Dengue is a mosquito-borne viral infection that is a major cause of illness and hospitalization in tropical and subtropical regions. Each year there are 50-100 million cases of dengue infection worldwide, with 500,000 cases resulting in hospitalization. The disease is caused by any of four related dengue virus serotypes. Dengue presents a spectrum of illness from mild fever to severe dengue which can include plasma leakage, bleeding, and organ impairment. There is no vaccine available and treatment focuses on fluid replacement and management of complications. Close monitoring is needed during the critical phase to guide fluid management and recognize bleeding or shock.

2.  DENGUE IS THE WORLD’S MOST COMMON MOSQUITO-
BORNE VIRALINFECTION AND A LEADING CAUSE OF MORBIDITY
THROUGHOUT THE TROPICS AND SUBTROPICS.1
 EACH YEAR, THERE ARE ABOUT 50-100 MILLION DENGUE
INFECTIONS AND ABOUT 5,00,000 INDIVIDUALS HOSPITALIZED
WITH DHF, MAINLY IN SOUTHEAST ASIA.2
GLOBALLY, DENGUE VIRUS TRANSMISSION HAS EXPANDED
IN RECENT YEARS, AND ALL FOUR DENGUE VIRUS SEROTYPES
ARE NOW CIRCULATING IN ASIA, AFRICA, AND THE AMERICAS,
REPRESENTING A GLOBAL PANDEMIC.3
 APPROXIMATELY 70% OF THE POPULATION AT RISK FOR
DENGUE WORLDWIDE LIVES IN THE WHO SOUTH EAST ASIAN
REGION AND WESTERN PACIFIC REGION, WHICH BEAR NEARLY
75% OF THE CURRENT GLOBAL DISEASE BURDEN DUE
TO DENGUE.4

3. EPIDEMIOLOGY
AGENT
 Dengue Virus
 There are four antigenetically related but distinct serotypes of
the dengue virus:
 DENV-1, DENV-2, DENV 3, and DENV-4.
 Each serotype has several genotypes. DENV-1 has three,
DENV-t2 has two, and DENV-3 and DENV-4 each have four. In
humans, one serotype produces lifelong immuniy against
reinfection but only temporary and partial immunity against
the other SEROTYPE
 Each serotype has unique characteristics and can present with
severe manifestations in a particular population depending
upon its interaction with the host response.

4. WHATS NEW
Dengue's D2 strain –DENV2
 the strain is particularly virulent and capable of inducing mortality. it
was one of the reasons behind the mysterious fever which had hit
the western UP districts of Firozabad, Agra, Mathura, and Aligarh
that led to the deaths of many people last monthin 2021`
DENV 2 or the strain D2 is considered to be the most severe and can
even lead to fatal internal bleeding and shocK
IT IS HIGHLY TRANSMISSIBLE AND SPREADS FASTER

5. HOST
 People of all ages and both genders are at risk of
being infected.
 Travel to dengue endemic areas is a very important risk
factor in transmission of disease- it is the commonest
cause of fever in the travelers returning from these
areas, overtaking malaria and typhoid.

6. VECTOR
 AEDES AEGYPTI
 AEDES ALBOPICTUS

7. SPECTRUM OF DENGUE
INFECTION
 The incubation period for dengue infection is 4-7 days
(range 3-14).
 Symptomatic dengue infection is a systemic and
dynamic disease with clinical, haematological and
serological profiles changing from day to day.
 These changes accelerate within hour or even minutes
during the critical phase, particularly in those with
plasma leakage

10. Febrile phase
 high-grade fever sudden onset-usually lasts 2-7 days
 facial flushing,
 skin erythema,
 generalized body ache, myalgia, arthralgia,.
 retro-orbital eye pain, photophobia.
 rubeliform exanthema RASHES and headache .
 Anorexia, nausea and vomiting are common

11. Confluent erythematosus
rash with island of
skinsparing
Rash in dengue fever is a
maculopapular or macular
confluent rash over the face,
thorax, and flexor surfaces,.with
islands of skin sparing
HERMAN
RASH

