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PITFALLS IN THE MANAGEMENT
OF DENGUE AND SOLUTIONS
ANJANA.K.S
ā€¢ Uncomplicated dengue cases
- ā€œmild disease of thrombocytopeniaā€
- no more than intravenous fluid therapy and
platelet transfusions for a couple of days.
ā€¢ Severe Dengue,
-unprepared for the changing clinical,
biochemical and haematological profiles during
febrile phase
-not step up their vigilance during the critical
period
PITFALL-1: Recognition of dengue at the
frontline
ā€¢ When the patient presents as a febrile illness- Fails
to recognize.
-no follow up
-D/d
-Upper respiratory tract infection /viral fever
-DENGUE patients-more ill and canā€™t do
routine works
ā€¢ SOLUTION:
-suspect dengue in every febrile patient.
-ask regarding dengue endemic locality or has
recently travelled there.
-take a detailed history and perform the step-
wise evaluation
-A positive tourniquet test ā€“may differentiate
dengue from non-dengue viral illness(high PPV)
-A patient with probable dengue- schedule
daily follow-up and advice immediate medical
attention should warning signs occur.
ā€¢ Pitfall 2: Missed Opportunity For FBC In Early
Febrile Period
ā€¢ Full blood count (FBC)
-to detect the falling platelet count
-to know changes in haematocrit levels
Solution:
-A full blood count should be done at the first visit
when dengue is suspected.
ā€¢ Pitfall 3: Not understanding the evolving FBC
ā€¢ The earlier the FBC done, the more likely it is
normal-Canā€™t rule out dengue .
ā€¢ Solution:
ā€¢ An early FBC is
- to establish the patientā€™s baseline haematocrit.
-early and progressive decrease in WBC and
platelet counts during febrile period is a useful
indicator of dengue.
ā€¢ Pitfall 4: Surge of hospital admissions during a
dengue outbreak
- because of fear and panic among patients and
-frontline physicians, or institutional directives to
admit all suspected dengue patients.
Solution:
-Clear guidelines for admissions need to be available.
-Integrating an OP management protocol within the
hospital
- Admission during febrile period
- for those who are unable to manage adequate
oral hydration at home,
- infants and those with co-morbid conditions.
HOME CARE
ā€¢ Give paracetamol for high fever if the patient is
uncomfortable.
- The recommended dose is 10 mg/kg/dose 6-8th hrly
ā€¢ Advise mothers to continue feeding and giving fluids to a child
patient.
ā€¢ Return to hospital if
-no clinical improvement
-deterioration around the time of defervescence,
-severe abdominal pain,
-persistent vomiting,
-cold and clammy extremities,
-lethargy or irritability/restlessness,
-bleeding (e.g. black stools or coffee ground vomiting)
- shortness of breath,
-not passing urine for more than 4āˆ’6 hours.
ā€¢ Follow-up and reassess the patient every day
until the patient has no fever on two consecutive
days without using paracetamol.
ā€¢ If fever persist for > 7 days, suspect bacterial
infections-refer to the hospital for further evaluation
ā€¢ Pitfall 5: Warning signs
ā€¢ If warning signs develop at night ā€“delay in seeking
medical attention.
ā€¢ During waiting period - plasma leakage and
deteriorate to hypovolaemic shock.
ā€¢ Solution:
ā€¢ Ambulatory patients should receive explicit advice
about the warning signs and the urgency of seeking
immediate medical attention.
At the emergency department
ā€¢ Pitfall 6: Triage based on fever
ā€¢ An afebrile dengue patient gets a non-urgent triage and
has to wait for medical attention or be sent home.
ā€¢ A subnormal temperature is seen in patients with
established plasma leakage or dengue shock.
ā€¢ At this stage the clinical outcome is extremely time-
sensitive; any delay in fluid resuscitation profound,
prolonged shock and a stormy course for the disease.
ā€¢ Solution:
ā€¢ Triage personnel should be taught assessment of
perfusion
ā€¢ A quick targeted history for nausea, vomiting and
lethargy will indicate the severity of illness.
ā€¢ Pitfall 7: Waiting for full blood count results
ā€¢ Waiting for FBC results to make decisions about
admission and intravenous fluid therapy will further
delay in recognition & treatment of dengue shock.
ā€¢ Solution:
ā€¢ IV fluid therapy should be initiated when warning
signs or clinical evidence of shock are present.
ā€¢ Better if haematocrit is obtained before
commencement of iv fluid therapy.
Shock and its many manifestations
ā€¢ Pitfall 8: Vital signs are ā€œstableā€
ā€¢ An alert patient with normal BP can present in
compensated shock.
ā€¢ The patient who is in shock is initially quietly
tachypneic; alert but lying down-difficult to recognize.
ā€¢ Unless you touch the patient, you will not be able to
detect the cold extremities, feeble peripheral pulses and
prolonged capillary refill time -earliest changes in
shock.
ā€¢ A patient in shock remains in alert state until
cerebral perfusion diminishes, and then develops a
ā€œsuddenā€ shortness of breath and restlessness or
seizures followed quickly by a ā€œsuddenā€ collapse.
ā€¢ Solution:
ā€¢ Make it a habit to touch and assess the peripheral
perfusion of every patient, not only dengue patients.
ā€¢ It takes less than 30 seconds to assess the four
parameters ā€“
-pulse volume,
-capillary refill time,
-colour and
-temperature of the extremities.
-Only trained humans can perform this vital function,
no machine can do it
ā€¢ Pitfall 9: Symptomatic treatment with
antispasmodic agents or antacid given to patients
with abdominal pain
ā€¢ Abdominal pain
-early sign of plasma leakage and
-becomes more severe as hypovolaemia
progresses.
ā€¢ The pain could be in the epigastrium and with
vomiting -misinterpreted as gastritis.
