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Systemic Inflammatory  Response Syndrome  (SIRS) PRANEE SITAPOSA, MD.
SEPSIS and It’s Disease spectrum ,[object Object],[object Object],[object Object],[object Object],[object Object]
Definition ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],American College of Chest Physicians/Society of Critical Care Medicine Consensus  Conference Committee. Crit Care Med. 1992;20:864-874.
SIRS  (Systemic Inflammatory Response Syndrome) ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],American College of Chest Physicians/Society of Critical Care Medicine Consensus  Conference Committee. Crit Care Med. 1992;20:864-874.
Severe Sepsis ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],American College of Chest Physicians/Society of Critical Care Medicine Consensus  Conference Committee. Crit Care Med. 1992;20:864-874.
MODS (Multiple Organ Dysfunction Syndrome) ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],American College of Chest Physicians/Society of Critical Care Medicine Consensus  Conference Committee. Crit Care Med. 1992;20:864-874.
Relationship between SIRS and Sepsis Bone RC et al, Chest1992;101:164-55.
The Sepsis Continuum ,[object Object],[object Object],[object Object],[object Object],[object Object],SIRS = systemic inflammatory  response syndrome SIRS with a presumed or confirmed  infectious process Chest 1992;101:1644. Sepsis with  organ failure Refractory hypotension Sepsis SIRS Severe  Sepsis Septic Shock
Mortality rate in SIRS   Rangel - Frausto, et al. JAMA 273:117-123, 1995.
The Response to Pathogens  “Cross-Talk” NEJM 2003;348:138-150.
Inflammatory Response to Sepsis NEJM 2006;355:1699-1713.
Procoagulant Response in Sepsis NEJM 2006;355:1699-1713.
Pathogenesis of sepsis and septic shock Angus DC, et al .  Crit Care Med 2001, 29:1303-1310.
Pathogenesis of Severe Sepsis Infection Microbial Products (exotoxin/endotoxin) Cellular Responses Oxidases Platelet Activation Kinins Complement Coagulopathy/DIC Vascular/Organ System Injury Multi-Organ Failure Death Endothelial   damage Endothelial damage Coagulation Activation Cytokines TNF, IL-1, IL-6
Normal Systemic Response to Infection and Injury   (1) ,[object Object],[object Object],[object Object],Mandell et al. Principals and Practice of Infectious Diseases6th ed;906:906-926.
Normal Systemic Response to Infection and Injury   (2) ,[object Object],[object Object],[object Object],[object Object],Mandell et al. Principals and Practice of Infectious Diseases6th ed;906:906-926.
Normal Systemic Response to Infection and Injury   (3) ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Mandell et al. Principals and Practice of Infectious Diseases6th ed;906:906-926.
Normal Systemic Response to Infection and Injury   (4) ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Mandell et al. Principals and Practice of Infectious Diseases6th ed;906:906-926.
Risk factors of sepsis   ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Angus DC, et al .  Crit Care Med 2001, 29:1303-1310.
Patients at increased risks of developing sepsis ,[object Object],[object Object],[object Object],[object Object],[object Object],Angus DC, et al .  Crit Care Med 2001, 29:1303-1310.
Source   ( usually an endogenous source of infection ) ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Angus DC, et al .  Crit Care Med 2001, 29:1303-1310.
Diagnosis ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Angus DC, et al .  Crit Care Med 2001, 29:1303-1310.
Specific Infectious agents ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],MacArthur RD, et al. Mosby, 2001:3-10. Wheeler AP, et al. NEJM 1999;340:207-214. Chaowagul W, et al. J Infect Dis 1989;159:890-899.
Specific Infectious agents ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],MacArthur RD, et al. Mosby, 2001:3-10. Wheeler AP, et al. NEJM 1999;340:207-214. Chaowagul W, et al. J Infect Dis 1989;159:890-899.
Diagnosis ,[object Object],[object Object],[object Object],[object Object],[object Object],Angus DC, et al .  Crit Care Med 2001, 29:1303-1310.
Signs and Symptoms ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Angus DC, et al .  Crit Care Med 2001, 29:1303-1310.
Complications   ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Angus DC, et al .  Crit Care Med 2001, 29:1303-1310.
