1 / 149

War Against Sepsis Case Based Sepsis Module (Based on Surviving Sepsis Guidelines 2008)

War Against Sepsis Case Based Sepsis Module (Based on Surviving Sepsis Guidelines 2008). Crit Care Med 2008 Vol. 36, No. 296-327. Surviving Sepsis Campaign Guidelines for Management of Severe Sepsis/Septic Shock. An Overview. Surviving Sepsis campaign. A Global program to:

iram
Download Presentation

War Against Sepsis Case Based Sepsis Module (Based on Surviving Sepsis Guidelines 2008)

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript


  1. War Against Sepsis Case Based Sepsis Module (Based on Surviving Sepsis Guidelines 2008) Crit Care Med 2008 Vol. 36, No. 296-327

  2. Surviving Sepsis CampaignGuidelines for Management of Severe Sepsis/Septic Shock An Overview

  3. Surviving Sepsis campaign A Global program to: Reduce mortality rates in severe sepsis

  4. A 50 yr old smoker presents to emergency with fever and acute shortness of breath of two days duration. • He has a respiratory rate of 35/min B.P of 90/40, pulse 120/min regular, Spo2 88% on 10L nasal cannula. • He is alert and communicating. • He has brought a chest x-ray which shows right lower zone opacity.

  5. What does this patient have? • Systemic inflammatory response syndrome (SIRS) • Sepsis • Severe sepsis • Septic shock

  6. SIRS AND SEPSIS Sepsis is defined as an infection plus 2 SIRS criteria Temperature >38°C or <36°C HR >90 beats/min Respirations >20/min WBC count >12,000/mm3or <4,000/mm3 or >10% immature neutrophils Other Pancreatitis SIRS Sepsis Infection Severesepsis Trauma Burns Septic shock Severesepsis SIRS Sepsis MODS Levy MM, et al. Crit Care Med. 2003;31:1250-1256.

  7. DEFINITIONS • Severe Sepsis • Sepsis + sepsis-induced organ dysfunction or • Tissue hypo-perfusion Crit Care Med 2008 Vol. 36, No. 296-327

  8. DEFINITIONS • Sepsis-induced hypotension • systolic blood pressure (SBP) <90 mm Hg Or • mean arterial pressure <70 mm Hg Or • SBP decrease >40 mm Hg Or • <2 SD below normal for age in the absence of other causes of hypotension Crit Care Med 2008 Vol. 36, No. 296-327

  9. DEFINITIONS • Septic shock • sepsis-induced hypotension persisting despite adequate fluid resuscitation Crit Care Med 2008 Vol. 36, No. 296-327

  10. DEFINITIONS • Sepsis-induced tissue hypo-perfusion: • septic shock • an elevated lactate Or • oliguria Crit Care Med 2008 Vol. 36, No. 296-327

  11. A 50 yr old smoker presents to emergency with fever and acute shortness of breath of two days duration. • He has a respiratory rate of 35/min B.P of 90/40, pulse 120/min regular, Spo2 88% on 10L nasal cannula. • He is alert and communicating. • He has brought a chest x-ray which shows right lower zone opacity.

  12. What does this patient have? • Systemic inflammatory response syndrome (SIRS) • Sepsis • Severe sepsis • Septic shock

  13. Epidemiology

  14. Severe Sepsis:Comparative Incidence and Mortality

  15. Pathophysiology

  16. Inflammation, Coagulation & Impaired Fibrinolysis In Severe Sepsis COAGULATION CASCADE Endothelium Tissue Factor Factor VIIIa PAI-1 IL-6 IL-1 TNF- Factor Va Monocyte Suppressed fibrinolysis THROMBIN Fibrin Neutrophil IL-6 Fibrin clot Tissue Factor Thrombotic Responseto Infection Fibrinolytic Responseto Infection Inflammatory Responseto Infection Adapted from Bernard GR, et al. N Engl J Med. 2001;344:699-709.

  17. Tissue Factor Factor VIII Coagulation cascade Monocyte Factor VIIIa Factor V Organisms Factor Va Thrombin Fibrin clot Fibrin Chemoattractants tissue factor Activation of Coagulation in Sepsis Adapted from Bernard GR, et al. N Engl J Med. 2001;344:699-709.

  18. Tissue Factor Factor VIII Coagulation cascade Monocyte IL-6 Factor VIIIa Inactivation Factor V Organisms Factor Va Inactivation Thrombin Reduced chemotactic response leading to less rolling of leukocytes on the endothelium aPC Inhibition of chemotactic response to chemokines Reduction of rolling Fibrin clot Fibrin Chemo attractants tissue factor Activation of Coagulation in Sepsis: Role of Endogenous APC Adapted from Bernard GR, et al. N Engl J Med. 2001;344:699-709.

