Dengue Clinical Practice Guidelines ppt.pdf

Dengue Clinical Practice Guidelines

1. linical Practice
Guidelines:
Dengue

Bo & UNICEF - UNDP + World Bank - WHO
CQ) World Health TP) PD) Sees
YY ay Organization wy poverty

2. O1
02
03
Table of contents
Diagnostics
Approach
Treatment
according to
Groups A-C
04
05
Complications
and ICU
Treatment in
specific risk
groups
Pitfalls

3. 01 = |
Dengue v yy
Diagnostics —i
for Clinician
—~ — > a
ely - l I

4. Dengue Diagnostics for Clinician
a
OBJECTIVES
e Toconfirm the clinical diagnosis
e To provide information for epidemiological surveillance
Dengue diagnosis
e Virological and serological markers in relation to the time of dengue
% infection
e Type of diagnostic method in relation to clinical illness
e Characteristic of clinical sample

5. Virological and Serological Markers
PRIMARY INFECTION
e IgM antibodies
o detected 3-6 days after fever
o Rises by day 6-10
e lgG antibodies
o Slowly increasing but low
o Elevates at days 9-10
SECONDARY INFECTION
e IgM antibodies
o Slower and lower levels
e l|gG antibodies
o Rapid and higher increase

vA



Viremia

a
Primary Infection Second Infection
IgG = immunoglobulin G; IgM = immunoglobulin M
Figure 1. Virological and serological markers of dengue infection according to time of
illness
Source: Dengue WHO Handbook, 2012, p. 16

6. Type of Dengue Diagnostic Method in relation to Time of Clinical Illness
FEBRILE PHASE
e = Inoculation
e RI-PCR
e NSA1Ag
CRITICAL AND CONVALESCENT
e MAC-ELISA
e IgM Rapid Test
s IgM/IgG optical density ratio

Clinical sample
Diagnostic
method
Methodology Time to results

Acute serum
Viral isolation
Mosquito or mosquito cell
culture inoculation
One week or more







5 Nucleic acid RT-PCR and real time RT- ore
Virus (1-5 days of detection PCR oie Saye
detection fever)
and its 4 NS1 Ag rapid tests Minutes
components an
necropsy tissues |} Antigen detection NS1 Ag ELISA 1 day
Immuno-histochemistry 2-5 days
Paired sera 1-2 days
(acute serum HIA
from1—5 days IgM or IgG
and second seroconversion
serum 15-21 Neutralization Test Minimum 7 days
Serological days after)
response

Serum after day
5 of fever


IgM detection ELISA 1 or 2 days
(recent infection) Rapid tests Minutes
IgG ELISA 1 or 2 days
IgG detection
HIA
Figure 2. Dengue Diagnostics and Sample Characteristics
Source: Dengue WHO Handbook, 2012, p. 15

7. Days of illness 1} 2 3 4 5 6 7 8 ¥ 10

Temperature
Dehydration Reabsorption
Potential clinical issues fluid overload
Organ impairment
Laboratory changes

IgM/IgG
Serology and virology Viraemia = eS
Course of dengue illness: Febrile ” Critical Recovery phases

8. Laboratory Confirmation of a Dengue Case
DIAGNOSTIC CONFIRMATION
yom DENGUE INFECTION
Detection of virus
Detection of viral genome
Detection of NS1Ag
Seroconversion of IgM or IgG
Positive IgM serology
HIA Antibody titre

9. Laboratory Confirmation of a Dengue Case
N «a

Method

Interpretation Sample characteristics

Confirmed
dengue
infection
Probable
Viral isolation


Virus isolated


Genome
detection


Positive RT-PCR or positive real-time
RT-PCR

Antigen detection

Positive NS1 Ag

Serum (collected at 1-5 days of
fever)
Necropsy tissues


Positive immunohistochemical Necropsy tissues


IgM From negative IgM to positive IgM in
seroconversion paired sera
IgG From negative IgG to positive IgG in
seroconversion





paired sera or 4-fold increase IgG
Acute serum (days 1-5) and
convalescent serum (15-21 days
after first serum)



Positive IgM Positive IgM
High IgG levels High IgG eo ee or HI


Figure 3. Confirmed and probable dengue diagnosis, interpretatiosn and sample
Single serum collected after
day 5

characteristics
Source: Dengue WHO Handbook, 2012, p. 19

10. Laboratory Confirmation of a Dengue Case










~












Primary health- District health Reference
NP centres centres centres
Virus isolation Yes
Genome detection Yes
NS1 Ag detection Rapid tests Yes Yes Yes
ELISA Yes Yes
IgM detection Rapid tests Yes Yes Yes
ELISA Yes Yes
IgG detection ELISA Yes
Xe IHA Yes
Neutralization assay Yes
Figure 4. Recommended diagnostic tool according to lab service level
Source: Dengue WHO Handbook, 2012, p. 19

11. O02

StepI StepII StepIII A Stepwise
| | [- Approach to the
Overall Diagnosis, Management
assessment 5Sessment of management of
disease phase
and severity
dengue
%

12. Stepwise approach to matlagemont

Step | - Overall assessment



1.1 History, including symptoms, past medical and family history
1.2 Physical examination, including full physical and mental assessment
13 Investigation, including routine laboratory tests and dengue-specific laboratory tests


Step Il - Diagnosis, assessment of disease phase and severity

Step Ill - Management

l.4 Disease notification

2 Management decisions. Depending on the clinical manifestations and other circumstances, patients
may (1):
- be sent home (Group A)
- be referred for in-hospital management (Group B)
- require emergency treatment and urgent referral (Group C)

13. Step 1: Overall Assessment \%
HISTORY
e Date of onset of fever/illness
® Quantity of oral fluid intake
e Diarrhea
e Urine output
@ Change in mental
State/seizure/dizziness
e History of travel to
dengue-endemic areas, coexisting
conditions
PHYSICAL EXAMINATION
Mental
Hydration status
Haemodynamic status
Checking for quiet tachypnea/acidotic
breathing
Checking for abdominal
tenderness/hepatomegaly/ascites
Examination for rash and bleeding
manifestation

14. Step 1: Overall Assessment \%

Clinical Abdominal pain or tenderness
Persistent vomiting
Lethargy, restlessness
Mucosal bleed
Liver enlargement > 2cm or tender enlarged liver
Clinical fluid accumulation

Laboratory Increase in haematocrit level concurrent with rapid decrease in platelet count

Figure 5. Warning signs
Source: Dengue WHO Handbook, 2012, p. 104

15. Step 1: Overall Assessment \%

Parameters Stable circulation Compensated shock Hypotensive shock

Conscious level Clear and lucid Clear and lucid (shock can be
missed if you do not touch
the patient)
Change of mental state
(restless, combative)

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


Extremities Warm and pink Cool peripheries Cold, clammy extremities
extremities
Peripheral pulse Good volume Weak and thready Feeble or absent
volume


