Limit IV fluids (refer to later slides for oral fluid advice) Early IV
therapy may lead to fluid overload especially with non-isotonic IV
fluid

Critical phase

IV fluids are usually required for 24–48 hours NOTE: For patients
who present with shock, IV therapy should be <48 hours

Recovery phase

IV fluids should be stopped so that extravasated fluids can be

reabsorbed

71

Intravenous fluid therapy in DHF

during critical period

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.

72
What type of intravenous fluid therapy should we use?
Use isotonic solutions (normal saline, Ringer’s lactate)
Colloids are preferred if the blood pressure has to be restored
urgently (e.g. Group C patients)1,2,3
Na K Cl Lactate Ca Osm Solution
mEq/L Normal saline (NS) 154 154 292 D5% NS 154 154 565
Ringer’s lactate 130 4 109 28 3 274 Hartmann’s solution 131 5 111 29
2 278
73

Calculations for normal maintenance of intravenous

 fluid infusion

Normal IV fluid maintenance per hour by Holliday-Segar

formula:

4 mL/kg/h for first 10 kg body weight

+ 2 mL/kg/h for next 10 kg body weight

+ 1 mL/kg/h for subsequent kg body weight

For overweight/obese patients, calculations for normal

maintenance of IV fluid should be based on ideal body weight
(IBW)

74
Skema 1. Tatalaksana Tersangka DBD derajat I & II
(tanpa syok)
75
Skema 2. Tatalaksana DBD Derajat I dan II

76
Box 15: Volume replacement flow chart for patients with DSS s
Skema 3. Tatalaksana DBD Derajat III
77

Management of
 prolonged/profound shock:
DHF Grade 4

• The scheme is similar with Skema 3

(Tatalaksana DBD derajat III) but the initial fluid
resuscitation in Grade 4 DHF is more vigorous
– 10-20 ml/kg of bolus fluid should be given as
fast as possible, ideally
within 10 to 15 minutes. When the blood pressure is
restored, further intravenous fluid may be given as in
Grade 3. – If shock is not reversible after the first
10 ml/ kg, a repeat bolus of 10
ml/kg and laboratory results should be pursued
and corrected as soon as possible.
• Laboratory investigations should be done as
soon as possible for ABCS as well as organ
involvement.
• Urgent blood transfusion should be
considered as the next step (after reviewing the
pre- resuscitation HCT) and followed up by
closer monitoring
78

• Profound shock
• Complication
• Adequate volume replacement →
no improvement → ABCS
A –B –C -S
A-Acidosis Blood gas LFT, BUN, Cr
S-Blood C-Calcium Electrolyte, Ca++
sugar BS (dextrostick)
Tatalaksana Fase Kritis
B-Bleeding Haematocrit
Hematocrit Summary of Monitoring IV fluid therapy And in

Dengue dengue
Inadequate Adequate Excessive
Hypovolaemia
Compensated shock
Improved circulation and tissue perfusion
• Capillaryrefill <2 seconds
• Normal heart rate
• Normal blood pressure
• Normal pulse pressure
• Urine0.5ml/kg/hr
• l HCT to normal
• Improving acid-base
Fluid overload:
• Pulmonary oedema
• Respiratory distress
•Worsening pleural effusion Hypotensive
and ascites shock
• Clinical deterioration
• Bleeding
• DIC
• Multi-organ failure
80