ā€¢ The patient will progress into full-blown shock if
definitive treatment for shock is not given promptly
ā€¢ Solution:
ā€¢ Development of gastrointestinal symptoms such as
nausea, vomiting or diarrhoea, during defervesence
should suggest dengue with warning signs or
dengue shock.
ā€¢ Patients with these symptoms should be carefully
assessed for signs of dehydration and hypovolaemic
shock
ā€¢ Pitfall 10: Patients presenting with severe
abdominal pain - referred to surgical team or for
USG
ā€¢ Plasma leakage is associated with abdominal pain
that may occur anywhere in the abdomen.
ā€¢ Guarding and rebound tenderness in the right iliac
fossa - due to serosal oedema and lymphoid
hyperplasia of the intestines.
ā€¢ The abdominal pain becomes more severe in the
shock state due to splanchnic vasoconstriction.
ā€¢ Referrals or ultrasound studies further delay
initiating fluid resuscitation.
ā€¢ Solution:
ā€¢ Evaluate the patientā€™s history for fever that preceded
the onset of abdominal pain.
ā€¢ Assess the patient for signs of shock.
ā€¢ Haemoconcentration and thrombocytopenia
should raise the suspicion of dengue diagnosis.
ā€¢ A bolus of intravenous fluid (5āˆ’10 ml/kg/ hour)
may lead to resolution of abdominal pain, making
the diagnosis of a surgical abdomen unlikely.
ā€¢ Pitfall 11: Shortness of breath misinterpreted as
fluid overload or pleural effusion or pneumonia.
ā€¢ As plasma leakage progresses undetected and
untreated-metabolic acidosis (lactic acidosis) that
initially appears as quiet tachypnoea.
ā€¢ This represents the respiratory compensation to
maintain the acid-base balance.
ā€¢ During shock, breathing becomes deeper and gives
the impression of shortness of breath.
ā€¢ Solution:
ā€¢ It is essential to be familiar with this breathing
pattern, which is seen in dengue shock as well as
diabetic ketoacidosis.
ā€¢ Do not be distracted by the patientā€™s dramatic
breathing pattern.
ā€¢ Look for features of shock: if unsure, a blood gas
(+ lactate) analysis should be done.
ā€¢ Start intravenous fluid resuscitation immediately
after sampling blood for haematocrit
determination
ā€¢ Pitfall 12: Seizures or altered sensorium ā€“ diagnosed
as meningitis or meningoencephalitis.
ā€¢ During febrile phase-affect young children who present
as febrile seizures
ā€¢ The child treated and followed up with vigilance for
warning signs and plasma leakage during defervesence.
ā€¢ A patient in critical phase with no fever, or low-
grade fever, but who are in severe shock-
seizures/altered sensorium
ā€¢ The brain is one of the last organs compromised by
perfusion in hypovolaemic shock- lead to acute
cerebral ischemia
ā€¢ Delay in fluid resuscitation - a detour to CT scan will
lead to cardiorespiratory collapse and irreversible shock
ā€¢ Solution:
ā€¢ A targeted history is essential to confirm that the
patient had fever preceding the seizures and might
not be febrile at the time of seizures.
ā€¢ The evidence of shock, such as narrowed pulse
pressure and tachycardia, should alert the
physician for urgent fluid resuscitation
ā€¢ A CT scan is not necessary if the patientā€™s
neurological state recovers together with a stable
haemodynamic state.
ā€¢ Pitfall 13: Bleeding versus plasma leakage
ā€¢ Focuses on monitoring the trend of platelet counts
alone to the exclusion of plasma leakage.
ā€¢ May administer platelet transfusions in addition to
the maintenance of intravenous fluid.
ā€¢ Fluid overload or inadequate fluid replacement may
ensue, depending on the severity of the plasma
leakage
ā€¢ Inadequate fluid replacement leads to prolonged and
profound shock characterized by bleeding
ā€¢ Platelet count may remain low/very low during
the first 1 or 2 days of recovery and that platelet
transfusion during this time will cause fluid
overload
ā€¢ Solution:
ā€¢ Should be alert to the onset of dengue vasculopathy
that causes plasma leakage and hypovolaemic shock
when the fever subsides.
ā€¢ Monitoring should be focused on manifestations of
plasma leakage, bleeding and shock.
ā€¢ The trend of haematocrit level together with
haemodynamic status is the main guide to fluid
management.
ā€¢ The usefulness of platelet count during the febrile
phase is to identify its rapid decrease, which marks
the beginning of plasma leakage.
ā€¢ Beyond this phase, trending of platelet counts has no
bearing on fluid management.
ā€¢ Pitfall 14: Pulse rate and BP
ā€¢ Frequently focus on the systolic BP and ignore the
rising diastolic pressure and pulse rate .
ā€¢ Solution:
ā€¢ Patients with compensated shock may be critically
ill despite being alert and having a ā€œnormalā€ systolic
BP.
ā€¢ Automated BP devices can provide normal BP
readings in severe shock and hypotension.
ā€¢ If you cannot palpate the radial or brachial pulse
and the central (femoral) pulses are weak or
absent, assume that the patient is hypotensive.
ā€¢ Do not rely on automated BP devices in patients
with clinical signs of shock.
Parenteral fluid therapy
ā€¢ Pitfall 15: Tachycardia and cold extremities during febrile
phase misinterpreted as shock & fluid resuscitation
ā€¢ Vasoconstriction resulting in cold extremities is normal
mechanism to conserve heat to increase core body
temperature.
ā€¢ Solution:
ā€¢ During the early febrile phase in addition fever, the
haematocrit and platelet count, pulse volume and urine
output will be normal.
ā€¢ Some may continue to have fever during the plasma leakage
phase- there may be tachycardia and cool peripheries despite a
good pulse volume.
ā€¢ Other parameters of intravascular volume should be
sought, e.g. capillary refill time, pulse pressure, urine
output and/or acid-base balance.
ā€¢ Pitfall 16: Starting intravenous fluids in the
febrile phase (because NS1 Ag is positive)
ā€¢ Studies have shown that plasma leakage is
detectable as early as day 2 of fever onset .
