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Dengue diagnosis, treatment, prevention and control

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Dengue diagnosis, treatment, prevention and control

  1. 1. Dengue: Diagnosis, Treatment, Prevention and Control Fadel Muhammad Garishah, MD Department of General Internal Medicine
  2. 2. Overview  Dengue is the most rapidly spreading mosquito-borne viral disease in the world.  Dengue has a wide spectrum of clinical presentations, often with unpredictable clinical evolution and outcome  In Indonesia, where more than 35% of the country’s population lives in urban areas, 150 000 cases were reported in 2007 (the highest on record) with over 25 000 cases reported from both Jakarta and West Java.  The case-fatality rate was approximately 1%.
  3. 3. Countries/Areas at Risk of Dengue Transmission
  4. 4. Clinical Course  dengue is one disease entity with different clinical presentations and often with unpredictable clinical evolution and outcome  Symptomatic dengue virus infections were grouped into three categories: undifferentiated fever, dengue fever (DF) and dengue hemorrhagic fever (DHF).
  5. 5. Suggested dengue case classification and levels of severity
  6. 6. Dengue Virus (DENV)  Dengue virus (DEN) is a small single-stranded RNA virus comprising four distinct serotypes (DEN-1 to-4).  It belongs to the genus Flavivirus, family Flaviviridae.  Among them, “Asian” genotypes of DEN-2 and DEN-3 are frequently associated with severe disease accompanying secondary dengue infections
  7. 7. Tiger Mosquito  Aedes mosquitoes, principally Ae. aegypti, is a tropical and subtropical species widely distributed around the world, mostly between latitudes 35 N and 35 S.  The immature stages are found in water filled habitats, mostly in artificial containers closely associated with human dwellings and often indoors.
  8. 8. The Host  an incubation period of 4--10 days  Individual risk factors determine the severity of disease and include secondary infection, age, ethnicity and possibly chronic diseases (bronchial asthma, sickle cell anaemia and diabetes mellitus).  Young children in particular may be less able than adults to compensate for capillary leakage and are consequently at greater risk of dengue shock.  Studies in the American region show the rates of severe dengue to be lower in individuals of African ancestry than those in other ethnic groups.
  9. 9. Immunology  Primary infection is thought to induce lifelong protective immunity to the infecting serotype but with no long-term cross-protective immunity to other serotypes  non-neutralizing, cross-reactive antibodies raised during a primary infection bind to epitopes on the surface of a heterologous infecting virus and facilitate virus entry into Fc-receptor-bearing cells.  The increased number of infected cells is predicted to result in a higher viral burden and induction of a robust host immune response that includes in inflammatory cytokines and mediators, some of which may contribute to capillary leakage  Activation of infected monocytes and T cells, the complement system and the production of mediators, monokines, cytokines and soluble receptors may also be involved in endothelial cell dysfunction.  During a secondary infection, cross-reactive memory T cells are also rapidly activated, proliferate, express cytokines and die by apoptosis in a manner that generally correlates with overall disease severity.
  10. 10. Hematology  Thrombocytopenia may be associated with alterations in megakaryocytopoieses by  the infection of human hematopoietic cells and impaired progenitor cell growth,  resulting in platelet dysfunction (platelet activation and aggregation),  increased destruction or  consumption (peripheral sequestration and consumption).  Hemorrhage may be a consequence of the thrombocytopenia and associated platelet dysfunction or disseminated intravascular coagulation.
  11. 11. Keyword  a transient and reversible imbalance of in inflammatory mediators, cytokines and chemokines occurs during severe dengue, probably driven by a high early viral burden, and leading to dysfunction of vascular endothelial cells, derangement of the hemocoagulation system then to plasma leakage, shock and bleeding.
  12. 12. Clinical Course of DVI
  13. 13. Phases of Dengue  Febrile Phase  Critical Phase  Recovery Phase
  14. 14. Febrile Phase  High grade fever (>3 first day)  Headache  Generalized body aches  Myalgia  Arthralgia  Anorexia  Epigastric Pain  Nausea/vomitus  Facial flushing  Skin erythema  Sore throat  injected pharynx  conjunctival injection  Petechiae  Epistaxis  Gum bleeding  GI/vaginal bleeding
