Dengue Mortality and Morbidity Conference

Mortality and Morbidity Conference

September 24, 2009

IDJ 34 years old, Female Dulonan, Arevalo, Iloilo City August 3, 2009 2:30 PM

General Data

Fever

Chief Complaint

2 days PTA◦ Low grade, intermittent fever◦ CBC requested

History of Present Illness

CBC Hemoglobin= 132 Hematocrit= 0.41 RBC= 4.59 WBC=3.6 Segmenters= 0.80 Lymphocytes= 0.18 Eosinophils= 0 Monocytes= 0 Basophils= 0.02 Platelet count= 216

4 hours PTA◦ Persistence of low grade, intermittent

fever◦ Repeat CBC – leukopenia and

thrombocytopenia◦ No bleeding problems

CBC Hemoglobin= 146 Hematocrit= 0.45 ↑ RBC= 5.15 WBC=2.3 Segmenters= 0.54 Lymphocytes= 0.45 Eosinophils= 0.01 Monocytes= 0 Basophils= 0 Platelet count= 78

Previous:Hemoglobin= 132 Hematocrit= 0.41 RBC= 4.59 WBC=3.6 Segmenters= 0.80 Lymphocytes= 0.18 Eosinophils= 0 Monocytes= 0 Basophils= 0.02 Platelet count= 216

Non hypertensive Non diabetic Non Asthmatic No history of bleeding dyscrasias No history of PTB No trauma/ surgical procedures Allergy to crustaceans

Past Medical History

Works as a school employee Non smoker, non alcoholic beverage drinker

Personal History

Family History

Unremarkable

Ambulatory, conscious, coherent, oriented, not in cardiopulmonary distress

BP=90/70 mm Hg CR=75 RR=23 Temp=36 C Weight= 71 kg Height= 5’2 Anicteric sclerae, pink palpebral

conjunctivae Good skin turgor, moist lips and buccal

mucosa No neck vein engorgement, no cervical

lymphadenopathy, no tonsillopharyngeal congestion

Physical Examination

Adynamic precordium, PMI at 5th ICS left midclavicular line, S1 and S2 normal, regular cardiac rate and rhythm, no murmurs

Symmetrical chest expansion, bronchovesicular breath sounds, no rales, no wheezes

Flat abdomen, normoactive bowel sounds, soft, non-tender, no palpable mass, non-palpable liver edge and spleen, Liver span= 10cm MSL, 6cm MCL

Grossly normal extremities, full peripheral pulses, no edema

Negative tourniquet test

Dengue Fever

Admitting Impression

Undifferentiated fever Classic dengue fever Dengue hemorrhagic fever Dengue shock syndrome

Dengue Clinical Syndromes

Center for Disease Control. Dengue: Clinical and Public Health Aspects, 2008

May be the most common manifestation of dengue

Prospective study found that 87% of students infected were either asymptomatic or only mildly symptomatic

Other prospective studies including all age-groups also demonstrate silent transmission

Source: DS Burke, et al. A prospective study of dengue infections in Bangkok. Am J Trop Med Hyg 1988; 38:172-80.

Undifferentiated Fever

Fever Headache Muscle and joint pain Nausea/vomiting Rash Hemorrhagic manifestations

Clinical Characteristics of Dengue Fever


Influenza Measles Rubella Malaria Typhoid fever Leptospirosis Meningococcemia Rickettsial infections Bacterial sepsis Other viral hemorrhagic fevers

Differential Diagnosis of Dengue


Clinical laboratory tests ◦ CBC—WBC, platelets, hematocrit◦ Albumin◦ Liver function tests◦ Urine—check for microscopic hematuria

Dengue-specific tests ◦ Virus isolation◦ Serology

Laboratory Tests in Dengue Fever


IVF= D5LR 1L x 125 cc/hour D5NSS 1L x 125 cc/hour

Diet: Full, no dark colored foods Laboratories:

◦ CBC◦ Serial platelet count Q4H◦ Dengue Rapid test◦ Typhidot◦ APTT, Protime◦ Chest X-ray PA view◦ ECG◦ Urinalysis