Heart rate Normal for age Tachycardia Severe tachycardia with
bradycardia in late shock
BP Normal for age Normal systolic pressure but Hypotension (see definition
Normal pulse pressure
for age
rising diastolic pressure
Narrowing pulse pressure
(¢ 20 mmHg in children)
Postural hypotension
below)
Unrecordable BP

Respiratory rate
(RR)
Normal for age Quiet tachypnoea Metabolic acidosis/hyperpnoea/
Kussmaul’s breathing

Urine output Normal Reducing trend

Figure 6. Hemodynamic Assessment
Oliguria/anuria
Source: Dengue WHO Handbook, 2012, p. 104

16. Step 1: Overall Assessment \%
INVESTIGATION
@ Full blood count on first visit
o Repeated daily until critical phase is over
o Decreasing WBC and platelet — dengue very likely
o Decrease in platelet + rising hematocrit — plasma leakage /
critical phase
e Additional tests
oO Liver function
o Serum electrolytes
oO Creatinine

17. Step 2: Diagnosis, assessment ofghase and severity

Warning signs Any of the warning signs (see Textbox C)

Signs and symptoms related to
hypotension (possible plasma
Dehydrated patient, unable to tolerate oral fluids
Dizziness or postural hypotension

leakage)
Profuse perspiration, fainting, prostration during defervescence
Hypotension or cold extremities
Difficulty in breathing/shortness of breath (deep sighing breaths)
Bleeding Spontaneous bleeding, independent of the platelet count

Organ impairment Renal, hepatic, neurological or cardiac
- enlarged, tender liver, although not yet in shock
— chest pain or respiratory distress, cyanosis

Findings through further
investigations
Rising haematocrit
Pleural effusion, ascites or asymptomatic gall-bladder thickening

Co-existing conditions Pregnancy
Co-morbid conditions, such as diabetes mellitus, hypertension, peptic ulcer,
haemolytic anemias and others
Overweight or obese (rapid venous access difficult in emergency)
Infancy or old age

Social circumstances
Living alone
Living far from health facility
Without reliable means of transport

Figure 7. Admission Criteria
Source: Dengue WHO Handbook, 2012, p. 105

18. Step 2: Diagnosis, assessment ofghase and severity
with warning
signs
1. Severe plasma leakage
2. Severe haemorrhage
3.Severe organ impairment

CRITERIA FOR DENGUE + WARNING SIGNS
Probable dengue
live in /travel to dengue endemic area.
Fever and 2 of the following criteria:
© Nausea, vomiting
© Rash
© Aches and pains
© Tourniquet test positive
© Leukopenia
e Any warning sign
Laboratory-confirmed dengue
(important when no sign of plasma leakage)
Warning signs*
¢ Abdominal pain or tenderness
© Persistent vomiting
® Clinical fluid accumulation
© Mucosal bleed
Lethargy, restlessness
@ Liver enlargment >2 cm
© Laboratory: increase in HCT
concurrent with rapid decrease
in platelet count
*(requiring strict observation and medical
intervention)
CRITERIA FOR SEVERE DENGUE
Severe plasma leakage
leading to:
© Shock (DSS}
© Fluid accumulation with respiratory
distress
Severe bleeding
as evaluated by clinician
Severe organ involvement
@ Liver: AST or ALT >=1000
e CNS: Impaired consciousness
© Heart and other organs

19. Step 3: Disease notification and idanagement decision
DISEASE NOTIFICATION
e Cases of suspected, probable, and confirmed dengue
should be notified
e@ Lab confirmation is not necessary but should be obtained
MANAGEMENT DECISIONS
e Group A — sent home
@ Group B — referred for in-hospital management
@ Group C > emergency treatment and urgent referral

20. a
sy
=
* 03
Treatment
According to
Groups A-C ,

21. Presumptive Diagnosis: ‘pat
Live in / travel to endemic area plus See
= Fever and two of the following:
c + Anorexia and nausea
oO + Rash
£ + Aches and pains v
+ Warning signs
2 “ Leucopenia Warning signs: em
o + Tourniquet test positive + Abdominal pain or tenderness
+ Persistent vomiting
4 + Clinical fluid accumulation Coa on
<x + Mucosal bleed ges an ere
Lab.confirmed dengue + Lethargy, restlessness aeasennaeiaiiceniemaaiaemaiiae
opt Wien am a eee renee
of plasma leakage) decrease of platelet count
f 1
<
° Co-existing conditions [postive |
= Social circumstances
oO
2
3
n
&
o Dengue without Dengue with s D
: = x . evere Vengue
warning signs warning signs g

22. GROUP CRITERIA
Group A
May be sent home
No warning sign
AND
Able to tolerate adequate
volumes of oral fluid
Able to pass urine at least
once every 6 hours
a
Group B
Referred for in-hospital care
Group C
Require emergency ufement
(immediately referred and admitted
within 24 hours
Any of the ff: Any of the ff:
- Co-existing condition (pregnancy, infancy, - Sever plasma leakage with
old age, DM) shock and/or fluid accumulation
- Social circumstances (living alone, far
from health facility) -
OR :
Existing warning signs (hepatic damage, renal
- Abdominal pain or tenderness impairment, cardiomyopathy,
- Persistent vomiting etc)
- Clinical fluid accumulation
- Mucosal bleeding
- lethargy/restlessness
- Liver enlargement >2 cm
- Lab = increased Hct
with respiratory distress
Severe bleeding
severe organ impairment

23. TREATMENT AND MONITORING: GROUP A

Treatment Monitoring

Advise for

e Adequate bed rest
e Adequate fluid intake
e Paracetamol

Daily review
o Temperature pattern
o Volume of fluid intake and losses
o Urine output
o Signs of plasma leakage
o Complete blood count
Advise immediate return to hospital if with warning
signs
Written advice of management

24. TREATMENT AND MONITORING: GROUP A

Home-care card for dengue
The patient should take this card with them to the health facility for each visit


What should be done?
Adequate bed rest
Adequate fluid intake (> 5 glasses for an average-sized adult, or accordingly in children)
e.g. milk, fruit juice (caution with diabetes patient), oral rehydration solution (ORS) or barley/rice
water/coconut water
Note: Plain water alone may cause electrolyte imbalance
Take paracetamol (not more than 3 grams per day for adults; 10 mg/ka/dose, not more than 3 to 4 times in
24 hours in children)
Tepid sponging
Look for mosquito breeding places in and around the home and eliminate them
What should be avoided?
* Do not take acetylsalicylic acid (aspirin), mefenemic acid (ponstan), ibuprofen or other NSAIDs or
steroids. If you are already taking these medications please consult your doctor
+ Antibiotics are not necessary
Laboratory results monitoring
If any of following is observed, the patient should be immediately taken to the nearest hospital; these are
warning signs for danger:
* Bleeding:
- fed spots or patches on the skin
- bleeding from nose or gums
— vomiting blood
- black-coloured stools
— heavy menstruation/vaginal bleeding
+ Frequent vomiting or not able to drink
* Severe abdominal pain
+ Drowsiness, mental confusion or seizures
+ Pale, cold or clammy hands and feet
* Difficulty in breathing
+ Postural dizziness
+ Nourine output for 4-6 hours