  19. Severe Sepsis Pathophysiology Microvascular dysfunction Inflammation Coagulation Fibrinolysis Hypoperfusion/hypoxia Microvascular thrombosis Endothelial dysfunction Organ dysfunction Global tissue hypoxia Direct tissue damage  

  20. DIC Redistribution of organ blood flow Cardiopulmonary pathology Endothelial activation Disturbance of red and white cell rheology Disturbed Microcirculation in Severe Sepsis Congestion and hemorrhage Viscosity alterations Vasoplegia Intravascular pooling Altered microvascular blood flow and vascular resistance Edema formation Increased microvascular permeability Opening of AV shunts Decreased red cell permeability Sepsis is a Disease of the …. Microcirculation Spronk, P., Zandstra, D., Ince, C. Bench-to-bedside review: Sepsis is a disease of the microcirculation. Critical Care. 2004; 8:462-468.

  21. Micro vascular Blood Flow Is Impaired in Severe Sepsis: Arterial blood SO2 - 0.65 SO2- 0.98 SO2 0.94 SO2 0.65 Venous blood SO2 -0 .83 SO2 -0 .86 SO2 -0 .65

  22. Lactate:An Indicator of Tissue Perfusion • Serum lactate levels are used to assess the disease severity and adequacy of global tissue perfusion • By-product of anaerobic metabolism if tissue hypoxia exists • Interpretation of elevated blood lactate levels in sepsis is limited by several important factors1: • Production of elimination • Increasing glycolysis • Inhibition of pyruvate metabolism • Global changes Bakker J, Gris P, Conerfils M, et al. Serial Blood Lactate Levels Can Predict the Development of Multiple Prgan Failure Following Septic Shock, Am J Surg 1996; 171:221-226.

  23. Identifying Acute Organ Dysfunction as a Marker of Severe Sepsis CNS: Altered consciousness Confusion Cardiovascular: Tachycardia Hypotension Altered CVP & PAOP Respiratory: Tachypnea  PaO2  PaO2/FiO2 ratio Renal: Oliguria Anuria  Creatinine Hepatic: Jaundice,  Liver enzymes  Albumin Hematologic:  Platelets  PT/INR,  aPTT  Protein C  D-dimer Metabolic: Metabolic Acidosis  Lactate level  Lactate Clearance Modified from criteria published in: Balk, R., Pathogenesis and management of multiple organ dysfunction or failure in severe sepsis and septic shock. Crit Care Clinics. 2000; 16(2):337-351; and Kleinpell, R. The role of the critical care nurse in the assessment and management of the patient with severe sepsis. Crit Care Nurs Clin N Am. 2003; 15:27-34.

  24. Severe Sepsis Pathophysiology: Summary • Severe sepsis is an inflammatory, prothrombotic, impaired fibrinolytic process associated with alterations in the microvasculature • Coagulopathy is prevalent in severe sepsis

  25. MANAGEMENT OF SEPSIS

  26. A 50 yr old smoker presents to emergency with fever and acute shortness of breath of two days duration. • He has a respiratory rate of 35/min B.P of 90/40, pulse 120/min regular, Spo2 88% on 10L nasal cannula. • He is alert and communicating. • He has brought a chest x-ray which shows right lower zone opacity.

  27. Clarifications • Recommendations grouped by category and not by hierarchy • Grading of recommendation implies literature support and not priority of importance

  28. SponsoringOrganizations • Infectious Disease Society of America • International Sepsis Forum • Indian Society of Critical Care Medicine • Society of Critical Care Medicine • Surgical Infection Society • Canadian Critical Care Society • Japanese Society of Critical Care Medicine • Japanese Association of Acute Medicine • German Sepsis Society • Latin American Sepsis Institute • American Association of Critical-care Nurses • American College of Chest Physicians • American College of Emergency Physicians • American Thoracic Society • Australian and New Zealand Intensive Care Society • European Society of Clinical Microbiology and Infectious Diseases • European Society of Intensive Care Medicine • European Respiratory Society

  29. Surviving Sepsis Campaign: 2008 Update • International effort to increase awareness and improve outcomes in severe sepsis • Endorsed by various organizations including SCCM, ACCP, ACEP, SHM, AACCN, and ESICM Crit Care Med 2008;36:296-327

  30. Modified GRADE System • Grading of Evidence • 1A: Strong recommendation, high quality evidence • 1B: Strong recommendation, moderate quality of evidence • 1C: Strong recommendation, low quality or very low quality evidence • 2A: Weak recommendation, high quality evidence • 2B: Weak recommendation, moderate quality evidence • 2C: Weak recommendation, low quality or very low quality of evidence Guyatt G, et al. Chest 2006;129:174-81

  31. Initial Resuscitation

  32. Severe Sepsis: Initial Resuscitation (1st 6 hours) • Should begin as soon as the syndrome is recognized and should not be delayed pending ICU admission. • Elevated serum lactate concentration identifies tissue hypo perfusion in patients at risk who are not hypotensive.