On Admission

CBC Hemoglobin= 146 Hematocrit= 0.45 RBC= 5.15 WBC=2.3 Segmenters= 0.54 Lymphocytes= 0.45 Eosinophils= 0.01 Monocytes= 0 Basophils= 0 Platelet count= 78

Dengue Rapid Test: IgM positive IgG positive

Typhidot Test: IgM negativeIgG negative

Temperature, Virus Positivity, and Anti-Dengue IgM, by Fever Day

APTT◦ 40.2

(Normal value: 26.1-36.3 s) Protime

◦ Control= 14.3◦ Patient= 14.6◦ PTA= 84.6◦ PTR= 1.24◦ ISI= 1.22◦ INR= 1.3

Why is APTT prolonged and Protime Normal in Dengue?

Intrinsic pathway of coagulation cascade is triggered by thrombin activating coagulation factor XI via positive feedback.

Factor XI generates additional thrombin by activation of factors IX and X.

Patients with DHF have a comparatively low level of thrombin-activatable fibrinolysis inhibitor (TAFI).

The function of TAFI is to down-regulate fibrinolysis by removing C-terminal lysine residues that are essential for binding and activation of plasminogen.

Thus, hemorrhagia in DHF results mainly from an inadequate factor XI/thrombin/TAFI feedback loop, which leads to an imbalance between coagulation and fibrinolysis.

Chest X-ray PA view

ECG

Urinalysis Color= straw Transparency= hazy Reaction= 6.5 acidic Specific Gravity= 1.020 Albumin= trace Sugar= negative WBC= 25-40 / hpf (2+) RBC= 8-12/ hpf (2+)

Plans Paracetamol 500 mg/tablet, 1 tablet Q4H

PRN for temp >37.5 C Ranitidine 50 mg IV Q8H Transfusion with 2 units platelet concentrate Referred to Infectious disease and

Hematology sections

First Hospital day (10 hours after)

S: ◦ Epigastric pain

O:◦ Awake, concious, not in cardiopulmonary distress◦ BP= 80/60- 90/70, CR: 80, RR: 20, T: 36.2 C◦ Anicteric sclerae, pinkish conjunctivae◦ (-) neck vein engorgement◦ Adynamic precordium, regular cardiac rate and rhythm,

no murmurs◦ Symmetrical chest expansion, bronchovesicular breath

sounds, (+) bibasal fine rales◦ Flat abdomen, normoactive bowel sounds, soft, (+) direct

tenderness epigastric area◦ Grossly normal extremities◦ (+) tourniquet test

Etiology of Abdominal Pain in Dengue FeverS. Khanna!, J.C. Vij, A. Kumar, D. Singal and R. Tandon

Pushpawati Singhania Research Institute for Liver, Renal and Digestive Diseases, Press Enclave Marg,

Sheikh Sarai, Phase-II, New Delhi-110017, India

Abdominal pain is a commonly reported symptom in DF. The reported causes of abdominal pain in DFinclude hepatitis, pancreatitis, acaculous cholecystitis and peptic ulcer disease. Till to date, there has been no planned study to evaluate the cause of pain abdomen in DF. This study was planned to evaluate the etiology of abdominal pain in DF.

The various causes of pain abdomen diagnosed in patients with DF were: acute hepatitis, acalculus cholecystitis, acute

pancreatitis, appendicitis, spontaneous bacterial peritonitis, enteritis, peptic ulcer disease and gastric erosions in 20 (36.4%), 9 (16.4%), 8 (14.5%), 3 (5.45%), 2 (3.63%), 8 (14.54%), 2 (3.63%) and 3 (5.45%) of the patients respectively.

In patients with dengue fever, the etiology of abdominal pain should be aggressively looked into for proper management.

