![Epidemiology
• An estimated 50 million dengue infections occur annually.
It occurs widely in the tropics, including the Southern
United States, northern Argentina, northern Australia,
Bangladesh, Barbados, Bolivia, Belize, Brazil, Cambodia,
Colombia, Costa Rica, Cuba, Dominican Republic, French
Polynesia, Guadeloupe, El Salvador, Grenada, Guatemala,
Guyana, Haiti, Honduras, India, Indonesia, Jamaica, Laos,
Malaysia, Melanesia, Mexico, Micronesia, Nicaragua,
Pakistan, Panama, Paraguay, The Philippines, Puerto Rico,
Samoa,[13] Western Saudi Arabia, Singapore, Sri Lanka,
Suriname, Taiwan, Thailand, Trinidad and Tobago,
Venezuela and Vietnam, and increasingly in southern China.
• India is an Endemic Region. Recurring outbreaks of DF/DHF
have been reported from various States/Uts namely Andhra
Pradesh, Delhi, Goa, Haryana, Gujarat, Karnataka, Kerala,
Maharashtra, Rajasthan, Uttar Pradesh, Pondicherry,
Punjab, Tamil Nadu, West Bengal and Chandigarh.](https://image.slidesharecdn.com/dengue-140906102808-phpapp01/75/Dengue-Fever-3-2048.jpg)
Uploaded byAnand Nambirajan
Dengue Fever
Dengue fever is a mosquito-borne tropical disease caused by the dengue virus. It is characterized by fever, headache, muscle and joint pains, and a skin rash. Some cases develop into life-threatening dengue hemorrhagic fever or dengue shock syndrome. It occurs widely in tropical areas and an estimated 50 million infections occur annually. The disease progresses through febrile, critical, and recovery phases. During the critical phase, increased capillary permeability can lead to life-threatening plasma leakage and shock.
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Dengue fever, transmitted by mosquitoes, causes fever, headache, muscle pain, and can lead to severe complications.
Approximately 50 million dengue infections per year; endemic regions include India and various tropical areas.
Presentation highlights geographic distribution of dengue cases.
Dengue virus is a Flavivirus with four serotypes, identifiable through structural proteins and genetic makeup.
Primary vectors of dengue are Aedes mosquitoes; survival and reproduction are key to outbreaks.
Humans are the primary hosts for dengue; secondary infection heightens risk for severe illness.
Individuals' age, ethnicity, and secondary infection influence dengue severity.
Dengue virus is transmitted from infected humans to mosquitoes, replicating within them to spread further.
Illustration of the dengue transmission cycle.
Dengue virus infects various cells, leading to immune response alterations and cell death.
High viral loads affect blood platelet production, correlating with severe dengue symptoms.
Infection triggers antibody responses; high IgG levels during secondary infections increase severity risks.
Clinical features of dengue infection categorized into severe and non-severe types.
WHO defines dengue types; criteria for probable and severe dengue provided.
Disease progresses through febrile, critical, and recovery phases.
Symptoms during the febrile phase include high fever, body aches, and possible hemorrhagic signs.
Typical rash presentation associated with dengue infection.
Utilizes capillary fragility test to assess bleeding tendency in suspected dengue cases.
Key characteristics during critical phase include plasma leakage and increased hematocrit.
Severe plasma loss leads to shock and organ impairment.
The recovery phase involves gradual fluid reabsorption and stabilizing health indicators.
Describes the progression of dengue infection through its various phases.
High fluid administration can lead to respiratory issues, necessitating careful monitoring.
Criteria for identifying severe dengue include plasma leakage and organ impairment.
Describes body’s response to maintain blood pressure during early shock stages.
Patterns of decompensatory shock can result in organ failure and further complications.
Identify severe dengue by recognizing plasma leakage and critical clinical signs.
Steps for assessing, diagnosing, and managing dengue patients effectively.
Key historical factors to evaluate in dengue cases which influence patient management.
Emphasizes thorough physical checks for hydration status and checking for bleeding.
Monitoring blood counts is crucial for assessing illness severity in dengue.
Other diseases that may mimic dengue presentations in patients are reviewed.
Various methods to confirm dengue infections and differentiate it from similar diseases.
