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Systemic Inflammatory Response Syndrome (SIRS)

Systemic Inflammatory Response Syndrome (SIRS). PRANEE SITAPOSA, MD. www.anaesthesia.co.in anaesthesia.co.in@gmail.com. SEPSIS and It’s Disease spectrum. Various stages of disease Bacteremia SIRS Sepsis syndrome Sepsis shock : early and refractory. Definition.

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Systemic Inflammatory Response Syndrome (SIRS)

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  1. Systemic Inflammatory Response Syndrome (SIRS) PRANEE SITAPOSA, MD. www.anaesthesia.co.inanaesthesia.co.in@gmail.com

  2. SEPSIS and It’s Disease spectrum • Various stages of disease • Bacteremia • SIRS • Sepsis syndrome • Sepsis shock : early and refractory

  3. Definition • Infection • Presence of microorganisms in a normally sterile site. • Bacteremia • Cultivatable bacteria in the blood stream. • Sepsis • The systemic response to infection. If associated with proven or clinically suspected infection, SIRS is called “sepsis”. American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference Committee. Crit Care Med. 1992;20:864-874.

  4. SIRS (Systemic Inflammatory Response Syndrome) • The systemic response to a wide range of stresses. • Temperature >38°C (100.4°) or <36°C (96.8°F). • Heart rate >90 beats/min. • Respiratory rate >20 breaths/min or PaCO2 <32 mmHg. • White blood cells > 12,000cells/ml or < 4,000 cells/ml or >10% immature (band) forms. • Note • Two or more of the following must be present. • These changes should be represent acute alterations from baseline in the absence of other known cause for the abnormalities. American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference Committee. Crit Care Med. 1992;20:864-874.

  5. Severe Sepsis • Sepsis with organ hypoperfusion one of the followings : • SBP < 90 mmHg • Acute mental status change • PaO2 < 60 mmHg on RA (PaO2 /FiO2 < 250) • Increased lactic acid/acidosis • Oliguria • DIC or Platelet < 80,000 /mm3 • Liver enzymes > 2 x normal American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference Committee. Crit Care Med. 1992;20:864-874.

  6. MODS(Multiple Organ Dysfunction Syndrome) • Sepsis with multiorgan hypoperfusion Two or more of the followings: • SBP < 90 mmHg • Acute mental status change • PaO2 < 60 mmHg on RA (PaO2 /FiO2 < 250) • Increased lactic acid/acidosis • Oliguria • DIC or Platelet < 80,000 /mm3 • Liver enzymes > 2 x normal American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference Committee. Crit Care Med. 1992;20:864-874.

  7. Relationship between SIRS and Sepsis Bone RC et al, Chest1992;101:164-55.

  8. Severe Sepsis Septic Shock SIRS Sepsis The Sepsis Continuum • A clinical response arising from a nonspecific insult, with 2 of the following: • T >38oC or <36oC • HR >90 beats/min • RR >20/min • WBC >12,000/mm3or <4,000/mm3 or >10% bands SIRS with a presumed or confirmed infectious process Sepsis with organ failure Refractory hypotension SIRS = systemic inflammatory response syndrome Chest 1992;101:1644.

  9. Mortality rate in SIRS Rangel-Frausto, et al. JAMA 273:117-123, 1995.

  10. The Response to Pathogens “Cross-Talk” NEJM 2003;348:138-150.

  11. Inflammatory Response to Sepsis NEJM 2006;355:1699-1713.

  12. Procoagulant Response in Sepsis NEJM 2006;355:1699-1713.

  13. Pathogenesis of sepsis and septic shock Angus DC, et al. Crit Care Med 2001, 29:1303-1310.

  14. Pathogenesis of Severe Sepsis Infection Microbial Products (exotoxin/endotoxin) Cellular Responses Platelet Activation Cytokines TNF, IL-1, IL-6 CoagulationActivation Kinins Complement Oxidases Coagulopathy/DIC Vascular/Organ System Injury Endothelial damage Endothelialdamage Multi-Organ Failure Death

  15. Normal Systemic Response to Infection and Injury (1) • Leukocytosis Mobilizes neutrophils into the circulation • Tachycardia Increases cardiac output, blood flow to injuried tissue • Fever Raises core temperature; peripheral vasoconstriction shunts blood flow to injuried tissue. Occurs much more often when infection is the trigger for systemic responses Mandell et al. Principals and Practice of Infectious Diseases6th ed;906:906-926.

  16. Normal Systemic Response to Infection and Injury (2) • Acute-Phase Responses • Anti-infective • Increases synthesis of complement factors, microbe pattern-recognition molecules(mannose-binding lectin, LBP, CRP, CD14, Others) • Sequesters iron (lactoferrin) and zinc (metallothionein) Mandell et al. Principals and Practice of Infectious Diseases6th ed;906:906-926.