CBC10 hours after

admission: Hemoglobin= 178 Hematocrit= 0.55 RBC= 6.23 WBC= 3.0 Segmentors= 0.63 Lymphocytes=

0.37 Eosinophils= 0 Basophils= 0 Platelet Count= 66

On Admission: Hemoglobin= 146 Hematocrit= 0.45 RBC= 5.15 WBC=2.3 Segmenters=

0.54 Lymphocytes=

0.45 Eosinophils= 0.01 Monocytes= 0 Basophils= 0 Platelet count=

78

1 day PTA: Hemoglobin= 132 Hematocrit= 0.41 RBC= 4.59 WBC=3.6 Segmenters= 0.80 Lymphocytes= 0.18 Eosinophils= 0 Monocytes= 0 Basophils= 0.02 Platelet count= 216

Protime

10 hours after:◦Control= 14.5◦Patient= 15.7◦PTA= 75.7◦PTR= 1.33◦ISI= 1.22◦INR= 1.42

On admission:◦ Control= 14.3◦ Patient= 14.6◦ PTA= 84.6◦ PTR= 1.24◦ ISI= 1.22◦ INR= 1.3

Chest X-ray

ABG FIO2= 52% pH= 7.35 pCO2= 28 pO2= 138 HCO3= 18 sO2= 99% pAO2/FI02 ratio=265.38 mm Hg Required FIO2= 22% HCO3 deficit= 56.8 meqs in 24 hours

Definition Criteria for ALI and ARDS Criteria for ALI

◦ Acute in onset ◦ Oxygenation: A partial pressure of arterial oxygen to fractional

inspired oxygen concentration ratio < 300 mm per Hg (regardless of PEEP)

◦ Bilateral pulmonary infiltrates on chest radiograph ◦ Pulmonary artery wedge pressure < 18 mm per Hg or no clinical

evidence of left atrial hypertension Criteria for ARDS

◦ Acute in onset ◦ Oxygenation: A partial pressure of arterial oxygen to fractional

inspired oxygen concentration ratio < 200 mm per Hg (regardless of PEEP)

◦ Bilateral pulmonary infiltrates on chest radiograph ◦ Pulmonary artery wedge pressure < 18 mm per Hg or no clinical

evidence of left atrial hypertension

Pathogenesis of ALI

Welbourn CR and Young Y. Endotoxin, septic shock and acute lung injury: neutrophils, macrophages and inflammatory mediators. Brit J Surg 1992; 79 (10):

998-1003.

SGPT= 298 SGOT= 253 Serum sodium= 136 Serum potassium= 3.31 Serum Calcium= 0.9

Hepatic changes in Dengue Alterations of hepatic functions and acute hepatitis

in some patients Aminotransferases peak on 9th day after

appearance of symptoms and go back to normal in 3 weeks.

Histopathological findings:◦ Centrotubular necrosis◦ Fatty alterations◦ Kupffer cells hyperplasia◦ Acidophilic bodies◦ Monocytic infiltrates of the portal tract,

Brazilian Journal of Infectious DiseasesBraz J Infect

Dis vol.6 no.6 Salvador Dec. 2002

First Day of Admission (10 hours PTA)

Assessment:◦ Dengue Hemorrhagic Fever Grade 3◦ Acute lung injury, secondary ◦ Acute hepatitis secondary◦ Hypokalemia◦ T/C Peptic Ulcer disease

4 Necessary Criteria: Fever, or recent history of acute fever Hemorrhagic manifestations Low platelet count (100,000/mm3 or less) Objective evidence of “leaky capillaries:”

◦ elevated hematocrit (20% or more over baseline)◦ low albumin◦ pleural or other effusions

Clinical Case Definition for Dengue Hemorrhagic Fever


Increase in vascular permeability

Dengue Hemorrhagic fever

Leakage of plasma from intravascular to extravascular space

Hypovolemia

Signs of circulatory compromise

Profound shock

Gubler DJ. Dengue and Dengue HaemorrhagicFever. Clinical Microbiology Reviews, 1998, 11:

480-496.

Grade 1 ◦ Fever and nonspecific constitutional symptoms◦ Positive tourniquet test is only hemorrhagic manifestation

Grade 2 ◦ Grade 1 manifestations + spontaneous bleeding

Grade 3 ◦ Signs of circulatory failure (rapid/weak pulse, narrow

pulse pressure, hypotension, cold/clammy skin) Grade 4

◦ Profound shock (undetectable pulse and BP)

Four Grades of DHF


Virus strain Pre-existing anti-dengue antibody

◦ previous infection◦ maternal antibodies in infants

Host genetics Age Higher risk in secondary infections Higher risk in locations with two or more serotypes

circulating simultaneously at high levels (hyperendemic transmission)

