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SEMINAR ON
DENGUE FEVER
DIAGNOSIS AND MANAGEMENT
MODERATOR PRESENTER
DR. D. KALITA NISHANT AGARWAL
ASST. PROF. PGT
DEPARTMENT OF PEDIATRICS, GMCH.
INTRODUCTION
 Dengue is a self limiting acute mosquito
transmitted disease characterized by fever ,
headache, muscle, joint pains, rash, nausea
and vomiting.
 The dengue viruses are the members of the
genus flavi virus. There are four virus
serotypes of which DEN1 and DEN2 widespread
in India.
 Dengue viruses are transmitted by the bite
of female Aedes (Ae) mosquitoes. other
species such as Ae albopictus, Ae.
polynesiensis and Ae. Niveus may also
transmit dengue.
 All ages and both sexes are susceptible
to dengue fever .
 Infected person can transmit the virus to
the mosquito 1 day before onset of febrile
episode and remain infectious for next 6-7
days.
 Migration of patient during viremia to a
non endemic area may introduce it into
the area.
CLINICAL CLASSIFICATION (old)
1. Dengue Fever :
An acute febrile illness of 2-7 days
duration with two or more of the following
manifestations:
Headache, retro-orbital pain, myalgia,
arthralgia, rash, haemorrhagic
manifestations.
2. Dengue Haemorrhagic Fever :
a). A probable or confirmed case of
dengue PLUS
b). Haemorrhagic tendencies evidenced
by one or more of the following –
 Positive tourniquet test.
 Petechiae, ecchymoses or purpura.
 Bleeding from mucosa, gastrointestinal
tract, injection sites or other sites.
 Haematemesis or malena
PLUS
c). Thrombocytopenia (<100,000 cells
per cumm) PLUS
d). Evidence of plasma leakage
 A rise in average haematocrit for
age and sex >/= 20%.
 A more than 20% drop in haematocrit
following volume replacement
treatment compared to baseline.
 Signs of plasma leakage (pleural
effusion, ascites , hypoproteinemia).
3. Dengue Shock Syndrome :
All the above criteria for DHF
PLUS
Evidence of circulatory failure manifested
by rapid and weak pulse and narrow
pulse pressure (<20 mm Hg) or
hypotension for age, cold and clammy skin
and restlessness.
• Grading of Dengue Fever
• DF : Fever of 2-7 days with two or more of the
following:
• Headache
• Retro orbital pain
• Myalgia
• Arthralgia with or without leukopenia
• Thrombocytopenia
and no evidence of plasma leakage
• DHF I: above criteria plus tourniquet test and
evidence of plasma leakage. Thrombocytopenia
with platelet count less than 100000/ cumm and
Hct rise more than 20% over baseline.
• Grading of Dengue Fever(contd)
• DHF II : above plus some evidence of
spontaneous bleeding in skin or other organs
(black tarry stool, epistaxis, gum bleeds) and
abdominal pain. Thrombocytopenia with
platelet count less than 100000/ cumm and
Hct rise more than 20% over baseline.
• DHF III (DSS): Above plus circulatory failure.
Thrombocytopenia with platelet count less
than 100000/ cumm and Hct rise more than
20% over baseline.
• Grading of Dengue Fever(contd.)
• DHF IV : Profound shock with undetectable
blood pressure or pulse. Thrombocytopenia
with platelet count less than 100000/ cumm
and Hct rise more than 20% over baseline.
THE TOURNIQUET TEST
Is performed by inflating a blood pressure cuff to
a midpoint between the systolic and diastolic
pressure for five minutes. The test is considered
positive when 10 or more petechiae per square
inch over the forearm.
• In DHF , the test usually gives a definite
positive test with 20 petechiae or more.
• The test may be negative or only mildly positive
during the phase of profound shock (DSS). If
tourniquet test is found negative it should be
repeated.
• Early diagnosis of disease and admission of DHF
patients in hospitals are important in order to
reduce case fatality rates.
Dengue Infection
symptomatic Asymptomatic
Mild
dengue
Severe
dengue
Mod
dengue
DF with risk factors
&co morbid condition
DF with warning signs
and symptoms
• Undifferentiat
ed DF
• Fever without
complication
• Without
capillary
leakage
• DF/DHF with
significant
hemorrhage
• DHF with
shock (DSS)
• Severe organ
involvement
• Severe met
disorder
• DF with
warning signs
and
symptoms
• DHF I and
DHF II with
minor bleeds
• Infants
• Haemoglobinop
athies
• Immunocomp
• Patients on
steroids,
anticoagulants
or
immunosuppres
ants
PATHOGENESIS
 Binding of the new virus to cross reactive non
neutralising antibody from the previous infection or
passively acquired antibodies in infant facilitating
the uptake by mononuclear phagocytes
 This enable amplified viral replication (ADE)the
resulting increase in viral load then drives an
immuno pathogenic cascade.
 The resultant exaggerated cytokine response
leads to a transient increase microvascular
permeability as well as activation of the
coagulating system.
THE COURSE OF DENGUE ILLNESS
Febrile phase—
 High-grade fever for 2-7 days with facial flushing,
skin erythema, generalized body ache, myalgia,
arthralgia and headache.
 Some patients may have sore throat, injected
pharynx and conjunctival injection, Anorexia,
nausea and vomiting
 Rash may be seen on the 3rd or 4th day which may
be rubelliform or maculopapular in nature.
 difficult to distinguish dengue clinically from non-
dengue febrile diseases.
 clinical features are indistinguishable between
severe and non-severe dengue cases.
Critical phase
Temperature drops,
Increase capillary permeability in parallel with
increasing haematocrit levels.
significant plasma leakage usually lasts 24–48
hours. Progressive leukopenia followed by a
rapid decrease in platelet count usually precedes
plasma leakage.
Pleural effusion and ascites may be clinically
detectable depending on the degree of plasma
leakage and the volume of fluid therapy.
Shock occurs when a critical volume of
plasma is lost. It is often preceded by
warning signs.
Mild haemorrhagic manifestations like
petechiae and mucosal membrane bleeding
may occurs. Massive bleeding may occur but
not common.
 With prolonged shock progressive organ
impairment, metabolic acidosis and DIC may
occurs.
 Severe organ impairment such as severe hepatitis,
encephalitis or myocarditis and/or severe bleeding
may also develop without obvious plasma leakage
or shock.
 Those who improve after defervescence are said to
have non-severe dengue. Those who deteriorate
will manifest with warning signs. This is called
dengue with warning signs. Some cases will
deteriorate to severe dengue.
