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![Epidemiology
Martin, G. S., Mannino, D. M., Eaton, S., & Moss, M. (2003). The
epidemiology of sepsis in the United States from 1979 through 2000.
New England Journal of Medicine, 348(16), 1546–1554.
Harrison, D. A., Welch, C. A., & Eddleston, J. M. (2006). The
epidemiology of severe sepsis in England, Wales and
Northern Ireland, 1996 to 2004: secondary analysis of a high
quality clinical database, the ICNARC Case Mix Programme
Database. Critical Care, 10(2), R42.
Brun-Buisson, C., Meshaka, P., Pinton, P., Vallet, B., EPISEPSIS
Study Group. (2004). EPISEPSIS: a reappraisal of the epidemiology
and outcome of severe sepsis in French intensive care units.
Intensive Care Medicine, 30(4), 580–588.
[1993 - 2001]...a 17%
reduction in mortality.
[1993-2001]...a
75% increase in... severe
sepsis...
Incidence
of Sepsis
Mortality
of Sepsis](https://image.slidesharecdn.com/survivingsepsis-180209184746/85/Surviving-sepsis-5-320.jpg)
![System-based Approaches to sepsis
Early-Goal Directed Therapy
INCLUSION = SEPSIS AND [BP < 90 after fluid OR Lactate > 4]
CVP 8-12 Fluids CVP 8-12
MAP > 65 Vasopressors MAP > 65
Transfusions
Dobutamine
ScvO2 > 70%
49%
mortality
33%
mortality
Rivers, E., Nguyen, B., Havstad, S., Ressler, J., Muzzin, A., Knoblich, B., Peterson, E., et al. (2001). Early goal-directed therapy in the treatment of severe sepsis and septic shock. New England Journal of Medicine, 345(19), 1368–1377.
Control Intervention EGDT](https://image.slidesharecdn.com/survivingsepsis-180209184746/85/Surviving-sepsis-33-320.jpg)
Uploaded byYouttam Laudari
Surviving sepsis
Three sentences: Sepsis is a life-threatening organ dysfunction caused by a dysregulated host response to infection. Mortality from sepsis is high, ranging from 30-60% depending on the presence of septic shock. New guidelines in 2016 defined sepsis as a life-threatening organ dysfunction represented by a SOFA score increase of 2 or more points from the patient's baseline.
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Surviving sepsis
- 1. Sepsis- overview and management2016 YUGAL LIMBU
- 2. Mortality Sepsis: 30% - 50% SepticShock: 50% - 60% Why are we spending time on sepsis?
- 3. Why are wespending time on sepsis? 0 50000 100000 150000 200000 250000 AIDS Breast Cancer AMI SEPSIS Mortality 0 50 100 150 200 250 300 AIDS Breast Cancer 1st MI sepsis Incidence Cases/100,000 Deaths/Year
- 4. The third InternationalConsensus 2016 Definition for Sepsis ( Sepsis 3) SEPSIS IS A LIFE THREATENING ORGAN DYSFUNCTION CAUSED BY A DYSREGULATED HOST RESPONSE TO INFECTION
- 5. Epidemiology Martin, G. S.,Mannino, D. M., Eaton, S., & Moss, M. (2003). The epidemiology of sepsis in the United States from 1979 through 2000. New England Journal of Medicine, 348(16), 1546–1554. Harrison, D. A., Welch, C. A., & Eddleston, J. M. (2006). The epidemiology of severe sepsis in England, Wales and Northern Ireland, 1996 to 2004: secondary analysis of a high quality clinical database, the ICNARC Case Mix Programme Database. Critical Care, 10(2), R42. Brun-Buisson, C., Meshaka, P., Pinton, P., Vallet, B., EPISEPSIS Study Group. (2004). EPISEPSIS: a reappraisal of the epidemiology and outcome of severe sepsis in French intensive care units. Intensive Care Medicine, 30(4), 580–588. [1993 - 2001]...a 17% reduction in mortality. [1993-2001]...a 75% increase in... severe sepsis... Incidence of Sepsis Mortality of Sepsis
- 6. Why the burdenof sepsis increasing? Increased geriatric population Increasing number of immunocompromised host Increasing drug resistant organism Increasing metabolic disorder
- 7. either Bacteraemia (orviraemia/fungaemia/protozoan) is the presence of bacteria within the bloodstream Septic focus (abscess / cavity / tissue mass) Infection
- 8. Sepsis is notmerely an infection THE CULPRIT HERE IS OVER REACTION OF OUR DEFENCE MECHANISM – NOT THE INVADER ALONE.