  33. Resuscitation Goals Goals in the first 6 hours: • CVP: 8-12 mm Hg • MAP > 65 mm Hg • Urine output > 0.5 ml/kg / hr. • Central venous (SVC) or mixed venous oxygen (SvO2) saturation > 70% GRADE 1C

  34. Figure B, page 948, reproduced with permission from Dellinger RP. Cardiovascular management of septic shock. Crit Care Med 2003;31:946-955.

  35. EGDT: Treatment Algorithm • EGDT subjects got more fluid, blood, and vasoactive meds • Less often ventilated or given PAC • Hospital mortality 30.5% vs. 46.5% (p=0.009) Rivers et al, NEJM 2001;345:1368

  36. NNT to prevent 1 event (death) = 6-8 Standard therapy 60 EGDT 50 40 Mortality (%) 30 20 10 0 In-hospital mortality (all patients) 28-day mortality 60-day mortality The Importance of Early Goal-DirectedTherapy for Sepsis Induced Hypo perfusion Adapted from Table 3, page 1374, with permission from Rivers E, Nguyen B, Havstad S, et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med 2001; 345:1368-1377

  37. What was done? • Supplemental oxygen started • IV line established, 1 liter NS given • Investigations sent • Blood cultures: two sets • Sputum for gram stain and culture • Complete blood count • Blood sugar ,urea creatinine, LFT • ABG with lactate and electrolytes • PT.PTT • Xray chest

  38. After initial resuscitation • Patient had pulse rate -110/mt • BP 90/60mmHg • Central line was put in on the right side • CVP was 8 cm H20

  39. Patient was given 500ml of normal saline over 30 mt • CVP was 12 • BP was 80/40 mmHg • Norepinephrine was started 8mcg/mt to maintain mean BP of 70mmHg • His PCV was 35 • Scvo2 was found to be 65% • Dobutamine was started at 6mcg/kg/mt • Urine output was .75ml/kg /hr

  40. Case After 2 hrs • Patient BP again dropped to 70/40mmHg • CVP – 10 cm H2O • So decided to give fluid challenge of 500 ml normal saline over 30 mts

  41. Fluid Therapy • Fluid resuscitation with either natural or artificial colloids or crystalloids. Grade 1B • Fluid challenge in patients with suspected hypovolemia may start with > 1000 ml of crystalloids or 300-500 ml of colloids over 30 mins. Grade 1D • Rate of fluid administration should be reduced substantially when cardiac filling pressures (CVP or PAOP) increase without concurrent hemodynamic improvement Grade 1D SSC Guidelines, Crit Care Med 2008

  42. Albumin and Saline for FluidResuscitation in the ICU (SAFE Trial) • RCT ~ 7,000 pts. in 16 Australian/NZ ICUs • Excluded pts. after cardiac surgery, liver transplant and burns • 4% albumin or NS • No significant difference: • 28-day mortality • New organ failure, duration of CRRT, or • mechanical ventilation • ICU and Hospital LOS Grade 1D NEJM 2004;350:2247-2256

  43. Fluid Challenge4 Aspects • Which fluid • What rate • Clinical End point • Stop fluid if reached • Pressure end-point • Stop fluid if reached • Safety limits

  44. FLUID CHALLENGE When To Stop When To Start

  45. FLUID CHALLENGE HOW TO GIVE IT 500 ml normal saline over 30 minutes Baseline 30mts AIM Pulse per min. 130 110 Mean BP mm Hg 50 70 CVP Cm HO2 10 16 SPO2 97% Chest Exam Clear

  46. FLUID CHALLENGE 500 ml normal saline over 30 minutes Baseline 30mts AIM Pulse per min. 130 128 110 Mean BP mm Hg 50 55 70 CVP Cm HO2 10 11 16 SPO2 97% 97% Chest Exam Clear Clear

  47. FLUID CHALLENGE 500 ml normal saline over 30 minutes Baseline 30mts AIM Pulse per min. 130 128 110 Mean BP mm Hg 50 55 70 CVP Cm HO2 10 11 16 SPO2 97% 97% Chest Exam Clear Clear Another fluid challenge

  48. FLUID CHALLENGE 500ml normal saline over 30 mint. Baseline AIM Pulse per min. 130 110 Mean BP mm Hg 50 70 CVP Cm H2O 10 16 Safety limits ↓SpO2 crepts at base

  49. FLUID CHALLENGE 500 ml normal saline over 30 minutes Baseline 10mts 30mts AIM Pulse per min. 130 110 125 Mean BP mm Hg 50 70 65 CVP Cm H2O 10 16 11 SPO2 97% 97%Continue Chest Clear Clear Clear

  50. FLUID CHALLENGE 500 ml normal saline over 30 minutes Baseline 10mts 30mts AIM Pulse per min. 130 110 125 Mean BP mm Hg 50 70 65 CVP Cm H2O 10 16 11 SPO2 97% 97%Continue Chest Clear Clear Clear continue

More Related