  15. 15. Critical Phase  Defervescence, restless, lethargy  Raising hematocrit (sign of plasma leakage)  Progressing leukopenia  Progressing thrombocytopenia and thrombocytopathy  Mild ascites/pleural effusion proved by RLD Xray  Cold clammy extremities  Prolonged shock leads to: metabolic acidosis, disseminated intravascular coagulation, organ impairment (hepatitis, encephalitis, myocarditis), severe bleeding
  16. 16. Improvement after defervescence  Non severe dengue  Some cases deteriorate to severe dengue
  17. 17. Recovery Phase  24-48 h post critical phase, following gradual reabsorption of extravascular fluid by 48-72 hours after  Hemodynamic issues stabilized  Gastrointestinal symptoms abate  WBC and platelets rise up
  18. 18. Primary Care Provider  Distinguishing dengue from other causes of fever  Recognizing plasma leakage and initiating appropriate fluid therapy
  19. 19. Overall Assessment  History:  fever analysis,  symptoms,  PMH,  FH  Physical Examination  Laboratory Studies  CBC  Serology
  20. 20. Management  Be sent home  Be referred to hospital  Emergency treatment
  21. 21. Referral centers  Early shock (2-3 days of illness)  Severe plasma leakage  Undetectable and blood pressure  Severe bleeding  Fluid overload  Unusual complications: hepatic damage, cardiomyopathy, encephalopathy, encephalitis
  22. 22. History  Date of onset of ever/illness  Oral intake  Assessment for warning signs  Diarrhea  Change in mental state/seizure  Urine output  Others: family/neighborhood/school mate with dengue, pregnancy, obesity, diabetes, hypertension, camping
  23. 23. Physical  General Appearance  Consciousness level  Vital signs  Hemodynamic assessment  Bleeding signs incl. torniquet test
  24. 24. Laboratory Studies  Full blood count  Hematocrit base  WBC count  Platelet count  Clinical chemistry: LFT, Glucose, Electrolytes, RFT, BGA, lactate, cardiac enzymes
  25. 25. Diagnostic  Living in endemic area  Fever over 3 days  Epigastric pain  Platelet lower than 100.000/uL  WBC < 4000/uL  NS1  Serology: Rapidtest, ELISA  Hemaglutination Inhibition Test  PCR
  26. 26. Laboratory Studies
  27. 27. Laboratory Studies
  28. 28. Patient A: Dengue Fever/DHF Grade I  No warning signs  Adequate oral intake  Adequate urine output  Have bed rest  Plenty fluids  Acetaminophen 10-15mg/kg/4-6 hours
  29. 29. Patient B: DHF Grade II-III  Warning signs (+)  Admission  Maintenance Fluid (Normal Saline/Lactate’s Ringer)  Monitoring urine output, warning signs
  30. 30. Patient C: DHF Grade IV/Dengue Shock Syndrome/Expanded Dengue Syndrome  Warning signs (+)  Severe plasma leakage  Severe bleeding  Severe organ impairment (expanded dengue syndrome)
  31. 31. Reduced Perfusion Maintained Systolic Pressure Crystalloid 5-10cc/kg 1 hour Improvement 5-7cc/kg/hr 1-2 hr 3-5cc/kg/hr 2-4 hr 2-3cc/kg/hr 2-4 hr Maintained max 48 hr Hct Monitoring/6-8 hr No Improvement HCt Check HCt Increase Bolus 10-20cc/kg 1 hr Improvement 5-7cc/kg/hr 1-2 hr 3-5cc/kg/hr 2-4 hr 2-3cc/kg/hr 2-4 hr Maintained max 48 hr Hct Monitoring/6-8 hr HCt decrease Suspect Bleeding Fresh Whole Blood No Improvement HCt Check
  32. 32. Better Perfusion  Decreasing HR  Improving BP  Pulse volume  Warm extremities  Capilary refill < 2’’  Alertness  Urine output > 0,5cc/kg/hr
  33. 33. Hypotensive Shock Crystalloid/Colloid 20cc/kg 15 minutes Hct High, no Improvement Colloid 20cc/kg 30min-1hr Hct High, no Improvement Colloid 20cc/kg 30min-1hr Hct Low, no Improvement FWB Transfusion Stable 7-2 cc/kg/hr Hct monitor/6hr Hct High, no Improvement Same Cycle Consider Vasopressors/Inotropes Stable 7-2 cc/kg/hr Hct monitor/6hr Hct Low, no Improvement FWB Transfusion Stable 7-2 cc/kg/hr Hct monitor/6hr Hct Low, no Improvement FWB Transfusion
  34. 34. Bleeding Risks  Prolonged/refractory shock  Hypotensive shock despite adequate fluid therapy (40- 60cc/kg)  Given NSAIDs  Preexisting Peptic Ulcer Disease
  35. 35. Blood Products  5-10cc/kg PRC  10-20cc/kg FWB
  36. 36. Fluid Overload  Signs: respiratory distress, wheezing, pleural effusion, ascites  Oxygen  Stopping IVFD  Furosemide 0.1-0.5mg/kg/12-24 hr
  37. 37. Differentials  Influenza,  measles,  chikungunya,  infectious mononucleosis,  leptospirosis,  typhoid,  typhus,  gastroenteritis,  Other virus infections
  38. 38. Admitting
  39. 39. Discharging
  40. 40. Mosquito Breeding Site
  41. 41. Vector Control  Environmental modification: piped water  Environmental manipulation: breeding sites, ovitrap  Human behavior: repellent, windows closed, bed nets  Chemical larvicides, insecticides  Biological: fish, copepods, Wolbachia

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