  17. Normal Systemic Response to Infection and Injury (3) • Anti-inflammatory • Releases anti-inflammatory neuroendocrine hormones (cortisol, ACTH, epinephrine, α-MSH) • Increases synthesis of proteins that help prevent inflammation within the systemic compartment • Cytokine antagonists (IL-1Ra, sTNF-Rs) • Anti-inflammatory mediators (e.g.,IL-4, IL-6, IL-6R, IL-10, IL-13, TGF-β) • Protease inhibitors (e.g.,α1-antiprotease) • Antioxidants (haptoglobin) • Reprograms circulating leukocytes (epinephrine, cortisol, PGE2, ?other) Mandell et al. Principals and Practice of Infectious Diseases6th ed;906:906-926.

  18. Normal Systemic Response to Infection and Injury (4) • Procoagulant • Walls off infection, prevents systemic spread • Increases synthesis or release of fibrinogen, PAI-1, C4b • Decreases synthesis of protein C, anti-thrombin III • Metabolic • Preserves euglycemia, mobilizes fatty acids, amino acids • Epinephrine, cortisol, glucagon, cytokines • Thermoregulatory • Inhibits microbial growth • Fever Mandell et al. Principals and Practice of Infectious Diseases6th ed;906:906-926.

  19. Risk factors of sepsis • aggressive oncological chemotherapy and radiation therapy • use of corticosteroid and immunosuppressive therapies for organ transplants and inflammatory diseases • longer lives of patients predisposed to sepsis, the elderly, diabetics, cancer patients, patients with major organ failure, and with granulocyopenia. • Neonates are more likely to develop sepsis (ex. group B Streptococcal infections). • increased use of invasive devices such as surgical protheses, inhalation equipment, and intravenous and urinary catheters. • indiscriminate use of antimicrobial drugs that create conditions of overgrowth, colonization, and subsequent infection by aggressive, antimicrobial-resistant organisms. Angus DC, et al. Crit Care Med 2001, 29:1303-1310.

  20. Patients at increased risks of developing sepsis • Underlying diseases: neutropenia, solid tumors, leukemia, dysproteinemias, cirrhosis of the liver, diabetes, AIDS, serious chronic conditions. • Surgery or instrumentation: catheters. • Prior drug therapy: Immuno-suppressive drugs, especially with broad-spectrum antibiotics. • Age: males, above 40 y; females, 20-45 y. • Miscellaneous conditions: childbirth, septic abortion, trauma and widespread burns, intestinal ulceration. Angus DC, et al. Crit Care Med 2001, 29:1303-1310.

  21. Source (usually an endogenous source of infection) • intestinal tract • oropharynx • instrumentation sites • contaminated inhalation therapy equipment • IV fluids. • Most frequent sites of infection: Lungs, abdomen, and urinary tract. • Other sources include the skin/soft tissue and the CNS. Angus DC, et al. Crit Care Med 2001, 29:1303-1310.

  22. Diagnosis • History • community or nosocomially acquired infection • immunocompromised patient • exposure to animals, travel, tick bites, occupational hazards, alcohol use, seizures, loss of consciousness, medications • underlying diseases ; specific infectious agents • Some clues to a septic event include • Fever or unexplained signs with malignancy or instrumentation • Hypotension • Oliguria or anuria • Tachypnea or hyperpnea • Hypothermia without obvious cause • Bleeding Angus DC, et al. Crit Care Med 2001, 29:1303-1310.

  23. Specific Infectious agents • Splenectomy (traumatic or functional) • S pneumoniae, H influenzae, N meningitidis • Neutropenia (<500 neutrophil/ml) • Gram-negative, including P aeruginosa, gram-positives, including S aureus • Fungi, especially Candida species • Hypogammaglobulinemia (e.g.,CLL) • S pneumoniae, E coli • Burns • MRSA, P aeruginosa, resistant gram-negatives 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.

  24. Specific Infectious agents • Aids • P aeuginosa (if neutropenic), S aureus, PCP pneumonia • Intravascular devices • S aureus, S epidermidis • Nosocomial infections • MRSA, Enterococcus species, resistant gram-negative, Candida species • Septic patients in NE of Thailand • Burkholderia pseudomallei 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.

  25. Diagnosis • Physical Examination • essential • In all neutropenic patients and in patients with as suspected pelvic infection the physical exam should include rectal, pelvic, and genital examinations • perirectal, and/or perineal abscesses • pelvic inflammatory disease and/or abscesses, or prostatitis Angus DC, et al. Crit Care Med 2001, 29:1303-1310.

  26. Signs and Symptoms • Nonspecific symptoms of sepsis : not pathognomonic • fever • chills • constitutional symptoms of fatigue, malaise • anxiety or confusion • absent symptoms in serious infections, especially in elderly individuals Angus DC, et al. Crit Care Med 2001, 29:1303-1310.

  27. Complications • Adult respiratory distress syndrome (ARDS) • Disseminated Intravascular Coagulation (DIC) • Acute Renal failure (ARF) • Intestinal bleeding • Liver failure • Central Nervous System dysfunction • Heart failure • Death Angus DC, et al. Crit Care Med 2001, 29:1303-1310.