Guidelines for confirming dengue through serological and PCR testing.
Comparison of diagnostic tests, advantages, and limitations for dengue detection.
Parameters to determine hospitalization needs for patients with warning signs.
Differentiates management strategies based on patient severity and warning signs.
Guidelines for stable dengue patients to manage symptoms at home.
Protocols for managing patients with warning signs through hospital care.
Critical management for severe dengue patients requiring intensive care.
Goals focused on improving patient circulation and end-organ perfusion.
Approaches to treating compensated shock through fluid resuscitation.
Instructions on managing hypotensive shock with appropriate fluid volumes.
Importance of haematocrit in guiding treatment decisions during dengue management.
Interventions based on haematocrit results and clinical status.
Approach for managing bleeding issues in stable dengue patients.
Identifies patients at highest risk for severe bleeding in dengue.
Protocols for effectively managing blood loss in severe dengue cases.
Risks of fluid overload highlighting causes and clinical features in dengue patients.
Strategies for addressing fluid overload in recovering dengue patients.
Links metabolic acidosis to shock and management strategies.
Monitoring and correcting electrolyte imbalances during dengue treatment.
Conditions required for safely discharging dengue patients from medical care.
Focus on vector control and potential vaccines under study to manage dengue.
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Dengue Fever
- 2. Dengue fever, alsoknown as Break Bone Fever, is a mosquito-borne tropical disease caused by the dengue virus. Symptoms include fever, headache, muscle and joint pains, and a characteristic skin rash. Some proportion of cases develop the life-threatening dengue hemorrhagic fever, resulting in bleeding, low levels of blood platelets and blood plasma leakage, or into dengue shock syndrome characterized by Shock.
- 3. Epidemiology • Anestimated 50 million dengue infections occur annually. It occurs widely in the tropics, including the Southern United States, northern Argentina, northern Australia, Bangladesh, Barbados, Bolivia, Belize, Brazil, Cambodia, Colombia, Costa Rica, Cuba, Dominican Republic, French Polynesia, Guadeloupe, El Salvador, Grenada, Guatemala, Guyana, Haiti, Honduras, India, Indonesia, Jamaica, Laos, Malaysia, Melanesia, Mexico, Micronesia, Nicaragua, Pakistan, Panama, Paraguay, The Philippines, Puerto Rico, Samoa,[13] Western Saudi Arabia, Singapore, Sri Lanka, Suriname, Taiwan, Thailand, Trinidad and Tobago, Venezuela and Vietnam, and increasingly in southern China. • India is an Endemic Region. Recurring outbreaks of DF/DHF have been reported from various States/Uts namely Andhra Pradesh, Delhi, Goa, Haryana, Gujarat, Karnataka, Kerala, Maharashtra, Rajasthan, Uttar Pradesh, Pondicherry, Punjab, Tamil Nadu, West Bengal and Chandigarh.
- 4.
- 5. The Virus Genus-Flavivirus Family -Flaviviridae Single-stranded RNA 4 serotypes (DEN-1 to 4) Dengue virus is spherical with a diameter of 50nm containing multiple copies of the three structural proteins, a host-derived membrane bilayer and a single copy of a positive-sense, single-stranded RNA genome. The genome encodes different gene prodcts: C(capsid),prM(matrix),E(envelope) and several NS Proteins(Non Strctural). NS1 protein is secreted in plasma and is useful in early Diagnosis.
- 6. VECTOR Female Aedesmosquitoes A.aegypti (primary) A. albopictus A.Polynesiensis Ae. aegypti ,the most common vector,has an average adult survival of fifteen days. The eggs can survive one year without water. It is a day time feeder. Dengue outbreaks have also been attributed to Aedes albopictus, Aedes polynesiensis and several species of the Aedes scutellaris complex. Each of these species has a particular ecology, behavior and geographical distribution
- 7. HOST • Denguevirus infects humans and several species of lower primates but in India man is the only natural reservoir of infection. Secondary dengue infection is a risk factor for DHF. • An incubation period of 4-10 days, infection by any of the four virus serotypes can produce a wide spectrum of illness, although most infections are asymptomatic or subclinical. Primary infection is thought to induce lifelong protective immunity to the infecting serotype but not for other serotypes.