1st visit


Haematocrit

White cell count

Platelet count
Figure XX. Home-care Card Dengue

Source: Dengue WHO Handbook, 2012, p. 106

25. TREATMENT AND MONITORING: GROUP A
Oral Fluid Intake *
@ Oral fluid intake to replace fluid loss from fever or
vomiting
e Choice of fluids based from culture (coconut water, rice
water, barley water, ORS)
e Avoid commercial carbonated drinks that exceed isotonic
level (sugar 5%)
a

26. TREATMENT AND MONITORING: GROUP A
%
Fever
@ Give paracetamol
o 10mg/kg/dose
O 3-4 times in 24 hours for children
o Not more than 3g/day in adults
e Sponge with tepid water
e DO NOT give aspirin, NSAIDS, or IM injections
a

27. TREATMENT AND MONITORING: GROUP B
%



Ringer Lactate)

Treatment Monitoring
e Encouragement for oral fluids Temperature
e If not tolerated, start IV fluid therapy (0.9% saline or Volume of fluid intake and
losses
Urine output
Warning signs
Hct, WBC, and platelet

28. TREATMENT AND MONITORING: GROUP B


Treatment Monitoring %
Obtain reference Hct first e VS and peripheral
Give isotonic solution ( 0.9% saline, Ringer’s lactate) perfusion (q 1-4h)
o 5-7 ml/kg/hr (1-2 hours) e Urine output (q 4-6h)
Oo 3-5 ml/kg/hr (2-4 hours) e Hct (before and after fluid
Oo 2-3 ml/kg/hr replacement then q 6h)
e Reassess clinical status e Blood glucose
o Hematocrit remains the same/rises minimally > e Other organ function
2-3ml/kg/hr for another 2-4 hours
o Rising Hct + worsening VS — 5-10mI/kg/hr for 1-2 hours
e Reassess clinical status, repeat Hct, and review infusion rate
e Reduce IVF gradually when plasma leakage decreases
a

29. TREATMENT AND MONITORING: GROUP B
%
Normal maintenance fluid per hour
@ 4Aml/kg/hr for 1st 10 kg body weight
@ +2 ml/kg/hr for next 10 kg body weight
e +1ml/kg/hr for subsequent kg body weight

30. TREATMENT AND MONITORING: GROUP B














5.9 Textbox I: Hourly maintenance fluid regime based on ideal body weight
Estimated ideal body weight (IBW) Normal maintenance fluid based on Holliday-Segar formula
(kg)
ml/hour ml/kg/hour
5 20 4
10 40 4
15 50 3.3
20 60 3
25 65 2.6
30 70 2.3
35 75 2.1
40 80 2
50 90 1.8
60 100 4:7
70 110 1.6
80 120 15

31. TREATMENT AND MONITORING: GROUP C
SEVERE DENGUE %
e Fluid resuscitation
Oo Improving central and peripheral circulation
o Improving end-organ perfusion
o Crystalloid solution without glucose
e Blood transfusion
o Given only in cases with established severe bleeding
o Blood typing and cross matching
a

32. TREATMENT AND MONITORING: GROUP C
Management of
Compensated Shock
in Adults
Compensated Shock:
° Clear and lucid
Prolonged CRT
Cool peripheries
Weak and thready
Tachycardia
Normal SBP bu rising DBP
Quiet tachypnea
Reducing UO
a

Yes
IV crystalloid, reduce
-7 for 1-2 hours
‘for 2-4 hours
r 2-4 hours
o

As clinical improvement
is noted, reduced fluids
accordingly



_ Further boluses may be
needed for the next
Stop IV fluids at 48
hours
*Reassess the patient's clinical condition, vital signs, pulse volume, capillary refill time and temperature of extremities.
**Colloid is preferable if the patient has already received previous boluses of crystalloid
-IV: intravenous, HCT: haematocrit, }: increased, |: decreased.

oF)
Start isotonic crystalloid
5-10 mi/ka/hr for 1 hour
No




Crystalloid (2* bolus) or
colloid**
10-20 mifkg/hr for 1 hour
Reduce IV crystalloids
7-10 mi/kg/hr for 1-2
hours

33. TREATMENT AND MONITORING: GROUP C
Management of
Compensated Shock
in Infants and
Children
Compensated Shock:
Clear and lucid
Prolonged CRT
Cool peripheries
Weak and thready
Tachycardia
Normal SBP bu rising DBP
Quiet tachypnea
Reducing UO
a







y

IV crystalloid, reduce gradually
10 miko/hr for 1-2 hours
7 mi/kg/hr for 2 hours
5 mi/ko/hr for 4 hours


Crystalloid (2° bolus) or

3 mi/kg/hr
¥
As clinical improvement is
noted, reduced fluids
accordingly
colloid
10-20 mi/kg/hr for 1 hour




Further boluses may be
ne for the next 24-48
Yes
Reduce IV crystalloids
7-10 mi/kg/hr for 1—2 hours
“Colloid is preferable if the patient has already received previous boluses of crystalloid
*Reassess the patient's clinical condition, vital signs, pulse volume, capillary refill time and temperature of
extremities.IV = intravenous; HCT = haematocrit; t = increased; | = decreased


¥v
Stop IV fluids at 48 hours

34. TREATMENT AND MONITORING: GROUP C
Management of eee an jotensiv eae ee
Profound Shock in —
Infants, Children, and
Adults
Profound Shock:
e restless/combative
Very prolonaed CRT
Mottled ski
Cold, clamr, 10MI/kg/hr for 1 hour
Feeble ora 7.5ml/kg/hr for 2 hours
Severe tact
late shock 5ml/kg/hr for 4 hours
hypotensio 3ml/kg/hr
Metabolic écssss:
e — oliguria/anuria


naan OE:







IV crystalloid/colloid*
(2 bolus)
10 mi/kg/hr for 30-60 min


As clinical improvement is
noted, reduced fluids
accordingly

PP










z Reduce IV crystalloids
Stop IV fluids at 48
eee reins ani
ay, “Colloid is preferable if the patient has already received previous boluses of crystalloid
*Reassess the patient's clinical condition, vital signs, pulse volume, capillary refill time and temperature of extremities.
IV = intravenous; HCT = haematocrit; { = increased; | = decreased

35. TREATMENT AND MONITORING: GROUP C
Management of
Profound Shock in
Infants, Children, and
Adults
Profound Shock:
restless/combative
Very prolonged CRT
Mottled skin
Cold, clammy extremities
Feeble or absent peripheral pulse
Severe tachycardia with bradycardia in
late shock
hypotension/unrecordable BP
Metabolic acidosis/hyperpnoea
oliguria/anuria
a



