Far Eastern University – Nicanor Reyes Medical Foundation TRANSMISSION

Internal Medicine 3A – Infectious Diseases Virus

 Dengue Virus (DEN) is a small single-stranded RNA virus
Dengue comprising four distinct serotypes (DEN-1 to -4), belongs to the
genus Flavivirus, family Flaviviridae.
WHO DENGUE GUIDELINES

DENGUE CASE CLASSIFICATION

 Dengue has a wide spectrum of clinical presentations, often with
unpredictable clinical evolution and outcome.
 While most patients recover following a self-limiting non-severe
clinical course, a small proportion progress to severe disease,
mostly characterized by plasma leakage with or without
hemorrhage.
 Intravenous hydration is the therapy of choice.
 Triage, appropriate treatment, and decision where treatment
should be given is influenced by the case classification of dengue.
 Symptomatic dengue virus infections were grouped into 3:
1. Undifferentiated Fever
2. Dengue Fever (DF)
3. Dengue Hemorrhagic Fever (DHF), classified further into 4:
 Grade I
 Grade II
 Grade III
Dengue Shock Syndrome (DSS)
 Grave IV
 For practical reasons, it was desirable to split the large group of
patients with non-severe dengue into 2 sub-groups:
 Patients with warning signs
 Patients without warning signs
 The mature particle of the dengue virus is spherical with a diameter
of 50nm containing multiple copies of 3 structural proteins, a host-
derived membrane bilayer and a single copy of a (+)-sense, single
stranded RNA genome
 The genome is cleaved by host and viral proteases in 3 structural
proteins:
 Capsid (C)
 Precursor of membrane (M)
 Envelope (E)
 7 non-structural proteins (NS)
 Asian genotypes of DEN-2 and DEN-3 are frequently associated
with severe disease accompanying secondary dengue infections.
Vector
 Dengue viruses are transmitted to humans through the bites of
infected Aedes mosquitoes, principally Aedes aegypti.
 This mosquito is a tropical and subtropical species widely
distributed around the world.
 These mosquitoes cannot survive in winters.
 Immature stages are found in water-filled habitats, mostly in
artificial containers closely associated with human dwellings and
often indoors.
 Dengue outbreaks have also been attributed to Aedes albopictus,
Aedes polynesiensis, and several species of Aedes scutellaris.

Host
 After an incubation of 4-10 days, infection by any of the 4
serotypes can produce a wide spectrum of illness, although most
PROBABLE DENGUE – live in WARNING SIGNS infections are asymptomatic or subclinical.
or travel to dengue endemic  Abdominal Pain / tenderness  Primary infection is thought to induce lifelong protective immunity
area with fever and 2 of the ff:  Persistent vomiting to the infecting serotype.
 Nausea, vomiting  Clinical fluid accumulation  Individuals suffering an infection are protected from clinical illness
with a different serotype within 2-3 months of the primary infection
 Rash  Mucosal bleeding
but with no long-term cross-protective immunity.
 Aches and pains  Lethargy, restlessness  Individual risk factors determine the severity of disease:
 (+) Tourniquet test  Liver enlargement (>2cm)  Secondary infection
 Leukopenia  Lab: increase in HCT  Age, ethnicity, chronic diseases
concurrent with rapid  Younger children may be less able to compensate for capillary
 Any warning sign decrease in platelet count leakage hence greater risk for dengue shock
 The dengue virus enters via the skin while an infected mosquito is
CRITERIA FOR SEVERE DENGUE taking a blood meal.
Severe Plasma Severe organ  During the acute phase, virus is present in the blood and its
Severe bleeding
Leakage leading to: involvement clearance from this compartment generally coincides with
 Shock (DSS)  AST/ALT ≥ 1,000 defervescence.
 Humoral and cellular immune responses are considered to
 Impaired
 Fluid accumulation As evaluate by a contribute to viral clearance via the generation of neutralizing
clinician consciousness
with respiratory antibodies and activation of CD4 and CD8 lymphocytes.
 Heart and other
distress  Endothelial activation could mediate plasma leakage associated
organs
with functional rather than destructive effects on the endothelium.