  28. Surviving Sepsis Campaign Guidelines for Management of Severe Sepsis and Septic Shock Dellinger RP, et al. Crit Care Med 2004; 32:858-873.

  29. Diagnosis • Before the initiation of antimicrobial therapy, at least two blood cultures should be obtained • At least one drawn percutaneously • At least one drawn through each vascular access device if inserted longer than 48 hours • Other cultures such as urine, cerebrospinal fluid, wounds, respiratory secretions or other body fluids should be obtained as the clinical situation dictates • Other diagnostic studies such as imaging and sampling should be performed promptly to determine the source and causative organism of the infection • may be limited by patient stability Weinstein MP. Rev Infect Dis 1983;5:35-53Blot F. J Clin Microbiol 1999; 36: 105-109. Dellinger, et. al. Crit Care Med 2004, 32: 858-873.

  30. Sepsis resuscitation bundle • Serum lactate measured • Blood cultures obtained before antibiotics administered • Improve time to broad-spectrum antibiotics • In the event of hypotension or lactate > 4 mmol/L (36 mg/dL) • a. Deliver an initial minimum of 20 mL/kg of crystaloid (or colloid equivalent) • b. apply vasopressors for ongoing hypotension • In the event of persistent hypotension despite fluid resuscitation or lactate > 4 mmol/L (36 mg/dL) • a. achieve central venous pressure of > 8 mmHg • b. achieve central venous oxygen saturation of > 70% Hurtado FJ. et al. Crit Care Clin;2006; 22:521-9.

  31. Sepsis management bundle • Fluid resuscitation • Appropriate cultures prior to antibiotic administration • Early targeted antibiotics and source control • Use of vasopressors/inotropes when fluid resuscitation optimized Surviving Sepsis Campaign Management Guidelines Committee. Crit Care Med 2004;32:858-873.

  32. Sepsis management bundle • Evaluation for adrenal insufficiency • Stress dose corticosteroid administration • Recombinant human activated protein C (xigris) for severe sepsis • Low tidal volume mechanical ventilation for ARDS • Tight glucose control Surviving Sepsis Campaign Management Guidelines Committee. Crit Care Med 2004; 32:858-873.

  33. Infection Control • Appropriate cultures prior to antibiotic administration • Early targeted antibiotics and source control Surviving Sepsis Campaign Management Guidelines Committee. Crit Care Med 2004; 32:858-873.

  34. Early Goal-Directed Therapy CVP : central venous pressure MAP : mean arterial pressure ScvO2: central venous oxygen saturation NEJM 2001;345:1368-77.

  35. Early Goal-Directed Therapy Results 28-day Mortality 60 49.2% P = 0.01* 50 40 33.3% 30 20 10 0 Standard Therapy n=133 EGDT n=130 *Key difference was in sudden CV collapse, not MODS NEJM 2001;345:1368-77.

  36. Antibiotic use in Sepsis (1) • The drugs used depends on the source of the sepsis • Community acquired pneumonia • third (ceftriaxone) or fourth (cefepime) generation cephalosporin is given with an aminoglycoside (usually gentamicin) • Nosocomial pneumonia • Cefipime or Imipenem-cilastatin and an aminoglycoside • Abdominal infection • Imipenem-cilastatin or Pipercillin-tazobactam and aminoglycoside Angus DC, et al. Crit Care Med 2001, 29:1303-1310.

  37. Antibiotic use in Sepsis (2) • Nosocomial abdominal infection • Imipenem-cilastatin and aminoglycoside or Pipercillin-tazobactam and Amphotericin B • Skin/soft tissue • Vancomycin and Imipenem-cilastatin or Piperacillin-tazobactam • Nosocomial skin/soft tissue • Vancomycin and Cefipime • Urinary tract infection • Ciprofloxacin and aminoglycoside Angus DC, et al. Crit Care Med 2001, 29:1303-1310.

  38. Antibiotic use in Sepsis (3) • Nosocomial urinary tract infection: • Vancomycin and Cefipime • CNS infection: • Vancomycin and third generation cephalosporin or Meropenem • Nosocomial CNS infection: • Meropenem and Vancomycin • Drugs will change depending on the most likely cause of the patient's sepsis • Single drug regimens are usually only indicated when the organism causing sepsis has been identified and antibiotic sensitivity testing Angus DC, et al. Crit Care Med 2001, 29:1303-1310.

  39. New Drug in Treating Severe Sepsis • It is the first agent approved by the FDA effective in the treatment of severe sepsis proven to reduce mortality. Activated Protein C (Xigris) mediates many actions of body homeostasis. It is a potent agent for the: • suppression of inflammation • prevention of microvascular coagulation • reversal of impaired fibrinolysis Angus DC, et al. Crit Care Med 2001, 29:1303-1310.

  40. NEJM;355:1699-1723.

  41. Sepsis Cascade

  42. Activated Protein C (Xigris) NEJM;355:1640, October 19, 2006.

  43. Thank you www.anaesthesia.co.inanaesthesia.co.in@gmail.com

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