Recovery phase
 A gradual reabsorption of extravascular
compartment fluid takes place in 2-3 days.
 General well-being, improves appetite returns,
gastrointestinal symptoms abate, haemodynamic
status stabilizes and diuresis ensues. Some
patients may have a rash of “isles of white in the
sea of red’’.
 Massive pleural effusion, Ascites, pulmonary
edema or CCF may occur at any time if excessive
intravenous fluids have been administered.
 The haematocrit stabilizes, White blood cell count
usually starts to rise but the recovery of platelet
count is typically later.
The course of dengue illness
Differential diagnosis of dengue fever
(febrile phase)
Flu-like syndromes--- Influenza, measles,
Chikungunya,
infectious mononucleosis ,
HIV seroconversion illness
Illnesses with a rash -- Rubella, measles, scarlet fever,
meningococcal infection,
Chikungunya, drug reactions
Diarrhoeal diseases -- Rotavirus, other enteric
infections
Illnesses with neurological
manifestations- ---- Meningo/encephalitis
Febrile seizures
Differential diagnosis of dengue fever
(critical phase )
Infectious---- Acute gastroenteritis, malaria, leptospirosis,
typhoid, typhus, viral hepatitis, acute HIV
seroconversion illness, bacterial sepsis,
septic shock
Malignancies---Acute leukaemia and other malignancies
Other clinical pictures
Acute abdomen( acute appendicitis, acute Cholecystitis,
perforated viscus), Diabetic ketoacidosis, Lactic acidosis,
Platelet disorders, Renal failure, Respiratory distress
(Kussmaul’s breathing), Systemic Lupus Erythematosus
APPROACH TO THE
MANAGEMENT OF
DENGUE
Step I—Overall assessment
History-- The history should include:
 date of onset of fever/illness;
 quantity of oral intake;
 assessment for warning signs.
 diarrhoea;
 seroconversion illness.
 change in mental state/seizure/dizziness;
 urine output (frequency, volume and time of last
voiding);
 Other relevant histories,--- such as family or
neighbourhood dengue, travel to dengue
endemic areas, co-existing conditions e.g.
infancy,
Physical examination-- should include:
assessment of mental state;
assessment of hydration status;
assessment of haemodynamic status
checking for 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).
INVESTIGATION
Complete blood count- Hb, TC, DLC, Platelet,
haematocrit, PBS study
A drop of platelet count <100000 cells/cumm
usullay found inbetween 3-10 days of illness.
A rise of haematocrit occurs in critcal phase
particularly in shock cases. Increase by 20%
or more is objective evidence of plasma
leakage. Haematocrit may become normal or
decrease if there is haemorrhage.
There is drop in tolal number of WBC and
neutrophil with relative lymphocytosis and
increase atypical lymphocyte towards the end
of febrile phase.
Additional tests when indicated include
 Liver function test—transaminase leve may be mildly
elevated.
Coagulation profile
Both APTT and PT may be prolong in severe
haemorrhagic manifestation.
Low fibrinogen and elevated fibrin degradation
product levels are signs of DIC.
Urea creatinine and serum electrolyte— ( Na+ K+ Ca2+
Bicaronate), lactate
BUN is elevated in prolong shock.
Hyponatremia is most common electrolyte
abnormality in DHS and DSS.
Hypocalcemia.
 Stool for occult blood-guaiac test.
 Hypoalbuminaemia
 Blood sugar.
 Cardiac enzyme and ECG
 Urine specific gravity.
 Chest x ray and USG.
Laboratory tests to confirm the
diagnosis.
Virus isolation
Viral nucleic acid detection(RT PCR).
NS1 antigen detection-
Serology
Haemoagglutination test.
Complement fixation test
Neutralization test
IgM capture-(MAC ELISA),
Indirect IgG ELISA
Within 5 days of illness
After 5 days of illness
 During the early stages of the disease, virus
isolation, nucleic acid or antigen detection can be
used to diagnose the infection.
 At the end of the acute phase of infection,
serology is the method of choice for diagnosis.
 To distinguish primary and secondary dengue
infections, IgM/IgG antibody ratios are now
more commonly used than the haemagglutination-
inhibition test (HI)
 NS1 antigen detection- NS1 antigen appears as
early as day 1 of life, hence used for early
diagnosis. Specificity is near 100% and sensitivity
in first 4 days of illness is 90% in primary and 70%
in secondary dengue.
 IgM/ IgG Ratios greater than 1.2 (using the
patient’s sera at 1/100 serum dilution) or 1.4
(using serum dilution of 1/20) suggest a
primary infection.
 IgG titres higher than 1/1280 by HIA or ELISA
are also suggestive of a secondary infection.
Step II—Diagnosis, assessment of disease
phase and severity
On the basis of evaluations of the history,
physical examination and/or full blood count
and haematocrit, determine whether the disease
is dengue, which phase it is in (febrile, critical
or recovery), whether there are warning signs,
the hydration and haemodynamic status of the
patient, and whether the patient requires
admission
CRITERIA FOR DENGUE ± WARNING SIGNS
CRITERIA FOR SEVERE DENGUE
Dengue Infection
symptomatic Asymptomatic
Mild
dengue
Severe
dengue
Mod
dengue
DF with risk factors
&co morbid condition
DF with warning signs
and symptoms
• Undifferentiat
ed DF
• Fever without
complication
• Without
capillary
leakage
• DF/DHF with
significant
hemorrhage
• DHF with
shock (DSS)
• Severe organ
involvement
• Severe met
disorder
• DF with
warning signs
and
symptoms
• DHF I and
DHF II with
minor bleeds
• Infants
• Haemoglobinop
athies
• Immunocomp
• Patients on
steroids,
anticoagulants
or
immunosuppres
ants
Home Mx Monitoring and possible hospitalization
Tertiary level
care
Admission criteria
• Any warning signs.
• Bleeding from any site independent of the platelet
count.
• Any signs of organ impairment--- renal, cardiac,
neurological or hepatic.
• Co existing condition ---peptic ulcer, haemolytic
anemias, Overweight or obese (rapid venous
access difficult in emergency), and Infancy.
• Sign and symptoms related to hypotension.
• Social circumstances-- Living far from health
facility, Without reliable means of transport.
• Findings through further investigations--Rising
haematocrit, Pleural effusion, ascites or
asymptomatic gall-bladder thickening.
Step III—Management
Disease notification
 In dengue-endemic countries, cases of
suspected, probable and confirmed
dengue should be notified as soon as
possible so that appropriate public health
measures can be initiated.