ā€¢ Early intravenous fluid therapy- exacerbate
accumulation of third space losses
ā€¢ Solution:
ā€¢ During the febrile phase hydration should be
maintained by the oral route .
ā€¢ Only in exceptional cases should intravenous
infusion be used, and should be kept at a minimal
infusion rate and be discontinued as soon as the
patient can take oral fluids.
ā€¢ Pitfall 17: Administering IV fluid at high rates for
several hours without review of the clinical state.
ā€¢ The management of dengue shock is centred on
intravenous fluid management.
ā€¢ In dengue,fluid is merely lost from the
intravascular to the extravascular compartments
through leaky capillary endothelium.
ā€¢ This state will continue for 24āˆ’48 hours during the
critical phase of illness.
ā€¢ Solution:
ā€¢ In a ā€œleakyā€ capillary state, beyond a certain
hydrostatic pressure, the more fluids are infused, the
more they will leak into the ā€œthird spaceā€
ā€¢ Massive pleural effusion and ascites are the
consequences -leads to respiratory distress 12āˆ’48
hours later.
ā€¢ Administer the minimum intravenous fluid
necessary to maintain a ā€œjust-enoughā€
circulation.
ā€¢ Placing a micro- haematocrit centrifuge facilitates
the use of haematocrit determinations to manage
fluid requirements.
ā€¢ Pitfall 18: Increased fluid therapy in a well perfused
patient with persistently elevated haematocrit.
ā€¢ The haematocrit may remain high towards the end of
the critical phase despite adequate fluid therapy.
ā€¢ A patient who remains well perfused will compensating
well for the ongoing plasma leakage.
ā€¢ An attempt to correct the haematocrit level by
increasing iv fluid will often lead to fluid overload.
ā€¢ Solution:
ā€¢ Continue close monitoring of this patient.
ā€¢ Do not increase the iv fluid ;
ā€¢ If well perfused then iv fluids can be gradually
reduced and even stopped, regardless of the
haematocrit level.
ā€¢ Pitfall 19: IVfluid therapy is continued into the
recovery phase because the patient is not drinking.
ā€¢ A careful examination of the patient and the fluid
intake and output chart -positive balance of fluid
ā€¢ The only way for the pleural effusion and ascites to
be reabsorbed into the circulation is to stop
intravenous therapy.
ā€¢ The patientā€™s own thirst mechanism will kick in after
the diuresis phase.
Urine output
ā€¢ Pitfall 20: During the febrile phase the urine
output is often ignored and not factored into the
evaluation of adequate oral fluids.
ā€¢ The urine output is a useful marker of the hydration
state during the febrile phase.
ā€¢ Solution:
ā€¢ Adequate oral intake of fluids should result in a
urinary output frequency of 4āˆ’6 times per day.
ā€¢ Pitfall 21: During the critical phase the urine
output of 1 ml/kg/hour is used as a criterion of
adequate IV therapy
ā€¢ During the critical phase the urine output is a useful
indicator of the intravascular volume state but
should not be used as the sole criterion.
ā€¢ Solution:
ā€¢ In severe shock, urine output should be monitored
hourly using an indwelling catheter.
ā€¢ Adequate urine output should be scaled down to
~ 0.5 ml/kg/hour to avoid fluid overload.
ā€¢ A urine output exceeding that may be an indication
to reduce intravenous fluid therapy
ā€¢ Pitfall 22: Use of furosemide for oliguria during
the critical phase.
ā€¢ Oliguria in this phase is due to ā€œpre-renalā€, i.e.
inadequate tissue-organ perfusion.
ā€¢ The use of furosemide will produce some urine but
will exacerbate the shock state.
ā€¢ Solution:
ā€¢ Adequate peripheral perfusion should be the main
end-point of intravenous fluid therapy.
ā€¢ Patients with oliguria should continue to receive
intravenous fluid therapy until peripheral
perfusion is established.
ā€¢ Pitfall 23:fluid bolus challenge followed by
furosemide may produce urine
ā€¢ This is detrimental in dengue with plasma leakage.
ā€¢ A large fluid bolus ā€“fluid will inevitably be
redistributed to the ā€œthird spaceā€.
ā€¢ Furosemide administration -fluid can only be drawn
out of intravascular compartment.
ā€¢ The net effect is that the ā€œthird spaceā€ gains
fluids while the intravascular compartment
remains depleted and the patient loses
electrolytes such as potassium.
ā€¢ Solution:
ā€¢ Urine will be produced by the kidneys when there is
adequate renal perfusion.
ā€¢ In established acute kidney injury - manifested in
anuria and high serum creatinine levels, volume
infusion should continue until the circulation is
established.
ā€¢ Urine output as a parameter of adequate
perfusion is very limited in this situation
ā€¢ Pitfall 25: Abdominal compartment syndrome.
ā€¢ Is the result of massive ascites accumulated in a
short time, and under tension.
ā€¢ It may be precipitated by using moderately high
PEEP during mechanical ventilation of dengue
patients.
ā€¢ Pressure on the retroperitoneal structures such as the
kidneys, renal veins and inferior vena cava, cause
reduced renal perfusion with consequent oliguria
even though peripheral perfusion may have been
adequate.
ā€¢ Solution:
ā€¢ Be cautious about using urine output as a parameter
of adequate perfusion.
ā€¢ If possible, nurse in a reclining or lateral position to
relieve pressure on the retroperitoneal structures.
ā€¢ At the end of the critical period, the intra-abdominal
tension will ease and urine may start flowing
gradually, spontaneously or with the help of an
infusion of furosemide.
ā€¢ The use of furosemide - commenced in the
recovery period when the patient is stable
without iv fluid infusion.
ā€¢ Premature use of furosemide may precipitate a
shock state
ā€¢ Pitfall 26: Use of renal replacement therapy during
the critical phase in a patient has severe metabolic
acidosis and oliguria.
