Dengue in special condition

in cases that need emergency surgery procedure. Guidelines for platelet transfusion thresholds in thrombocytopenic surgical patients and patients undergoing invasive procedures are largely based on expert opinion and clinical experience. Consensus guidelines commonly used for thrombocytopenic patients requiring surgery are summarized in Table 4. When treatment is indicated, a single adult therapeutic dose ATD of platelets should be transfused shortly before the procedure and the post- transfusion count checked 10 minutes after transfusion gives a reliable indication. 19 Table 4. Platelet transfusion threshold in surgery and invasive procedure Indication Transfusion threshold or target Most invasive surgery including post- cardiopulmonary bypass 50×10 3 uL Neurosurgery or posterior eye surgery 100×10 3 uL Prevention of bleeding associated with invasive procedures Lumbar puncture 50×10 3 uL Central-line insertion 50×10 3 uL Liver, renal or transbronchial biopsy 50×10 3 uL Gastrointestinal endoscopy with biopsy 50×10 3 uL Spinal anaesthesia 50×10 3 uL Epidural anaesthesia 80×10 3 uL

6. Antiviral for treatment of dengue infection

Despite estimated one third of world population currently at risk for dengue infection, the approved antiviral treatment still unavailable. Two drugs were under investigation the study will start on July 2016 in Singapore namely Celgosivir, an alpha glucosidase inhibitor phase 1b and Modipafant a platelet activating factor receptor PAFR antagonist phase 2b. Conclusion Dengue infection still possess as a global threat for one third of world population at risk for contracting dengue. Clinical manifestation range from asymptomatic to severe and live threatening manifestations. The mainstay of management is supportive with special strict monitoring should be done during critical phase to prevent further worsening morbidity and mortality. References 1. Anders KL, Nguyet NM, Chau NV, et al. Epidemiological factors associated with dengue shock syndrome and mortality in hospitalized dengue patients in Ho Chi Minh City, Vietnam. Am J Trop MedHyg 2011;84:127-34. 2. Khor CC, Chau TN, Pang J, et al. Genome- wide association study identifies susceptibility loci for dengue shock syndrome at MICB and PLCE1. Nat Genet 2011;43:1139-41. 3. Nguyen TH, Nguyen TL, Lei HY, et al. Association between sex, nutritional status, severity of dengue hemorrhagic fever, and immune status in infants with dengue hemorrhagic fever. Am J Trop Med Hyg 2005;72:370-4. 4. Nisalak A, Endy TP, Nimmannitya S, Kalanayarooj S, Thisayakorn U, Scott RM, Burke DS, Hoke CH, Innis BL, Vaughn DW. Serotype – specific dengue virus circulation and dengue disease in Bangkok, Thailand from 1973 to 1999. Am J Trop Med Hyg 2003; 68 2: 191-202 5. Rigau-Pérez JG et al., Dengue and dengue haemorrhagic fever. Lancet, 1998, 352:971 –977. 6. Yip WCL. Dengue haemorrhagic fever: current approaches to management. Medical Progress , 1980, 7:13. 7. World Health Organization. Dengue guidelines for diagnosis, treatment, prevemtion and control. Geneva.WHO 2009. WHOHTMNTDDEN2009 8. Gunzman MG, Rosario D, Kouri G. In: Kalitzky M and Borowski P, eds. Diagnosis of dengue virus infection. Molecular Biology of the flaviviruses . Horizon Bioscience, UK, 2009. 9. Buchy F et al., Laboratory tests for the diagnosis of dengue virus infection. Geneva, TDRScientific Working Group, 2006. TDRSWG08. Guzman MG, Kouri G. Dengue diagnosis, advances and challenges. International Journal of Infectious Diseases , 2004, 8:69 –80. 10. World Health Organization. Handbook for clinical management of dengue. Geneva. WHO 2012 11. Wichmann O, Stark K, Shu P-Y, et al. Clinical features and pitfalls in the laboratory diagnosis in travelers. BMC Infectious Diseases. 2006;6120: 1-8. 12. Lam SK, Ew CL, Mitchell JL, et al. Evaluation of a capture screening enzyme-linked immunosorbent assay for combined determination of immunoglobulin M and G antibodies produced during dengue infection. Clin.Diagn. Lab. Immunol. 