 Laboratory confirmation is not
necessary before notification, but
should be obtained.
Management decisions
Depending on the clinical manifestations
and other circumstances, patients may be
 Sent home (Group A),
 Be referred for in-hospital management
(Group B), or
 Require emergency treatment and
urgent referral (Group C).
Group A
Patients who do not have warning signs
AND
who are able:
 Totolerate adequate volumes of oral fluids
 Topassurine at least once every 6 hours
Action plan
 Oral intake of ORS, fruit juice and other fluids
containing electrolytes and sugar. Plain water alone
may cause electrolyte imbalance.
 Paracetamol for high fever. Tepid sponge if the
patient still has high fever.
 Avoid acetylsalicylic acid (aspirin), ibuprofen or
other NSAIDs as these drugs may aggravate
gastritis or bleeding. Acetylsalicylic acid (aspirin)
may be associated with Reye’s Syndrome.
Instruction for the care-givers
• no clinical improvement,
• deterioration around the time of
defervescence,
• severe abdominal pain,
• persistent vomiting,
• cold and clammy extremities,
• lethargy or irritability/restlessness,
• bleeding,
• not passing urine for more than 4–6 hours.
MONITORING daily for
temperature pattern,
volume of fluid intake and losses,
urine output (volume and frequency),
warning signs,
signs of plasma leakage and bleeding,
haematocrit, and white blood cell and
platelet counts.
Group B –
Patients with
• warning signs,
• co-existing conditions ( infancy, obesity,
renal failure, chronic haemolytic
diseases), and
• certain social circumstances (living far
from a health facility without reliable
means of transport).
DENGUE FEVER WITH RISK FACTOR
RL 7 ml/kg/hr
Assessment at 1 hours
Discharge when stable
for 24-48 hrs
RL 3 ml/kg/hr
Further improvement
RL 5ml/kg/hr
improvement
RL 15 ml/kg/hr
No improvement
No improvement
RL 10 ml/kg/hr
Assessment at 2 hours
Look for aneamia, acidosis, and myocardial dysfunction
No improvement
Colloids 10 ml/kg/hr
Continue IVF until table
for 24 hs
No improvement
Assessment at 3 hrs
• Patients may be able to take oral fluids
after a few hours of intravenous fluid
therapy. Thus, it is necessary to revise the
fluid infusion frequently.
• For infants < 6 months old, D5 0.45 NaCI
is preferable if available (D5 0.45 NaCI is
prepared by mixing equal volumes of D5
0.9 NaCL and D5W.
Monitor
• vital signs and peripheral perfusion (1–4
hourly until the patient is out of the critical
phase),
• urine output (4–6 hourly),
• haematocrit (before and after fluid
replacement, then 6–12 hourly),
• blood glucose, and other organ functions
(such as renal profile, liver profile,
coagulation profile, as indicated).
Group C
• severe plasma leakage leading to dengue
shock and/or fluid accumulation with
respiratory distress;
• severe haemorrhages;
• severe organ impairment (hepatic
damage, renal impairment,
cardiomyopathy, encephalopathy or
encephalitis).
FLUID MANAGEMENT
IN SHOCK
Choice of IVF for resuscitation
• Crystalloids (Ringer's lactate or 0.9 NaCI solutions)
have been shown to be safe and as effective as
colloid solutions (dextran, starch, or gelatin) in
reducing the recurrence of shock and mortality.
• Crystalloids should be used as first line in fluid
resuscitation in compensated dengue shock.
• Colloids have been shown to restore the cardiac
index and reduce the level of haematocrit faster
than crystalloids in patients with intractable shock.
colloids may be the preferred choice if the blood
pressure has to be restored urgently, i.e. in those
with pulse pressure less than 10 mm Hg.
Normal Saline
 0.9% Saline is a suitable option for initial
fluid resuscitation, but repeated large
volumes of 0.9% saline may lead to
hyperchloraemic acidosis.
 Hyperchloraemic acidosis may aggravate
or be confused with lactic acidosis from
prolonged shock.
 Monitoring the chloride and lactate levels
will help to identify this problem. When serum
chloride level exceeds the normal range, it is
advisable to change to other alternatives
such as Ringer’s Lactate.
Ringer’s Lactate
 Ringer’s Lactate has lower sodium (131
mmol/L) and chloride (115 mmol/L) contents
and an osmolality of 273 mOsm/L.
 It is not be suitable for resuscitation of
patients with severe hyponatremia. However, it
is a suitable solution after 0.9 Saline has been
given and the serum chloride level has
exceeded the normal range.
 Ringer’s Lactate should probably be
avoided in liver failure.
Colloids
 The types of colloids are gelatin-based,
dextran-based and starch-based solutions.
 Of all the colloids, gelatine has the least
effect on coagulation but the highest risk of
allergic reactions.
 Allergic reactions such as fever, chills and
rigors have also been observed in Dextran
70.
 Dextran 40 can potentially cause an
osmotic renal injury in hypovolaemic patients.
Assessment of improvement
Compensated Shock
(Systolic Pressure maintained + signs of reduced perfusion)
Start isotonic crystalloid^
10-20 mL/kg/hr for 1 hour
IV crystalloid, reduce gradually 10
mL/kg/hr for 1-2 hrs
7 mL/kg/hr for 2 hrs
5 ml/ kg/hr for 4 hrs
3mL/kg/hr
As clinical improvement is noted,
reduce fluids accordingly
Further boluses may be needed for
the next 24- 48 hrs
Stop IV fluids at 48 hrs
IMPROVEMENT*
Check HCT
Crytalloid (2nd bolus ) or colloid 10-
20 mL/kg/hr for 1 hr
IMPROVEMENT*
Reduce IV crystalloids 7-10 mL /kg/hr
for 1-2 hours
Severe
overt bleed
Urgent blood
transfusion
Colloid 10-20
mL/kg/hr
.evaluate to
consider blood
transfusion if no
clinical
improvement
^ Colloid is preferable if the patient has already received previous boluses of crystalloid
*Reasses the patient’s clinical condition, vital signs, pulse volume, CRT and temp of extremities
IV: intravenous, HCT : haematocrit,↑ : increased ,↓ : decreased
YES
NO
YES
NO
HCT↑
HCT↓
YES NO
Hypotensive shock
• Patients with dengue shock should be frequently
monitored until the danger period is over.
• A detailed fluid balance of all input and output
should be maintained.
• Parameters that should be monitored include vital
signs and peripheral perfusion (every 15–30
minutes until the patient is out of shock, then 1–2
hourly).