ā€¢ Severe metabolic acidosis and oliguria are the
consequences of uncorrected and prolonged shock.
ā€¢ The haemodialysis machine will face technical
problems with drawing blood from the hypovolaemic
patient.
ā€¢ Solution:
ā€¢ Reserved for patients who are already in the recovery
phase, who are haemodynamically stable, are fluid
overloaded and have oliguria not responding to
furosemide therapy.
-haemodialysis works very well and effective in
preventing life threatening pulmonary oedema.
Blood transfusions for severe bleeding
ā€¢ Pitfall 28: Not transfusing blood until the
haematocrit has decreased to low levels in
unstable patients.
ā€¢ Severe but occult bleeding can be difficult to
recognize .
ā€¢ The haematocrit will only decrease to low levels
after several boluses of fluid resuscitation
(especially with colloids), or if the bleeding has
been very severe.
ā€¢ During fluid resuscitation the patient remains
unstable while the ā€œthird spaceā€ fluid accumulation
increases
ā€¢ Solution:
ā€¢ Lower the haematocrit in dengue shock , the more
likely the significant bleeding, and therefore it is
vital to change from crystalloid/colloid infusion to
blood transfusion.
ā€¢ This change in strategy will prevent excessive
infusion of non-blood fluids and accumulation of
ā€œthird spaceā€ fluid.
ā€¢ Bleeding should always be considered as a possible
cause of prolonged/profound shock.
ā€¢ On the contrary, haematocrit is very useful in
recognizing severe bleeding, provided that it is
interpreted together with other clinical parameters.
ā€¢ Pitfall 29: DIC regime for severe bleeding.
ā€¢ The causes of severe bleeding in dengue are not well
understood.
ā€¢ These patients have thrombocytopenia, deranged
coagulation and disseminated intravascular
coagulopathy.
ā€¢ Therapy with multiple transfusions of fresh frozen
plasma, platelet concentrates and cryoprecipitate.
ā€¢ Unless transfusion with fresh whole blood is
given urgently, the patient will succumb to
haemorrhagic shock with massive third space
accumulation.
ā€¢ Solution:
ā€¢ Repeated blood transfusions should be guided by
clinical assessment, haematocrit levels, blood gas
and lactate analysis.
ā€¢ Bleeding will usually decrease once the critical
phase is over, as manifested by decreasing
tachycardia and improved peripheral perfusion.
ā€¢ It is important to request fresh whole blood.
ā€¢ Stored blood does not have the same properties as
fresh whole blood and may not reverse the clinical
situation
ā€¢ Pitfall 30: Blood transfusion when the
haematocrit is on the rise in a shocked patient.
ā€¢ Fluid boluses that are administered aggressively in
compensated shock may give impression of
refractory shock and prompt the physician into
changing from crystalloid fluid to blood transfusion.
ā€¢ The subsequent haematocrit will rise even more
sharply after the blood transfusion and prompt the
physician to give more crystalloids even though the
haemodynamic situation is stable.
ā€¢ The patient will become fluid overloaded.
ā€¢ Solution:
ā€¢ If haematocrit continues to rise despite fluid
resuscitation, consider using a colloid bolus at 10 to
20 ml/kg.
ā€¢ If the shock patient has a normal systolic BP, there is
no need to rush the fluid resuscitation.
ā€¢ Aggressive fluid resuscitation over 15 minutes
should be reserved for those with hypotension
ā€¢ Pitfall 31: Blood transfusion in a stable patient
with low haematocrit.
ā€¢ This usually occurs during the recovery period when
re-absorption causes haemodilution.
ā€¢ A blood transfusion at this stage may precipitate
life-threatening pulmonary oedema.
ā€¢ Solution:
ā€¢ If the patient has a stable circulation they do not
need blood transfusion.
ā€¢ The haematocrit will increase after the excess fluid
has been diuresed.
ā€¢ Pitfall 32: Severe shock and inotropes.
ā€¢ 40āˆ’60 ml/kg of fluid administration and have failed
to reverse the shock state-initiate inotropes such as
dobutamine or dopamine and norepinephrine .
ā€¢ Refractory shock is the most common cause of
death within 24āˆ’48 hours of admission.
ā€¢ There is usually a combination of plasma leakage
and bleeding following prolonged uncorrected shock
accompanied by renal and liver impairment.
ā€¢ Solution:
ā€¢ After every bolus infusion of 10āˆ’20 ml/kg, there should be
a re-evaluation of the haemodynamic state.
ā€¢ If there is no clinical improvement, a repeat haematocrit
should be done.
ā€¢ A rising haematocrit or an haematocrit that is still high,
would suggest ongoing plasma leakage and change to
colloid solution.
ā€¢ A decrease in haematocrit suggests significant bleeding and
proceed to transfuse matched fresh whole blood as soon as
possible
ā€¢ Colloids and inotropes should be used as a temporary
measure.
ā€¢ Pitfall 33: Liver enzymes and multi-organ
involvement may prompt multi-specialty
referrals resulting in several ā€œsingle organā€
treatments.
ā€¢ The multi-organ involvement is mainly due to shock
with tissue hypoperfusion and diminished oxygen
delivery.
ā€¢ Solution
ā€¢ Prioritize achievement of haemodynamic stability
and improved tissue oxygenation by fluid, colloid,
or blood administration
ā€¢ All other outstanding clinical issues (except
hypoglycaemia and electrolyte imbalances) should
await achievement of haemodynamic stability
SUMMARY
ā€¢ Intravenous fluid therapy is life-saving in dengue shock.
However, there is a ā€œnarrow therapeutic indexā€.
ā€¢ Fluids have to be given timely, at the appropriate
volume, rate, of the appropriate type (crystalloids,
colloid and/or blood) and for the appropriate duration.
ā€¢ Progression of the disease through the critical phase should
be tracked in hours of plasma leakage.