- 10. Dysregulated host responseleads to..
- 11. Immune system Vs.mortality
- 12. How to suspectsepsis?
- 13.
- 14. Altered mental status Edemaor increased fluid balance Hyperglycemia (absent diabetes) Hypoglyemia Increased CRP or procalcitonin Hypotension Increased SvO2 CI > 3.5 L/min/m2 Arterial hypoxemia (PaO2/FiO2 < 300) Acute oliguria (> 2 hours) Increased serum Cr (> 0.5 mg/dL) Coagulopathy (INR > 1.5) Ileus (absent bowel sounds) Thrombocytopenia (< 100,000/uL) Hyperbilirubinemia (> 40 mg/dL or 70 mmol/L) Hyperlactatemia (> 1 mmol/L) Decreased capillary refill or mottling Levy MM, et al. Crit Care Med. 2003. How to recognize organ dysfunction?
- 15. Change in internationalguideline Sepsis 2 Sepsis = SIRS + Infection Infection sepsis severe sepsis septic shock MODS Sepsis 3 Sepsis= infection + >2 SOFA score from baseline NO Severe sepsis
- 16.
- 17. Sequential Organ FailureAssessment (SOFA) ► Previously known as Sepsis-related Organ Failure Assessment because it was initially developed in 1994 to describe the degree of organ dysfunction associated with sepsis in a mixed, medical-surgical ICU patients. ► Nowadays, it has since been validated to describe the degree of organ dysfunction in various ICU patient groups with organ dysfunctions not due to sepsis. ► The SOFA score involves six organ systems (respiratory, cardiovascular, renal, hepatic, central nervous, coagulation), and the function of each is scored from 0 (normal function) to 4 (most abnormal), giving a possible score of 0 to 24.
- 18.
- 19. Sequential Organ FailureAssessment (SOFA) ► Mortality rate increases as number of organs with dysfunction increases. ► Unlike other scores, the worst value on each day is recorded. ► A key difference is in the cardiovascular component; instead of the composite variable, the SOFA score uses a treatment-related variable (dose of vasopressor agents).
- 20. Organ failure insepsis Vincent, J.-L., Sakr, Y., Sprung, C. L., Ranieri, V. M., Reinhart, K., Gerlach, H., Moreno, R., et al. (2006). Sepsis in European intensive care units: results of the SOAP study. Critical Care Medicine, 34(2), 344–353. P/F Platelets Bili BP GCS Cr/UOP
- 21. Sequential Organ FailureAssessment (SOFA) ► Maximal (highest total) SOFA score: is the sum of highest scores per individual during the entire ICU stay. A score of >15 predicted mortality of 90%. ► Mean SOFA score (ΔSOFA): is the average of all total SOFA scores in the entire ICU stay. ΔSOFA for 1st 10 days is significantly higher in non-survivors. ► Delta SOFA score: maximum SOFA – admission SOFA Crit Care Med 1998;26:1793-1800
- 22. qSOFA for NonICU patients with Infection – early recognition of severity
- 23. SEPTIC SHOCK Septicshock is a subset of sepsis in which profound circulatory, cellular and metabolic abnormalities are associated with a greater risk of mortality than sepsis alone
- 24. CLINICAL CRITERIA FORSEPTIC SHOCK 2016 DESPITE ADEQUATE FLUID RESUSCITATION VASOPRESSOR NEEDED TO MAINTAIN MAP >_65mm Of Hg AND LACTATE >2 MMOL/LIT
- 25. Basal lactate production MuscleBrain RBC WBC Platelets Renal medulla Gut mucosa Skin 0.13 mmol/ kg/hr 0.14 mmol/ kg/hr 0.18 mmol/ kg/hr 0.11 mmol/kg/hr 0.11 mmol/ kg/hr Total = 1290 mmol / 24 hours for 70 kg
- 26.