• In general, the higher the fluid infusion rate, the
more
frequently the patient should be monitored and
reviewed in order to avoid fluid overload while
ensuring adequate volume replacement.
Hypotensive Shock
Try to obtain an HCT level before fluid resuscitation
Start isotonic crystalloid or colloid^
20mL/kg over 15-30 mins
IV crystalloid or colloid 10mL
/kg/hr for 1 hour
IV colloid 10 mL/kg/hr for 1 hour
reduce gradually
7.5 mL/kg/hr for 2 hrs
5 mL/kg/hr for 4 hrs
3 ml/ kg/hr for 4 hours which can
continue till 24- 48 hours
As clinical improvement is noted,
reduce fluids accordingly
Stop IV fluids at 48 hrs
IMPROVEMENT*
Check HCT
IV Crytalloid /colloid^ (2nd bolus) or
colloid
10 mL/kg/hr for 30-60 min
IMPROVEMENT*
Reduce IV crystalloids 7-10 mL /kg/hr
for 1-2 hours
Severe
overt bleed
Urgent blood
transfusion
Colloid 10-20
mL/kg/hr
.evaluate to
consider blood
transfusion if no
clinical
improvement
^ Colloid is preferable if the patient has already received previous boluses of crystalloid
*Reasses the patient’s clinical condition, vital signs, pulse volume, CRT and temp of extremities
IV: intravenous, HCT : haematocrit,↑ : increased ,↓ : decreased
YES
NO
YES
NO
HCT↑
HCT↓
YES NO
Treatment of haemorrhagic complications
Mucosal bleeding may occur in any patient with
dengue but, if the patient remains stable with
fluid resuscitation/replacement, it should be
considered as minor. In patients with profound
thrombocytopaenia,
 ensure strict bed rest and
 protect from trauma to reduce the risk of
bleeding.
 Do not give intramuscular injections to avoid
haematoma.
prophylactic platelet transfusions for severe
thrombocytopaenia in otherwise hemodynamically
stable patients have not been shown to be
effective and are not necessary.
Risk of major bleeding
• have prolonged/refractory shock;
• have hypotensive shock and renal or liver
failure and/or severe and persistent metabolic
acidosis;
• are given non-steroidal anti-inflammatory
agents;
• have pre-existing peptic ulcer disease;
• are on anticoagulant therapy;
• have any form of trauma, including
intramuscular injection.
Severe bleeding can be recognized by:
• a decrease in haematocrit after 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 low/normal
haematocrit before fluid resuscitation;
Action plan
 Give 5–10ml/kg of fresh-packed red cells or
10–20 ml/kg of fresh whole blood at an
appropriate rate and observe the clinical
response. It is important that fresh whole
blood or fresh red cells are given.
 Consider repeating the blood transfusion if
there is further blood loss or no
appropriate rise in haematocrit after blood
transfusion.
 Transfuse platelet concentrates when
massive bleeding can not be managed with
just fresh whole blood/fresh-packed cells.
Causes of fluid overload :-
excessive and/or too rapid intravenous fluids;
incorrect use of hypotonic;
inappropriate use of large volumes of IVF in
patients with unrecognized severe bleeding;
inappropriate transfusion of fresh-frozen plasma,
platelet concentrates and cryoprecipitates;
continuation of IVF after plasma leakage has
resolved;
co-morbid conditions such as congenital heart
disease.
Treatment of Fluid overload
Early signs fluid overload :
– respiratory distress, difficulty in breathing;
– rapid breathing;
– chest wall in-drawing;
– wheezing;
– large pleural effusions;
– tense ascites;
– increased jugular venous pressure (JVP).
Late signs fluid overload :
– pulmonary oedema (cough with pink or frothy
sputum ± crepitations, cyanosis);
– irreversible shock (heart failure, often in
combination with ongoing hypovolaemia).
Treatment of fluid overload (cont.)
 Oxygen therapy should be given immediately.
 If the patient has stable haemodynamic status and
is out of the critical phase, discontinue IVF. If
necessary, give oral or intravenous furosemide.
 If the patient has stable haemodynamic status but
is still within the critical phase, reduce the intravenous
fluid accordingly.
 Avoid diuretics during the plasma leakage phase.
 If in shock despite clinical signs and symptoms of
fluid overload Give 10ml/kg/hr of colloid. Once with BP
is stable, administer IV furosemide 0.5 to 1mg/kg/dose;
 If BP is unstable, check ABCS and other electrolyte
imbalance.
Cardiac complication
 Cardiac involvement may be seen during the
period of shock and convalescence.
 Variable manifestations may be seen from
myocarditis, arrhythmias to evidence of systolic
or diastolic dysfunction presenting as heart
failure and/or shock.
 Investigation should include an
echocardiogram, ECG, chest x-ray and CPKMB.
Management of Myocardial dysfunction.
• Systolic dysfunction should be treated with
inotropes like dopamine, dobutamine or their
combination and diastolic dysfunction should be
treated with milrinone.
• fluids should be computed 50-75% of maintenance
depending on the degree of heart failure.
• In patients with uncompensated shock due to
hypovolemia but with heart failure, the
recommendation for fluid boluses should be
followed.
• At any point if fluid overload is considered,
furosemide should be given once BP is stable.
Management of myocarditis
 If DF or DHF is complicated by myocarditis in the
convalescent phase, bed rest is recommended. In
addition, physical activity after discharge is restricted
anywhere from 2 to 4 weeks up to 6 months depending
on severity of the myocarditis .
Management of Cardiac Arrhythmias
 During the period of convalescence, variable
arrhythmias observed range from sinus node
dysfunction (sinus bradycardia, junctional rhythm),
conduction abnormalities like first degree AV block,
Wencheback.
 In patients with cardiac arrhythmia but with no signs of
heart failure, Usually no treatment is needed.
Other complications of dengue
 Electrolyte and acid-base imbalances are also
common observations in severe dengue and
are probably related to gastrointestinal losses
through vomiting and diarrhoea or to the use of
hypotonic solutions for resuscitation and
correction of dehydration.
 Hyponatraemia, hypokalaemia, hyperkalaemia,
serum calcium imbalances and metabolic
acidosis can occur.
 Patients who present with convulsion and/or
coma may have Encephalopathy
Laboratory Investigations (ABCS) for patients who present with profound shock
or have complications, and in cases with no clinical improvement inspite of
adequate volume replacement
Criteria for discharge
All of the following must be present:
A. Clinical
•No fever for 48 hrs
•Improvement in clinical status (general well-being,
appetite, hemodynamic status, urine output, no
respiratory distress).