Yes




Start isotonic crystalloid or
colloid*



py a or colloid




As clinical improvement is
noted, reduced fluids
accordingly


‘


Stop IV fluids at 48
hours



IV crystalloid/colloid*
(2 bolus)
10 mi/kg/hr for 30-60 min



Reduce IV crystalloids
7-10 mikg/hr for 1-2 hours
“Colloid is preferable if the patient has already received previous boluses of crystalloid
*Reassess the patient's clinical condition, vital signs, pulse volume, capillary refill time and temperature of extremities.
IV = intravenous; HCT = haematocrit; { = increased; | = decreased

36. TREATMENT AND MONITORING: GROUP C






Management of ————
Profound Shock in ——
.
Start isotonic gaa or
Infants, Children, and costs
Adults
Profound Shock:






e restless/combative py separ ox colloid
Very prolonged CRT
Mottled skin
Cold, clammy extremities
Feeble or absent peripheral pulse
Severe tachycardia with bradycardia in
late shock
hypotension/unrecordable BP
Metabolic acidosis/hyperpnoea
e — oliguria/anuria




- lloid, reduce
ay IV crystalloid/colloid”
(2 bolus)
10 mi/kg/hr for 30-60 min


As clinical improvement is
noted, reduced fluids


accordingly
¥ z Reduce IV crystalloids
aay pores 7-10 mi/kg/hr for 1-2 hours


ay, “Colloid is preferable if the patient has already received previous boluses of crystalloid
*Reassess the patient's clinical condition, vital signs, pulse volume, capillary refill time and temperature of extremities.
IV = intravenous; HCT = haematocrit; { = increased; | = decreased

37. When to stop intravenous fluid therapy?
g Signs of cessation of plasma leakage
g Stable BP, pulse, and peripheral perfusion
g Decreased Hct with good pulse volume
g Apyrexia for 24-48 hours
g Resolving bowel/abdominal symptoms
g Improving urine output

38. Hemorrhagic complications
At-risk patients
profound/prolonged/refractory shock
Hypotensive shock and multi-organ failure or persistent metabolic
acidosis
Are given non-steroidal anti-inflammatory agents
Have preexisting peptic ulcer disease
Are on anticoagulant therapy
PP er BS Have any form of trauma (inlucing IM injection)

39. Hemorrhagic complications
Situations
ay
ey
Gq
GG
Persistent and/or severe overt bleeding in the presence of unstable
haemodynamic status, regardless of the haematocrit level
A decrease in haematocrit after boluses of fluid resuscitation together with
unstable haemodynamic status;
Refractory shock that fails to respond to consecutive fluid resuscitation of 40-60
ml/kg;
Hypotensive shock with inappropriately low/normal haematocrit;
Persistent or worsening metabolic acidosis in patients with a well-maintained
systolic BP, especially in those with severe abdominal tenderness and distension

40. Hemorrhagic complications
MANAGEMENT
e Identify source of bleed and attempt to stop it
@ Give aliquots of 5-10 ml/kg of fresh pRBC or 10-20 ml/kg of fresh whole
blood
@ Precaution when inserting NGT or bladder catheter

41. Glucose Control
Cause
Effect
Management
HYPERGLYCEMIA
Due to neuroendocrine stress response or
administration of glucose-fluid during
resuscitation
Osmotic diuresis
Use of appropriate isotonic non-glucose
fluid during resuscitation
Use of glucose-isotonic fluid during
maintenance
HYPOGLYCEMIA
Due to starvation in young
children, DM patients on
hypoglycemic agents, and severe
liver involvement
Seizures, mental confusion,
tachycardia
Treated emergency with
0.1-0.5g/kg of glucose

42. Electrolyte and Acid-Base Imbalances
Cause Management
HYPONATREMIA Can be related to Gl losses or use of Use of isotonic solution
hypotonic solution
HYPERKALEMIA Associated with metabolic acidosis or | Appropriate volume resuscitation
acute renal injury Resonium A and calcium
gluconate and insulin-dextrose
HYPOKALEMIA Gl losses and stress-induced Potassium supplement in
hypercortisol state parenteral fluid

43. Metabolic Acidosis
Compensated Metabolic Acidosis
e Early sign of hypovolemia and shock
e Common cause: tissue hypoxia and hypoperfusion
@ Maybe managed through correction of shock and adequate fluid
replacement
o If remains uncorrected — assess for severe bleeding and check Hct — transfuse pRBC or
fresh whole blood
e Bicarbonate therapy
o NOT recommended for pH > 7-10
o Associated with sodium and fluid overload, increase in lactate, decreased serum ionized
calcium

44. * 04 °
Complications& /. Ia. \
Intensive Care 7 A\
Management, "0

45. Causes of complications in dengue include:
Missed diagnosis at the frontline a
Inadequate monitoring and misinterpretation of vital
signs
Inadequate monitoring of fluid intake and urine output
Late recognition of shock leading to profound and/or
prolonged shock
Late recognition of severe bleeding
Too much or too little intravenous fluids i.e. not
following/understanding the treatment guidelines
Careless attitude towards aseptic techniques

46. Outcome: These lead to a life-threatening situation
a
e Prolonged and/or profound shock;
e Severe bleeding with severe disseminated
intravascular coagulopathy;
e@ Fluid overload;
e Respiratory distress and failure;
e Multi-organ dysfunction of liver, kidneys and
%& neurological system;
e Irreversible shock and death.

47. Clinical evaluation of these patients
should include: x
@ General inspection of the mental state
e Airway and breathing
e Circulation
e Monitoring

48. General inspection of the mental state
e Shock patients remain quiet but alert A
e Irritable combative dengue patient indicates
severe shock
e Other causes:
Oo Fulminant hepatic failure
o Hypoglycemia
Oo Electrolyte abnormalities
o Intracranial bleeding and encephalitis
AS

49. Airway and breathing:
Early compensated shock has quiet tachypava
Shock progresses, the breathing becomes
deeper and faster.
Patients with Kussmaul’s breathing: lie
horizontal because of hypovolaemia
Patients with true respiratory distress from
pulmonary causes will most probably be
sitting up

50. Airway and breathing:
Combination of metabolic acidosis and fluid a
overload may be seen in patients who have received
inappropriate fluid therapy.
Patients cannot get comfortable lying down or
sitting up and are very restless.
Diminished air entry in a drowsy patient indicates
impending respiratory failure.
Cyanosis and gasping respiration is seen in an
imminent respiratory arrest.

51. Circulation
e The peripheral perfusion should be assessed Bh
examination and palpation of the extremities and
the radial pulse - pulse volume, capillary refill time,
temperature, colour of extremities and pulse
pressure
e Examine for bleeding (orogastric tube insertion, if
%& indicated), jaundice, evidence of plasma leakage and
abdominal tenderness and distension.

52. Monitoring:
e Continuous heart rate (ECG), respiration and oul
oximetry should be monitored.
e Intermittent BP (measured every 5-30 minutes),
peripheral perfusion and four-hourly temperature
checks should be maintained for these critically ill
patients.