- 27. How is lactateproduced? If pyruvate production > oxidation in CAC then lactate formation increases PDH
- 28. Hypoxia blocks oxidativephosphorylation prevents NADH re-oxidation to NAD increases the NADH/NAD ratio increases the lactate/pyruvate ratio Normal ratio around 10:1
- 29. Prognostic value Sourcedoesn’t matter High lactate still a marker of severe physiological stress and risk of death High lactate often not hypoxia related but represents metabolic changes of severe stress
- 31. Management of SEPSIS FLUIDS ANTIBIOTICS SOURCE IDENTIFICATION AND CONTROL VASOACTIVE DRUGS TO MAINTAIN MAP EARLY ORGAN SUPPORT LUNG PROTECTIVE VENTILATION Etc. BUT THE MOST IMPORTANT IS A SYSTEMATIC APPROACH
- 32. System-based Approaches tosepsis Rivers, E., Nguyen, B., Havstad, S., Ressler, J., Muzzin, A., Knoblich, B., Peterson, E., et al. (2001). Early goal-directed therapy in the treatment of severe sepsis and septic shock. New England Journal of Medicine, 345(19), 1368–1377.
- 33. System-based Approaches tosepsis Early-Goal Directed Therapy INCLUSION = SEPSIS AND [BP < 90 after fluid OR Lactate > 4] CVP 8-12 Fluids CVP 8-12 MAP > 65 Vasopressors MAP > 65 Transfusions Dobutamine ScvO2 > 70% 49% mortality 33% mortality Rivers, E., Nguyen, B., Havstad, S., Ressler, J., Muzzin, A., Knoblich, B., Peterson, E., et al. (2001). Early goal-directed therapy in the treatment of severe sepsis and septic shock. New England Journal of Medicine, 345(19), 1368–1377. Control Intervention EGDT
- 34. System-based Approaches tosepsis Rivers, E., Nguyen, B., Havstad, S., Ressler, J., Muzzin, A., Knoblich, B., Peterson, E., et al. (2001). Early goal-directed therapy in the treatment of severe sepsis and septic shock. New England Journal of Medicine, 345(19), 1368–1377. Used to promote: 1. CVP > 8 as an initial target 2. Use of Svo2 monitoring and use of blood/dobutamine
- 35. A Multidisciplinary CommunityHospital Program for Early and Rapid Resuscitation of Shock in Non-trauma Patients Sebat, F., Johnson, D., Musthafa, A. A., Watnik, M., Moore, S., Henry, K., & Saari, M. (2005). A multidisciplinary community hospital program for early and rapid resuscitation of shock in nontrauma patients. Chest, 127(5), 1729–1743.
- 36. Early Goal-Directed Therapyin the Treatment of Severe Sepsis and Septic Shock Control EGDT Relative Risk (95% Confidence Interval) P In-Hospital 46.5 30.5 0.58 (0.38-0.87) 0.009 28-day Mortality 49.2 33.3 0.58 (0.39 – 0.87) 0.01 60-day Mortality 56.9 44.3 0.67 (0.46-0.96) 0.03 Rivers E. N Engl J Med. 2001;345: 1368-1377.