•Minimum of 2-3 days have elapsed after recovery
from shock
B. Laboratory
• Increasing trend of platelet count. (> 50000/cumm)
• Stable hematocrit without IVF.
REFERENCES
• WHO guidelines for diagnosis, treatment,
prevention and control.
• NVDCP guidelines for clinical management of
dengue fever, dengue haemorrhagic fever
and dengue shock syndrome.
• Immunopathogenesis of dengue virus
infection journal.
• Nelson Textbook of PEDIATRICS(19th
edition).
• IAP guidelines for management of dengue
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dengue diagnosis and management

  • 1. SEMINAR ON DENGUE FEVER DIAGNOSIS AND MANAGEMENT MODERATOR PRESENTER DR. D. KALITA NISHANT AGARWAL ASST. PROF. PGT DEPARTMENT OF PEDIATRICS, GMCH.
  • 2. INTRODUCTION  Dengue is a self limiting acute mosquito transmitted disease characterized by fever , headache, muscle, joint pains, rash, nausea and vomiting.  The dengue viruses are the members of the genus flavi virus. There are four virus serotypes of which DEN1 and DEN2 widespread in India.  Dengue viruses are transmitted by the bite of female Aedes (Ae) mosquitoes. other species such as Ae albopictus, Ae. polynesiensis and Ae. Niveus may also transmit dengue.
  • 3.  All ages and both sexes are susceptible to dengue fever .  Infected person can transmit the virus to the mosquito 1 day before onset of febrile episode and remain infectious for next 6-7 days.  Migration of patient during viremia to a non endemic area may introduce it into the area.
  • 4. CLINICAL CLASSIFICATION (old) 1. Dengue Fever : An acute febrile illness of 2-7 days duration with two or more of the following manifestations: Headache, retro-orbital pain, myalgia, arthralgia, rash, haemorrhagic manifestations.
  • 5. 2. Dengue Haemorrhagic Fever : a). A probable or confirmed case of dengue PLUS b). Haemorrhagic tendencies evidenced by one or more of the following –  Positive tourniquet test.  Petechiae, ecchymoses or purpura.  Bleeding from mucosa, gastrointestinal tract, injection sites or other sites.  Haematemesis or malena PLUS
  • 6. c). Thrombocytopenia (<100,000 cells per cumm) PLUS d). Evidence of plasma leakage  A rise in average haematocrit for age and sex >/= 20%.  A more than 20% drop in haematocrit following volume replacement treatment compared to baseline.  Signs of plasma leakage (pleural effusion, ascites , hypoproteinemia).
  • 7. 3. Dengue Shock Syndrome : All the above criteria for DHF PLUS Evidence of circulatory failure manifested by rapid and weak pulse and narrow pulse pressure (<20 mm Hg) or hypotension for age, cold and clammy skin and restlessness.
  • 8. • Grading of Dengue Fever • DF : Fever of 2-7 days with two or more of the following: • Headache • Retro orbital pain • Myalgia • Arthralgia with or without leukopenia • Thrombocytopenia and no evidence of plasma leakage • DHF I: above criteria plus tourniquet test and evidence of plasma leakage. Thrombocytopenia with platelet count less than 100000/ cumm and Hct rise more than 20% over baseline.
  • 9. • Grading of Dengue Fever(contd) • DHF II : above plus some evidence of spontaneous bleeding in skin or other organs (black tarry stool, epistaxis, gum bleeds) and abdominal pain. Thrombocytopenia with platelet count less than 100000/ cumm and Hct rise more than 20% over baseline. • DHF III (DSS): Above plus circulatory failure. Thrombocytopenia with platelet count less than 100000/ cumm and Hct rise more than 20% over baseline.
  • 10. • Grading of Dengue Fever(contd.) • DHF IV : Profound shock with undetectable blood pressure or pulse. Thrombocytopenia with platelet count less than 100000/ cumm and Hct rise more than 20% over baseline.
  • 11. THE TOURNIQUET TEST Is performed by inflating a blood pressure cuff to a midpoint between the systolic and diastolic pressure for five minutes. The test is considered positive when 10 or more petechiae per square inch over the forearm. • In DHF , the test usually gives a definite positive test with 20 petechiae or more. • The test may be negative or only mildly positive during the phase of profound shock (DSS). If tourniquet test is found negative it should be repeated. • Early diagnosis of disease and admission of DHF patients in hospitals are important in order to reduce case fatality rates.
  • 12. Dengue Infection symptomatic Asymptomatic Mild dengue Severe dengue Mod dengue DF with risk factors &co morbid condition DF with warning signs and symptoms • Undifferentiat ed DF • Fever without complication • Without capillary leakage • DF/DHF with significant hemorrhage • DHF with shock (DSS) • Severe organ involvement • Severe met disorder • DF with warning signs and symptoms • DHF I and DHF II with minor bleeds • Infants • Haemoglobinop athies • Immunocomp • Patients on steroids, anticoagulants or immunosuppres ants
  • 13. PATHOGENESIS  Binding of the new virus to cross reactive non neutralising antibody from the previous infection or passively acquired antibodies in infant facilitating the uptake by mononuclear phagocytes  This enable amplified viral replication (ADE)the resulting increase in viral load then drives an immuno pathogenic cascade.  The resultant exaggerated cytokine response leads to a transient increase microvascular permeability as well as activation of the coagulating system.
  • 14.
  • 15.
  • 16. THE COURSE OF DENGUE ILLNESS Febrile phase—  High-grade fever for 2-7 days with facial flushing, skin erythema, generalized body ache, myalgia, arthralgia and headache.  Some patients may have sore throat, injected pharynx and conjunctival injection, Anorexia, nausea and vomiting  Rash may be seen on the 3rd or 4th day which may be rubelliform or maculopapular in nature.  difficult to distinguish dengue clinically from non- dengue febrile diseases.  clinical features are indistinguishable between severe and non-severe dengue cases.
  • 17. Critical phase Temperature drops, Increase capillary permeability in parallel with increasing haematocrit levels. significant plasma leakage usually lasts 24–48 hours. Progressive leukopenia followed by a rapid decrease in platelet count usually precedes plasma leakage. Pleural effusion and ascites may be clinically detectable depending on the degree of plasma leakage and the volume of fluid therapy.
  • 18. Shock occurs when a critical volume of plasma is lost. It is often preceded by warning signs. Mild haemorrhagic manifestations like petechiae and mucosal membrane bleeding may occurs. Massive bleeding may occur but not common.  With prolonged shock progressive organ impairment, metabolic acidosis and DIC may occurs.