Risk Factors Reported for DHF


Antibody-dependent enhancement is the process in which certain strains of dengue virus, complexed with non-neutralizing antibodies, can enter a greater proportion of cells of the mononuclear lineage, thus increasing virus production

Hypothesis on Pathogenesis of DHF


Persons who have experienced a dengue infection develop serum antibodies that can neutralize the dengue virus of that same (homologous) serotype

In a subsequent infection, the pre-existing heterologous antibodies form complexes with the new infecting virus serotype, but do not neutralize the new virus



Infected monocytes release vasoactive mediators, resulting in increased vascular permeability and hemorrhagic manifestations that characterize DHF and DSS



Homologous Antibodies Form Non-Infectious Complexes


Heterologous Antibodies Form Infectious Complexes


Heterologous Complexes Enter More Monocytes, Where Virus Replicates


Virus strain (genotype) ◦ Epidemic potential: viremia level, infectivity

Virus serotype ◦ DHF risk is greatest for DEN-2, followed by DEN-3,

DEN-4 and DEN-1

Viral Risk Factors for DHF Pathogenesis


Plans Referred for CVP insertion

◦Initial CVP= 3-4 cm◦IVF: D5LR 1 L x 150 cc/hr

Transfusion with 4 units platelet concentrate and 4 units FFP

Hydrocortisone 200 mg IV given as loading dose then 100 mg IV Q6H

Furosemide 20 mg IV every 12 hours for 4 doses

Treatment of ALI

MacNaughton PD, and Ewans, TW. Adult respiratory Distress Syndrome. Recent advances in respiratory

medi cine Edinburgh. Churchill Livingstone. First edition. 1991. P. 1-22.

The use of corticosteroids in severe sepsis and acute respiratory distress syndrome.

Chadda K, Annane D.,Medical Intensive Care Unit, Raymond Poincaré University Hospital, School of MedicineGarches, France

In practice, a high dose of corticosteroids (i.e. one to four boluses of 30 mg/kg of methylprednisolone, or equivalent) had no effects on survival in severe sepsis or acute respiratory distress syndrome. There are at least seven randomised controlled trials reporting the benefits and risks of low dose corticosteroids (i.e. 200 to 300 mg daily of hydrocortisone or equivalent) given for a prolonged period in severe sepsis or in the late phase of acute respiratory distress syndrome. These trials showed consistently that, in these patients, the use of low dose of corticosteroids alleviated inflammation, restored cardiovascular homeostasis, reduced organ dysfunction, improved survival and was safe. Further studies are ongoing to better identify the target population. In the meantime, cortisol replacement (i.e. 200 to 300 mg daily of hydrocortisone or equivalent) should be considered as standard care for these patients.

No good evidence that corticosteroids are helpful in dengue shock syndrome

The current treatment for dengue shock syndrome is to give fluids directly into the bloodstream, but corticosteroids have been suggested as drugs that may help due to their anti-inflammatory properties. This review of trials found only four small trials (with 284 participants) that were not of good quality and which showed no benefit overall. Further trials would be needed before this drug were used in these patients, as there is the potential for adverse effects due to the drugs' properties of suppressing the immune system and potentially leaving people open to other infections.

Corticosteroids for treating dengue shock syndromePanpanich R, Sornchai P, Kanjanaratanakorn K Cochrane Database of Systematic Reviews 2006, Issue 3. Art. No.: CD003488. DOI: 10.1002/14651858.CD003488.pub2

Rapid potassium replacement done Ranitidine IV discontinued Omeprazole 40 mg IV OD started Ciprofloxacin 200mg IV Q12H Blood culture and TPAG requested

Acute Lung Injury and Bacterial Infection

Didier Dreyfuss,Service de Réanimation Médicale, Hôpital Louis Mourier, Assistance Publique—Hôpitaux de Paris, Colombes 92700, France

28 March 2005.

The relationships between acute lung injury and bacterial infection are complex. Indeed, sepsis and in particular pneumonia are leading causes of acute lung injury. Bacterial superinfection of the lung is a frequent complication of acute lung injury. Because of impaired host defenses and prolonged mechanical ventilation, more than one third of patients with the acute respiratory distress syndrome acquire ventilator-associated pneumonia, with resistant pathogens in most instances. This complication is responsible for more than a doubling of the time on mechanical ventilation but does not seem to increase mortality.