53. Evaluate the history and prior treatment:
@ What was the date of onset of fever? A
@ Which phase of dengue illness is the patient in? Is the
patient in the critical phase?
e@ Is there evidence of plasma leakage? How many more
hours of plasma leakage do you envisage?
e Review the fluid intake, output and balance since the
Me Start of parenteral fluid therapy.

54. Evaluate the history and prior treatment:
e@ What types of fluids have been administered a
e When was the last urine output? What is the amount of
urine?
e How much is the positive fluid balance?
e Review the haemodynamic response to the volume and
type of intravenous fluid therapy, and the corresponding
trends of hematocrit.

55. Additional investigations:
e Full blood count, haematocrit, blood glucose, blood gas aiAysis
and lactate - tachypnoea and shock.
e Serum electrolytes and calcium, liver function tests, blood urea and
creatinine is indicated in all cases of severe dengue shock.
e Coagulation profile - prothrombin time (PT), partial thromboplastin
time (PTT), (INR), fibrinogen degradation products and fibrinogen
level is indicated in severe bleeding.
% Chest radiography
® Determine blood group and match
e Blood culture and sensitivity (if indicated)
e Dengue diagnostic tests

56. KEY QUESTIONS:
e ls the patient alert and cooperative or restless, combative a
drowsy?
e ls the patient in respiratory distress or failure?
e Does the patient have stable hemodynamics?
e Has the fluid therapy been adequate to maintain the circulation and
tissue organ perfusion?
e ls the patient in the beginning or nearing the end of the critical
Mh phase or in the recovery phase?

57. KEY QUESTIONS:
e Does the patient have intravascular and extravascular fluid
overload?
e Is the shock prolonged? Has it been missed?
e Is there multi-organ dysfunction?
e Is there hyperglycemia? If there is, is it related to stress,
inappropriate fluids or undiagnosed or uncontrolled diabetes
mellitus?
% Is there electrolyte disturbances?
@ Does the patient have severe overt bleeding?.
e Does the patient have severe internal/occult bleeding?

58. Prolonged/profound shock:
Prolonged/profound shock is characterized by severe metabolic
acidosis + multi-organ failure: x

59. Acute respiratory distress and failure
Severe metabolic acidosis from severe shock a
Fluid overload - large pleural effusions and ascites
Acute pulmonary oedema
@
@
@
e Acute respiratory distress syndrome (ARDS)
AS

60. Fluid overload:
Excessive and/or too rapid intravenous fluids dur the
critical phase;
Incorrect use of hypotonic crystalloid solutions e.g. 0.45%
sodium chloride solutions;
Inappropriate use of large volumes of intravenous fluids
in patients with unrecognized severe bleeding;

61. Fluid overload:
Inappropriate transfusion of fresh-frozen plasma, Bhatelet
concentrates and cryoprecipitates;
Prolonged intravenous fluid therapy, i.e., continuation of
intravenous fluids after plasma leakage has resolved (> 48
hours from the start of plasma leakage);
Co-morbid conditions such as congenital or ischaemic
heart disease, heart failure, chronic lung and renal
diseases.

62. Early clinical features of fluid
overload are: E
Sapid breathing;
Suprasternal in-drawing and intercostal recession (in children);
Respiratory distress, difficulty in breathing;
Wheezing, crepitations;
Large pleural effusions;
Tense ascites, persistent abdominal discomfort/pain/tenderness
(this should not be
e@ interpreted as warning signs of shock);
e@ Increased jugular venous pressure (JVP).

63. Late clinical features are:
@ Pulmonary oedema (cough with pink or frothy sputum,
wheezing and crepitations, cyanosis) - this may be
mistaken as pulmonary haemorrhage
e lrreversible shock (heart failure, often in combination with
ongoing hypovolemia).

64. Additional investigations are:
a
Blood gas and lactate analysis
Chest X-ray
ECG
Echocardiogram
Cardiac enzymes.
aS

65. Action plan:
AS
Oxygen therapy should be given immediately.
The further action plan for the treatment of fluid
overload is dependent on the patient's haemodynamic
Stability, intravascular volume status and the timing of
this event with respect to the timeline of the critical
phase.

66. Pulmonary edema and acute
respiratory distress syndrome (ARDS)
The goals of therapy are to optimize oxygenation and ventilation with
respiratory support and stabilize the haemodynamic situation.
e Positive end-expiratory pressure (PEEP) is essential to
maintain adequate oxygenation and reduce the work of
breathing. PEEP can be delivered through such as continuous
positive airway pressure (CPAP) and mechanical ventilation.
¥ Patients who are alert, cooperative and hemodynamically
stable with no, or mild, metabolic acidosis may benefit from
non-invasive ventilation

67. Pulmonary edema and acute
respiratory distress syndrome (ARDS)
e intravenous fluid therapy should be discontinued and diuretic
therapy can be commenced cautiously.
e Indications for mechanical ventilation include:
Oo patients who have shock and are restless, combative or
confused;
Me oO respiratory failure from acute pulmonary edema/ARDS +
shock;
Oo patients who fail to respond to non-invasive ventilation

68. Undertaking a tracheal intubation in a dengue shock
patient is a risky procedure for the ¥
following reasons:
e Sedation and induction agents
e Unless the tidal volume and respiratory rate (RR) are increased to
match those of the patient's own respiratory effort, muscle relaxants
will worsen the metabolic acidosis
e The compliance of the respiratory system will be diminished by the
pleural effusion and ascites, so higher pressures will be required to
Ke achieve adequate ventilation and oxygenation.
e Trauma to the airway will cause bleeding which will block the
tracheal tube.

69. Possible benefits of sedation and mechanical
ventilation are: x
@ easier monitoring of the hemodynamic status;
@ adequate respiratory support will decrease the oxygen
demand of the body.
AS

70. Urine output should not be used as an indicator of
organ perfusion under the circumstances nested
below:
e The urine volume is a reliable indicator of end-organ
perfusion as fluid repletion gets underway.
e Urine output should not be used as an indicator of
organ perfusion under the circumstances listed below
%

71. Urine output should not be used as an indicator of
organ perfusion under the circumstances nested
below:
e Blood glucose exceeds the renal threshold of 10 mmol/L;
e There is acute kidney injury, as manifested by elevated serum
creatinine levels;
e There is underlying chronic renal failure, or uncontrolled
hypertension or diabetes mellitus;
% Moderately high PEEP is used;
e |ntra-abdominal pressure is elevated;
e Administration of furosemide or hyperoncotic fluids.

72. Co-infections and nosocomial infections
Co-infections with gram-negative bacteria have been Aorted
in patients with diabetes mellitus and renal failure.
Prolonged fever, pulmonary haemorrhage, unexplained renal
failure or liver failure in the absence of shock.
Those with severe dengue and when intravenous therapy has
been prolonged.
Careful attention to aseptic techniques is necessary in
procuring and accessing intravascular devices. Prompt and
appropriate antibiotic therapy will be crucial to prevent
morbidity and mortality.