- 8. Individual risk factorsdetermine the severity of disease and include secondary infection,younger 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.
- 9. Transmission Humans arethe 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. Ae. aegypti is one of the most efficient vectors for arboviruses because it is highly anthropophilic, frequently bites several times before completing oogenesis, and thrives in close proximity to human
- 10.
- 11. Pathogenesis Upon inoculationof DENV into the dermis, Langerhans cells and keratinocytes will primarily be infected. The virus then via blood spreads and infects tissue macrophages in several organs, especially the macrophages in the spleen. Essentially, infection of macrophages, hepatocytes, and EC influences the hemostatic and the immune responses to DENV. Infected cells die predominantly through apoptosis and to a lesser extent through necrosis. Necrosis results in release of toxic products,which activate the coagulation and fibrinolytic systems
- 12. Depending on theextent of infection of bone marrow stromal cells and the levels of IL-6, IL-8, IL-10, and IL-18, hemopoiesis is suppressed, resulting in decreased blood platelets. Platelets interact closely with EC, and a normal number of functioning platelets is necessary to maintain vascular stability. A high viral load in blood and possibly viral tropism for EC, severe thrombocytopenia, and platelet dysfunction may result in increased capillary fragility, clinically manifested as petechiae, easy bruising, and gastrointestinal mucosal bleeding which is characteristic of DHF.
- 13. Infection stimulates developmentof specific antibody and cellular immune responses to DENV. IgM antibodies that crossreact with EC, platelets, and plasmin are produced, resulting in increased vascular permeability and coagulopathy. Enhancing IgG antibodies bind heterologous virus during secondary infection and enhance infection of APCs, thereby contributing to the increased viral load that is seen during secondary viremia in some patients. A high viral load overstimulates Cross-Reactive T cells. These leads to production of high levels of proinflammatory cytokines and other mediators which induce changes in EC leading to the coagulopathy and plasma leakage characteristic of DSS.
- 15.
- 16. WHO Classifies Denguein to Non-Severe Dengue(with and without Warning Signs) and Severe Dengue PROBABLE DENGUE live in /travel to dengue endemic area. Fever and 2 of the following criteria: • Nausea, vomiting • Rash • Aches and pains • Tourniquet test positive • Leukopenia • Any warning sign Laboratory-confirmed dengue WARNING SIGNS • Abdominal pain or tenderness • Persistent vomiting • Clinical fluid accumulation • Mucosal bleed • Lethargy, restlessness • Liver enlargment >2 cm • Laboratory: increase in HCT concurrent with rapid decrease in platelet count SEVERE DENGUE Severe plasma leakage leading to: • Shock (DSS) • Fluid accumulation with respiratory distress Severe bleeding as evaluated by clinician Severe organ involvement • Liver: AST or ALT >=1000 • CNS: Impaired consciousness • Heart and other organs
- 17. After the incubationperiod, the illness begins abruptly and is followed by the three phases -- febrile, critical and recovery Febrile Phase Critical Phase Recovery Phase
- 19. Febrile Phase HighGrade Fever lasting 2-7 days Facial Flushing, Skin Erythema, Generalized Body ache, Myalgia, Arthralgia, Severe Backache(Break Bone Fever),Retro-Orbital Pain ,Headache,Pharyngitis,Conjuctival injection. Anorexia,Nausea and vomiting. A positive tourniquet test in this phase increases the probability of dengue Mild Hemmorhagic manifestations like petechiae and mucosal bleeding Tender Hepatomegaly Indistinguishable from Non-Severe dengue and Severe Dengue Lab Parameters – Progressive Decrease in White Cell Count
- 20.
- 21. Tourniquet test /Rumpel-LeedeCapillary- Fragility Test/Hess test • It is a clinical diagnostic method to determine a patient's haemorrhagic tendency. It has good sensitivity but a low specificity • A blood pressure cuff is applied and inflated to the midpoint between the systolic and diastolic blood pressures for five minutes. The test is positive if there are more than 10 to 20 petechiae per square inch.