S/O:◦ Drowsy◦ BP: 0-50 palpatory CR= 120s RR= 25 Temp= 36.6 C◦ Anicteric sclerae, pinkish conjunctivae◦ (+) Neck vein engorgement◦ Symmetrical chest expansion, harsh breath sounds(+)

fine rales, mid to base lung fields◦ Adynamic precordium, regular cardiac rate and

rhythm, tachycardic, no murmurs◦ Flat abdomen, normoactive bowel sounds, soft, (+)

direct tenderness epigastric area◦ CVP= 9cm◦ Platelet count= 36

Second Hospital Day (25 hours after admission)

Chest X-ray

ABG FIO2=52% pH= 7.33 pCO2= 24 PO2= 119 HCO3= 16 SO2= 98% HCO3 deficit=60 meqs in 24 hours Required FIO2=36.35 PaO2/FIO2= 228.84

Serum Creatinine= 78. 10 BUN= 3.43 Troponin I: 0.53 ug/ L

(borderline)

Assessment◦ Dengue Hemorrhagic Fever Grade 4◦ Acute lung injury, secondary ◦ Acute hepatitis secondary◦ Hypokalemia◦ T/C Peptic Ulcer disease

Plans Summary of Fluids

◦ CVP line= PNSS 1 L x 10 cc/hr◦ Mainline=D5NSS 1L x 60 cc / hr◦ Dopamine 400 mg/250 cc at 10 ugtts/min◦ Dobutamine 500mg/250 cc at 10 ugtts/min◦ Levophed 8mg/250 cc at 100 ugtts/minTOTAL= 190 cc/hr or 4560 cc/ 24 hours

Dextran 250 cc to run for 2 hours Transfusion with FFP Hydrocortisone shifted to

Methylprednisolone 500 mg IV q8H Comanagement with Nephrology Section

and Cardiology Section

S/O:◦ Drowsy, no urine output◦ BP= 80 palpatory CR=150s-170s RR=25

Temp=36.5 C◦ Anicetric sclerae, pinkish conjunctivae◦ (+) Neck vein engorgement◦ Symmetrical chest expansion, harsh breah

sounds, (+) rales, mid to base lung fields◦ Adynamic precordium, tachycardic, no murmurs◦ CVP= 9 cm◦ ECG at cardiac monitor= non-sustained

ventricular tachycardia

Second Hospital Day (28 hours after admission)

Assessment◦ Dengue Hemorrhagic Fever Grade 4◦ Acute lung injury, secondary ◦ Cardiac Arrhythmia– ventricular tachycardia◦ T/C Viral encephalopathy◦ Acute kidney injury secondary to dengue shock

syndrome

Myocardial depression in dengue hemorrhagic fever: prevalence and clinical description.

Khongphatthanayothin A, Lertsapcharoen P, Supachokchaiwattana P, La-Orkhun V, Khumtonvong A, Boonlarptaveechoke C, Pancharoen C.

King Chulalongkorn Memorial Hospital, Bangkok, Thailand.

OBJECTIVES: To determine the prevalence of myocardial depression and its effect on the clinical severity in patients with dengue hemorrhagic fever.

MEASUREMENTS AND MAIN RESULTS: EF during toxic stage was significantly lower in patients with DSS than DHF, and lower in DHF than DF (p = .05) with rapid recovery within 24-48 hrs. EF <50% was found in 6.7%, 13.8%, and 36% of patients with DF, DHF, and DSS during the toxic stage, respectively (p = .01). DSS patients with poor ventricular function had significantly more tachycardia and hepatomegaly. While end-diastolic volumes were similarly reduced, patients with lower EF tended to have lower cardiac output, required more aggressive intravenous fluid resuscitation, developed larger pleural effusion, and had higher incidence of respiratory embarrassment. No patient had elevated troponin T level. CONCLUSIONS: Transient myocardial depression is not uncommon in patients with DSS. Cardiac dysfunction in children with DSS may contribute to the clinical severity and the degree of fluid overload in these patients.