ā€¢ Recognizing the cues to discontinue IV fluid therapy is just
as important as knowing when to start it.
ā€¢ Given time and haemodynamic stability, other issues such
as thrombocytopenia, coagulopathy and raised liver
enzymes will recover spontaneously or with supportive
care.
THANK YOU

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PITFALLS IN THE MANAGEMENT OF DENGUE AND SOLUTIONS.pptx

  • 1. PITFALLS IN THE MANAGEMENT OF DENGUE AND SOLUTIONS ANJANA.K.S
  • 2. ā€¢ Uncomplicated dengue cases - ā€œmild disease of thrombocytopeniaā€ - no more than intravenous fluid therapy and platelet transfusions for a couple of days. ā€¢ Severe Dengue, -unprepared for the changing clinical, biochemical and haematological profiles during febrile phase -not step up their vigilance during the critical period
  • 3. PITFALL-1: Recognition of dengue at the frontline ā€¢ When the patient presents as a febrile illness- Fails to recognize. -no follow up -D/d -Upper respiratory tract infection /viral fever -DENGUE patients-more ill and canā€™t do routine works
  • 4. ā€¢ SOLUTION: -suspect dengue in every febrile patient. -ask regarding dengue endemic locality or has recently travelled there. -take a detailed history and perform the step- wise evaluation -A positive tourniquet test ā€“may differentiate dengue from non-dengue viral illness(high PPV) -A patient with probable dengue- schedule daily follow-up and advice immediate medical attention should warning signs occur.
  • 5. ā€¢ Pitfall 2: Missed Opportunity For FBC In Early Febrile Period ā€¢ Full blood count (FBC) -to detect the falling platelet count -to know changes in haematocrit levels Solution: -A full blood count should be done at the first visit when dengue is suspected.
  • 6. ā€¢ Pitfall 3: Not understanding the evolving FBC ā€¢ The earlier the FBC done, the more likely it is normal-Canā€™t rule out dengue . ā€¢ Solution: ā€¢ An early FBC is - to establish the patientā€™s baseline haematocrit. -early and progressive decrease in WBC and platelet counts during febrile period is a useful indicator of dengue.
  • 7. ā€¢ Pitfall 4: Surge of hospital admissions during a dengue outbreak - because of fear and panic among patients and -frontline physicians, or institutional directives to admit all suspected dengue patients. Solution: -Clear guidelines for admissions need to be available. -Integrating an OP management protocol within the hospital - Admission during febrile period - for those who are unable to manage adequate oral hydration at home, - infants and those with co-morbid conditions.
  • 8.
  • 9. HOME CARE ā€¢ Give paracetamol for high fever if the patient is uncomfortable. - The recommended dose is 10 mg/kg/dose 6-8th hrly ā€¢ Advise mothers to continue feeding and giving fluids to a child patient. ā€¢ Return to hospital if -no clinical improvement -deterioration around the time of defervescence, -severe abdominal pain, -persistent vomiting, -cold and clammy extremities, -lethargy or irritability/restlessness, -bleeding (e.g. black stools or coffee ground vomiting) - shortness of breath, -not passing urine for more than 4āˆ’6 hours.
  • 10. ā€¢ Follow-up and reassess the patient every day until the patient has no fever on two consecutive days without using paracetamol. ā€¢ If fever persist for > 7 days, suspect bacterial infections-refer to the hospital for further evaluation
  • 11. ā€¢ Pitfall 5: Warning signs ā€¢ If warning signs develop at night ā€“delay in seeking medical attention. ā€¢ During waiting period - plasma leakage and deteriorate to hypovolaemic shock. ā€¢ Solution: ā€¢ Ambulatory patients should receive explicit advice about the warning signs and the urgency of seeking immediate medical attention.
  • 12. At the emergency department ā€¢ Pitfall 6: Triage based on fever ā€¢ An afebrile dengue patient gets a non-urgent triage and has to wait for medical attention or be sent home. ā€¢ A subnormal temperature is seen in patients with established plasma leakage or dengue shock. ā€¢ At this stage the clinical outcome is extremely time- sensitive; any delay in fluid resuscitation profound, prolonged shock and a stormy course for the disease. ā€¢ Solution: ā€¢ Triage personnel should be taught assessment of perfusion ā€¢ A quick targeted history for nausea, vomiting and lethargy will indicate the severity of illness.
  • 13. ā€¢ Pitfall 7: Waiting for full blood count results ā€¢ Waiting for FBC results to make decisions about admission and intravenous fluid therapy will further delay in recognition & treatment of dengue shock. ā€¢ Solution: ā€¢ IV fluid therapy should be initiated when warning signs or clinical evidence of shock are present. ā€¢ Better if haematocrit is obtained before commencement of iv fluid therapy.
  • 14. Shock and its many manifestations ā€¢ Pitfall 8: Vital signs are ā€œstableā€ ā€¢ An alert patient with normal BP can present in compensated shock. ā€¢ The patient who is in shock is initially quietly tachypneic; alert but lying down-difficult to recognize. ā€¢ Unless you touch the patient, you will not be able to detect the cold extremities, feeble peripheral pulses and prolonged capillary refill time -earliest changes in shock. ā€¢ A patient in shock remains in alert state until cerebral perfusion diminishes, and then develops a ā€œsuddenā€ shortness of breath and restlessness or seizures followed quickly by a ā€œsuddenā€ collapse.