- 22. Positive Tourniquet test Right Side Positive
- 23. Critical Phase Thetemperature drops to 37.5-38 C (days 3-7) An increase in capillary permeability in parallel with increasing haematocrit levels Clinically significant plasma leakage lasting 24–48 hours Progressive leukopenia followed by a rapid decrease in platelet count usually precedes plasma leakage Increase in capillary permeability leads to loss of plasma volume Pleural effusion and ascites may be clinically detectable depending on the degree of plasma leakage and the volume of fluid therapy.
- 24. • Shock occurswhen a critical volume of plasma is lost through leakage. Prolonged shock, the consequent organ hypoperfusion results in progressive Organ Impairment, Metabolic Acidosis and Disseminated Intravascular Coagulation • DIC leads to severe haemorrhage causing the haematocrit to decrease further in severe shock • Severe organ impairment such as severe Hepatitis, Encephalitis or Myocarditis and/or severe bleeding may also develop without obvious plasma leakage or shock
- 25. Recovery Phase Ifthe patient survives the 24–48 hour critical phase, a gradual reabsorption of extravascular compartment fluid takes place in the following 48–72 hours General well-being improves, appetite returns, gastrointestinal symptoms abate, hemodynamic status stabilizes and diuresis ensues Some patients may have a rash of “isles of white in the sea of red” Some may experience generalized pruritus. Bradycardia is common during this stage The haematocrit stabilizes or may be lower due to the dilutional effect of reabsorbed fluid. White blood cell count usually starts to rise soon after defervescence but the recovery of platelet count is typically later than that of white blood cell count.
- 26.
- 27. Respiratory Distress frommassive Pleural Effusion and Ascites may occur due to excessive intravenous fluids administertration. During the critical and/or recovery phases, excessive fluid therapy is associated with Pulmonary Oedema or Congestive Heart Failure Those who improve after defervescence are said to have non-severe dengue. Some patients progress to the critical phase of plasma leakage without defervescence and, in these patients, changes in the full blood count should be used to guide the onset of the critical phase and plasma leakage. Those who deteriorate will manifest with warning signs. Cases of dengue with warning signs will probably recover with early intravenous rehydration. Some cases will deteriorate to severe dengue
- 28. Severe Dengue Severedengue is defined by one or more of the following: • Plasma Leakage that may lead to shock (dengue shock) and/or fluid accumulation, with or without Respiratory Distress • Severe Bleeding • Severe Organ Impairment Dengue shock syndrome (DSS) is a form of hypovolaemic shock and results from continued vascular permeability and plasma leakage. This usually takes place around defervescence, i.e. on days 4−5 of illness (range of days 3−8), and is often preceded by warning signs. Patients who do not receive prompt intravenous fluid therapy progress rapidly to a state of shock.
- 29. Compensatory Phase Duringthe initial stage of shock,the compensatory mechanism which maintains a normal systolic blood pressure. Tachycardia and Peripheral Vasoconstriction with reduced skin perfusion, resulting in Cold Extremities ,Delayed Capillary Refill time and weak volume peripheral pulses . The diastolic pressure rises towards the systolic pressure and the Pulse Pressure narrows as the peripheral vascular resistance increases. Compensated Metabolic Acidosis is observed when the pH is normal with low carbon dioxide tension and a low bicarbonate level.
- 30. Decompensatory Phase Thereis decompensation and Blood pressure disappears abruptly. Prolonged hypotensive shock and hypoxia leads to Metabolic Acidosis and Multi Organ Failure Rapid and increased depth of breathing − a compensation for the metabolic acidosis (Kussmaul’s breathing) The patient becomes restless, confused and extremely lethargic. Seizures may occur and agitation may alternate with lethargy Acute Liver and Renal Failure and Encephalopathy may be present in severe shock Cardiomyopathy and Myocarditis have also been reported in a few dengue cases.
- 31. Severe dengue shouldbe considered if the patient is from an area of dengue risk presenting with fever of 2–7 days plus any of the following features: • There is evidence of plasma leakage, such as: – high or progressively rising haematocrit; – pleural effusions or ascites; – circulatory compromise or shock (tachycardia, cold and clammy extremities, capillary refill time greater than three seconds, weak or undetectable pulse, narrow pulse pressure or, in late shock, unrecordable blood pressure). • There is significant Bleeding • There is an altered level of consciousness (lethargy or restlessness, coma, convulsions). • There is severe gastrointestinal involvement (persistent vomiting, increasing or intense abdominal pain, jaundice). • There is severe organ impairment (acute liver failure, acute renal failure, encephalopathy or encephalitis, or other unusual manifestations, cardiomyopathy) or other unusual manifestations
- 32.
