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Leanna R. Miller, RN, MN, CCRN-CMC, PCCN-CSC, CEN, CNRN, NP Education Specialist LRM Consulting

Critical Care Immunology. Leanna R. Miller, RN, MN, CCRN-CMC, PCCN-CSC, CEN, CNRN, NP Education Specialist LRM Consulting Nashville, TN. Critical Care Immunology. Learning Outcomes

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Leanna R. Miller, RN, MN, CCRN-CMC, PCCN-CSC, CEN, CNRN, NP Education Specialist LRM Consulting

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  1. Critical Care Immunology Leanna R. Miller, RN, MN, CCRN-CMC, PCCN-CSC, CEN, CNRN, NP Education Specialist LRM Consulting Nashville, TN lrmmiller@msn.com

  2. Critical Care Immunology • Learning Outcomes • Analyze the mediators (cytokines) responsible for cellular and clinical changes during the inflammatory response. • Correlate the clinical significance of immunoparalysis to trauma, sepsis and open heart surgery. • Evaluate strategies used to manage patients with immunoparalysis. lrmmiller@msn.com

  3. Critical Care Immunology • recovery from critical illness requires proper immunologic balance between pro- and anti-inflammatory forces • persistence of a marked compensatory anti-inflammatory innate immune response following an insult such as sepsis, surgery, or trauma is termed immunoparalysis lrmmiller@msn.com

  4. Critical Care Immunology • an acquired immunodeficiency can be quantified through the measurement of: • monocyte cell-surface HLA-DR expression • analysis of the capacity of whole blood to produce TNFα upon ex vivo stimulation with endotoxin lrmmiller@msn.com

  5. Critical Care Immunology • during critical illness, there is a systemic anti-inflammatory state intended to avoid the spread of the local proinflammatory response lrmmiller@msn.com

  6. Critical Care Immunology • resulting immunosuppression increases the risk of nosocomial infections • related to an increase in morbidity and mortality in critically ill patients lrmmiller@msn.com

  7. Critical Care Immunology • Host Defenses • exposed to injury & infection • defense mechanisms • inflammation • thrombosis • healing lrmmiller@msn.com

  8. Critical Care Immunology • Stages of Inflammation • destruction & removal • containment • stimulation & amplification of the immune response • promotion of healing lrmmiller@msn.com

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  11. Critical Care Immunology lrmmiller@msn.com

  12. Critical Care Immunology lrmmiller@msn.com

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  14. Critical Care Immunology • Nonspecific Immunity • natural killer cells (NK) • kill viruses, bacteria, neoplastic cells • regulate production of erythrocytes & granulocytes lrmmiller@msn.com

  15. Critical Care Immunology • Complement • activated by: • antigen/antibody complex • tissue injury • tissue ischemia • coagulation lrmmiller@msn.com

  16. Critical Care Immunology • Complement • activated by: • cell debris • kinins • endotoxin • bacterial cell debris lrmmiller@msn.com

  17. Critical Care Immunology • Complement • opsonization • mediator release • histamine • leukotrienes lrmmiller@msn.com

  18. Critical Care Immunology • Coagulation • activated by: • Intrinsic pathway • Extrinsic pathway lrmmiller@msn.com

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  20. Critical Care Immunology • Coagulation • excessive intravascular coagulation leads to: • vascular damage • tissue ischemia lrmmiller@msn.com

  21. Critical Care Immunology • Fibrinolysis • Hemorrhage leads to: • decreased O2 delivery • tissue ischemia lrmmiller@msn.com

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  23. Arachidonic Acid Metabolism lrmmiller@msn.com

  24. Critical Care Immunology lrmmiller@msn.com

  25. Critical Care Immunology • Tumor Necrosis Factor • fever • endothelial damage • anorexia • procoagulant activity •  responsiveness to catecholamine lrmmiller@msn.com

  26. Critical Care Immunology • Triggers to IIR • infection • hypoperfusion • hypoxemia • injury lrmmiller@msn.com

  27. Critical Care Immunology • Etiology • ARDS • Sepsis • DIC • ATN • Shock lrmmiller@msn.com

  28. COAGULATION CASCADE Tissue Factor Factor VIIIa PAI-1 IL-6 IL-1 TNF- Monocyte Factor Va Suppressed fibrinolysis TAFI THROMBIN Neutrophil Fibrin IL-6 Fibrin clot Tissue Factor Inflammatory Responseto Infection Thrombotic Responseto Infection Fibrinolytic Responseto Infection Activation of the Immune Response Endothelium lrmmiller@msn.com