2000. 7:850 –852. 13. Berlioz-Arthaud A. Evaluation of reagents for the serological diagnosis of Dengue EPINET II Workshop. InstitutPasteir de Nouvelle Caledonie. March 2002. 14. Pesaro AE, D‟Amico E, Aranha LFC. Dengue: cardiac manifestations and implications in antithrombotic treatment. Arq Bras Cardiol. 2007;892:e12-5. 15. Bonow RO, Carabello BA, Kanu C, de Leon AC Jr, Faxon DP, Freed MD, et al. ACCAHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of CardiologyAmerican Heart Association Task Force on Practice Guidelines Circulation. 2006; 114: e84-231. 16. Lum L, Chan M, Leo Y. Strategy in managing anticoagulation therapy following prosthetic heart valve replacement in a patient with dengue fever. Int Jour of Cardiol 2015. 199: 432 – 434 17. Joob B, Wiwanitkit W. Dengue in HIV infected patients: clinical profiles. Asian Pac J Trop Biomed 2014; 4Suppl 2: S568-S569 18. Sharma S, Seth T, Mishra P, Gupta N, et al. Clinical profile of dengue infection in patients with hematological diseases. Mediterr J Hematol Infect Dis. 2011; 31: e2011039. 19. JPAC. Guidelines for the blood transfusion services. JPAC UK 2015. Update Diagnostic and Management of Septic Shock Dewi Dian Sukmawati Division of Tropical and Infectious Disease Department of Internal Medicine Udayana University School of Medicine-Sanglah Hospital Denpasar Reducing mortality due to severe sepsis requires an organized process that guarantees early recognition and consistent application of the evidence-based practices in the 2012 Surviving Sepsis Campaign guidelines. DIAGNOSTIC CRITERIA International sepsis definition 1. Definitive diagnosis requires clinical identification of infection in a patient who also meets the clinical criteria for the Systemic Inflammatory Response Syndrome SIRS. According to a revised consensus conference definition in 2001, SIRS is defined by the presence of 2 or more criteria from a collection of clinical signs and laboratory investigations as follows: a. Temperature 38.3°C 101°F or 36.0°C 96.8°F b. Tachycardia 90 bpm c. Tachypnoea 20 breathsminute d. PCO2 4.3 kPa 32 mmHg e. Hyperglycaemia blood glucose 6.66 mmolL [120 mgdL] in absence of diabetes mellitus f. Acutely altered mental status g. WBC count 12×109L 12,000microlitre or 4×109L 4000microlitre, or normal WBC count with 10 immature forms. 2. Sepsis: when SIRS is present in an individual patient and the cause is thought likely to be an infection, sepsis is present. 3. Severe sepsis: present when sepsis leads to dysfunction of 1 or more organ systems, and includes the subset septic shock. Organ dysfunction variables are: a. Arterial hypoxaemia PaO2FiO2 ratio 300 with new pulmonary infiltrates b. A new or increased oxygen requirement to maintain SpO2 90 c. Acute oliguria urine output 0.5 mLkghour for at least 2 hours d. Serum creatinine 176.8 micromolL 2.0 mgdL e. Coagulation abnormalities INR 1.5 or aPTT 60 seconds f. Thrombocytopenia platelets 100 × 109L [100,000microlitre] g. Hyperbilirubinaemia total bilirubin 68.42 micromolL [4 mgdL] h. Arterial hypotension systolic BP 90 mmHg, mean BP 65 mmHg, or reduction in systolic BP 40 mmHg from baseline i. Serum lactate 2 mmolL. 4. Septic Shock defined as a. Arterial hypotension systolic BP 90 mmHg, mean BP 65 mmHg, or reduction in systolic BP 40 mmHg from baseline persisting for at least 1 hour, despite adequate fluid resuscitation, or b. Serum lactate 4 mmolL after adequate fluid resuscitation. The use of vasopressor agents to correct hypotension does not exclude shock. INITIAL RESUSCITATION AND INFECTION ISSUES Initial Resuscitation Protocolized, quantitative resuscitation of patients with sepsis induced tissue hypoperfusion defined as hypotension persisting after initial fluid challenge or blood lactate concentration ≥ 4 mmolL. Goals during the first 6 hrs of resuscitation: a Central venous