- 33. An Approach StepI − Overall assessment History, including symptoms, past medical and family history Physical examination, including full physical and mental assessment Investigation, including routine laboratory tests and dengue-specific laboratory tests Step II − Diagnosis, assessment of disease phase and severity Step III − Management Disease notification Management decisions.
- 34. History The historyshould include: i. – date of onset of fever/illness ii. – quantity of oral intake iii. – assessment for warning signs iv. – diarrhoea v. – change in mental state/seizure/dizziness vi. – urine output (frequency, volume and time of last voiding) vii. – other important relevant histories, such as family or neighbourhood dengue,travel to dengue endemic areas, co-existing conditions (e.g. infancy,pregnancy, obesity, diabetes mellitus, hypertension), jungle trekking and swimming in waterfall (consider leptospirosis, typhus, malaria), recent unprotected sex or drug abuse (consider acute HIV seroconversion illness)
- 35. Physical examination Thephysical examination should include: i. assessment of mental state ii. assessment of hydration status iii. assessment of haemodynamic status iv. checking for tachypnoea/acidotic breathing/pleural effusion; v. checking for abdominal tenderness/hepatomegaly/ascites vi. examination for rash and bleeding manifestations vii. tourniquet test (repeat if previously negative or if there is no bleeding manifestation)
- 36. Investigations A fullblood count should be done at the first visit (it may be normal); and this should be repeated daily until the critical phase is over. The haematocrit in the early febrile phase could be used as the patient’s own baseline Leukopenia (≤ 5000 cells/mm3). Dengue-specific laboratory tests. Liver function, glucose, serum electrolytes, urea and creatinine, bicarbonate or lactate, cardiac enzymes, electrocardiogram (ECG)
- 37. Conditions that mimicthe febrile phase of dengue infection Flu-like syndromes Influenza, Measles, Chikungunya, Infectious Mononucleosis, HIV seroconversion illness Illnesses with a rash Rubella, measles, scarlet fever, meningococcal infection, Chikungunya, drug reactions Diarrhoeal diseases Rotavirus, other enteric infections Illnesses with neurological Meningoencephalitis manifestations Febrile seizures Conditions that mimic the critical phase of dengue infection Infectious Acute gastroenteritis, malaria, leptospirosis, typhoid, typhus, viral hepatitis, Acute HIV-seroconversion illness, bacterial sepsis, septic shock Malignancies Acute leukaemia and other malignancies
- 38.
- 41. CLINICAL SAMPLE DIAGNOSTICMETHOD METHODOLOGY Virus detection and its components Acute serum (1–5 days of fever) Whole blood and Tissues Viral isolation Mosquito or mosquito cell Culture inoculation Nucleic acid Detection RT-PCR and real time RT PCR Antigen detection NS1 Ag rapid tests NS1 Ag ELISA Immuno- histochemistry Serological response Paired sera (acute serum from1–5 days and second serum 15–21 days after) IgM or IgG seroconversion ELISA HIA Neutralization Test Serum after day 5 of fever IgM detection (recent infection) IgG detection IgM antibody-capture enzyme-linked Immunosorbent assay (MAC-ELISA),Rapid Test IgG ELISA HIA
- 42. INTERPRETATION OF RESULTS INTERPRETATION CONFIRMED DENGUE INFECTION One of the following: 1. PCR + 2. Virus culture + 3. IgM seroconversion in paired sera 4. IgG seroconversion in paired sera or fourfold IgG titer increase in paired sera PROBABLE DENGUE INFECTION IgM + in a single serum sample IgG + in a single serum sample with a HI titre of 1280 or greater
- 43. Diagnostic Tests AdvantagesLimitations Nucleic acid detection Most sensitive and specific Early detection Expensive Not possible to differentiate between primary and secondary infection Isolation in cell culture and identification using immuno-fluorescence Specific Takes more than 1 week Need expertise and facility Not possible to differentiate between primary and secondary infection Antigen detection in clinical specimens Easy to perform Early diagnosis Not as sensitive as virus isolation Serologic tests: IgM tests Seroconversion: 4-fold rise in HI or ELISA IgG titres between acute and convalescent samples Confirmation of acute infection Least expensive Easy to perform distinguish between primary and secondary infection May miss cases because IgM levels may be low or undetectable Delay in confirming diagnosis