12. Critical phase
 During the transition from the febrile to afebrile phase,
patients without an increase in capillary permeability will
improve without going through the critical phase. Instead of
improving with the subsidence of high fever.
 The warning signs mark the beginning of the critical phase.
These patients become worse around the time of
defervescence, when the temperature drops to 37.5-38°C or
less and remains below this level, usually on days 3–8 of
illness.
 Progressive leukopenia followed by a rapid decrease in
platelet count usually precedes plasma leakage. An increasing
haematocrit above the baseline may be one of the earliest
additional sign. The period of clinically significant plasma
leakage usually lasts 24-48 hours. A rising haematocrit
precedes changes in blood pressure (BP) and pulse volume

13.  thrombocytopaenia and haemoconcentration are
usually detectable in this phase. The haematocrit (HCT)
level correlates well with plasma volume loss and
disease severity
 Leucopaenia with relative lymphocytosis,
 clotting abnormalities,
 elevation of transaminases [typically the level of
aspartate aminotransaminase (AST) is higher than the
level of alanine aminotransaminase (ALT)],
 hypoproteinaemia
 hypoalbuminaemia
 hyponatremia

14. Recovery Phase
 Plasma leakage stops followed by reabsorption of extravascular
fluid
 General well being improves
 appetite returns, gastrointestinal symptoms improve,
haemodynamic status stabilises and diuresis ensues
 The recovery of platelet count is typically preceded by recovery
of white cell count.

17. Severe dengue
 A case of severe dengue is defined as a suspected
dengue patient with one or more of the following
severe plasma leakage that leads to shock
(dengue shock) and/or fluid accumulation
with respiratory distress;
severe bleeding;
severe organ impairment.


18.  Dengue shock syndrome (DSS)
 a form of hypovolaemic shock and results from continued vascular
permeability and plasma leakage
IN the initial stage of shock, the compensatory mechanism that
maintains a normal systolic BP produces tachycardia, quiet
tachypnoea (tachypnoea without increased effort) and peripheral
vasoconstriction with reduced skin perfusion
 As peripheral vascular resistance increases, the diastolic pressure rises
towards the systolic pressure and the pulse pressure (the difference
between the systolic and diastolic pressures) narrows.

20. history
 date of onset of fever/illness;
 quantity of oral fluid intake;
 diarrhoea;
 urine output (frequency, volume and time of last voiding);
 assessment of warning signs (Textbox C);
 change in mental state/seizure/dizziness;
 other important relevant history, such as family or
neighbourhood dengue, travel to dengue-endemic areas, co-
existing conditions (e.g. infancy, pregnancy, obesity, diabetes
mellitus, hypertension), jungle trekking and swimming in
waterfalls (consider leptospirosis, typhus, malaria), recent
unprotected sex or drug abuse (consider acute HIV-
seroconversion illness).

21. Physical examination
 assessment of mental state;
 assessment of hydration status;
 assessment of haemodynamic status (Textbox D);
 checking for quiet tachypnoea/acidotic
breathing/pleural effusion;
 checking for abdominal
tenderness/hepatomegaly/ascites;
 examination for rash and bleeding manifestations;
 tourniquet test (repeat if previously negative or if there
is no bleeding manifestation).

22. INVESTIGATIONS
 COMPLETE BLOOD COUNT
 RENAL FUNCTION TEST
 LIVER FUNCTION TEST
 URINE ROUTINE
 RANDOM BLOOD SUGAR
 ECG
 CHEST XRAY PA VIEW
 USG ABDOMEN AND PELVIS

24. DIFFERENTIAL DIAGNOSIS

25. Electrolyte and acid-base imbalances
 Hyponatraemia is a common observation in severe
dengue. gastrointestinal losses through vomiting and
diarrhoea or the use of hypotonic solutions for
resuscitation and correction of dehydration. The use of
isotonic solutions for resuscitation will prevent and
correct this condition.
 Hyperkalaemia is observed in association with severe
metabolic acidosis or acute renal injury. Appropriate
volume resuscitation will Hypokalaemia is often
associated with gastrointestinal fluid losses and the
stress-induced hypercortisol state; it is usually
encountered towards the later part of the critical phase. It
should be corrected with potassium supplements in the
parenteral fluids.
 Serum calcium levels should be monitored and corrected
when large quantities of blood have been transfused or if
sodium bicarbonate has been used.