  • 15. ā€¢ Solution: ā€¢ Make it a habit to touch and assess the peripheral perfusion of every patient, not only dengue patients. ā€¢ It takes less than 30 seconds to assess the four parameters ā€“ -pulse volume, -capillary refill time, -colour and -temperature of the extremities. -Only trained humans can perform this vital function, no machine can do it
  • 16. ā€¢ Pitfall 9: Symptomatic treatment with antispasmodic agents or antacid given to patients with abdominal pain ā€¢ Abdominal pain -early sign of plasma leakage and -becomes more severe as hypovolaemia progresses. ā€¢ The pain could be in the epigastrium and with vomiting -misinterpreted as gastritis. ā€¢ The patient will progress into full-blown shock if definitive treatment for shock is not given promptly
  • 17. ā€¢ Solution: ā€¢ Development of gastrointestinal symptoms such as nausea, vomiting or diarrhoea, during defervesence should suggest dengue with warning signs or dengue shock. ā€¢ Patients with these symptoms should be carefully assessed for signs of dehydration and hypovolaemic shock
  • 18. ā€¢ Pitfall 10: Patients presenting with severe abdominal pain - referred to surgical team or for USG ā€¢ Plasma leakage is associated with abdominal pain that may occur anywhere in the abdomen. ā€¢ Guarding and rebound tenderness in the right iliac fossa - due to serosal oedema and lymphoid hyperplasia of the intestines. ā€¢ The abdominal pain becomes more severe in the shock state due to splanchnic vasoconstriction. ā€¢ Referrals or ultrasound studies further delay initiating fluid resuscitation.
  • 19. ā€¢ Solution: ā€¢ Evaluate the patientā€™s history for fever that preceded the onset of abdominal pain. ā€¢ Assess the patient for signs of shock. ā€¢ Haemoconcentration and thrombocytopenia should raise the suspicion of dengue diagnosis. ā€¢ A bolus of intravenous fluid (5āˆ’10 ml/kg/ hour) may lead to resolution of abdominal pain, making the diagnosis of a surgical abdomen unlikely.
  • 20. ā€¢ Pitfall 11: Shortness of breath misinterpreted as fluid overload or pleural effusion or pneumonia. ā€¢ As plasma leakage progresses undetected and untreated-metabolic acidosis (lactic acidosis) that initially appears as quiet tachypnoea. ā€¢ This represents the respiratory compensation to maintain the acid-base balance. ā€¢ During shock, breathing becomes deeper and gives the impression of shortness of breath.
  • 21. ā€¢ Solution: ā€¢ It is essential to be familiar with this breathing pattern, which is seen in dengue shock as well as diabetic ketoacidosis. ā€¢ Do not be distracted by the patientā€™s dramatic breathing pattern. ā€¢ Look for features of shock: if unsure, a blood gas (+ lactate) analysis should be done. ā€¢ Start intravenous fluid resuscitation immediately after sampling blood for haematocrit determination
  • 22. ā€¢ Pitfall 12: Seizures or altered sensorium ā€“ diagnosed as meningitis or meningoencephalitis. ā€¢ During febrile phase-affect young children who present as febrile seizures ā€¢ The child treated and followed up with vigilance for warning signs and plasma leakage during defervesence. ā€¢ A patient in critical phase with no fever, or low- grade fever, but who are in severe shock- seizures/altered sensorium ā€¢ The brain is one of the last organs compromised by perfusion in hypovolaemic shock- lead to acute cerebral ischemia ā€¢ Delay in fluid resuscitation - a detour to CT scan will lead to cardiorespiratory collapse and irreversible shock
  • 23. ā€¢ Solution: ā€¢ A targeted history is essential to confirm that the patient had fever preceding the seizures and might not be febrile at the time of seizures. ā€¢ The evidence of shock, such as narrowed pulse pressure and tachycardia, should alert the physician for urgent fluid resuscitation ā€¢ A CT scan is not necessary if the patientā€™s neurological state recovers together with a stable haemodynamic state.
  • 24. ā€¢ Pitfall 13: Bleeding versus plasma leakage ā€¢ Focuses on monitoring the trend of platelet counts alone to the exclusion of plasma leakage. ā€¢ May administer platelet transfusions in addition to the maintenance of intravenous fluid. ā€¢ Fluid overload or inadequate fluid replacement may ensue, depending on the severity of the plasma leakage ā€¢ Inadequate fluid replacement leads to prolonged and profound shock characterized by bleeding ā€¢ Platelet count may remain low/very low during the first 1 or 2 days of recovery and that platelet transfusion during this time will cause fluid overload
  • 25. ā€¢ Solution: ā€¢ Should be alert to the onset of dengue vasculopathy that causes plasma leakage and hypovolaemic shock when the fever subsides. ā€¢ Monitoring should be focused on manifestations of plasma leakage, bleeding and shock. ā€¢ The trend of haematocrit level together with haemodynamic status is the main guide to fluid management. ā€¢ The usefulness of platelet count during the febrile phase is to identify its rapid decrease, which marks the beginning of plasma leakage. ā€¢ Beyond this phase, trending of platelet counts has no bearing on fluid management.
  • 26. ā€¢ Pitfall 14: Pulse rate and BP ā€¢ Frequently focus on the systolic BP and ignore the rising diastolic pressure and pulse rate . ā€¢ Solution: ā€¢ Patients with compensated shock may be critically ill despite being alert and having a ā€œnormalā€ systolic BP. ā€¢ Automated BP devices can provide normal BP readings in severe shock and hypotension. ā€¢ If you cannot palpate the radial or brachial pulse and the central (femoral) pulses are weak or absent, assume that the patient is hypotensive. ā€¢ Do not rely on automated BP devices in patients with clinical signs of shock.
  • 27. Parenteral fluid therapy ā€¢ Pitfall 15: Tachycardia and cold extremities during febrile phase misinterpreted as shock & fluid resuscitation ā€¢ Vasoconstriction resulting in cold extremities is normal mechanism to conserve heat to increase core body temperature. ā€¢ Solution: ā€¢ During the early febrile phase in addition fever, the haematocrit and platelet count, pulse volume and urine output will be normal. ā€¢ Some may continue to have fever during the plasma leakage phase- there may be tachycardia and cool peripheries despite a good pulse volume. ā€¢ Other parameters of intravascular volume should be sought, e.g. capillary refill time, pulse pressure, urine output and/or acid-base balance.