73. Hemophagocytic syndrome
e Evidence of hemophagocytosis in dengue a
e The unusual incidence of phagocytic reticulum cells which
phagocytosed all blood elements has been reported
e The clinical significance of reactive hemophagocytosis in
dengue has not been studied.

74. Supportive care and adjuvant therapy:
Vasopressor and inotropic therapy x
e Temporary measure to prevent life-threatening hypotension in
dengue shock and during induction for intubation, while
correction of intravascular volume is being vigorously carried
out.
e Recommended choice of vasopressor is dopamine
e Evidence of cardiogenic shock due to myocarditis or ischemic
%& heart disease. Dobutamine is the recommended choice.

75. Supportive care and adjuvant therapy:
Vasopressor and inotropic therapy x
e In concomitant septic shock, dopamine or norepinephrine are
the vasopressors of choice.
e The most essential and effective strategy is the correction of
intravascular volume with the appropriate types of fluids.
AS

76. Supportive care and adjuvant therapy:
Central venous pressure monitoring x
e Reliability in predicting left ventricular filling volume and
hemodynamic response to fluid challenge has been contested
e The risks of severe bleeding and pneumothorax due to
placement of the central venous line could be minimized with
the use of ultrasound guidance.
e Amore reliable method with severe dengue is
Ke echocardiography.

77. Supportive care and adjuvant therapy:
Renal replacement therapy x
e Renal replacement therapy may be indicated in acute kidney
injury after haemodynamic stability has been achieved and
maintained without further fluid resuscitation.
e Preferred choice of renal replacement therapy is continuous
veno-venous haemodialysis (CVVH).
e Peritoneal dialysis may be considered if CVVH is not available,
‘& but there is a risk of bleeding.
e The placement of a large dialysis catheter in a hypovolaemic
patient may cause unnecessary trauma and severe bleeding.

78. Supportive care and adjuvant therapy:
Other organ impairment x
e Drug toxicity
e Liver enzymes have increased disproportionate to the severity
of shock.
e Paracetamol should be discontinued in patients with liver
enlargement or raised liver enzymes.
e The most critical issue for recovery is stabilization of the
‘& hemodynamic state
e tis essential to stop or reduce intravenous fluids to the
minimum and to maintain euglycemia.

79. 05 *
Treatment of
Dengue In
Specific Risk
* Groups

80. Adults: Clinical manifestations and laboratory
findings
Petechiae, melaena, headache, retro-orbital pain, joint pain,
myalgia, nausea and vomiting; Higher baseline haematocrit
levels, haematuria and menorrhagia
o More common in Adults
e Epistaxis, oliguria and liver enlargement, haematemesis and
melaena
o More common among Children
e Most susceptible to plasma leakage and thrombocytopenia
o Infants

81. Adults: Issues in management
Recognition of plasma leakage
e Clinicians should familiarize - warning signs of severe dengue
and early signs of shock.
Recognition of shock
e Young adult patients- compensate for hypovolemic shock
e Children -mental status is clear and they may even be able to
work until the stage of profound shock.
e A pulse pressure of s 20 mmHg that defines shock in children
often indicates a far more advanced state of shock in adults.

82. Adults: Issues in management
Recognition of shock
e Self-medication: Paracetamol, NSAIDs, Antiemetics etc.
o Worsen liver and platelet functions.
e Adult- Take no more than 3 g per day of paracetamol
Dual-infection
e Concurrent bacteraemia or dual-infections
e Failure to make a timely diagnosis = increased morbidity and
mortality.

83. Elderly: Clinical manifestations, Risk and Death
Clinical manifestations
e Similar to those of younger adults
o Rash, hepatomegaly and mucocutaneous haemorrhage are
less frequent
o Gastrointestinal tract bleeding and microhematuria are
more common.
Risk of severe dengue and death
e Ahigher incidence of plasma leakage and case fatalities

84. Elderly: Issues on Management
Non-febrile elderly with dengue
e About 10% of - NO complaints of fever
Higher rate of acute renal failure
e Ageing on the kidneys - More susceptible
The impact of increased comorbidities
e Ageing-related decline in cardiopulmonary function - congestive
heart failure and acute pulmonary oedema may occur.
o Frequent assessments and adjustments of the fluid regime

85. Pregnancy: Issues on Management
e Clinical manifestations, Treatment and Outcome of Dengue in
pregnant women are similar to those of non-pregnant women

e Misdiagnosis or delayed diagnosis are not uncommon
o Overlapping clinical and/or laboratory features
e Better recognized conditions in pregnancy:
o Eclampsia or preeclampsia, haemolysis, elevated liver enzymes
and low platelet count (HELLP) syndrome, pneumonia,
pulmonary embolism, various obstetric causes of per-vaginal
bleeding and other infectious diseases.

86. Pregnancy: Impact
Adverse pregnancy outcome
e Uncertain -significant factor for adverse pregnancy outcomes
o Preterm birth, low-birth weight and caesarean deliveries
Risk of vertical transmission
e The risk is well established during the perinatal period
Significant impact of dengue at parturition
e Severe bleeding may complicate delivery and/or surgical
procedures

87. Pregnancy: Management and Challenges
Management of dengue during pregnancy:
e Early admission for close monitoring
o Close to full-term/labour.
e Conservative medical and obstetrical management TOC
Challenges in recognition of dengue disease and plasma leakage
e Hyperemesis -1st Trimester
e Increase in circulating blood volume + vasodilatation -2nc
Trimester

88. Pediatric: Management
Management of dengue in infants
e Severe dengue is less common in infancy
o But risk of dying is higher
o Should be referred for in-hospital management
Management of dengue infants WITHOUT warning signs
e Treatment is supportive.
e Oral rehydration - ORS, fruit juice, fluids with electrolytes and sugar,
breastfeeding or formula feeding and/or solid food.
Febrile seizures are more frequent in infants and young children
Fever control with antipyretics and tepid sponging.

89. Pediatric: Management
Management of dengue infants WITH warning signs
e IV fluid therapy
e Judicious volume replacement of lost plasma
o Modify the course and severity of disease
e Only isotonic crystalloid solutions such as:
o Ringer's lactate (RL), Ringer's acetate (RA), or 0.9% saline
solution
e Start with 5-7 ml/kg/hour for 1-2 hours and then adjust the
rate according to the patient's clinical response.

90. Pediatric: Management
Management of Neonatal dengue
e Pregnant woman with signs of dengue = neonate consideration for
dengue
o Suspected on clinical grounds and then confirmed in the
laboratory, but may be confused with:
= Bacterial sepsis, birth trauma and other causes of neonatal
illness.
e Symptomatic and supportive treatment under close observation is
the mainstay of treatment.