26. 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
extremities
Cool peripheries Cold, clammy extremities
Peripheral pulse
volume
Good volume Weak and thready Feeble or absent
Heart rate Normal for age Tachycardia Severe tachycardia with
bradycardia in late shock
BP Normal for age
Normal pulse pressure
for age
rising diastolic pressure
Narrowing pulse pressure
(≤ 20 mmHg in children)
Postural hypotension
Hypotension (see
below)
Unrecordable BP
Respiratory rate
(RR)
Normal for age Quiet tachypnoea Metabolic
acidosis/hyperpnoea/
Kussmaul’s breathing
Urine output Normal Reducing trend Oliguria/anuria

27. INTERPRETATION OF HEMATOCRIT
 A rising or persistently high haematocrit together with unstable vital
signs (such as narrowed pulse pressure) indicates active plasma leakage
and the need for a further bolus of fluid replacement.
 However, a rising or persistently high haematocrit together with stable
haemodynamic status and adequate urine output does not require extra
intravenous fluid. continue to monitor closely and it is likely that the
haematocrit will start to fall within the next 24 hours as plasma leakage
stops.
 A decrease in haematocrit (for example from 50% to 40% or below the
patient’s known baseline) together with unstable vital signs (narrowed
pulse pressure, tachycardia, metabolic acidosis and poor urine output),
may indicate major haemorrhage.
 If there is severe haemorrhage, urgent blood transfusion should be
given. If there is no clinical sign of bleeding, then a further bolus of 10–
20 ml/kg of colloid should be given, followed by repeat clinical
assessment and haematocrit level determination plus a review by senior
staff to consider blood transfusion.

28. Dengue without warning
signs-GROUP A
 Patients who do not have warning signs
 AND
who are able:
 T o tolerate adequate volumes of oral fluids
 T o pass urine at least once every 6 hours
treatment
 Adequate bed rest
 Adequate fluid intake
 Paracetamol, 4 gram max. per day in adults

29. Group B- Dengue with warning signs
 These are patients who should be admitted for in-hospital
management for close observation as they approach the critical
phase.
 These include patients with warning signs
 those with co-existing conditions that may make dengue or its
management more complicated (such as pregnancy, infancy, old
age, obesity, diabetes mellitus, hypertension, heart failure, renal
failure, chronic haemolytic diseases such as sickle-cell disease
and autoimmune diseases
 those with certain social circumstances (such as living alone, or
living far from a health facility without reliable means of
transport
 PLUS WARNING SIGNS OF DENGUE

30. HIGH RISK GROUP

31. TREATMENT
 G i v e isotonic solutions such as 0,9% saline, Ringer lactate,
 start with 5-7 ml/kg/hr for 1-2 hours,
then reduce to 3- 5 ml/kg/hr for 2-4 hr,
and then reduce to 2-3 ml/kg/hr or less according to clinical
response
 Reassess clinical status and repeat Hct
 I f Hct remains the same or rises only minimally -> continue with
2-3 ml/kg/hr for another 2-4 hours
 I f worsening of vital signs and rapidly rising Hct -> increase rate
to 5-10 ml/kg/hr for 1-2 hours
 Reassess clinical status, repeat Hct and review fluid infusion
rates accordingly
 Reduce intravenous fluids gradually when the rate of plasma
leakage decreases towards the end of the critical phase.

