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9.dengue seminar
 

9.dengue seminar

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3rd year 3rd rotation

3rd year 3rd rotation

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    9.dengue seminar 9.dengue seminar Presentation Transcript

    • DENGUE PRESENTED BY: NOR AINI BINTI MOHAMAD NADIAH BINTI MOHD NASIR SHARIFAH MAISARAH BINTI SYED OTHMAN SEMINAR PRESENTATION INFECTION IN CHILDREN
    • In June 2001, a girl aged 5 years was taken to an ED in Missouri with a 3-day history of intermittent fever, headache, mild nausea, and a sore throat. On physical examination, the patient had a fever of 105 ° F (40.6 º C) and a maculopapular rash on her legs, including the soles of her feet.
    • What additional information would assist with the diagnosis? The parent noticed the rash, which began on the arms and legs, on the same day that the child was taken to the ED. They did not own a dog, and no history of recent travel out of the local area and no history of a tick bite were noted, although the parent said that ticks were in the area around their house.
    • Introduction Dengue fever is caused by a virus belonging to the Flaviviridae family. It is a RNA virus, ecosahedral shape There are four serotypes of dengue virus (Den 1, Den 2, Den 3, Den 4) that can be distinguished serologically. While infection by one serotype produces life-long immunity against re-infection by that same serotype, there is only temporary and partial protection against other serotypes. The incubation period of dengue varies from 3-10 days with an average of 4-6 days (WHO, 1997, level 6; Kabra et al, 1999, level 8).
    • Expert consensus groups in Latin America (Havana, Cuba, 2007), (Kuala Lumpur, Malaysia, 2007), and at WHO headquarters in Geneva, Switzerland in 2008 agreed that: “ dengue is one disease entity with different clinical presentations and often with unpredictable clinical evolution and outcome”;
    • Epidemiology WHO 2009: Dengue is the most rapidly spreading mosquito-borne viral disease in the world. In the last 50 years, incidence has increased 30-fold with increasing geographic expansion to new countries and, in the present decade, from urban to rural settings
    • Mode of transmission Humans are the main amplifying host of the virus. Dengue virus circulating in the blood of viraemic humans is ingested by female mosquitoes during feeding. The virus then infects the mosquito mid-gut and subsequently spreads systemically over a period of 8--12 days. After this extrinsic incubation period, the virus can be transmitted to other humans during subsequent probing or feeding. The extrinsic incubation period is influenced in part by environmental conditions, especially ambient temperature. Thereafter the mosquito remains infective for the rest of its life.
    • WHO DENGUE CLASSIFICATION Based on current WHO dengue classification scheme the key differentiating feature between DF and DHF is the presence of plasma leakage in DHF. However, in the early febrile phase of dengue infection, the symptoms can overlap and one cannot differentiate DF and DHF. DHF is further classified as mild (grades I and II) or severe (grades III and IV), the presence of shock being the main difference. Grades III and IV are classified as Dengue Shock Syndrome.
    • Dengue Virus Infection asymptomatic symptomatic Undifferentiated fever Dengue fever syndrome Dengue haemorrhagic fever Without haemorrhage With unusual haemorrhage No shock Dengue shock Syndrome Dengue fever (DF) Dengue Haemorrhagic Fever (DHF)
    • CASE DEFINITION FOR DENGUE FEVER An acute febrile viral disease frequently presenting with: Headache Bone / joint pain Muscular pain Rash Leukopenia
    • CASE DEFINITION FOR DENGUE HAEMORRHAGIC FEVER The following must ALL be present : • Fever, or history of acute fever, lasting 2–7 days, occasionally biphasic. • Haemorrhagic tendencies , evidenced by at least one of the following : - a positive tourniquet test - petechiae, ecchymoses or purpura - bleeding from the mucosa, gastrointestinal tract, injection sites or other locations - haematemesis or melaena. • Thrombocytopenia (100,000 cells per mm3 or less). • Evidence of plasma leakage due to increased vascular permeability, manifested by at least one of the following: - a rise in the HCT equal to or greater than 20% above average for age, sex and population; - a drop in the HCT following volume-replacement treatment equal to or greater than 20% or baseline; - signs of plasma leakage such as pleural effusion, ascites and hypoproteinaemia.
    • CASE DEFINITION FOR DENGUE SHOCK SYNDROME All of the above four criteria for DHF must be present, plus evidence of circulatory failure manifested by : • Rapid and weak pulse , and • Narrow pulse pressure [<20mmHg (2.7 kPa)] OR manifested by : • Hypotension for age, and • Cold, clammy skin and restlessness .
