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Strategizing  against  Systemic Inflammatory Syndrome Trey Rumph
Objectives ,[object Object],[object Object],[object Object],[object Object],[object Object]
Prevalence ,[object Object],[object Object]
Inflammation ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Infection ,[object Object]
SIRS ,[object Object],[object Object],[object Object]
Sepsis ,[object Object]
Severe Sepsis ,[object Object]
Septic Shock ,[object Object],[object Object]
Classification system for Sepsis ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Pathophysiology of Septic Shock ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Neuroendocrine reflex ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Inflammatory Response
Inflammatory Response ,[object Object],[object Object],[object Object],[object Object],[object Object]
Liver ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Gastrointestinal Tract ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Gastrointestinal Tract ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Gastrointestinal Tract ,[object Object]
Nutritional Clinical Effects ,[object Object],[object Object],[object Object]
TPN Formulation ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
TPN Formulation ,[object Object],[object Object],[object Object],[object Object],[object Object]
TPN Formulation ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Summary
Consequences Overfeeding ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
[object Object],[object Object]
Clinical Pearls ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Questions??? ,[object Object],[object Object],Germs NEJM 1972;287:553-5
bpm = beats per minute; MAP = mean arterial pressure; SBP = systolic blood pressure; s.d. = standard deviations; SVO 2  = venous oxygen saturation; WBC = white blood cell count. Table 6-1 Criteria for Systemic Inflammatory Response Syndrome General variables Hemodynamic variables    Fever [core temp >38.3°C (100.9°F)]    Arterial hypotension (SBP <90 mmHg, MAP <70, or SBP decrease >40 mmHg)    Hypothermia [core temp <36°C (96.8°F)]    SVO 2  >70%      Heart rate >90 bpm     Cardiac index >3.5 L/min per square meter    Tachypnea Organ dysfunction variables    Altered mental status    Arterial hypoxemia    Significant edema or positive fluid balance (>20 mL/kg over 24 h)    Acute oliguria     Hyperglycemia in the absence of diabetes    Creatinine increase Inflammatory variables    Coagulation abnormalities    Leukocytosis (WBC >12,000)    Ileus    Leukopenia (WBC <4000)    Thrombocytopenia    Bandemia (>10% band forms)    Hyperbilirubinemia    Plasma C-reactive protein > 2 s.d. above normal value Tissue perfusion variables    Plasma procalcitonin >2 s.d. above normal value    Hyperlactatemia    Decreased capillary filling

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Strategizing SIRS in nutrition

  • 1. Strategizing against Systemic Inflammatory Syndrome Trey Rumph
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  • 28. bpm = beats per minute; MAP = mean arterial pressure; SBP = systolic blood pressure; s.d. = standard deviations; SVO 2  = venous oxygen saturation; WBC = white blood cell count. Table 6-1 Criteria for Systemic Inflammatory Response Syndrome General variables Hemodynamic variables    Fever [core temp >38.3°C (100.9°F)]    Arterial hypotension (SBP <90 mmHg, MAP <70, or SBP decrease >40 mmHg)    Hypothermia [core temp <36°C (96.8°F)]    SVO 2  >70%      Heart rate >90 bpm    Cardiac index >3.5 L/min per square meter    Tachypnea Organ dysfunction variables    Altered mental status    Arterial hypoxemia    Significant edema or positive fluid balance (>20 mL/kg over 24 h)    Acute oliguria    Hyperglycemia in the absence of diabetes    Creatinine increase Inflammatory variables    Coagulation abnormalities    Leukocytosis (WBC >12,000)    Ileus    Leukopenia (WBC <4000)    Thrombocytopenia    Bandemia (>10% band forms)    Hyperbilirubinemia    Plasma C-reactive protein > 2 s.d. above normal value Tissue perfusion variables    Plasma procalcitonin >2 s.d. above normal value    Hyperlactatemia    Decreased capillary filling

Editor's Notes

  1. The normal endothelial tissue has tight junctions but in inflammation the vessels are dilated and become disjointed and it allows for fluid to pass that barrier easier than normal. The increased fluid to the area is what causes the swelling and pain associated with inflammation
  2. Excessive triggering of the bodys natural defense mechanisms
  3. Despite adequate fluid resuscitation in the absence of other causes of hypotension ex: Medications (BP, cholinergic drugs, CA-I, EtOH)
  4. Seems to be a acronym to remember what signs to look for in sepsis P: immunocompromised states I: Bacterial introduced R: The inflammatory response couple with the coagulation response, the feed off each other, and amplify the response O: hypoperfusion, that causes (liver, kidney, GI, myocardial) dysfunction
  5. Gram (-) Enterobacteriaceae E. Coli Klebsiella species Pseudomonas aeruginosa Gram (+) Staphylococci S. aureus Coagulase-negative staphylococcus Streptococci Strep. pyrogens Strep. pneumoniae Fungal Candida
  6. APP: a type of protein whose plasma concentration either increases or decreases in response to inflammation , during the acute-phase response - 2 groups: (Positive and Negative) Positive associated with anti-inflammatory response: [destroy and inhibit microbes/neg feedback of inflammatory response} vs Negative associated with pro-inflammatory response
  7. Toxic stimulus activates macrophages “recognition cells” and produce cytokines (TNF and IL-1) Neutrophils “effector cells” are then activated and adhere to epithelial cells, aggregate and formation of the microthrombus begins During this time more cytokines are formed and cause alterations to the microvascular wall Results in microvascular injury
  8. Sepsis in different organ systems
  9. Hepatocytes, Kupffer cells, and sinusoidal cells  interactions Early: tx  infection control, oxygenation, ample fluid administration and eventually transfusion and use of vasoactive drugs (like pressors and dobutamine)
  10. The digestive tract&apos;s immune system is often referred to as  gut-associated lymphoid tissue (GALT)  and works to protect the body from invasion. GALT is an example of  mucosa-associated lymphoid tissue
  11. Boitano, Megan. “Hypocaloric Feeding of the Critically Ill”. December 2006, ASPEN. 2006. 21:617-622 Stress Response  trauma, cardiogenic shock, sepsis, MOF and Severe acute pancreatitis
  12. JPEN May/June 2009 Guidelines
  13. Septic Autocannabalism Malnutrition compromised the bodys ability to mount a adequate inflammatory response to stressors
  14. Reports of non-occlusive bowel necrosis, which suggest that early initiation of EN can be harmful Inappropriate EN into a dysfunctional gut plays a pathogenic role
  15. http://www.accessmedicine.com.swilley-proxy.mercer.edu/popup.aspx?aID=5013634&amp;searchStr=systemic%20inflammatory%20response%20syndrome