32. MONITORING-GROUP B
 Temperature pattern
 Volume of fluid intake and losses
 Warning signs
 Hct, white blood cell and platelet counts
Vital signs and peripheral perfusion (1-4 hourly until patient is
out of critical phase
 Urine output (4-6 hourly)
 Hct (before and after fluid replacement, then 6-12 hourly)
 Blood glucose
 Other organ functions (renal profile, liver profile, coagulation
profile, as indicated)

33. GROUP C
 Patients with any of the following features.
 Severe plasma leakage with shock and/or fluid
accumulation with respiratory distress
 Severe bleeding
 Severe organ impairment


34. Treatment of compensated
shock:
 Start I.V. fluid resuscitation with isotonic crystalloid Solution at 5-
10ml/kg/hr
patient improves:
 I . V. fluids should be reduced gradually to 5-7 ml/kg/hr for 1-2 hr,
then to 3- 5 ml/kg/hr for 2-4 hr, then to 2-3 ml/kg/hr for 2-4 hr
and then reduced further depending on haemodynamic status
 I . V. fluids can be maintained for up to 24 - 48 hours
If patient still unstable:
 C h eck Hct after first bolus
 If Hct increases/ still high (>50%), repeat a second bolus of
crystalloid solution at 10-20 ml/kg/hr for 1 hr.
 I f improvement after second bolus, reduce rate to 7-10 ml/kg/hr
for 1-2 hr, continue to reduce as above.
 If Hct decreases, this indicates bleeding and need to cross-match
and transfuse blood as soon as possible

36. Treatment of hypotensive
shock
 I nitiate I.V. fluid resuscitation with crystalloid or colloid
solution at 20 ml/kg as a bolus for 15 min
 If patient improves
 G i v e a crystalloid / colloid solution of 10 ml/kg/hr for 1
hr, then reduce gradually as above
 If patient still unstable
 R e view the Hct taken before the first bolus

37.  If Hct was low (<40% in children and adult females, < 45% in
adult males) this indicates bleeding, the need to crossmatch
and transfuse
 o If HCT was high compared to the baseline value, change to
I.V. colloids at 10-20 ml/kg as a second bolus over to 1 hour;
reassess after second bolus
 If improving reduce the rate to 7-10 ml/kg/hr for 1-2 hours,
then back to I.V. crystalloids and reduce rates as above
 If Hct increases/ remains high (> 50%), continue colloid
infusion at 10-20 ml/kg as athird bolus over 1 hr, then reduce
to 7-10 ml/kg /hr for 1-2 hours, then change back to
solution and reduce rate as above

39. INDICATIONS FOR BLOOD
TRANSFUSION
 LOSS OF BLOOD-OVERT GI BLEED;MUCOSAL BLEED-
MORE THAN 10%
 REFRACTORY SHOCK DESPITE ADEQUATE FLUID
THERAPY AND HEMATOCRIT DECLINE

40. INDICATIONS FOR PLATELET
TRANSFUSION
 PLATELET TRANSFUSION NOT THE MAIN STAY OF
TREATMENT IN DENGUE
 IF PLT COUNT>10000 WITH NO BLEED-NO NEED OF
PROPHYLACTIC TRANSFUSION
 IF<10000-CAN BE GIVEN
 ABNORMAL COAGULATION PROFILEWITH
PROLONGED SHOCK

42. CNS manifestations
 Intra-cerebral haemorrhage
 Encephalitis
 Aseptic meningitis
 ADEM
 Cerebral infarct
 Cortical venous thrombosis
 Myelitis
 Hypokalemic periodic paralysis
 G.B. syndrome
 Opsoclonus myoclonus
 Optic neuropathy
 Myalgia cruris
 Rhabdomyolysis
 Dysarthria clumsy-hand syndrome

43. Cardiovascular
manifestations
 Asymptomatic myocarditis
 Symptomatic myocarditis
 Pericarditis
 Myocardial infarction
 S-A nodal block A-V nodal block
 Acute atrial fibrillation
 Cardiomyopathy

44. Gastrointestinal
manifestations
 Hepatic dysfunction (without ALF)
 Acalculus cholecystitis
 Fulminant hepatic failure
 Acute pancreatitis
 Diffuse peritonitis
 Acute appendicitis
 Acute parotitis
 Spleen rupture