  • 28. ā€¢ Pitfall 16: Starting intravenous fluids in the febrile phase (because NS1 Ag is positive) ā€¢ Studies have shown that plasma leakage is detectable as early as day 2 of fever onset . ā€¢ Early intravenous fluid therapy- exacerbate accumulation of third space losses ā€¢ Solution: ā€¢ During the febrile phase hydration should be maintained by the oral route . ā€¢ Only in exceptional cases should intravenous infusion be used, and should be kept at a minimal infusion rate and be discontinued as soon as the patient can take oral fluids.
  • 29. ā€¢ Pitfall 17: Administering IV fluid at high rates for several hours without review of the clinical state. ā€¢ The management of dengue shock is centred on intravenous fluid management. ā€¢ In dengue,fluid is merely lost from the intravascular to the extravascular compartments through leaky capillary endothelium. ā€¢ This state will continue for 24āˆ’48 hours during the critical phase of illness.
  • 30. ā€¢ Solution: ā€¢ In a ā€œleakyā€ capillary state, beyond a certain hydrostatic pressure, the more fluids are infused, the more they will leak into the ā€œthird spaceā€ ā€¢ Massive pleural effusion and ascites are the consequences -leads to respiratory distress 12āˆ’48 hours later. ā€¢ Administer the minimum intravenous fluid necessary to maintain a ā€œjust-enoughā€ circulation. ā€¢ Placing a micro- haematocrit centrifuge facilitates the use of haematocrit determinations to manage fluid requirements.
  • 31. ā€¢ Pitfall 18: Increased fluid therapy in a well perfused patient with persistently elevated haematocrit. ā€¢ The haematocrit may remain high towards the end of the critical phase despite adequate fluid therapy. ā€¢ A patient who remains well perfused will compensating well for the ongoing plasma leakage. ā€¢ An attempt to correct the haematocrit level by increasing iv fluid will often lead to fluid overload. ā€¢ Solution: ā€¢ Continue close monitoring of this patient. ā€¢ Do not increase the iv fluid ; ā€¢ If well perfused then iv fluids can be gradually reduced and even stopped, regardless of the haematocrit level.
  • 32. ā€¢ Pitfall 19: IVfluid therapy is continued into the recovery phase because the patient is not drinking. ā€¢ A careful examination of the patient and the fluid intake and output chart -positive balance of fluid ā€¢ The only way for the pleural effusion and ascites to be reabsorbed into the circulation is to stop intravenous therapy. ā€¢ The patientā€™s own thirst mechanism will kick in after the diuresis phase.
  • 33. Urine output ā€¢ Pitfall 20: During the febrile phase the urine output is often ignored and not factored into the evaluation of adequate oral fluids. ā€¢ The urine output is a useful marker of the hydration state during the febrile phase. ā€¢ Solution: ā€¢ Adequate oral intake of fluids should result in a urinary output frequency of 4āˆ’6 times per day.
  • 34. ā€¢ Pitfall 21: During the critical phase the urine output of 1 ml/kg/hour is used as a criterion of adequate IV therapy ā€¢ During the critical phase the urine output is a useful indicator of the intravascular volume state but should not be used as the sole criterion. ā€¢ Solution: ā€¢ In severe shock, urine output should be monitored hourly using an indwelling catheter. ā€¢ Adequate urine output should be scaled down to ~ 0.5 ml/kg/hour to avoid fluid overload. ā€¢ A urine output exceeding that may be an indication to reduce intravenous fluid therapy
  • 35. ā€¢ Pitfall 22: Use of furosemide for oliguria during the critical phase. ā€¢ Oliguria in this phase is due to ā€œpre-renalā€, i.e. inadequate tissue-organ perfusion. ā€¢ The use of furosemide will produce some urine but will exacerbate the shock state. ā€¢ Solution: ā€¢ Adequate peripheral perfusion should be the main end-point of intravenous fluid therapy. ā€¢ Patients with oliguria should continue to receive intravenous fluid therapy until peripheral perfusion is established.
  • 36. ā€¢ Pitfall 23:fluid bolus challenge followed by furosemide may produce urine ā€¢ This is detrimental in dengue with plasma leakage. ā€¢ A large fluid bolus ā€“fluid will inevitably be redistributed to the ā€œthird spaceā€. ā€¢ Furosemide administration -fluid can only be drawn out of intravascular compartment. ā€¢ The net effect is that the ā€œthird spaceā€ gains fluids while the intravascular compartment remains depleted and the patient loses electrolytes such as potassium.
  • 37. ā€¢ Solution: ā€¢ Urine will be produced by the kidneys when there is adequate renal perfusion. ā€¢ In established acute kidney injury - manifested in anuria and high serum creatinine levels, volume infusion should continue until the circulation is established. ā€¢ Urine output as a parameter of adequate perfusion is very limited in this situation
  • 38. ā€¢ Pitfall 25: Abdominal compartment syndrome. ā€¢ Is the result of massive ascites accumulated in a short time, and under tension. ā€¢ It may be precipitated by using moderately high PEEP during mechanical ventilation of dengue patients. ā€¢ Pressure on the retroperitoneal structures such as the kidneys, renal veins and inferior vena cava, cause reduced renal perfusion with consequent oliguria even though peripheral perfusion may have been adequate.
  • 39. ā€¢ Solution: ā€¢ Be cautious about using urine output as a parameter of adequate perfusion. ā€¢ If possible, nurse in a reclining or lateral position to relieve pressure on the retroperitoneal structures. ā€¢ At the end of the critical period, the intra-abdominal tension will ease and urine may start flowing gradually, spontaneously or with the help of an infusion of furosemide. ā€¢ The use of furosemide - commenced in the recovery period when the patient is stable without iv fluid infusion. ā€¢ Premature use of furosemide may precipitate a shock state
  • 40. ā€¢ Pitfall 26: Use of renal replacement therapy during the critical phase in a patient has severe metabolic acidosis and oliguria. ā€¢ Severe metabolic acidosis and oliguria are the consequences of uncorrected and prolonged shock. ā€¢ The haemodialysis machine will face technical problems with drawing blood from the hypovolaemic patient. ā€¢ Solution: ā€¢ Reserved for patients who are already in the recovery phase, who are haemodynamically stable, are fluid overloaded and have oliguria not responding to furosemide therapy. -haemodialysis works very well and effective in preventing life threatening pulmonary oedema.