- 44. Step II –Diagnosis, assessment of disease phase and severity Warning signs Hydration Haemodynamic state ADMISSION CRITERIA WARNING SIGNS Any Signs and symptoms related to hypotension (possible plasma leakage) Dehydrated patient, unable to tolerate oral fluids Dizziness or postural hypotension Profuse perspiration, fainting, prostration during defervescence Hypotension or cold extremities Difficulty in breathing/shortness of breath (deep sighing breaths)
- 45. Bleeding Spontaneous bleeding,independent of the platelet count Organ impairment Renal, hepatic, neurological or cardiac enlarged, tender liver, although not yet in shock chest pain or respiratory distress, cyanosis Investigations Rising haematocrit Pleural effusion, ascites or asymptomatic gall-bladder thickening Co-existing conditions Pregnancy Co-morbid conditions, such as diabetes mellitus, hypertension, peptic ulcer, haemolytic anemias and others Overweight or obese (rapid venous access difficult in emergency) Infancy or old age Social circumstances Living alone,Living far from health facility Without reliable means of transport
- 46. Step III—Management Dependingon the clinical manifestations and other circumstances, patients may be • Sent home (Group A) • Be referred for in-hospital management (Group B) • Require emergency treatment and urgent referral (Group C)
- 47. Group A •Encourage intake of ORS, fruit juice and other fluids • Paracetamol and tepid sponge for fever • Advise to come back if : no clinical improvement severe abdominal pain persistent vomiting cold and clammy extremities, lethargy or irritability or restlessness, bleeding not passing urine for more than 4–6 hours. • Don’t give NSAIDS,Aspirin
- 48. Group B ThesePatients should be referred for in-hospital management. These include patients with warning signs, those with co-existing conditions that may make dengue or its management more complicated (such as pregnancy, infancy, old age, obesity, diabetes mellitus, renal failure, chronic haemolytic diseases) If the patient has dengue with warning signs, the action plan should be as follows: • Obtain a reference haematocrit before fluid therapy. • Give only isotonic solutions such as 0.9% saline, Ringer’s lactate, or Hartmann’s solution. • Start with 5–7 ml/kg/hour for 1–2 hours, then reduce to 3–5 ml/kg/hr for 2–4 hours, and then reduce to 2–3 ml/kg/hr or less according to the clinical response. • Reassess the clinical status and repeat the haematocrit. If the haematocrit remains the same or rises only minimally, continue with the same rate (2–3 ml/kg/hr) for another 2–4 hours. If the vital signs are worsening and haematocrit is rising rapidly, increase the rate to 5–10 ml/kg/hour for 1–2 hours. Reassess the clinical status, repeat the haematocrit and review fluid infusion rates accordingly • Intravenous fluids are usually needed for only 24–48 hours. • Reduce intravenous fluids gradually when the rate of plasma leakage decreases towards the end of the critical phase as indicated by urine output and/or oral fluid intake or haematocrit decreasing below the baseline value in a stable patient
- 49. Group C Allpatients with severe dengue should be admitted to a hospital with access to intensive care facilities Judicious intravenous fluid resuscitation is the essential. Plasma losses should be replaced immediately and rapidly with isotonic crystalloid solution or, in the case of hypotensive shock, colloid solutions Blood transfusion: with suspected/severe bleeding
- 50. Goals of fluidresuscitation: • Improving central and peripheral circulation (decreasing tachycardia, improving BP, warm and pink extremities, and capillary refill time <2 secs) • Improving end-organ perfusion – i.e. stable conscious level (more alert or less restless), urine output ≥ 0.5 ml/kg/hour, decreasing metabolic acidosis.
- 51.