91. * O6 C
Pitfalls in the
Management
of Dengue
& Solutions*

92. Pitfall 1: Recognition of dengue at the frontline
e Usually misdiagnosed as URTI or viral fever
Solution: Suspect dengue in every febrile
patient.
e Direct questioning to reveal residence or
travel in a dengue endemic locality
e Detailed history and stepwise evaluation
e Tourniquet test; negative test does not
exclude dengue

93. Pitfall 1: Recognition of dengue at the frontline
e Usually misdiagnosed as URTI or viral fever
Solution: Suspect dengue in every febrile
patient.
For probable dengue patients: Schedule daily
follow-up and advice immediate medical
attention for warning signs

94. Pitfall 2: Missed opportunity for FBC in early
febrile period
e FBC is not determined until day 4 of illness
o To detect falling PC
o Changes in hematocrit levels
Solution: A full blood count should be done at
the first visit when dengue is suspected.

95. Pitfall 3: Not understanding the evolving FBC
e The earlier the FBC is done, the more likely the
results seem normal
Solution: Establish patient’s baseline
hematocrit using an early FBC.
e The early and progressive decrease in WBC
and PC during the febrile period is a useful
indicator of dengue.

96. Pitfall 4: Surge of hospital admissions during a
dengue outbreak
e Fear and panic to admit all suspected dengue
patients
Solution: Clear guidelines for admissions
e Outpatient management protocol
e Admission during the febrile period should be
for those who are unable to manage adequate
oral hydration at home, infants and with
co-morbids

97. Assessment Classification Management

Indicators of shock:
¢ Cold, clammy extremities and
¢ Prolonged capillary refill time and
e Weak pulse
¢ Severe bleeding
¢ Impaired consciousness
Severe dengue e Give intravenous crystalloid
fluids if the patient has shock
¢ Refer URGENTLY to hospital

¢ Abdominal pain or tenderness
e¢ Persistent vomiting or
e¢ Lethargy or restlessness or
¢ Bleeding from nose or gum or
¢ Blood in vomit or stool or
¢ Petechiae on the skin
Dengue with warning
signs
e Refer URGENTLY to hospital


None of the above signs and no other
infectious causes of fever, able to drink
enough (refer section 5.7, Textbox G)

Dengue

Instructions for:
- home care
- follow-up
- warning signs

*for a patient from a dengue endemic locality, with fever, or history of fever, which lasts 2—7 days, and fulfils
criteria for probable dengue (refer to Figure 2: Dengue classification)

98. Pitfall 5: Patients who develop warning signs
at night usually wait until their next scheduled
morning appointment to seek medical attention.
Solution: Ambulatory patients should receive
explicit advice about the warning signs and the
urgency of seeking immediate medical
attention.

99. Pitfall 6: Triage based on fever
e Afebrile dengue patient: non-urgent triage and
has to wait
e Subnormal temperature seen in patients with
established plasma leakage or dengue shock.
Solution: Triage personnel should be taught
assessment of perfusion.
e History of nausea, vomiting and lethargy

100. Pitfall 7: Waiting for full blood count results
(for thrombocytopenia)
e Further delay in recognition and treatment of
dengue shock.
Solution: IVF should be initiated when warning
signs or clinical evidence of shock are
present.
e Sample blood for CBC and hematocrit before
commencement of IVF.

101. Pitfall 8: Vital signs are “stable”
e Compensated shock - patient is alert and has a
stable BP
e Patient in shock ts initially quietly tachypneic,
and remain so until cerebral perfusion
diminishes
Solution: Touch and assess the peripheral
perfusion of every patient.

102. Pitfall 9: Symptomatic treatment with
antispasmodic agents or antacid Is being given
to patients with abdominal pain.
e Abdominal pain is an early sign of plasma
leakage
e Pain inthe epigastrium + vomiting
o Misinterpreted as gastritis
e Full-blown shock if definitive treatment for shock
Is not given promptly.

103. Pitfall 9: Symptomatic treatment with
antispasmodic agents or antacid Is being given
to patients with abdominal pain.
Solution: Know the pattern of fever and
GI symptoms of dengue shock.
e Transitioning from fever to no-fever and the
development of GI symptoms such as nausea,
vomiting or diarrhea, should suggest dengue
with warning signs or dengue shock.

104. Pitfall 10: Patients who present with severe
abdominal pain are referred to the surgical
team or for ultrasound studies.
e Guarding and rebound tenderness in the tliac
fossa
o Due to serosa edema and lymphoid
hyperplasia of the intestines
e Abdominal pain becomes more severe
o Due to splanchnic vasoconstriction

105. Pitfall 10: Patients who present with severe
abdominal pain are referred to the surgical
team or for ultrasound studies.
Solution: Evaluate the patient's history for
fever that preceded the onset of abdominal
pain.
e Signs of shock
e Hematocrit and thrombocytopenia

106. Pitfall 10: Patients who present with severe
abdominal pain are referred to the surgical
team or for ultrasound studies.
Solution: Evaluate the patient's history for
fever that preceded the onset of abdominal
pain.
e A bolus of IVF (5-19 mL/kg/ over 1 hour) may
lead to resolution of abdominal pain, making
the diagnosis of a surgical abdomen unlikely

107. Pitfall 11: Shortness of breath is
misinterpreted as fluid overload or due to
pleural effusion or pneumonia.
e As plasma leakage progresses, patient
develops metabolic acidosis.
e Further deterioration leads to breathing more
deeper and gives the impression of shortness
of breath.

108. Pitfall 11: Shortness of breath is misinterpreted
as fluid overload or due to pleural effusion or
pneumonia.
Solution: Familiarize with the breathing pattern
seen in dengue shock as well as diabetic
ketoacidosis. Look for features of shock.
e If unsure, do ABG (+ lactate) analysis. Start IVF
immediately after sampling blood for hematocrit.

109. Pitfall 12: Seizures or altered sensorium —
diagnosed as meningitis or
meningoencephalitis.
e Seizures occur during:
o 1) Febrile phase (febrile seizures)
o 2) Critical phase (no to low-grade, but with
shock

110. Pitfall 12: Seizures or altered sensorium —
diagnosed as meningitis or
meningoencephalitis.
Solution: Targeted history to confirm had
fever preceding seizures and might not be
febrile at the time of seizure.
e ACT scan is not necessary if patient's
neurological state recovers with stable
hemodynamic state.

111. Pitfall 13: Focusing on bleeding versus plasma
leakage
e May result in administering platelet
transfusions — Fluid overload or inadequate
fluid replacement may ensue
Solution: Use the platelet count trend during the
febrile phase to identify rapid decrease, which
marks the beginning of plasma leakage.

112. Pitfall 14: Focusing on the systolic BP and
ignoring the rising diastolic BP and pulse rate
Solution: In general, assume hypotension when
the radial or brachial pulse are not palpable,
and femoral pulses are weak or absent. Do not
rely on automated BP devices tn patients with
clinical signs of shock.