  29. Critical Care Immunology • Pathophysiology • role of initial insult in promoting INFECTION • Immunosuppression • downregulation • blood products • stress response • hypercatabolism lrmmiller@msn.com

  30. Critical Care Immunology • Pathophysiology • Transluminal migration • SIRS • nosocomial pneumonia lrmmiller@msn.com

  31. Critical Care Immunology • Pathophysiology • Flow dependent O2 consumption • DO2 > 600 • VO2 > 150 lrmmiller@msn.com

  32. Critical Care Immunology • Pathophysiology • tissue ischemia and reperfusion • xanthine oxidase  O2 free radicals (ROS)  tissue injury lrmmiller@msn.com

  33. Critical Care Immunology • Mortality rates • One organ = 1% • Two organs = 11% • Three organs = 50% • Four organs = 75% lrmmiller@msn.com

  34. Critical Care Immunology • Nurse’s Role in Treatment • assessing system failure • early identification • minimizing complications lrmmiller@msn.com

  35. Critical Care Immunology • SIRS Criteria (2 or more) • Temperature > 38 °C or < 36 °C • Heart rate > 90 beats • RR > 20 or paCO2 < 32 • WBC > 12,000 or < 4,000 or > 10% bands SIRS??? Levy et al. 2001 International Sepsis Definitions Conference lrmmiller@msn.com

  36. Critical Care Immunology • Definitions • SIRS • SIRS + Infection = Sepsis • Sepsis + Acute Organ Dysfunction or hypoperfusion = Severe Sepsis • Severe Sepsis + CV failure = Septic Shock

  37. Critical Care Immunology • Most common sites of origin • Urinary tract • GI system • Respiratory tract • Skin & wounds

  38. Critical Care Immunology • Predisposing Factors • extremes in age • granulocytopenia • prior antibiotic use • severe burn, trauma, surgery • functional asplenia

  39. Critical Care Immunology • Predisposing Factors • immunosuppression • malnutrition & TPN • alcohol & drug abuse • prolonged ICU stay

  40. Critical Care Immunology • Assessing Acute Immune Inflammatory Response • Procalcitonin (PCT) 0.12 – 0.26 ng/mL • C – reactive protein (CRP) 0 – 5 mg/L • IL – 60 – 28 pg/mL Hermann et al;(2000) Procalcitonin in septic shock. Clin Chem Lab Med 38(1):41 - 46 lrmmiller@msn.com

  41. Critical Care Immunology 1st Six Hours Resuscitation = Cultures + Antibiotics + Early Goal – Directed Therapy

  42. Critical Care Immunology 1st Six Hours • Delays in management of the SIR result in higher mortality rates and increased utilization of hospital resources lrmmiller@msn.com

  43. Critical Care Immunology Transition from Sepsis to Severe Sepsis • occurs most often during the 1st 24 hours of hospitalization • increase in mortality of 20 – 46% lrmmiller@msn.com

  44. Critical Care Immunology Transition •  tissue O2 delivery & CV insufficiency accompanies transition • usually not detected by VS nor SIRS criteria lrmmiller@msn.com

  45. Critical Care Immunology O2 Transport & Utilization • O2 delivery is insufficient to meet O2 demands @ cell level • results in increased lactate levels lrmmiller@msn.com

  46. Critical Care Immunology O2 Transport & Utilization • SvO2 < 65% or ScvO2 < 70% result in increased lactate and suggest the presence of global tissue hypoxia – greater extraction by tissues lrmmiller@msn.com

  47. Critical Care Immunology lrmmiller@msn.com

  48. Critical Care Immunology O2 Transport & Utilization • high SvO2, ScvO2 & lactate indicates that despite adequate global systemic O2 delivery, the tissues are unable to extract the O2 lrmmiller@msn.com

  49. Sepsis Pathophysiology lrmmiller@msn.com

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