    • Grade 1 Fever with constitutional symptoms. A positive Hess test. Grade 2 Spontaneous bleeding (skin ± other bleeds) in addition to manifestations of grade 1 Grade 3 Circulatory failure (rapid weak pulse, pulse pressure < 20mmHg) but systolic BP still normal Grade 4 Profound shock (hypotension, undetectable blood pressure and heart rate) WHO Grading Of DHF/DSS
    • Limitation of WHO classification 1. Many case reports of patients with severe dengue with shock who do not fulfil all the 4 criteria for DHF 2. Patients with severe organ impairment such as liver, respiratory and cardiac are not captured as having severe disease based on the existing classification. 3. Requirement 20% plasma leakage Baseline HCT is not available in most patients and therefore, the interpretation of plasma leak can only be made retrospectively Early fluid administration may affect the level of HCT Bleeding will affect the HCT level
    • CLINICAL COURSE OF DENGUE INFECTION incubation period 3 phases: Febrile Critical Recovery phase
    • Febrile Phase Abrupt onset of high grade fever (2-7 days) Rash - discrete macularpapular rash or generalized flushing, common on lower limbs and chest. Generalized body ache Myalgia Arthalgia Headache - usually frontal or retroorbital pain, particularly when pressure applied to the eyes Sore throat Injected pharynx and conjunctival Anorexia, nausea and vomitting This clinical features are indistinguishable from DHF/DSS Earliest abnormality in FBC Progressive decrease in TWC Positive history of neighborhood dengue
    • 2. Critical Phase (Late febrile) When a rapid drop in temperature Often on the 3 rd day of fever Coincidence with increase capillary permeability Plasma leak may occur (minimal or worse) Last about 24 – 48 hours Circulatory disturbances (minimal and transient patient recover spontaneously with fluids or electrolyte therapy) Severe plasma leakage sweat Restlessness Cool extrimities Prolong capillary time Pulse rate increase Diastolic blood pressure increase Pulse pressure narrow Abdominal pain Persistent vomitting Altered concious level Mucosal bleed Tender enlarged liver Pleural effusion, ascites
    • 3. Recovery Phase (after 24-48 hours of defervescence ) Plasma leakage stops followed by reabsorption of extravascular fluid General well being improved May have classical rash “ isles of white in the sea of red”
    • ONSET OF DEFERVESCENCE USUALLY OCCURS BETWEEN DAY 3 AND DAY 5 OF ILLNESS
    • Increase in vascular permeability Leads to leakage of plasma to extravascular compartment Haemoconcentration (> 20%) and hypovolaemic shock Hypovolemia lead to reflex tachycardia and generalized vasoconstriction due to increase sympathetic output
    • Clinical manifestation of vasoconstriction ↑ d BP narrowing of pulse pressure ↓↓ urine output Vomiting Abdominal pain Lethargy Restlessness Apprehension Reduced level of consciousness tachypnoea Coolness Pallor Delayed capillary refill time
    • The pathogenetic mechanism responsible for the increased vascular permeability in DHF/DSS is not known Abnormal immune response involving the production of cytokines or chemokines, activation of T-lymphocytes and disturbances of haemostatic system are the major changes seen in DHF. Secondary infection with a heterotypic dengue virus is associated with increased risk of developing DHF. It is believed to be due to the antibodydependent enhancement phenomenon.
    • antibodydependent enhancement phenomenon
    • infected with dengue develop an immune response to that dengue subtype produced specific antibodies to that subtype specific surface proteins that prevents the virus from binding to macrophage cells and gaining entry another subtype of dengue virus infects the individual virus will activate the immune system to attack it as if it was the first subtype The antibodies bind to the surface proteins but do not inactivate the virus. The immune response attracts numerous macrophages, which the virus proceeds to infect because it has not been inactivated viral infection much more acute The body releases cytokines that cause the endothelial tissue to become permeable which results in DHF and fluid loss from the blood vessels.
    • PRINCIPLES OF MANAGEMENT
    • Ambulatory monitoring of suspected dengue : Clinical parameters: T emperature O ral fluid intake U rine output B leeding tendencies H ydration status
    • Lab parameters: - Hemoglobin/ haematocrit - Total white count, platelet count IgM
    • Indication for hospitalization: Shock - feeble pulses, cold extremities, crt >2s, hypotension Altered conscious level- lethargy, delirium, combativeness Bleeding Inability to tolerate oral fluids / vomiting Abdominal tenderness/ hepatomegaly Obese / overweight Falling platelet/ rising haematocrit Social factors; live far from hospital