  • 19.  Severe organ impairment such as severe hepatitis, encephalitis or myocarditis and/or severe bleeding may also develop without obvious plasma leakage or shock.  Those who improve after defervescence are said to have non-severe dengue. Those who deteriorate will manifest with warning signs. This is called dengue with warning signs. Some cases will deteriorate to severe dengue.
  • 20. Recovery phase  A gradual reabsorption of extravascular compartment fluid takes place in 2-3 days.  General well-being, improves appetite returns, gastrointestinal symptoms abate, haemodynamic status stabilizes and diuresis ensues. Some patients may have a rash of “isles of white in the sea of red’’.  Massive pleural effusion, Ascites, pulmonary edema or CCF may occur at any time if excessive intravenous fluids have been administered.  The haematocrit stabilizes, White blood cell count usually starts to rise but the recovery of platelet count is typically later.
  • 21. The course of dengue illness
  • 22. Differential diagnosis of dengue fever (febrile phase) Flu-like syndromes--- Influenza, measles, Chikungunya, infectious mononucleosis , HIV seroconversion illness Illnesses with a rash -- Rubella, measles, scarlet fever, meningococcal infection, Chikungunya, drug reactions Diarrhoeal diseases -- Rotavirus, other enteric infections Illnesses with neurological manifestations- ---- Meningo/encephalitis Febrile seizures
  • 23. Differential diagnosis of dengue fever (critical phase ) Infectious---- Acute gastroenteritis, malaria, leptospirosis, typhoid, typhus, viral hepatitis, acute HIV seroconversion illness, bacterial sepsis, septic shock Malignancies---Acute leukaemia and other malignancies Other clinical pictures Acute abdomen( acute appendicitis, acute Cholecystitis, perforated viscus), Diabetic ketoacidosis, Lactic acidosis, Platelet disorders, Renal failure, Respiratory distress (Kussmaul’s breathing), Systemic Lupus Erythematosus
  • 25. Step I—Overall assessment History-- The history should include:  date of onset of fever/illness;  quantity of oral intake;  assessment for warning signs.  diarrhoea;  seroconversion illness.
  • 26.  change in mental state/seizure/dizziness;  urine output (frequency, volume and time of last voiding);  Other relevant histories,--- such as family or neighbourhood dengue, travel to dengue endemic areas, co-existing conditions e.g. infancy,
  • 27. Physical examination-- should include: assessment of mental state; assessment of hydration status; assessment of haemodynamic status checking for 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).
  • 28. INVESTIGATION Complete blood count- Hb, TC, DLC, Platelet, haematocrit, PBS study A drop of platelet count <100000 cells/cumm usullay found inbetween 3-10 days of illness. A rise of haematocrit occurs in critcal phase particularly in shock cases. Increase by 20% or more is objective evidence of plasma leakage. Haematocrit may become normal or decrease if there is haemorrhage. There is drop in tolal number of WBC and neutrophil with relative lymphocytosis and increase atypical lymphocyte towards the end of febrile phase.
  • 29. Additional tests when indicated include  Liver function test—transaminase leve may be mildly elevated. Coagulation profile Both APTT and PT may be prolong in severe haemorrhagic manifestation. Low fibrinogen and elevated fibrin degradation product levels are signs of DIC. Urea creatinine and serum electrolyte— ( Na+ K+ Ca2+ Bicaronate), lactate BUN is elevated in prolong shock. Hyponatremia is most common electrolyte abnormality in DHS and DSS. Hypocalcemia.
  • 30.  Stool for occult blood-guaiac test.  Hypoalbuminaemia  Blood sugar.  Cardiac enzyme and ECG  Urine specific gravity.  Chest x ray and USG.
  • 31. Laboratory tests to confirm the diagnosis. Virus isolation Viral nucleic acid detection(RT PCR). NS1 antigen detection- Serology Haemoagglutination test. Complement fixation test Neutralization test IgM capture-(MAC ELISA), Indirect IgG ELISA Within 5 days of illness After 5 days of illness
  • 32.
  • 33.  During the early stages of the disease, virus isolation, nucleic acid or antigen detection can be used to diagnose the infection.  At the end of the acute phase of infection, serology is the method of choice for diagnosis.  To distinguish primary and secondary dengue infections, IgM/IgG antibody ratios are now more commonly used than the haemagglutination- inhibition test (HI)  NS1 antigen detection- NS1 antigen appears as early as day 1 of life, hence used for early diagnosis. Specificity is near 100% and sensitivity in first 4 days of illness is 90% in primary and 70% in secondary dengue.
  • 34.  IgM/ IgG Ratios greater than 1.2 (using the patient’s sera at 1/100 serum dilution) or 1.4 (using serum dilution of 1/20) suggest a primary infection.  IgG titres higher than 1/1280 by HIA or ELISA are also suggestive of a secondary infection.
  • 35.
  • 36. Step II—Diagnosis, assessment of disease phase and severity On the basis of evaluations of the history, physical examination and/or full blood count and haematocrit, determine whether the disease is dengue, which phase it is in (febrile, critical or recovery), whether there are warning signs, the hydration and haemodynamic status of the patient, and whether the patient requires admission
  • 37. CRITERIA FOR DENGUE ± WARNING SIGNS
  • 39. Dengue Infection symptomatic Asymptomatic Mild dengue Severe dengue Mod dengue DF with risk factors &co morbid condition DF with warning signs and symptoms • Undifferentiat ed DF • Fever without complication • Without capillary leakage • DF/DHF with significant hemorrhage • DHF with shock (DSS) • Severe organ involvement • Severe met disorder • DF with warning signs and symptoms • DHF I and DHF II with minor bleeds • Infants • Haemoglobinop athies • Immunocomp • Patients on steroids, anticoagulants or immunosuppres ants Home Mx Monitoring and possible hospitalization Tertiary level care
  • 40. Admission criteria • Any warning signs. • Bleeding from any site independent of the platelet count. • Any signs of organ impairment--- renal, cardiac, neurological or hepatic. • Co existing condition ---peptic ulcer, haemolytic anemias, Overweight or obese (rapid venous access difficult in emergency), and Infancy. • Sign and symptoms related to hypotension. • Social circumstances-- Living far from health facility, Without reliable means of transport. • Findings through further investigations--Rising haematocrit, Pleural effusion, ascites or asymptomatic gall-bladder thickening.
  • 41. Step III—Management Disease notification  In dengue-endemic countries, cases of suspected, probable and confirmed dengue should be notified as soon as possible so that appropriate public health measures can be initiated.  Laboratory confirmation is not necessary before notification, but should be obtained.