  • 41. Blood transfusions for severe bleeding ā€¢ Pitfall 28: Not transfusing blood until the haematocrit has decreased to low levels in unstable patients. ā€¢ Severe but occult bleeding can be difficult to recognize . ā€¢ The haematocrit will only decrease to low levels after several boluses of fluid resuscitation (especially with colloids), or if the bleeding has been very severe. ā€¢ During fluid resuscitation the patient remains unstable while the ā€œthird spaceā€ fluid accumulation increases
  • 42. ā€¢ Solution: ā€¢ Lower the haematocrit in dengue shock , the more likely the significant bleeding, and therefore it is vital to change from crystalloid/colloid infusion to blood transfusion. ā€¢ This change in strategy will prevent excessive infusion of non-blood fluids and accumulation of ā€œthird spaceā€ fluid. ā€¢ Bleeding should always be considered as a possible cause of prolonged/profound shock. ā€¢ On the contrary, haematocrit is very useful in recognizing severe bleeding, provided that it is interpreted together with other clinical parameters.
  • 43. ā€¢ Pitfall 29: DIC regime for severe bleeding. ā€¢ The causes of severe bleeding in dengue are not well understood. ā€¢ These patients have thrombocytopenia, deranged coagulation and disseminated intravascular coagulopathy. ā€¢ Therapy with multiple transfusions of fresh frozen plasma, platelet concentrates and cryoprecipitate. ā€¢ Unless transfusion with fresh whole blood is given urgently, the patient will succumb to haemorrhagic shock with massive third space accumulation.
  • 44. ā€¢ Solution: ā€¢ Repeated blood transfusions should be guided by clinical assessment, haematocrit levels, blood gas and lactate analysis. ā€¢ Bleeding will usually decrease once the critical phase is over, as manifested by decreasing tachycardia and improved peripheral perfusion. ā€¢ It is important to request fresh whole blood. ā€¢ Stored blood does not have the same properties as fresh whole blood and may not reverse the clinical situation
  • 45. ā€¢ Pitfall 30: Blood transfusion when the haematocrit is on the rise in a shocked patient. ā€¢ Fluid boluses that are administered aggressively in compensated shock may give impression of refractory shock and prompt the physician into changing from crystalloid fluid to blood transfusion. ā€¢ The subsequent haematocrit will rise even more sharply after the blood transfusion and prompt the physician to give more crystalloids even though the haemodynamic situation is stable. ā€¢ The patient will become fluid overloaded.
  • 46. ā€¢ Solution: ā€¢ If haematocrit continues to rise despite fluid resuscitation, consider using a colloid bolus at 10 to 20 ml/kg. ā€¢ If the shock patient has a normal systolic BP, there is no need to rush the fluid resuscitation. ā€¢ Aggressive fluid resuscitation over 15 minutes should be reserved for those with hypotension
  • 47. ā€¢ Pitfall 31: Blood transfusion in a stable patient with low haematocrit. ā€¢ This usually occurs during the recovery period when re-absorption causes haemodilution. ā€¢ A blood transfusion at this stage may precipitate life-threatening pulmonary oedema. ā€¢ Solution: ā€¢ If the patient has a stable circulation they do not need blood transfusion. ā€¢ The haematocrit will increase after the excess fluid has been diuresed.
  • 48. ā€¢ Pitfall 32: Severe shock and inotropes. ā€¢ 40āˆ’60 ml/kg of fluid administration and have failed to reverse the shock state-initiate inotropes such as dobutamine or dopamine and norepinephrine . ā€¢ Refractory shock is the most common cause of death within 24āˆ’48 hours of admission. ā€¢ There is usually a combination of plasma leakage and bleeding following prolonged uncorrected shock accompanied by renal and liver impairment.
  • 49. ā€¢ Solution: ā€¢ After every bolus infusion of 10āˆ’20 ml/kg, there should be a re-evaluation of the haemodynamic state. ā€¢ If there is no clinical improvement, a repeat haematocrit should be done. ā€¢ A rising haematocrit or an haematocrit that is still high, would suggest ongoing plasma leakage and change to colloid solution. ā€¢ A decrease in haematocrit suggests significant bleeding and proceed to transfuse matched fresh whole blood as soon as possible ā€¢ Colloids and inotropes should be used as a temporary measure.
  • 50. ā€¢ Pitfall 33: Liver enzymes and multi-organ involvement may prompt multi-specialty referrals resulting in several ā€œsingle organā€ treatments. ā€¢ The multi-organ involvement is mainly due to shock with tissue hypoperfusion and diminished oxygen delivery. ā€¢ Solution ā€¢ Prioritize achievement of haemodynamic stability and improved tissue oxygenation by fluid, colloid, or blood administration ā€¢ All other outstanding clinical issues (except hypoglycaemia and electrolyte imbalances) should await achievement of haemodynamic stability
  • 51. SUMMARY ā€¢ Intravenous fluid therapy is life-saving in dengue shock. However, there is a ā€œnarrow therapeutic indexā€. ā€¢ Fluids have to be given timely, at the appropriate volume, rate, of the appropriate type (crystalloids, colloid and/or blood) and for the appropriate duration. ā€¢ Progression of the disease through the critical phase should be tracked in hours of plasma leakage. ā€¢ Recognizing the cues to discontinue IV fluid therapy is just as important as knowing when to start it. ā€¢ Given time and haemodynamic stability, other issues such as thrombocytopenia, coagulopathy and raised liver enzymes will recover spontaneously or with supportive care.