pressure CVP 8 –12 mm Hg b Mean arterial pressure MAP ≥ 65 mm Hg c Urine output ≥ 0.5 mLkghr d Central venous superior vena cava or mixed venous oxygen saturation 70 or 65, respectively. In patients with elevated lactate levels targeting resuscitation to normalize lactate. Screening for Sepsis and Performance Improvement Routine screening of potentially infected seriously ill patients for severe sepsis to allow earlier implementation of therapy Diagnosis  Cultures as clinically appropriate before antimicrobial therapy if no significant delay 45 mins in the start of antimicrobials. At least 2 sets of blood cultures both aerobic and anaerobic bottles be obtained before antimicrobial treatment with at least 1 drawn percutaneously and 1 drawn through each vascular access device, unless the device was recently 48 hours inserted.  Use of the 1,3 beta-D-glucan assay, mannan and anti-mannan antibody assays, if available, and invasive candidiasis is in differential diagnosis of cause of infection.  Imaging studies performed promptly to confirm a potential source of infection UG Antimicrobial Therapy • Administration of effective intravenous antimicrobials within the first hour of recognition of septic shock and severe sepsis without septic shock as the goal of therapy. a Initial empiric anti-infective therapy of one or more drugs that have activity against all likely pathogens bacterial andor fungal or viral and that penetrate in adequate concentrations into tissues presumed to be the source of sepsis b Antimicrobial regimen should be reassessed daily for potential de-escalation  Use of low procalcitonin levels or similar biomarkers to assist the clinician in the discontinuation of empiric antibiotics in patients who initially appeared septic, but have no subsequent evidence of infection  Combination empirical therapy for neutropenic patients with severe sepsis and for patients with difficult-to-treat, multidrug-resistant bacterial pathogens such as Acinetobacter and Pseudomonas spp.. For patients with severe infections associated with respiratory failure and septic shock, combination therapy with an extended spectrum beta-lactam and either an aminoglycoside or a fluoroquinolone is for P. aeruginosa bacteremia. A combination of beta-lactam and macrolide for patients with septic shock from bacteremic Streptococcus pneumoniae infections.  Empiric combination therapy should not be administered for more than 3–5 days. De-escalation to the most appropriate single therapy should be performed as soon as the susceptibility profile is known  Duration of therapy typically 7–10 days; longer courses may be appropriate in patients who have a slow clinical response, undrainable foci of infection, bacteremia with S. aureus; some fungal and viral infections or immunologic deficiencies, including neutropenia.  Antiviral therapy initiated as early as possible in patients with severe sepsis or septic shock of viral origin. Antimicrobial agents should not be used in patients with severe inflammatory states determined to be of noninfectious cause Source Control  A specific anatomical diagnosis of infection requiring consideration for emergent source control be sought and diagnosed or excluded as rapidly as possible, and intervention be undertaken for source control within the first 12 hr after the diagnosis is made, if feasible.  When infected peripancreatic necrosis is identified as a potential source of infection, definitive intervention is best delayed until adequate demarcation of viable and nonviable tissues has occurred.  When source control in a severely septic patient is required, the effective intervention associated with the least physiologic insult should be used eg, percutaneous rather than surgical drainage of an abscess  If intravascular access devices are a possible source of severe sepsis or septic shock, they should be removed promptly after other vascular access has been established UG.