Surviving Sepsis Campaign Guidelines for Management of  Severe Sepsis and Septic Shock Dellinger RP, et al. Crit Care Med 2004; 32:858-873.
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Weinstein MP. Rev Infect  Dis  1983;5:35-53 Blot F.  J  Clin   Microbiol  1999; 36: 105-109. Diagnosis Dellinger, et. al.  Crit Care Med 2004, 32: 858-873.
Sepsis resuscitation bundle ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Hurtado FJ. et al. Crit Care Clin;2006;   22:521-9.
Sepsis management bundle ,[object Object],[object Object],[object Object],[object Object],[object Object],Surviving Sepsis Campaign Management Guidelines Committee. Crit Care Med 2004;   32:858-873.
Sepsis management bundle ,[object Object],[object Object],[object Object],[object Object],[object Object],Surviving Sepsis Campaign Management Guidelines Committee. Crit Care Med 2004; 32:858-873.
Infection Control ,[object Object],[object Object],[object Object],Surviving Sepsis Campaign Management Guidelines Committee. Crit Care Med 2004; 32:858-873.
Early Goal-Directed Therapy CVP  : central  venous  pressure MAP  : mean  arterial  pressure ScvO 2 : central  venous  oxygen  saturation NEJM  2001;345:1368-77 .
Early Goal-Directed Therapy Results 49.2% 33.3% 0 10 20 30 40 50 60 Standard Therapy n=133 EGDT n=130 P = 0.01* *Key difference was in sudden CV collapse, not MODS 28-day Mortality NEJM 2001;345:1368-77.
Antibiotic use in Sepsis (1) ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Angus DC, et al .  Crit Care Med 2001, 29:1303-1310.
Antibiotic use in Sepsis (2) ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Angus DC, et al .  Crit Care Med 2001, 29:1303-1310.
Antibiotic use in Sepsis (3) ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Angus DC, et al .  Crit Care Med 2001, 29:1303-1310.
New Drug in Treating Severe Sepsis   ,[object Object],[object Object],[object Object],[object Object],Angus DC, et al .  Crit Care Med 2001, 29:1303-1310.
NEJM;355:1699-1723.
Sepsis Cascade
Activated Protein C  ( Xigris ) NEJM;355:1640, October 19, 2006.
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  1. Do not need to draw a blood culture through vascular access devices that were recently inserted (<48 hrs) Appropriate cultures should always be obtained before antimicrobial therapy is initiated Recovering the same organism from both cultures enhances the likelihood that the organism is causing the severe sepsis. If the culture for the peripheral access device (PAD) is positive much earlier than the peripheral blood culture (i.e., >2hrs) then the PAD might be the source of infection. Volume of blood may also be important
  2. BACK-UP SLIDE: This slide shows specifically how the monitored parameters in EGDT were maintained. “ The protocol was as follows: A 500-ml bolus of crystalloid was given every 30 minutes to achieve a central venous pressure of 8 to 12 mm Hg. If the mean arterial pressure was less than 65 mm Hg, vasopressors were given to maintain a mean arterial pressure of at least 65 mm Hg. If the mean arterial pressure was greater than 90 mm Hg, vasodilators were given until it was 90 mm Hg or below. If the central venous oxygen saturation was less than 70 percent, red cells were transfused to achieve a hematocrit of at least 30 percent. After the central venous pressure, mean arterial pressure, and hematocrit were thus optimized, if the central venous oxygen saturation was less than 70 percent, dobutamine administration was started at a dose of 2.5 µg per kilogram of body weight per minute, a dose that was increased by 2.5 µg per kilogram per minute every 30 minutes until the central venous oxygen saturation was 70 percent or higher or until a maximal dose of 20 µg per kilogram per minute was given. Dobutamine was decreased in dose or discontinued if the mean arterial pressure was less than 65 mm Hg or if the heart rate was above 120 beats per minute. To decrease oxygen consumption, patients in whom hemodynamic optimization could not be achieved received mechanical ventilation and sedatives. ” (p. 1370)
  3. Cause of in-hospital death: --Sudden Cardiovascular collapse Standard Tx= 25/119 (21%) EGDT 12/117 (10.3%) --MODS Standard Tx 26/119(21.8%) EGDT 19/117 (16.2%) P. 1374 in New England Journal of Medicine