 Activation of infected monocytes and T cells, the complement, and
LABORATORY-CONFIRMED DENGUE: Important when there are
production of mediators may be involved in endothelial cell
no signs of plasma leakage.
dysfunction.
 Thrombocytopenia may be associated with alterations in
megakaryocytes by the infection of human hematopoietic cells and
impaired progenitor growth.
 Hemorrhage may be a consequence of the thrombocytopenia and
platelet dysfunction, or DIC.
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Viral Transmission
 Dengue virus circulating in the blood of the humans is ingested by
the female mosquitoes during feeding.
 The virus infects the mosquito mid-gut and subsequently spreads
systematically over a period of 8-12 days.
 After the extrinsic incubation period, the virus can be transmitted to
other humans by subsequent probing or feeding.
 The mosquito remains infective for the rest of its life.
 Vertical transmission has been demonstrated in the laboratory
but rarely in the field.
CLINICAL MANAGEMENT
 After the incubation period, the illness begins abruptly and is
followed by three phases:
 Febrile
 Critical
 Recovery
 Key is early recognition and understanding of the clinical problems
during the different phase of the disease, leading to a rational
approach to case management and good clinical outcome.
FEBRILE PHASE
 Patients develop high-grade fever suddenly.
 Usually lasts 2-7 days and is often accompanied by facial flushing,
skin erythema, generalized body ache, myalgia, arthralgia, and
headache.
 Some have sore throat, injected pharynx, and conjunctival injection
 Anorexia, nausea, and vomiting are common.
 Monitor for warning signs and other clinical parameters.
 Mild hemorrhagic manifestations like petechiae and mucosal
membrane bleeding may be seen.
 Massive vaginal bleeding (in women of childbearing age) and GI
bleeding may occur in this phase, but is not common.
 Liver is usually enlarged and tender after few days of fever.
 Earliest abnormality in CBC is progressive decrease in total WBC
count, which should alert the physician of possibility of dengue.
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CRITICAL PHASE
 Around the time of defervescence, when the temperature drops to
37.5 – 38oCor less and remains below this level, usually on days
3-7 of illness, an increase in capillary permeability in parallel with
increasing hematocrit levels may occur.
 This marks the beginning of critical phase.
 The period of clinically significant plasma leakage usually lasts
for 24-48 hours.
 Progressive leukopenia followed by a rapid decrease in platelet
count usually precedes plasma leakage.
 At this point, patients without an increase in capillary
permeability will improve.
 While those with increased capillary permeability may become
worse as a result of lost plasma volume.
 Pleural effusion and ascites may be clinically detectable.
 Degree of increase above the baseline hematocrit reflects the
severity of the plasma leakage.
 Shock occurs when a critical volume is lost through leakage, it is
often preceded by warning signs.
 The body temperature may be subnormal when shock occurs.
 With prolonged shock, consequent organ hypoperfusion results
in progressive organ impairment, metabolic acidosis, and DIC.
 This in turn leads to severe hemorrhage causing the hematocrit
to decrease in severe shock.
 WBC count may increase in patients with severe bleeding.
 Severe hepatitis, encephalitis, or myocarditis or severe
bleeding may also develop without obvious plasma leakage or
shock.
 Those who improve after defervescence are said to have, non-
severe dengue.
 Some patients progress to critical phase of plasma leakage without
defervescence and, in these patients, changes in full blood count
should be used to guide the onset of critical phase and plasma
leakage.
 Those who deteriorate will manifest warning signs, this is called
dengue with warning signs, and they will probably recover with
early IV rehydration.
 Some cases will deteriorate to severe dengue.
RECOVERY PHASE
 If the patient survives the 24-48 hour critical phase, a gradual
reabsorption of the extravascular compartment fluid takes place in
the following 48-72 hours.
 General well-being improves, appetite returns, GI symptoms abate,
hemodynamic status stabilizes, and diuresis ensues.
 Some may have rash of isles of white in the sea of red.
 Some may experience generalized pruritus.
 Bradycardia and ECG changes are common during this stage.
 Hematocrit may normalize or become lower due to dilution effect of
reabsorbed fluid.
 WBC count may start to rise soon after defervescence, but platelet
count increase is typically later than that of the WBC.