  • 42. Management decisions Depending on the clinical manifestations and other circumstances, patients may be  Sent home (Group A),  Be referred for in-hospital management (Group B), or  Require emergency treatment and urgent referral (Group C).
  • 43. Group A Patients who do not have warning signs AND who are able:  Totolerate adequate volumes of oral fluids  Topassurine at least once every 6 hours
  • 44. Action plan  Oral intake of ORS, fruit juice and other fluids containing electrolytes and sugar. Plain water alone may cause electrolyte imbalance.  Paracetamol for high fever. Tepid sponge if the patient still has high fever.  Avoid acetylsalicylic acid (aspirin), ibuprofen or other NSAIDs as these drugs may aggravate gastritis or bleeding. Acetylsalicylic acid (aspirin) may be associated with Reye’s Syndrome.
  • 45. Instruction for the care-givers • no clinical improvement, • deterioration around the time of defervescence, • severe abdominal pain, • persistent vomiting, • cold and clammy extremities, • lethargy or irritability/restlessness, • bleeding, • not passing urine for more than 4–6 hours.
  • 46. MONITORING daily for temperature pattern, volume of fluid intake and losses, urine output (volume and frequency), warning signs, signs of plasma leakage and bleeding, haematocrit, and white blood cell and platelet counts.
  • 47. Group B – Patients with • warning signs, • co-existing conditions ( infancy, obesity, renal failure, chronic haemolytic diseases), and • certain social circumstances (living far from a health facility without reliable means of transport).
  • 48. DENGUE FEVER WITH RISK FACTOR RL 7 ml/kg/hr Assessment at 1 hours Discharge when stable for 24-48 hrs RL 3 ml/kg/hr Further improvement RL 5ml/kg/hr improvement RL 15 ml/kg/hr No improvement No improvement RL 10 ml/kg/hr Assessment at 2 hours Look for aneamia, acidosis, and myocardial dysfunction No improvement Colloids 10 ml/kg/hr Continue IVF until table for 24 hs No improvement Assessment at 3 hrs
  • 49. • Patients may be able to take oral fluids after a few hours of intravenous fluid therapy. Thus, it is necessary to revise the fluid infusion frequently. • For infants < 6 months old, D5 0.45 NaCI is preferable if available (D5 0.45 NaCI is prepared by mixing equal volumes of D5 0.9 NaCL and D5W.
  • 50. Monitor • vital signs and peripheral perfusion (1–4 hourly until the patient is out of the critical phase), • urine output (4–6 hourly), • haematocrit (before and after fluid replacement, then 6–12 hourly), • blood glucose, and other organ functions (such as renal profile, liver profile, coagulation profile, as indicated).
  • 51. Group C • severe plasma leakage leading to dengue shock and/or fluid accumulation with respiratory distress; • severe haemorrhages; • severe organ impairment (hepatic damage, renal impairment, cardiomyopathy, encephalopathy or encephalitis).
  • 53. Choice of IVF for resuscitation • Crystalloids (Ringer's lactate or 0.9 NaCI solutions) have been shown to be safe and as effective as colloid solutions (dextran, starch, or gelatin) in reducing the recurrence of shock and mortality. • Crystalloids should be used as first line in fluid resuscitation in compensated dengue shock. • Colloids have been shown to restore the cardiac index and reduce the level of haematocrit faster than crystalloids in patients with intractable shock. colloids may be the preferred choice if the blood pressure has to be restored urgently, i.e. in those with pulse pressure less than 10 mm Hg.
  • 54. Normal Saline  0.9% Saline is a suitable option for initial fluid resuscitation, but repeated large volumes of 0.9% saline may lead to hyperchloraemic acidosis.  Hyperchloraemic acidosis may aggravate or be confused with lactic acidosis from prolonged shock.  Monitoring the chloride and lactate levels will help to identify this problem. When serum chloride level exceeds the normal range, it is advisable to change to other alternatives such as Ringer’s Lactate.
  • 55. Ringer’s Lactate  Ringer’s Lactate has lower sodium (131 mmol/L) and chloride (115 mmol/L) contents and an osmolality of 273 mOsm/L.  It is not be suitable for resuscitation of patients with severe hyponatremia. However, it is a suitable solution after 0.9 Saline has been given and the serum chloride level has exceeded the normal range.  Ringer’s Lactate should probably be avoided in liver failure.
  • 56. Colloids  The types of colloids are gelatin-based, dextran-based and starch-based solutions.  Of all the colloids, gelatine has the least effect on coagulation but the highest risk of allergic reactions.  Allergic reactions such as fever, chills and rigors have also been observed in Dextran 70.  Dextran 40 can potentially cause an osmotic renal injury in hypovolaemic patients.
  • 58. Compensated Shock (Systolic Pressure maintained + signs of reduced perfusion) Start isotonic crystalloid^ 10-20 mL/kg/hr for 1 hour IV crystalloid, reduce gradually 10 mL/kg/hr for 1-2 hrs 7 mL/kg/hr for 2 hrs 5 ml/ kg/hr for 4 hrs 3mL/kg/hr As clinical improvement is noted, reduce fluids accordingly Further boluses may be needed for the next 24- 48 hrs Stop IV fluids at 48 hrs IMPROVEMENT* Check HCT Crytalloid (2nd bolus ) or colloid 10- 20 mL/kg/hr for 1 hr IMPROVEMENT* Reduce IV crystalloids 7-10 mL /kg/hr for 1-2 hours Severe overt bleed Urgent blood transfusion Colloid 10-20 mL/kg/hr .evaluate to consider blood transfusion if no clinical improvement ^ Colloid is preferable if the patient has already received previous boluses of crystalloid *Reasses the patient’s clinical condition, vital signs, pulse volume, CRT and temp of extremities IV: intravenous, HCT : haematocrit,↑ : increased ,↓ : decreased YES NO YES NO HCT↑ HCT↓ YES NO
  • 59. Hypotensive shock • Patients with dengue shock should be frequently monitored until the danger period is over. • A detailed fluid balance of all input and output should be maintained. • Parameters that should be monitored include vital signs and peripheral perfusion (every 15–30 minutes until the patient is out of shock, then 1–2 hourly). • In general, the higher the fluid infusion rate, the more frequently the patient should be monitored and reviewed in order to avoid fluid overload while ensuring adequate volume replacement.
