Anda di halaman 1dari 6

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.


 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.  The mature particle of the dengue virus is spherical with a diameter
 Intravenous hydration is the therapy of choice. of 50nm containing multiple copies of 3 structural proteins, a host-
 Triage, appropriate treatment, and decision where treatment derived membrane bilayer and a single copy of a (+)-sense, single
should be given is influenced by the case classification of dengue. stranded RNA genome
 Symptomatic dengue virus infections were grouped into 3:  The genome is cleaved by host and viral proteases in 3 structural
1. Undifferentiated Fever proteins:
2. Dengue Fever (DF)  Capsid (C)
3. Dengue Hemorrhagic Fever (DHF), classified further into 4:  Precursor of membrane (M)
 Grade I  Envelope (E)
 Grade II  7 non-structural proteins (NS)
 Grade III  Asian genotypes of DEN-2 and DEN-3 are frequently associated
Dengue Shock Syndrome (DSS)
 Grave IV with severe disease accompanying secondary dengue infections.
 For practical reasons, it was desirable to split the large group of
patients with non-severe dengue into 2 sub-groups: Vector
 Patients with warning signs  Dengue viruses are transmitted to humans through the bites of
 Patients without warning signs 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.

 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
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.
 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.
Page 1 of 6
Viral Transmission CRITICAL PHASE
 Dengue virus circulating in the blood of the humans is ingested by  Around the time of defervescence, when the temperature drops to
the female mosquitoes during feeding. 37.5 – 38oCor less and remains below this level, usually on days
 The virus infects the mosquito mid-gut and subsequently spreads 3-7 of illness, an increase in capillary permeability in parallel with
systematically over a period of 8-12 days. increasing hematocrit levels may occur.
 After the extrinsic incubation period, the virus can be transmitted to  This marks the beginning of critical phase.
other humans by subsequent probing or feeding.  The period of clinically significant plasma leakage usually lasts
 The mosquito remains infective for the rest of its life. for 24-48 hours.
 Vertical transmission has been demonstrated in the laboratory  Progressive leukopenia followed by a rapid decrease in platelet
but rarely in the field. count usually precedes plasma leakage.
 At this point, patients without an increase in capillary
CLINICAL MANAGEMENT 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
 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
 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.

 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,
 After the incubation period, the illness begins abruptly and is hemodynamic status stabilizes, and diuresis ensues.
followed by three phases:  Some may have rash of isles of white in the sea of red.
 Febrile  Some may experience generalized pruritus.
 Critical  Bradycardia and ECG changes are common during this stage.
 Recovery  Hematocrit may normalize or become lower due to dilution effect of
 Key is early recognition and understanding of the clinical problems reabsorbed fluid.
during the different phase of the disease, leading to a rational  WBC count may start to rise soon after defervescence, but platelet
approach to case management and good clinical outcome. count increase is typically later than that of the WBC.
 Respiratory distress and ascites may occur at any time if excessive
FEBRILE PHASE IV fluids have been administered.
 Patients develop high-grade fever suddenly.
 Usually lasts 2-7 days and is often accompanied by facial flushing, The following problems arise during the different phases of dengue:
skin erythema, generalized body ache, myalgia, arthralgia, and
 Some have sore throat, injected pharynx, and conjunctival injection
 Anorexia, nausea, and vomiting are common.  Dehydration  Shock from  Hypervolemia (if IV
 Monitor for warning signs and other clinical parameters.  High grade fever plasma leakage therapy has been
 Mild hemorrhagic manifestations like petechiae and mucosal may cause  Severe excessive or has
neurological hemorrhage extended into this
membrane bleeding may be seen.
 Massive vaginal bleeding (in women of childbearing age) and GI
disturbances and  Organ impairment period)
febrile seizures in
bleeding may occur in this phase, but is not common.
young children
 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.

Page 2 of 6
 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
pulse pressure narrows as the peripheral vascular resistance
 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
 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
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
 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
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.

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

Page 4 of 6
 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
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-
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.
 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

Repeat 3rd Hct

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