Plans Cordarone 150 mg IV given Cordarone drip started Furosemide 40 mg IV given Request for 5 units FFP Joint Service with Department of Neurology

Furosemide drip started Repeat platelet count= 34 Request 6 units platelet concentrate Nephrosteril drip 500 cc to run for 24 hours Nebulization with Salbutamol 1 neb Q 4H

S/O:◦ Drowsy , in cardiorespiratory distress◦ GCS 10 (E= to pain, V=confused, M=localizing)◦ BP= 80 palpatory CR=120s RR=36 Temp= 36.5 C◦ On and off desaturation at 10 lpm◦ (+) Neck vein engorgement (+) supraclavicular

retractions◦ Harsh breath sounds(+) rales, mid to base lung fields,

(+) diffuse wheezing◦ Adynamic precordium, regular cardiac rate and

rhythm, tachycardic, no murmurs◦ (+) Flat abdomen, (+) abdominal retractions, normoactive

bowel sounds, soft◦ Grossly normal extremities

Second hospital day (31 hours after)

ABG pH= 7.22 PCO2= 29 PO2= 127 HCO3= 14 SO2= 98% FIO2= 68% Required FIO2=45. 15% PAO2/FIO2=186.76

Assessment◦ Dengue Hemorrhagic Fever Grade 4◦ Acute respiratory distress syndrome, secondary ◦ Encephalopathy, secondary◦ Acute kidney injury secondary to dengue shock

syndrome

Encephalopathy Hepatic damage Cardiomyopathy Severe gastrointestinal hemorrhage

Unusual Presentations of Severe Dengue Fever

ARDS Presence of bilateral pulmonary infiltrates

on chest radiograph Impaired oxygenation resulting in a PaO2 to

fraction of inspired oxygen (FIO2) ratio of less than 200

The presence of pulmonary edema in the absence of volume overload or depressed left ventricular function.

Evangelos Briasoulis, Nicholas Pavlidis, Noncardiogenic Pulmonary Edema: An Unusual and Serious Complication of Anticancer Therapy. Department of Medical Oncology, University of Ioannina, Ioannina, Greece

Hormones in Sepsis and ARDS

Activation of hypothalamic pituitary adrenal axis through a systemic pathway, i.e. by circulating pro-inflammatory cytokines and through the vagus nerve

Adrenal glands release cortisol which counteracts inflammatory process and restores cardiovascular homeostasis.

BLOCKED BY SEPSIS

Inadequate hypothalamic pituitary adrenal axis response to stress

Shock and organ dysfunction in sepsis and acute respiratory distress syndrome.

Warning Signs for Dengue Shock

Plans Intubation done VR set-up:

◦ FIO2= 100%◦ TV= 500◦ PFR= 50◦ BUR= 18◦ Mode=A/C◦ PEEP= 3 cm

Fentanyl 0.5 cc Q6H In-line nebulization with Salbutamol, 1 neb

Q 4H Nebulization with Budesonide respule, 1

respule Q8H

S/O: No urine output◦ Drowsy, bloody ET aspirate◦ BP= 30 palpatory CR=120-130 Temp=36 C O2

sat=94◦ (+) Neck vein engorgement (+) supraclavicular

retractions◦ Harsh breath sounds, (+) coarse rales, mid to base

lung fields, (+) diffuse wheezing◦ Adynamic precordium, regular cardiac rate and

rhythm, tachycardic, no murmurs◦ (+) Flat abdomen, (+) abdominal retractions,

normoactive bowel sounds, soft◦ Grossly normal extremities◦ CVP= 8 cm

Second hospital day (31 hours after

Chest X-ray

ABG

FIO2= 100%PH= 7.21PCO2= 32PO2= 59HCO3= 14So2= 83%Required FIO2= 133%HCO3 deficit= 90 meqs in 24 hours

Assessment T/C Pulmonary hemorrhage Dengue Hemorrhagic Fever Stage 4 Multiorgan failure secondary to viral sepsis Acute Respiratory Distress Syndrome

Repeat CBC requested STAT 1 unit Fresh whole blood requested

2 hours laterS/O:

◦ Unresponsive◦ BP= 0 CR=0 O2 sat= not appreciated◦ Pupils fixed dilated

A: ◦ Cardiopulmonary arrest secondary to

pulmonary hemorrhage◦ Dengue Hemorrhagic fever Stage IV◦ Multiorgan failure secondary to viral sepsis