 Respiratory distress and ascites may occur at any time if excessive
IV fluids have been administered.
The following problems arise during the different phases of dengue:
FEBRILE PHASE CRITICAL PHASE RECOVERY PHASE
 Dehydration  Shock from  Hypervolemia (if IV
 High grade fever plasma leakage therapy has been
may cause  Severe excessive or has
neurological hemorrhage extended into this
disturbances and  Organ impairment period)
febrile seizures in
young children
SEVERE DENGUE
 Defined by 1 or more of the following:
 Plasma leakage that may lead to shock (dengue shock) and/or
fluid accumulation with or without respiratory distress, and/or;
 Severe bleeding, and/or;
 Severe organ impairment.
 As dengue vascular permeability progresses, hypovolemia
worsens and results in shock.
 It usually takes around defervescence phase, usually on day 4 or 5
(range days 3-7) of illness, preceded by warning signs.
 During initial stage, compensatory mechanisms maintain normal
systolic BP producing tachycardia and peripheral vasoconstriction
with reduced skin perfusion, resulting in cold extremities and
delayed capillary refill time.
 The diastolic pressure rises towards the systolic pressure and the
RECOMMENDATIONS FOR TREATMENT
pulse pressure narrows as the peripheral vascular resistance
increases.
STEPWISE APPROACH FOR MANAGEMENT
 Patients often remain conscious and lucid.
STEP I – Overall Assessment
 Patient is considered to have shock if the pulse pressure (SBP-
 History
DBP) is:
 Date of onset of fever/illness
 ≤20 mmHg in children or has signs of poor capillary perfusion.
 Quantity of oral intake
 ≤20mmHg in adults may indicate a more severe shock.
 Warning signs
 Patients with severe dengue may have coagulation abnormalities,
 Diarrhea
but these are usually not sufficient to cause major bleeding.
 Change in mental status
 When major bleeding occurs, it is almost always associated
with profound shock, since this is in combination with  Urine output (frequency, volume, time of last void)
thrombocytopenia, hypoxia, and acidosis.  Relevant histories (travel, neighborhood dengue, co-existing
 Can lead to multiple organ failure and DIC. conditions, recent unprotected sex or drug abuse).
 Massive bleed can occur in patients taking aspirin, ibuprofen,  Physical Examination
or steroids.  Mental State
 Unusual manifestations include:  Hydration Status
 Acute liver failure and encephalopathy.  Hemodynamic Status (table below)
 Cardiomyopathjy  Check for tachypnea, acidotic breathing, pleural effusion
 Encephalitis  Check for abdominal tenderness, hepatomegaly, ascites
 Examination of rash or bleeding manifestations
Severe dengue should be considered if the patient is from an area of  Tourniquet test (repeat if previously negative or no bleeding).
dengue risk with fever of 2-7 days plus any of the ff:
 Evidence of plasma leakage Hemodynamic Status Assessment:
 High or progressively increasing hematocrit COMPENSATED HYPOTENSIVE
PARAMETER STABLE
 Pleural effusion or ascites SHOCK SHOCK
 Circulatory compromise
 Significant bleeding Hypotensive Change of mental
Clear, Lucid Clear, Lucid
 Altered mental status (lethargy, restlessness, coma, seizures) Shock state
 Severe GI involvement Capillary Refill Very prolonged
 Severe organ impairment (unusual manifestations) Brisk <2s Prolonged >2s
Time Mottled Skin
Extremities Warm, Pink Cool Cold, Clammy
CLINICAL SERVICES AND MANAGEMENT Peripheral
Good Weak, Thready Feeble, Absent
 Activities at the first level of care: Pulse Volume
 Recognizing the febrile patient could have dengue. Severe tachy with
Heart Rate Normal Tachycardia
 Notify early to public health authorities. brady in late shock
 Manage patients in the early febrile phase. Normal systolic
 Recognize early stage of plasma leakage or critical phase and Rising diastolic Narrowed PP <20
initiating fluid therapy. Blood
Normal Narrowing PP Hypotension
Pressure
 Recognizing patients with warning signs needed to be referred Postural Unrecordable BP
for admission or IV fluid therapy to a secondary health facility hypotension
 Recognizing and managing severe plasma leakage and shock, Metabolic acidosis
severe bleeding, and severe organ impairment promptly. Respiratory
Normal Tachypnea Hyperpnea
Rate
Kussmaul’s
PRIMARY AND SECONDARY HEALTH CARE CENTERS
Hypotension – SBP <90, MAP <70 or SBP decrease of >40 or <2SD below
 Responsible for emergency or ambulatory triage. normal in adults. In children up to 10, the 5th percentile for SBP can be
 Triage is the process of rapidly screening patients soon after their determined by the formula: 70+(age in yearsx2).