  • 60. Hypotensive Shock Try to obtain an HCT level before fluid resuscitation Start isotonic crystalloid or colloid^ 20mL/kg over 15-30 mins IV crystalloid or colloid 10mL /kg/hr for 1 hour IV colloid 10 mL/kg/hr for 1 hour reduce gradually 7.5 mL/kg/hr for 2 hrs 5 mL/kg/hr for 4 hrs 3 ml/ kg/hr for 4 hours which can continue till 24- 48 hours As clinical improvement is noted, reduce fluids accordingly Stop IV fluids at 48 hrs IMPROVEMENT* Check HCT IV Crytalloid /colloid^ (2nd bolus) or colloid 10 mL/kg/hr for 30-60 min IMPROVEMENT* Reduce IV crystalloids 7-10 mL /kg/hr for 1-2 hours Severe overt bleed Urgent blood transfusion Colloid 10-20 mL/kg/hr .evaluate to consider blood transfusion if no clinical improvement ^ Colloid is preferable if the patient has already received previous boluses of crystalloid *Reasses the patient’s clinical condition, vital signs, pulse volume, CRT and temp of extremities IV: intravenous, HCT : haematocrit,↑ : increased ,↓ : decreased YES NO YES NO HCT↑ HCT↓ YES NO
  • 61. Treatment of haemorrhagic complications Mucosal bleeding may occur in any patient with dengue but, if the patient remains stable with fluid resuscitation/replacement, it should be considered as minor. In patients with profound thrombocytopaenia,  ensure strict bed rest and  protect from trauma to reduce the risk of bleeding.  Do not give intramuscular injections to avoid haematoma. prophylactic platelet transfusions for severe thrombocytopaenia in otherwise hemodynamically stable patients have not been shown to be effective and are not necessary.
  • 62. Risk of major bleeding • have prolonged/refractory shock; • have hypotensive shock and renal or liver failure and/or severe and persistent metabolic acidosis; • are given non-steroidal anti-inflammatory agents; • have pre-existing peptic ulcer disease; • are on anticoagulant therapy; • have any form of trauma, including intramuscular injection.
  • 63. Severe bleeding can be recognized by: • a decrease in haematocrit after 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 low/normal haematocrit before fluid resuscitation;
  • 64. Action plan  Give 5–10ml/kg of fresh-packed red cells or 10–20 ml/kg of fresh whole blood at an appropriate rate and observe the clinical response. It is important that fresh whole blood or fresh red cells are given.  Consider repeating the blood transfusion if there is further blood loss or no appropriate rise in haematocrit after blood transfusion.  Transfuse platelet concentrates when massive bleeding can not be managed with just fresh whole blood/fresh-packed cells.
  • 65. Causes of fluid overload :- excessive and/or too rapid intravenous fluids; incorrect use of hypotonic; inappropriate use of large volumes of IVF in patients with unrecognized severe bleeding; inappropriate transfusion of fresh-frozen plasma, platelet concentrates and cryoprecipitates; continuation of IVF after plasma leakage has resolved; co-morbid conditions such as congenital heart disease. Treatment of Fluid overload
  • 66. Early signs fluid overload : – respiratory distress, difficulty in breathing; – rapid breathing; – chest wall in-drawing; – wheezing; – large pleural effusions; – tense ascites; – increased jugular venous pressure (JVP). Late signs fluid overload : – pulmonary oedema (cough with pink or frothy sputum ± crepitations, cyanosis); – irreversible shock (heart failure, often in combination with ongoing hypovolaemia).
  • 67. Treatment of fluid overload (cont.)  Oxygen therapy should be given immediately.  If the patient has stable haemodynamic status and is out of the critical phase, discontinue IVF. If necessary, give oral or intravenous furosemide.  If the patient has stable haemodynamic status but is still within the critical phase, reduce the intravenous fluid accordingly.  Avoid diuretics during the plasma leakage phase.  If in shock despite clinical signs and symptoms of fluid overload Give 10ml/kg/hr of colloid. Once with BP is stable, administer IV furosemide 0.5 to 1mg/kg/dose;  If BP is unstable, check ABCS and other electrolyte imbalance.
  • 68. Cardiac complication  Cardiac involvement may be seen during the period of shock and convalescence.  Variable manifestations may be seen from myocarditis, arrhythmias to evidence of systolic or diastolic dysfunction presenting as heart failure and/or shock.  Investigation should include an echocardiogram, ECG, chest x-ray and CPKMB.
  • 69. Management of Myocardial dysfunction. • Systolic dysfunction should be treated with inotropes like dopamine, dobutamine or their combination and diastolic dysfunction should be treated with milrinone. • fluids should be computed 50-75% of maintenance depending on the degree of heart failure. • In patients with uncompensated shock due to hypovolemia but with heart failure, the recommendation for fluid boluses should be followed. • At any point if fluid overload is considered, furosemide should be given once BP is stable.
  • 70. Management of myocarditis  If DF or DHF is complicated by myocarditis in the convalescent phase, bed rest is recommended. In addition, physical activity after discharge is restricted anywhere from 2 to 4 weeks up to 6 months depending on severity of the myocarditis . Management of Cardiac Arrhythmias  During the period of convalescence, variable arrhythmias observed range from sinus node dysfunction (sinus bradycardia, junctional rhythm), conduction abnormalities like first degree AV block, Wencheback.  In patients with cardiac arrhythmia but with no signs of heart failure, Usually no treatment is needed.
  • 71. Other complications of dengue  Electrolyte and acid-base imbalances are also common observations in severe dengue and are probably related to gastrointestinal losses through vomiting and diarrhoea or to the use of hypotonic solutions for resuscitation and correction of dehydration.  Hyponatraemia, hypokalaemia, hyperkalaemia, serum calcium imbalances and metabolic acidosis can occur.  Patients who present with convulsion and/or coma may have Encephalopathy
  • 72. Laboratory Investigations (ABCS) for patients who present with profound shock or have complications, and in cases with no clinical improvement inspite of adequate volume replacement
  • 73. Criteria for discharge All of the following must be present: A. Clinical •No fever for 48 hrs •Improvement in clinical status (general well-being, appetite, hemodynamic status, urine output, no respiratory distress). •Minimum of 2-3 days have elapsed after recovery from shock B. Laboratory • Increasing trend of platelet count. (> 50000/cumm) • Stable hematocrit without IVF.
  • 74. REFERENCES • WHO guidelines for diagnosis, treatment, prevention and control. • NVDCP guidelines for clinical management of dengue fever, dengue haemorrhagic fever and dengue shock syndrome. • Immunopathogenesis of dengue virus infection journal. • Nelson Textbook of PEDIATRICS(19th edition). • IAP guidelines for management of dengue MISSION UDAY