- 37. Surviving Sepsis Campaign Suggestsbundled initiative for hospitals to reduce sepsis related mortality. 0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9 1 Resuscitation Bundle Management Bundle Compliant Non-Compliant
- 38. TO BE COMPLETEDWITHIN 3 HOURS OF TIME OF PRESENTATION*:1. Measure lactate level 2. Obtain blood cultures prior to administration of antibiotics 3. Administer broad spectrum antibiotics 4. Administer 30ml/kg crystalloid for hypotension or lactate ≥4mmol/L * “Time of presentation” is defined as the time of triage in the emergency department or, if presenting from another care venue, from the earliest chart annotation consistent with all elements of severe sepsis or septic shock ascertained through chart review.
- 39. TO BE COMPLETEDWITHIN 6 HOURS OF TIME OF PRESENTATION:5. Apply vasopressors (for hypotension that does not respond to initial fluid resuscitation) to maintain a mean arterial pressure (MAP) ≥65mmHg 6. In the event of persistent hypotension after initial fluid administration (MAP < 65 mm Hg) or if initial lactate was ≥4 mmol/L, re-assess volume status and tissue perfusion and document findings 7. Re-measure lactate if initial lactate elevated
- 40. DOCUMENT REASSESSMENT OF VOLUMESTATUS AND TISSUE PERFUSION WITH EITHER • Repeat focused exam (after initial fluid resuscitation) by licensed independent practitioner including vital signs, cardiopulmonary, capillary refill, pulse, and skin findings. OR TWO OF THE FOLLOWING: • Measure CVP • Measure ScvO2 • Bedside cardiovascular ultrasound • Dynamic assessment of fluid responsiveness Bedside sonologic assessment of Volume status is prioritized.
- 42. fluid in septicshock, How much ?
- 43. IVF recommendation Initialfluid challenge ≥ 1000 mL of crystalloids or minimum of 30 mL/kg of crystalloids in the 1st 4-6 hours (Strong recommendation; Grade 1C). Crystalloids is the initial fluid for resuscitation (Strong recommendation; Grade 1A). Adding albumin to the initial fluid resuscitation (Weak recommendation; Grade 2B). Against hydroxyethyl starches (hetastarches) with MW >200 dalton (Strong recommendation; Grade 1B).
- 44. Timing of AntibioticAdministration
- 45. Septic Shock: Timingof Antibiotics Kumar Crit Care Med 2006 0.0 .20 .40 .60 .80 1.00 % Survival % Total receiving antibiotics Percent Time, hrs 14 ICUs; n = 2,731 Only 50% of patients in Septic Shock received antibiotics w/in 6 hrs.
- 46. G. Fluid Therapyof Severe Sepsis H. Vasopressors I. Inotropic Therapy J. Corticosteroids 2. Hemodynamic Support and Adjunctive Therapy
- 47.
- 48. Which Inotropes touse? Norepinephrine as the first choice ( Grade 1B) Adding or substituting epinephrine when an additional drug is needed (Strong recommendation; Grade 1B). Vasopressin 0.03 units/min may be added (Weak recommendation; Grade 2A) Dopamine only in highly selected patients at very low risk of arrhythmias or low heart rate (Weak recommendation; Grade 2C). Dobutamine infusion be started or added with low cardiac output) or ongoing signs of hypoperfusion, even after adequate intravascular volume (Strong recommendation; Grade 1C)
- 49. Inotropic Therapy • Werecommend that a trial of dobutamine infusion up to 20 μg/kg/min be administered or added to vasopressor (if in use) in the presence of: • myocardial dysfunction as suggested by elevated cardiac filling pressures and low cardiac output, or • ongoing signs of hypoperfusion, despite achieving adequate intravascular volume and adequate mean arterial pressure. (Grade 1C) • We recommend against the use of a strategy to increase cardiac index to predetermined supranormal levels. (Grade 1B)
- 50. Diagnosis of Infection Appropriate cultures before antimicrobial therapy as soon as possible (<45 minutes) (Grade 1C). At least two sets of blood cultures (both aerobic and anaerobic bottles) before antimicrobial therapy, with at least one drawn percutaneously and one drawn through each vascular access device, unless the device was recently (<48 hours) inserted. Blood cultures can be drawn at the same time if from a different anatomic site (Grade 1C).