arrival in order to identify those with severe dengue (who should be  Investigation
given emergency treatment), those with warning signs (who should  Full CBC should be done.
be given priority while waiting), and non-urgent cases (who have  Hematocrit in the early febrile phase establishes baseline
neither severe dengue nor warning signs).  Decreasing WBC makes dengue very likely
 Healthcare workers should apply a stepwise approach:  Rapid decrease platelet in parallel with a rising hematocrit
compared to baseline is suggestive of progressive to the
plasma leakage / critical phase.

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  If baseline hematocrit is not present, age-specific population
hematocrit can be used as surrogate during critical phase.
STEP II – DIAGNOSIS, ASSESSMENT
 Determine whether the disease is dengue and which phase is it in.
 Determined if there are warning signs.
 Determine the hydration status and hemodynamic status and
whether the patient requires admission.
STEP III - MANAGEMENT
Treatment according to group
GROUP A
 Patients who may be sent home.
 Able to tolerate adequate volumes of oral fluids.
 Able to pass urine at least once every 6 hours.
 DO NOT have any of warning signs particularly when fever subside
 Should be reviewed daily for disease progression until they are
out of the critical period.
 Those with stable hematocrit can be sent home and advised to
return to hospital immediately if they develop warning signs.
 Encourage intake of ORS, fruit juices, other fluids containing
electrolytes and sugars to replace losses from fever and vomiting.
 Give paracetamol for high grade fever, interval dosing should not
be less than 6 hours.
 Tepid sponge if the patient still has high fever.
 Do not give aspirin or any NSAID.
 Bring to hospital if any of the following occurs:
 No clinical improvement
 Deterioration at time of defervescence
 Severe abdominal pain
 Persistent vomiting
 Cold and clammy extremities
 Lethargy, irritability, restlessness
 Bleeding (melena or hematemesis)
 Not passing urine for more than 4-6 hours
 Monitor daily for fluid intake, temperature pattern, urine output,
warning signs.
GROUP B
 Patients who should be referred for in-hospital management.
 Patients may need to be admitted for close monitoring as they
approach the critical phase, these include patients with:
 Warning signs
 Co-existing conditions that may make dengue more
complicated (pregnancy, infancy, old age, obesity, DM, renal
failure, chronic hemolytic diseases)
 Social circumstances (living alone or far from health facilities)
 If dengue patient HAS WARNING SIGNS, the action plan should
be followed:
 Obtain reference hematocrit before fluid therapy.
 Give only isotonic solutions
 0.9% Saline
 Ringer’s Lactate
 Hartmann’s Solution
 Start with 5-7ml/kg/hr for 1-2 hours, then reduce to 3-5
ml/kg/hr for 24 hours, and then reduce to 2-3 ml/kg/hr or less
according to the clinical response.
 Reassess the clinical status and repeat the hematocrit.
 If hematocrit remains the same or rises only minimally,
continue with same rate 2-3 ml/kg/hr for another 24 hrs.
 If vital signs are worsening and hematocrit is rising rapidly,
increase to 5-10 ml/kg/hr for 1-2 hours
 Reassess clinical status, repeat hematocrit, and review fluid
infusion rates accordingly.
 Give minimum IV fluid required to maintain good perfusion and
urine output of about 0.5ml/kg/hr.
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 IV fluids are usually only needed for 24-48 hours, reduce
gradually when the rate of plasma leakage decreases towards
the end of critical phase.
 This is indicated by urine output and/or oral fluid intake that is
adequate or hematocrit decreasing below the baseline value in
a stable patient.