P:◦ CPR done◦ Patient expired 4:42 AM August 5, 2009

Cardiopulmonary arrest secondary to pulmonary hemorrhage

Dengue Hemorrhagic Fever Stage IV Multiorgan failure secondary to viral sepsis Acute Respiratory Distress Syndrome (Non

Cardiogenic Pulmonary edema Stage IV) Septic shock

Final Diagnosis

Fluids Rest Antipyretics (avoid aspirin and non-steroidal

anti-inflammatory drugs) Monitor blood pressure, hematocrit, platelet

count, level of consciousness

Treatment of Dengue Fever

Continue monitoring after defervescence If any doubt, provide intravenous fluids,

guided by serial hematocrits, blood pressure, and urine output

The volume of fluid needed is similar to the treatment of diarrhea with mild to moderate isotonic dehydration (5%-8% deficit)


Avoid invasive procedures when possible Unknown if the use of steroids, intravenous

immune globulin, or platelet transfusions to shorten the duration or decrease the severity of thrombocytopenia is effective

Patients in shock may require treatment in an intensive care unit


Source: Adapted from Guidelines for Treatment of Dengue Fever/Dengue Haemorrhagic Fever in Small Hospitals, WHO, 1999.

Fluid for Moderate Dehydration (Intravenous)

weight in lb ml/lb/day weight in kg

ml/kg/day

<15 100 <7 220

16-25 75 7-11 165

26-40 60 12-18 132

41-88 40 19-40 88

Volume required for rehydration is twice the recommended maintenance requirement

Formula for calculating maintenance volume: 1500 + 20 x (weight in kg - 20)

For example, maintenance volume for 55 kg patient is: 1500 + 20 x (55-20) = 2200 ml

For this patient, the rehydration volume would be 2 x 2200, or 4400 ml

Source: Pan American Health Organization: Dengue and Dengue Hemorrhagic Fever: Guidelines for Prevention and Control. PAHO: Washington, D.C., 1994: 67.

Rehydrating Patients Over 40 kg

Actual Fluid maintenance requirement of our patient 1500 + 20 x (weight in kg – 20)Weight= 71 kg

1500 + 20 x (71 – 20) = 2520x 2--------5040 ml/ 24 hours OR 210 cc/ hour

Dengue + bleeding = DHF ◦ Need 4 WHO criteria, capillary permeability

DHF kills only by hemorrhage ◦ Patient dies as a result of shock

Poor management turns dengue into DHF ◦ Poorly managed dengue can be more severe, but

DHF is a distinct condition, which even well-treated patients may develop

Positive tourniquet test = DHF ◦ Tourniquet test is a nonspecific indicator of

capillary fragility

Common Misconceptions about Dengue Hemorrhagic Fever

No licensed vaccine at present Effective vaccine must be tetravalent Field testing of an attenuated tetravalent

vaccine currently underway Effective, safe and affordable vaccine will

not be available in the immediate future

Dengue Vaccine?

Comparison of three fluid solutions for resuscitation in dengue shock syndrome.

Wills BA, Nguyen MD, Ha TL, Dong TH, Tran TN, Le TT, Tran VD, Nguyen TH, Nguyen VC, Stepniewska K, White NJ, Farrar JJ.Oxford University Clinical Research Unit, Hospital for

Tropical Diseases, Ho Chi Minh City, Vietnam. A double-blind, randomized comparison of three fluids for

initial resuscitation of Vietnamese children with dengue shock syndrome.

The primary outcome measure--requirement for rescue colloid--was similar for the different fluids in the two severity groups. Although treatment with Ringer's lactate resulted in less rapid improvement in the hematocrit and a marginally longer time to initial recovery than did treatment with either of the colloid solutions, there were no differences in all other measures of treatment response.

Initial resuscitation with Ringer's lactate is indicated for children with moderately severe dengue shock syndrome. Dextran 70 and 6 percent hydroxyethyl starch perform similarly in children with severe shock, but given the adverse reactions associated with the use of dextran, starch may be preferable for this group.

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Dengue Mortality and Morbidity Conference