- 52. Compensated shock (systolicpressure maintained but has signs of reduced perfusion) Fluid resuscitation with isotonic crystalloid 5–10 ml/kg/hr over 1 hour Improving Not Improving IV crystalloid 5–7 ml/kg/hr for 1–2 hours, then: reduce to 3–5 ml/kg/hr for 2–4 hours; reduce to 2–3 ml/kg/hr for 2–4 hours. If patient continues to improve, fluid can be further reduced. Monitor HCT 6–8 hourly. If the patient is not stable, act according to HCT levels: if HCT increases, consider bolus fluid administration or increase fluid administration; if HCT decreases, consider transfusion with fresh whole transfusion. Stop at 48 hours Check HCT HCT High Administer 2nd bolus of fluid 10–20 ml/kg/hr for 1 hour Improving If patient improves, reduce to 7–10 ml/kg/hr for 1–2 hours Then reduce further HCT Low Consider significant occult/overt bleed Initiate transfusion with fresh whole blood Not Improving
- 53. HYPOTENSIVE SHOCK Fluidresuscitation with 20 ml/kg isotonic crystalloid or colloid over 15 minutes Try to obtain a HCT level before fluid resuscitation Improving Not Improving Crystalloid/colloid 10 ml/kg/hr for 1 hour, then continue with: IV crystalloid 5–7 ml/kg/hr for 1– 2 hours; reduce to 3–5 ml/kg/hr for 2– 4 hours; reduce to 2–3 ml/kg/hr for 2– 4 hours. If patient continues to improve, fluid can be further reduced. Monitor HCT 6-hourly. If the patient is not stable, act according to HCT levels: if HCT increases, consider bolus fluid administration or increase fluid administration; if HCT decreases, consider transfusion with fresh whole transfusion. Stop at 48 hour Review 1st HCT HCT High HCT Low Administer 2nd bolus fluid (colloid) 10–20 ml/kg over ½ to 1 hour Improving Not Improving Repeat 2nd HCT HCT High Administer 3rd bolus fluid HCT Low (colloid) 10–20 ml/kg over 1 hour Improving Not Improving Repeat 3rd HCT Consider significant occult/overt bleed Initiate transfusion with fresh whole blood
- 54. Changes in thehaematocrit are a useful guide to treatment and must be interpreted in parallel with the haemodynamic status, the clinical response to fluid therapy and the acid-base balance. • A rising or persistently high haematocrit together with unstable vital signs (particularly narrowing of the pulse pressure , tachycardia, metabolic acidosis, poor urine output) indicates active plasma leakage and the need for a further bolus of fluid replacement. • A rising or persistently high haematocrit together with stable haemodynamic status and adequate urine output does not require extra intravenous fluid but need close monitoring and it is likely that the haematocrit will start to fall within the next 24 hours as the plasma leakage stops.
- 55. • A decreasein haematocrit together with unstable vital signs indicates major haemorrhage and the need for urgent blood transfusion. • A decrease in haematocrit together with stable haemodynamic status and adequate urine output indicates haemodilution and/or reabsorption of extravasated fluids, so in this case intravenous fluids must be discontinued immediately to avoid pulmonary oedema
- 56.