 Parameters that should be monitored include:
 Vital Signs
 Peripheral Perfusion (1-4 hourly until out of critical phase)
 Urine output (4-6 hourly)
 Hematocrit (before and after fluids, then 6-12 hourly)
 Blood Glucose
 Other organ functions (renal, liver, coagulation profiles)
 If the patient has dengue WITHOUT WARNING SIGNS the action
plan should be as follows:
 Encourage oral fluids.
 If not tolerated, start IV fluids of 0.9% saline or Ringer’s lactate
with or without dextrose at maintenance rate.
 For obese and overweight, use IBW for calculation of infusion.
 Give the minimum volume required to maintain good perfusion
and urine output, IV fluids are usually needed for 24-48 hours.
 Patients should be monitored by health care providers.
GROUP C
 Patients who require emergency treatment and urgent referral
when they have severe dengue:
 Severe plasma leakage leading to dengue shock and/or fluid
accumulation with respiratory distress
 Severe hemorrhages
 Severe organ impairment
 All patients with severe dengue should be admitted to a hospital
with access to intensive care facilities and blood transfusion.
 Judicious fluid resuscitation is the essential and usually sole
intervention required.
 Crystalloid solution should be isotonic and the volume just
sufficient to maintain an effective circulation during the period of
plasma leakage.
 In case of hypotensive shock, colloid solutions can be used to
immediately replace plasma losses.
 Continued replacement of plasma losses to maintain effective
circulation for 24-48 hours.
 Group and cross-match should be done for all shock patients.
 Fluid resuscitation must be clearly separated from simple fluid
administration. This is a strategy in which larger volumes of fluids
(e.g. 10-20ml boluses) are administered for a limited period of time
under close monitoring.
 Goals of resuscitation include:
 Improving central and peripheral circulation (decrease
tachycardia, improve BP, pulse volume, warm and pink
extremities, and capillary refill time <2 seconds).
 Improving end-organ perfusion
 Urine output >0.5 ml/kg/hour
 Decreasing metabolic acidosis.
Treatment of Shock
 Start IV fluid resuscitation with isotonic crystalloid at 5-10 ml/kg/hr
over one hour, then reassess.
 If the patient’s condition improves, IV fluid should be gradually
reduced to 5-7ml/kg/hr for 2 hours, then 3-5ml/kg/hr for 2-4
hours, then to 2-3ml/kg/hr, and then further depending on
hemodynamic status, can be maintained for 24-48 hours.
 If the vital signs are unstable, check hematocrit after first bolus.
 If Hct increases or still high (>50%), repeat a second bolus of
crystalloid at 10-20ml/kg/hr for 1 hour.
 If there is improvement, reduce to 7-10ml/kg/hr for 1-2 hrs, then
continue to reduce as above.
 If Hct decreases (<40% in children and female, <45% males),
this indicates bleeding, cross-match and transfuse as soon as
possible.
  Further boluses of crystalloid or colloid may be given during the
next 24-48 hours.  Patients should be frequently monitored until the danger period is
over, parameters to measure include:
Algorithm for Fluid Management in Compensated Shock  Vital Signs
 Peripheral perfusion (every 15-30 minutes until out of shock,
COMPENSATED SHOCK then 1-2 hourly).
(Systolic pressure maintained, but has signs of reduced perfusion)  If possible, use indwelling arterial catheter for continuous
 Fluid resuscitation - isotonic crystalloid (5-10 ml/kg/hr over 1 hr) monitoring and reproducible BP measurements and frequent
 FBC, HCT, before and after fluid resuscitation, BUSEC, LFT, RBS, blood sampling.
PT/APTT, Lactate/HCO3, GXM  Monitor ECG and pulse oximetry
 Urine output check regularly (hourly till patient is out of shock
then 1-2 hourly), continuous bladder catheter enables close
YES NO monitoring, acceptable output would be 0.5 ml/kg/hr
IMPROVEMENT  Hematocrit must be monitored (before and after fluid boluses
until stable, then 4-6 hourly).
 Monitor blood gases, lactate, total CO2/HCO3 (every 30
minutes to 1 hour until stable, then as indicated.