- 51. Diagnosis Cultures ofother sites (preferably quantitative where appropriate), such as urine, cerebrospinal fluid, wounds, respiratory secretions, or other body fluids that may be the source of infection, should also be obtained before antimicrobial therapy if doing so does not cause significant delay in antibiotic administration (Grade 1C). We suggest the use of the 1,3 β-D-glucan assay (Grade 2B), mannan and anti-mannan antibody assays (Grade 2C) when invasive candidiasis is in the differential diagnosis of infection.
- 52. Diagnosis Imaging studiesbe performed promptly in attempts to confirm a potential source of obscure infection. and aggressive monitoring if the decision is made to transport for a CT-guided needle aspiration) . Bedside studies, such as ultrasound, may avoid patient transport (Ungraded).
- 53. Antimicrobial Therapy Theadministration of effective intravenous antimicrobials as soon as possible , but never beyond the first hour of recognition of SEPSIS Initial empiric anti-infective therapy include one or more drugs that have activity against all likely pathogens (bacterial and/or fungal or viral) and that penetrate in adequate concentrations into the tissues presumed to be the source of sepsis (Grade 1B). The antimicrobial regimen should be reassessed daily for potential de-escalation to prevent the development of resistance, to reduce toxicity, and to reduce costs (Grade 1B).
- 54. Antibiotics • Abx within1 hr hypotension: 79.9% survival • Survival decreased 7.6% with each hour of delay • Mortality increased by 2nd hour post hypotension • Time to initiation of Antibiotics was the single strongest predictor of outcome
- 55. Antimicrobial Therapy … Duration of therapy typically be 7 to 10 days if clinically indicated; longer courses may be appropriate in patients who have a slow clinical response, Undrainable foci of infection, Bacteremia with Staphylococcus aureus, some fungal and viral Infections, or Immunologic deficiencies, including neutropenia
- 56. Source Control Whensource 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.
- 57. Corticosteroids Only whenBlood Pessure is not maintained with adquate fluid resuscitation and vasoacive Intravenous hydrocortisone alone at a dose of 200 mg per day. Continuous Infusion preferred over bolus doses. Taper steroid when vasopressors are no longer required
- 58. Blood product Administration Transfuse PRBC only when Hb%v<7.0 g/dL to target a hemoglobin concentration of 7.0 to 9.0 g/dL in adults (Grade 1B). Exceptions are myocardial ischemia, severe hypoxemia, acute hemorrhage, or ischemic coronary artery disease. NO Erythropoetin in sepsis No FFP to correct lab abnormality in absence of Bleeding or planned invasive procedure. Platelet transfusion – <10,000 in absence of bleeding <20000 if bleeding risk high <50,000 if planned procedure, active bleeding or surgery
- 59. Glucose Control • Werecommend protocolized approach to blood glucose management, commencing insulin dosing when two consecutive blood glucose levels are >180 mg/dL. • This protocolized approach should target upper blood glucose <180 mg/dL rather than <110 mg/dL (Grade 1A). • Treatment should avoid hyperglycemia (>180 mg/dL), hypoglycemia, and wide swings in glucose levels
- 60. Glucose control… Glucometermeasured capillary blood be interpreted with caution, as such measurements may not accurately estimate arterial blood or plasma glucose values Capillary point-of-care testing found to be inaccurate with frequent false glucose elevations over range of glucose levels, but especially in hypoglycemic and hyperglycemic glucose ranges and in hypotensive patients or patients receiving catecholamines.
- 61. Bicarbonate Therapy • Noto sodium bicarbonate therapy for the purpose of improving hemodynamics or reducing vasopressor requirements in patients with hypoperfusion-induced lactic acidemia with pH ≥7.15 (Grade 2B), in absence of Renal acidosis.