- 57. Treatment of haemorrhagiccomplications Mucosal bleeding occuring in dengue is considered as a minor issue as long as the patient remains stable with fluid replacement. The bleeding usually improves rapidly during the recovery phase. In patients with profound thrombocytopenia, ensure strict bed rest and protection from trauma. Do not give intramuscular injections. Prophylactic platelet transfusions for severe thrombocytopaenia in otherwise haemodynamically stable patients have not been shown to be effective and are unnecessary
- 58. Patients at riskof major bleeding are those who: – have prolonged/refractory shock; – have hypotensive shock and renal or liver failure and/or severe and persistent metabolic acidosis; – are given non-steroidal anti-inflammatory agents; – have pre-existing peptic ulcer disease; – are on anticoagulant therapy; – have any form of trauma, including intramuscular injection
- 59. • Give 5–10ml/kgof fresh-packed red cells or 10– 20 ml/kg of fresh whole blood at an appropriate rate and observe the clinical response. Fresh whole blood or fresh red cells are given as stored ones lose 2,3 DPG. • Consider repeating the blood transfusion if there is further blood loss or no appropriate rise in haematocrit after blood transfusion • Transfusing platelet concentrates and/or fresh-frozen plasma for severe bleeding is not recommended as it may paradoxically worsen fluid overload
- 60. Fluid overload Fluidoverload with large pleural effusions and ascites is a common cause of acute respiratory distress and failure in severe dengue Causes of fluid overload are: – excessive and/or too rapid intravenous fluids; – incorrect use of hypotonic rather than isotonic crystalloid solutions; – inappropriate use of large volumes of intravenous fluids in patients with unrecognized severe bleeding; – inappropriate transfusion of fresh-frozen plasma, platelet concentrates and cryoprecipitates; – continuation of intravenous fluids after plasma leakage has resolved (24–48 hours from defervescence); – co-morbid conditions such as congenital or ischaemic heart disease, chronic lung and renal diseases
- 61. Clinical Features ofFluid Overload Early clinical features Late clinical features Respiratory distress, difficulty in breathing; Rapid breathing; Chest wall in-drawing; Wheezing (rather than crepitations); Large pleural effusions; Tense ascites; Increased jugular venous pressure (JVP Pulmonary oedema (cough with pink or frothy sputum ± crepitations, cyanosis); Irreversible shock (heart failure, often in combination with ongoing Hypovolaemia)
- 62. Treatment of FluidOverload • Oxygen therapy • If the patient has stable haemodynamicstatus and is out of the critical phase (more than 24–48 hours of defervescence), stop intravenous fluids but continue close monitoring. If necessary, give oral or intravenous furosemide 0.1–0.5 mg/kg/dose once or twice daily, or a continuous infusion of furosemide 0.1 mg/kg/hour • If the patient has stable haemodynamic status but is still within the critical phase, reduce the intravenous fluid accordingly. Avoid diuretics during the plasma leakage phase because they may lead to intravascular volume depletion • Stopping intravenous fluid therapy during the recovery phase will allow fluid in the pleural and peritoneal cavities to return to the intravascular compartment.
- 63. Metabolic acidosis •Compensated metabolic acidosis is an early sign of hypovolaemia and shock. Lactic acidosis due to tissue hypoxia and hypoperfusion is the most common cause of metabolic acidosis in dengue shock. Correction of shock and adequate fluid replacement will correct it. • If metabolic acidosis remains persistent, one should suspect severe bleeding and check the haematocrit. Transfuse fresh whole blood or fresh packed red cells urgently. • Sodium bicarbonate for metabolic acidosis caused by tissue hypoxia is not recommended for pH ≥ 7.10. • Hyperchloraemia, caused by the administration of large volumes of 0.9% NaCl solution (chloride concentration of 154 mmol/L), may cause metabolic acidosis with normal lactate levels. If serum chloride levels increase, use Ringer’s lactate as crystalloid.
- 64. Dyselectrolytemia • Hyponatremiais in severe dengue could be related to gastrointestinal losses through vomiting and diarrhoea or the use of hypotonic solutions for resuscitation .The use of isotonic solutions for resuscitation will prevent and correct this condition. • Hyperkalemia is observed with severe metabolic acidosis or acute renal injury. Appropriate volume resuscitation will reverse the metabolic acidosis and the associated hyperkalemia. • Hypokalemia is often associated with gastrointestinal fluid losses and the stress-induced hypercortisol state, usually encountered towards the later part of the critical phase and should be corrected with potassium supplements in the parenteral fluids. • Serum calcium levels should be monitored and corrected when large quantities of blood have been transfused or if sodium bicarbonate has been used
- 65. Discharge Criteria Allof the following conditions must be present: • Clinical No fever for 48 hours Improvement in clinical status (general well-being, appetite, haemodynamic status, urine output, no respiratory distress) • Laboratory Increasing trend of platelet count Stable haematocrit without intravenous fluids
- 66.
- 67. • Vector Control • Vaccines While no licensed dengue vaccine is available, several vaccine candidates are currently being evaluated in clinical studies. Live-Attenuated Tetravalent Vaccine based on chimeric yellow fever-dengue virus (CYD-TDV), has progressed to phase III efficacy studies Several other live-attenuated vaccines, as well as subunit, DNA and purified inactivated vaccine candidates, are at earlier stages of clinical development.