 IV crystalloid 5-7ml/kg/hr Check Hct
 Monitor other organ functions
for 1-2 hours then:
 Reduce to 3-5 for 2-4h
Algorithm for Fluid Management in Hypotensive Shock
 Reduce to 2-3 for 2-4h ↑ Hct ↓ Hct
 If patient improves, fluid HYPOTENSIVE SHOCK
can be further reduced.  Fluid resuscitation - isotonic crystalloid or colloid (10-20
 Monitor Hct 4-6 hourly Administer 2nd Consider
ml/kg/hr over 15 minutes)
 If patient is not stable, act bolus of fluid at significant
 Try to obtain Hct level before resuscitation.
according to Hct: 10-20ml/kg/hr for occult or
 If Hct increases, 1 hour. overt bleed,
consider bolus fluids or transfuse
YES NO
increase fluid blood IMPROVEMENT
administration IMPROVEMENT
 If Hct decreases, NO
consider transfusion YES
 IV crystalloid 5-7ml/kg/hr Review 1st Hct
with fresh whole blood. If patient improves, for 1-2 hours then:
 Consider to stop IV at 48 reduce to 7-10ml/kg/hr.  Reduce to 3-5 for 2-4h
hours of plasma leakage or for 1-2 hours, and then  Reduce to 2-3 for 2-4h ↑ Hct ↓ Hct
defervescence reduce further  If patient improves, fluid
can be further reduced.
Administer Consider
 Monitor Hct 4-6 hourly
2nd bolus of significant
Treatment for patients with Hypotensive Shock  If patient is not stable, act
 Initiate IV fluid with crystalloid or colloid (if available) at 20 ml/kg as fluid at 10- bleeding,
according to Hct: 20ml/kg/hr transfuse
bolus given over 15 minutes to bring patient out of shock as  If Hct increases,
quickly as possible. for 30m- 1h whole blood
consider bolus fluids or
 If patients improves, give crystalloid or colloid at 10ml/kg/hr for 1
increase fluid
hours, then continue with crystalloid, and gradually reduce at 5-
administration
7ml/kg/hour for 1-2 hours, then 3-5ml/ml/hr for 2-4 hours, and IMPROVEMENT
 If Hct decreases,
then 2-3 ml/kg/hr or less, which can be maintained for up to 48h.
 If vital signs are still unstable, review the hematocrit obtained consider transfusion NO
before the first bolus. with fresh whole blood.
YES
 If Hct was low (<40% children, females and <45% males),  Consider to stop IV at 48
Repeat 2nd Hct
this indicates bleeding, cross-match then transfuse blood. hours of plasma leakage or
 If Hct was high (>50%), change IV fluid to colloid at 10-20 defervescence
ml/kg as a second bolus over 30 minutes to 1 hr.
 After second bolus, reassess the patient, if patient improves,
reduce rate to 7-10ml/kg/hr then return to crystalloid. ↑ Hct ↓ Hct
 If still unstable, repeat hematocrit after second bolus.
 If decreasing hematocrit, transfuse blood.
 If remains increased, continue colloid at 10-20ml/kg/hr as Administer 3rd bolus of
third bolus, reduce to 7-10ml/kg/hour for 1-2 hours then fluid at 10-20ml/kg/hr
change back to crystalloid and reduce rate of infusion. for 1h
 Further boluses may need to be given during the next 24 hours.
 Patients with severe dengue should be admitted to the high
dependency or intensive care area. IMPROVEMENT
YES
NO

Repeat 3rd Hct

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TREATMENT OF HEMORRHAGIC COMPLICATIONS
 Mucosal bleeding may occur in any patients with dengue, but itf the
patient remains stable, it should be considered as minor.
 Bleeding usually improves rapidly during the recovery phase.
 In patients with profound thrombocytopenia, ensure strict bed rest
and protect from trauma.
 Do not give IM injections to avoid hematoma.
 Prophylactic platelet transfusion has NOT BEEN shown to be
effective and necessary.
 If major bleeding occurs, it is usually from the GIT or vagina.
Internal bleeding may not become apparent for many hours until
the first black stool is passed.
 Patients at risk for major bleeding:
 Prolonged/Refractory shock
 Hypotensive shock
 Renal or liver failure and persistent metabolic acidosis
 Given NSAIDs
 Preexisting PUD
 On anticoagulant therapy
 Have any form of trauma, including IM injection.
 Patients with hemolytic conditions are at risk for acute hemolysis
with hemoglobinuria, and will require blood transfusion.
 Severe bleeding can be recognized by:
 Overt bleeding in the presence of unstable hemodynamic
status, regardless of hematocrit level
 Decrease in hematocrit after fluid resuscitation with unstable
hemodynamic status.
 Refractory shock that fails to respond to 40-60 ml/kg fluid
 Hypotensive shock with low/normal hematocrit after fluids
 Persistent or worsening metabolic acidosis +/- a well
maintained systolic pressure, especially those with severe
abdominal tenderness and distention.
 Action plan for hemorrhagic complications:
 Give 5-10 ml/kg of fresh packed red cells or 10-20ml/kg of
fresh whole blood at an appropriate rate and observe the
clinical response (improving hemodynamic status and acid-
base balance).
 Oxygen delivery is optimal with high levels of 2,3 DPG, with
stored blood, 2,3 DPG levels decrease which impede
oxygen-releasing capacity of hemoglobin
 Consider repeating transfusion if there is further blood loss or
no appropriate rise in hematocrit
 Great care should be taken when inserting NGT which may
cause severe hemorrhage, a lubricated oro-gastric tube may
minimize trauma.
TREATMENT OF COMPLICATIONS
FLUID OVERLOAD
 Fluid overload with large pleural effusions and ascites is a common
cause of acute respiratory distress and failure in severe dengue.
 Causes are:
 Excessive or too rapid infusion
 Incorrect use hypotonic rather than isotonic
 Inappropriate use of large volumes with unrecognized severe
bleeding.
 Inappropriate transfusion of FFP, platelet concentrates
 Continuation of IV after leakage has resolved
 Co-morbid conditions (heart, lung, and renal diseases)
 Early clinical features of fluid overload are:
 Respiratory distress, DOB
 Rapid breathing
 Chest wall in-drawing
 Wheezing (rather than crepitations)
 Large pleural effusions
 Tense ascites
 Increased JVP
Page 6 of 6
 Late clinical features are:
 Pulmonary edema (cough with pink frothy sputum with or
without crepetations, cyanosis).
 Irreversible shock (heart failure with hypovolemia)
 Additional investigations:
 Chest X-ray – cardiomegaly, upward displacement of the
diaphragm, bat’s wings appearance, Kerley B lines.
 ECG
 ABG
 2D Echo
 Cardiac Enzyme
 Action plan for treatment of fluid overload
 Oxygen therapy should be given immediately
 Stop IV fluid during recovery phase, resulting to diuresis and
resolution of ascites and effusion.
 When the ff. signs are present, IV fluids should be discontinued
or reduced to minimum rate necessary to maintain euglycemia:
 Signs of cessation of plasma leakage
 Stable BP, pulse, peripheral perfusion
 Hct decreases with good pulse volume
 Afebrile for more than 24-48h without use of antipyretics
 Resolve bowel/abdominal symptoms
 Improving urine output
 If patient is hemodynamically stable and is out of critical phase,
STOP intravenous fluid infusion but closely monitor
 If necessary, can give oral or IV furosemide 0.1-0.5 mg/kg per
dose once or twice daily, or a continuous infusion at
0.1mg/kg/hour.
 Monitor serum potassium and correct ensuing hypokalemia
 If patient is hemodynamically stable but is still within critical
phase, reduce the IV fluid accordingly, avoid diuretics.
 Patients who remain in shock with low or normal hematocrit but
show signs of fluid overload may have occult hemorrhage.
Other Complications of Dengue
 Hyperglycemia/Hypoglycemia
 Hyponatremia, hypokalemia, hyperkalemia, serum calcium
imbalances, and metabolic acidosis (sodium bicarbonate for
acidosis is not recommended for pH >7.15).
 Watch out for co-infections or nosocomial infections.
Supportive Care and Adjuvant Therapy
 Renal replacement therapy, preference for continuous veno-
venous hemodialysis (CVVH), since peritoneal dialysis has risks of
bleeding.
 Vasopressor and inotropic therapies for hypotension.
 Further treatment of organ impairment.
 Treatment of cardiac abnormalities.