Strategizing  against  Systemic Inflammatory Syndrome Trey Rumph
Objectives <ul><li>Define SIRS and Sepsis, and understand the difference between the two </li></ul><ul><li>Identify those ...
Prevalence <ul><li>Leading cause of death in critically ill patients, claiming approximately 225,000 deaths annually in th...
Inflammation <ul><li>The Role of inflammation is to contain the site of damage, localize the response and restore tissue f...
Infection <ul><li>A pathological process involving a sterile or colonized site that becomes over run with a pathogenic par...
SIRS <ul><li>Systemic Inflammatory Response Syndrome </li></ul><ul><ul><li>1+ symptoms </li></ul></ul><ul><ul><li>*Can be ...
Sepsis <ul><li>Must meet criteria for Infection +  > 2 SIRS criteria </li></ul>
Severe Sepsis <ul><li>Sepsis complicated by organ dysfunction, organ hypoperfusion or hypotension </li></ul>
Septic Shock <ul><li>Persistent arterial hypotension in a septic patient </li></ul><ul><ul><li>Defined: systolic arterial ...
Classification system for Sepsis <ul><li>PIRO System </li></ul><ul><ul><li>P : predisposing conditions </li></ul></ul><ul>...
Pathophysiology of Septic Shock <ul><li>Pathogenic micro-organism </li></ul><ul><li>Body illicit a response to fight off i...
Neuroendocrine reflex <ul><li>The response initiated by recognition of free LPS in the body. </li></ul><ul><ul><li>Fever <...
Inflammatory Response
Inflammatory Response <ul><li>Hyper-inflammatory state    SIRS “Systemic inflammatory response syndrome” </li></ul><ul><u...
Liver <ul><li>The liver actively modulates inflammatory processes by filtering, inactivating, and clearing bacteria, bacte...
Gastrointestinal Tract <ul><li>Instigator and victim of MOF </li></ul><ul><li>Estimated ~70% of immune system </li></ul><u...
Gastrointestinal Tract <ul><li>Disuse of the gut </li></ul><ul><ul><li>Leads to ileus formation, colonization of new patho...
Gastrointestinal Tract <ul><li>Figure 20.1 “conceptual framework for the role of the gut in late MOF.” </li></ul>
Nutritional Clinical Effects <ul><li>Protein,  Carbohydrates and Lipids </li></ul><ul><li>Risks associated with overfeedin...
TPN Formulation <ul><li>Protein  Aminosyn 15% </li></ul><ul><ul><li>GOAL: attenuate the loss of lean body mass (high prote...
TPN Formulation <ul><li>Carbohydrates  Dextrose 70% </li></ul><ul><ul><li>GOAL: reduce excess glucose </li></ul></ul><ul><...
TPN Formulation <ul><li>Lipids  Liposyn 20%/30% </li></ul><ul><ul><li>GOAL: limit serum FFA </li></ul></ul><ul><ul><li>Dur...
Summary
Consequences Overfeeding <ul><li>Protein </li></ul><ul><ul><li>Impair kidney function due to the following: </li></ul></ul...
<ul><li>During a stress response the patient will have increase  glucose  circulation along with  FFA mobilization    inc...
Clinical Pearls <ul><li>Tight Glycemic control (BG  <  150) </li></ul><ul><ul><li>No more than 3.0mg/kg/min </li></ul></ul...
Questions??? <ul><li>“ The microorganisms…turn out…to be rather more like bystanders. It is our response to their presence...
bpm = beats per minute; MAP = mean arterial pressure; SBP = systolic blood pressure; s.d. = standard deviations; SVO 2  = ...
Upcoming SlideShare
Loading in …5
×

Strategizing SIRS in nutrition

1,276 views

Published on

A presentation to pharmacist on how to properly manage patients in the pre-stages of sepsis in regards to nutritional support

Published in: Health & Medicine, Technology
  • