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Sepsis

Sepsis. Rebecca Linstead. SIRS vs. Sepsis vs. Septic Shock. SIRS (systemic inflammatory response syndrome) The inflammatory response that occurs from a variety of insults including infection, pancreatitis, burns, shock, organ injury, etc Presence of at least two of the following:

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Sepsis

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  1. Sepsis Rebecca Linstead

  2. SIRS vs. Sepsis vs. Septic Shock • SIRS (systemic inflammatory response syndrome) • The inflammatory response that occurs from a variety of insults including infection, pancreatitis, burns, shock, organ injury, etc • Presence of at least two of the following: • Body temperature >38C or <36C • Heart rate >90 beats/minute • Respiratory rate >20 breaths/min (tachypnea) • WBC count >12,000/mm3 • Hypermetabolic

  3. SIRS vs. Sepsis vs. Septic Shock • Sepsis • SIRS with the presence or presumed presence of an infectious source • Severe Sepsis • Sepsis with one or more organ dysfunction • Septic Shock • Presence of sepsis with hemodynamic instability • systolic peak pressure less than 90 mmHg, mean arterial pressures less than 65 mmHg or a drop of greater than 40mmHg from baseline • Unresponsive to crystalloid volume resuscitation

  4. SIRS vs. Sepsis vs. Septic Shock

  5. Pathophysiology of SIRS • Stage 1 • Cytokine production at the site of insult to initiate inflammatory response and promote wound healing (+) • Macrophages • Interleukin-1 (IL-1) and tissue necrosis factor-a (TNF-a) • Stage 2 • Local cytokines spill into circulation in small quantities to improve the local response (+/-) • Balance is retained by dampening effects of anti-inflammatory cytokines • Stage 3 • Massive pro-inflammatory swing as balance between anti-inflammatory and pro-inflammatory cytokines is lost (-)

  6. Nutrition – a Critical Component • Maintenance of immune function • Wound healing • Maintenance of mucosal barrier function • Slow/counteract skeletal muscle catabolism

  7. Metabolic Response to Sepsis • Increase in energy expenditure • 20-60% above basal energy expenditure • Protein catabolism • both from visceral and skeletal sources • Oxidation of stored lipids • Significant alterations in the body’s ability to metabolize carbohydrate

  8. Carbohydrate Metabolism • Mechanism to maintain glucose homeostasis is interrupted • Hyperglycemia due to increased insulin resistance and increase of blood glucose

  9. Protein Metabolism • Net negative nitrogen balance • Accelerated peripheral protein breakdown results in diminished protein uptake • Efflux of amino acids from muscle • Delivery to liver results in increase of creatinine and ammonia • As systemic response to sepsis continues, protein catabolism increases and results in loss of skeletal and visceral proteins

  10. Lipid Metabolism • Lipolysis stimulated by catabolic hormones glucagon, epinephrine and norepinephrine • Intracellular transport metabolism affected • Acyl-carnitine carrier impaired • Long chain fatty acids accumulate in the cell, inhibiting the function of pyruvate dehydrogenase • Aerobic respiration decreases • Lactic acid builds up

  11. When to Start Nutrition Support • Varies by patient • Age, metabolic state, vasopressor administration and organ function • Recently, several studies have been reporting the benefits of initiating nutrition support early • Prevent adverse structural and functional alterations of mucosal barrier • Enhance visceral blood flow • Support of local and systemic immune response • Always make sure GI tract is functioning properly first!

  12. Common vasopressors • -Epinephrine • -Phenylephrine • -Vasopressin • -Dobutamine • -Midodrine

  13. Providing Adequate Nutrition • Currently, the calorie delivery that is considered to be safe is 25-35 kcal/kg • CHO • 50-60 % of total energy requirements • Lipids • 1.0g/kg/d • Protein • Optimal range is 1.5-2.0 g/kg

  14. Labs to Monitor • Electrolytes • At risk for refeeding • ABGs • Acidosis/alkalosis • Lactate • Glucose/accuchecks • Ins, Outs, Residuals

  15. References • http://www.systemswiki.org/index.php?title=Glucose_Insulin_Glucagon_Loops • http://www.buzzle.com/articles/inflammation-of-the-heart.html • http://www.jped.com.br/conteudo/07-83-s128/ing.asp?cod=1721 • http://emedicine.medscape.com/article/168943-treatment • http://www.rcsed.ac.uk/RCSEDBackIssues/journal/vol45_3/4530010.htm • Martindale RG, Sawai R, Warren M. Sepsis and Infection. A.S.P.E.N. 2007: 440-451.

  16. Thank you!

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