113. Pitfall 15: During the febrile stage, tachycardia
and cold extremities could be misinterpreted as
shock and fluid resuscitation commenced.
e Vasoconstriction resulting in cold extremities
IS anormal mechanism to conserve heat and
increase core body temperature

114. Pitfall 15: During the febrile stage, tachycardia
and cold extremities could be misinterpreted as
shock and fluid resuscitation commenced.
Solution: Assess intravascular volume using
more than 2 parameters.
e Febrile phase: Normal Hct, PC, pulse volume,
urine output
e CRT, pulse pressure, urine output, acid-base
balance

115. Pitfall 16: Starting IVF in the febrile phase
(because NS1 Ag is positive)
e Plasma leakage is detectable as early as day 2 of
fever onset
e Early IVF will exacerbate accumulation third
space losses
Solution: During the febrile phase, hydration
Should be maintained by the oral route

116. Pitfall 17: Administering IVF at high rates for
several hours without review of clinical state
e In dengue, there is no loss of fluid from the
body.
e Ina “leaky” capillary state, beyond a certain
hydrostatic pressure, the more fluids infused,
the more they will leak.

117. Pitfall 17: Administering IVF at high rates for
several hours without review of clinical state
Solution: Administer the minimum IVF
necessary to maintain a “just enough”
circulation.

118. Pitfall 18: Increased fluid therapy ina
well-perfused patient with persistently elevated
hematocrit.
e Hematocrit may remain elevated towards the end of
the critical phase despite adequate fluid therapy
e Anattempt to correct it will lead to fluid overload
Solution: Do not increase the IVF therapy. If
patient continues to be well perfused in the next
2-3 hours, IVF should be gradually reduced and
stopped, regardless of hematocrit level.

119. Pitfall 19: IVF therapy is continued into the
recovery phase because the patient Is not
drinking.
Solution: Stop IVF therapy. The patient's own
thirst mechanism will kick in after the diuresis.

120. Pitfall 20: During the febrile phase, the urine
output Is ignored and not factored into the
evaluation of adequate oral fluids.
Solution: Note that adequate oral fluid intake of
fluids should result in a urinary output
frequency of 4-6 times per day.

121. Pitfall 21: During the critical phase, the urine
output of 1 mL/g/hr is used as a criterion of
adequate intravenous therapy or might not be
monitored at all.
Solution: In severe shock, urine output should
be monitored hourly using an indwelling
catheter. Adequate urine output should be
scaled down to ~ 0.5 mL/kg /h to avoid overload.
Urine output exceeding that may indicate
reduction of IVF

122. Pitfall 22: Use of furosemide for oliguria during
the critical phase
e Oliguria is due to “pre-renal”. Use of loop
diuretics will produce some urine but will
exacerbate shock state
Solution: Adequate peripheral perfusion should
be the main end-point of IVF therapy

123. Pitfall 23: The practice of a fluid bolus challenge
followed by furosemide may produce urine; the
physician may think they have averted an
oliguric renal failure.
Solution: Recognize that urine output as a
parameter of adequate perfusion Is very limited
in this situation.

124. Pitfall 24: Worsening or persistent abdominal
pain/tenderness appearing after 24 hours of
large volumes of fluid replacement,
misinterpreted as “warning sign for shock”
e May be due to tense ascites and/or enlarged
and congested liver from the fluid overload
Solution: Assess the intravascular volume
through different parameters, not just by
abdominal symptoms.

125. Pitfall 24: Worsening or persistent abdominal
pain/tenderness appearing after 24 hours of
large volumes of fluid replacement,
misinterpreted as “warning sign for shock”
Solution: Assess the intravascular volume
thoroughly based on peripheral perfusion, pulse
pressure and volume, urine output 9(~0.5
mL/kg/h) and acid-base balance, not just by
abdominal symptoms.

126. Pitfall 25: Abdominal compartment syndrome.
e Result of massive ascites accumulated ina
short time, hence Is under tension
e May be precipitate by using high PEEP during
mechanical ventilation
e Reduced perfusion in the retroperitoneal
structures — oliguria, even though with
adequate peripheral perfusion

127. Pitfall 25: Abdominal compartment syndrome.
Solution: Be cautious about using urine output
as a parameter of adequate perfusion
e Reclining/lateral position to relieve pressure
e With time, ease of intra-abdominal tension—
urine will start flowing, soontaneously or with
furosemide
e Furosemide should be commenced tn the
recovery period when the patient is stable
without IVF infusion

128. Pitfall 26: Use of renal replacement therapy
such as continuous venous hemodialysis during
the critical phase when the patient has severe
metabolic acidosis and oliguria.
Solution: Reserve renal replacement for patients
who are already in recovery phase, who are
hemodynamically stable, are fluid overloaded
and have oliguria not responding to furosemide
therapy.

129. Pitfall 28: Not transfusing blood until the
hematocrit has decreased low levels In
unstable patients
e Low levels of hematocrit only after several
boluses of fluid resuscitation or if bleeding is
very severe
Solution: Recognize that the lower the
hematocrit in dengue shock, the more significant
the bleeding. Change strategy from
crystalloid/colloid to blood transfusion.

130. Pitfall 30: Blood transfusion when the
hematocrit is on the rise in a shocked patient.
e Subsequent hematocrit will rise even more
sharply after blood transfusion and prompt use
of crystalloids even with stable hemodynamics,
leading to fluid overload

131. Pitfall 30: Blood transfusion when the
hematocrit is on the rise in a shocked patient.
Solution: Consider using colloid bolus 10-20
mL/kg if hematocrit continues to rise despite
resuscitation. Do not resuscitate if systolic BP Is
normal. Reserve aggressive fluid resuscitation
over 15 minutes for those with hypotension.

132. Pitfall 31: Blood transfusion ina stable patient
with low hematocrit
e Recovery phase: re-absorption causes
hemodilution
e Blood transfusion may precipitate
life-threatening pulmonary edema
Solution: Do not transfuse blood if the patient
has a stable circulation; the hematocrit will
increase after the excess fluid has been
diuresed.

133. Pitfall 32: Severe shock and inotropes
Solution: Re-evaluate hemodynamic state after
every bolus infusion of 10-20 mL/kg, and repeat
hematocrit If no clinical improvement.
e Arising/high hematocrit suggests ongoing
plasma leakage -— change to a colloid solution.
e Adecrease in hematocrit suggests significant
bleeding — proceed to transfuse matched fresh
whole blood ASAP

134. Pitfall 33: Liver enzymes and multi-organ
involvement may prompt multi-specialty referrals
that result in several “single organ” treatments
Solution: Do not be distracted in prioritizing
achievement of hemodynamic stability and
improved tissue oxygenation. All other outstanding
clinical issues (except hypoglycemia and
electrolyte imbalances should await hemodynamic
stability

135. Pitfall 34: Dengue shock treated “aggressively”
as in septic shock
Solution: Limit aggressive fluid resuscitation to
dengue shock with hypotension as it may be
harmful. Once peripheral pulses are established,
rate of parenteral fluid replacement should be
reduced.

136. Thank.”
you! =