45. Renal manifestations
 Myoglobinuric acute renal failure
 Rhabdomyolysis
 AKI associated with DHF
 AKI with DSS/DHF
 IgA nephropathy
 Hemolytic-uremic syndrome

47. Challenges when managing dengue patients with pre-
existing hypertension
Interpretation of BP Hypotension is a late sign of shock. in patients with uncontrolled. Patients with chronic
hypertension should beconsidered to be hypotensive when the mean arterial pressure
declines by 40 mmHg from the baseline, even if it still exceeds 60 mmHg. (For example, if
baseline MAP is 110 mmHg, a MAP reading of 65 mmHg should be considered as
hypotension.) Look for other manifestations of shock (see Section
: Bradycardia:
Tachycardia:
End-organ damage
from chronic
hypertension:
ß-blockers, a common antihypertensive medication, cause bradycardia and may block the
tachycardic response in shock. The heart rate should not be used as anassessment of
perfusion in patients on ß-blockers.
calcium channel blockers may cause tachycardia.Tachycardia in these patients may not
indicate hypovolemia. Knowing the baseline heart rate before the dengue illness is helpful
the haemodynamic assessment
Heart failure and renal failure are common complications of chronic uncontrolled
Clinicians should be aware if there is pre-existing or new onset of end-organ damage.
Interpretation of urine output as a marker of renal perfusion has to
be revoked in these situations.

48. Challenges when managing dengue patients with pre-
existing diabetes mellitus
Hyperglycaemia
Osmotic diuresis:
Increased risk of
concomitant sepsis:
Diabetic
and hyperosmolar
hyperglycaemia:
dengue can precipitate diabetic ketoacidosis or hyperosmolar
hyperglycaemia.
Hyperglycaemia results in osmotic diuresis and worsens intravascular
hypovolaemia.
patients at risk of bacterial infection.
Clinical manifestations of diabetic ketoacidosis and hyperosmolar
(nausea, vomiting and abdominal pain) are similar to the warning signs of
dengue. It is not uncommon for dengue shock to be misdiagnosed as
diabeticketoacidosis.
Hypoglycaemia: Hypoglycaemia may occur in those patients taking oral hypoglycaemic agents .
Hypoglycaemia could beaggravated by severe hepatitis from dengue.
Oral hypoglycaemic
agents:
Gastrointestinal absorption of oral hypoglycaemic agents is unreliable .Some
hypoglycaemic agents suchas metformin may aggravate lactic acidosis,
particularly in dengue shock syndrome

49.  Dengue patients with known diabetes mellitus should be admitted for closer
monitoring of the diabetic as well as dengue states. If the patient has
gastrointestinal disturbances, blood glucose should be controlled with
intravenous short-acting insulin during the dengue illness.
 A validated protocol for insulin dose adjustments to a target glucose level of
< 150 mg/dl (8.3 mmol/L) should be used.
 A source of glucose may be maintained once the target is achieved while
receiving intravenous insulin. Blood glucose should be monitored every 1–2
hours until glucose values and insulin rates are stable and then every 4 hours
thereafter

50. CHRONIC KIDNEY DISEASE
 Dengue patients with chronic Kidney disease(CKD) have
a significantly higher risk of severe dengue and mortality.
 The warning signs of severe dengue are similar to those
of uraemia in CRF. Ascites and/or pleural effusion, and
signs of plasma leakage in dengue, are not uncommon
findings in patients with CRF and fluid retention. The
ambiguity of these symptoms and signs could delay the
recognition of plasma leakage and severe dengue.
 Low baseline haematocrit and platelet count
 Patients with CRF have a low baseline haematocrit.

51. CKD –DENGUE MANAGEMENT
CHALLENGES
 Narrow window of fluid tolerance
 Urine output
The urine output should not be used as an indicator of
the intravascular volume status because patients with
CRF can have either low or high urine-output renal failure
 Limited effect of diuretics
 Acid base balance and electrolyte balance
 Platelet dysfunction