- 62. Nutrition • We suggestadministering oral or enteral feedings, as tolerated, rather than complete fasting or provision of only intravenous glucose within the first 48 hours after a diagnosis of severe sepsis/septic shock (Grade 2C). • We suggest avoiding mandatory full caloric feeding in the first week, but rather suggest low-dose feeding (e.g., up to 500 kcal per day), advancing only as tolerated Marik and Zaloga. Crit Care Med. 2001;29:2264–2270 Heyland et al. JPEN J Parenter Enteral Nutr. 2003;27:355-373 Doig et al. Intensive Care Med. 2009;35:2018–2027
- 63. • Enteral nurtritioncombined with IV Glucose supplementation is preferred than Total parenteral Nutrition • Use of Selenium, Arginine, Glutamine and Omega 3 fatty acid therapy during acute illness with sepsis NOT recommended Nutrition…
- 64. Mechanical Ventilation ofSepsis- Induced ARDS • Target a tidal volume of 6 mL/kg predicted body weight in patients with sepsis-induced ARDS (grade 1A vs. 12 mL/kg). • Positive end-expiratory pressure (PEEP) be applied to avoid alveolar collapse at end expiration (grade 1B). ° Strategies based on higher rather than lower levels of PEEP be used for patients with sepsis-induced moderate or severe ARDS (grade 2C).
- 65. ° Recruitmentmaneuvers be used in sepsis patients with severe refractory hypoxemia (grade 2C). ° Prone positioning be used in sepsis-induced ARDS patients with a Pao2/Fio2 ratio ≤ 100 mm Hg in facilities that have experience with such practices (grade 2B). • That mechanically ventilated sepsis patients be maintained with the head of the bed elevated to 30-45 degrees to limit aspiration risk and to prevent the development of ventilator-associated pneumonia (grade 1B).
- 66. discontinue mechanical ventilationwhen they satisfy the following criteria: a) arousable; b) b) hemodynamically stable (without vasopressor agents); c) c) no new potentially serious conditions; d) d) low ventilatory and end-expiratory pressure requirements; and e) e) low Fio2 requirements which can be met safely delivered with a face mask or nasal cannula. If the spontaneous breathing trial is successful, consideration should be given for extubation (grade 1A).
- 67. • Aconservative rather than liberal fluid strategy for patients with established sepsis-induced ARDS who do not have evidence of tissue hypoperfusion (grade 1C).
- 68. Renal Replacement Therapy •Continuous renal replacement therapies and intermittent hemodialysis are equivalent in patients with sepsis and acute renal failure because they achieve similar short-term survival rates (Grade 2B). • We suggest the use of continuous therapies to facilitate management of fluid balance in hemodynamically unstable septic patients (Grade 2D). Slide 69 Copyright 2014 SCCM/ESICM
- 69. Prophylaxis for VTE We recommend that patients with severe sepsis receive daily pharmacoprophylaxis against VTE (Grade 1B). We recommend that septic patients who have a contraindication to heparin not receive pharmacoprophylaxis (Grade 1B). Rather, we suggest they receive mechanical prophylactic treatment, such as graduated compression stockings or intermittent compression devices, unless contraindicated (Grade 2C). When the risk decreases, we suggest starting pharmacoprophylaxis (Grade 2C).
- 70. Stress Ulcer Prophylaxis •We recommend that stress ulcer prophylaxis using H2 blocker or proton pump inhibitor be given to patients with sepsis/septic shock who have bleeding risk factors (Grade 1B). • We suggest that patients without risk factors should not receive prophylaxis (Grade 2B).
- 71. Setting Goals ofCare We recommend that goals of care and prognosis be discussed with patients and families (Grade 1B). Goals of care be incorporated into treatment and end-of-life care planning, utilizing palliative care principles where appropriate Goals of care be addressed as early as feasible, but no later than within 72 hours of ICU admission
- 72.
- 73. Take home message… Identify sepsis early More and faster fluid Send cultures early Antibiotic Fast <1 hr, consider early antifungals, use biomarkers to deescalate or stop Earlier Inotropes, Use norepineprine Chase Lactic acid clearance Sonologic volume assessment is better than CVP Higher PEEP
- 74.