    • ICU admission indications: Impending respiratory failure Persistent shock not responding to 60ml/kg fluid resuscitation
    • Monitoring of Suspected Dengue Patients in Wards Clinical parameters: • Hydration mucosa and skin turgor oral fluid intake urine volume, and other fluid losses such as vomiting or diarrhoea. • Haemodynamics skin perfusion – temperature of extremities capillary refill time pulse volume heart rate blood pressure pulse pressure level of consciousness. • Body Temperature
    • Investigations Haematocrit Hb, TWBC, Platelet count Creatinine Dengue Serology
    • Management of the Acute Phase 1. Fluid management Prompt and adequate fluid resuscitation -maintain an effective circulation, avoid over-replacement that could lead to massive pleural effusion and ascites. Fluid therapy has to be adjusted according to: • haematocrit level • urine volume – 0.5 to 1.0 ml/kg/hour • vital signs and tissue perfusion
    • For children with signs of shock , two fluid therapy lines should be established : • First Fluid Line for replacement of fluid lost in the plasma leakage in decompensated shock, rapid bolus of normal saline based on 20ml/kg body weight should be given in compensated shock, normal saline based on 10-20 ml/kg body weight should be given over 30-60 minutes volume and infusion rate has to be adjusted every 2-6 hours based on clinical assessment and haematocrit of the patient
    • Second Fluid Line - to administer maintenance fluids - 5% Dextrose ½ saline with or without KCl, in the maintenance volume according to the child’s weight for height-centile-for-age - most children with DSS will be physiologically stressed, and some may not be able to handle the glucose load. Blood glucose should be checked regularly and if found to be high, dextrose should be omitted or infusion rate reduced.
    • If patient still in shock, a second rapid normal saline bolus dose should be administered . ⇩ If no improvement, rapid fluid bolus is repeated with colloids or blood/blood products depending on whether there is a rise or fall in haematocrit . ⇩ When patient improves (warm and good pulse volume), fluid therapy is reduced to maintenance, and tapered off, finally discontinuing IV therapy, usually 24 to 48 hours after the start of plasma leakage. This is to avoid fluid overload and pulmonary oedema. ⇩ For obese patients, the weight adjusted to height-centile-for-age should be closely followed to avoid fluid overload. The use of albumin and plasma is not recommended.
    • Physiologic status assesment: • Heart rate • Pulse volume and pulse pressure • Peripheral colour • Temperature • Capillary refill time • Blood pressure
    • 2. Blood transfusion Significant haemorrhage ⇨ prompt transfusion of fresh whole blood administered at 10 to 20 ml/kg. fresh whole blood due to plasma loss from plasma leakage.
    • Bleeding: signs • shock • GIT bleeding; occult or obvious • a drop in haematocrit with no clinical improvement e.g. a drop from 50% to 45% (or from 0.50 to 0.45) • decompensated shock after infusion of 40 ml/kg of isotonic crystalloids or colloids • worsening metabolic acidosis. • history of prolonged shock • presence of multi-organ failure e.g. high creatinine, restlessness A delay in blood transfusion and continued infusion of crystalloids or non-blood colloids (such as FFP and platelets) will give rise to more plasma leakage and a poor outcome
    • Management of the Convalescent Phase Most cases of DHF will enter into the convalescent phase 24 – 48 hours after the onset of plasma leakage, and recover spontaneously with appropriate management Signs patient is in convalescent phase: • Stable vital signs - wide pulse pressure, strong pulse, no tachycardia (warm extremities, sinus bradycardia and hypertension). • Return of haematocrit to baseline values. • Increase in urine output • Confluent petechial rash with multiple small, white, round areas among the rash over the extremities (islands of white in a sea of red). • Improvement in general condition with gradual return of appetite • Afebrile
    • Treatment • Discontinuation of iv fluids • Hypokalaemia may occur during the diuretic phase. This can be corrected with fruits and fruit juices. • Potassium chloride supplementation- if patient refuses or is unable to take these. • Invasive procedures; dental extractions or intramuscular injections are not advisable during this period
    • Discharge Criteria for Hospitalized Patients • visible improvement in clinical picture • absence of fever for 24 hours without the use of antipyretics • complete recovery from shock (after 3 days) • stable haematocrit • rising platelet counts greater than 50, 000/mm3 • return of appetite • absence of respiratory distress • normal urine output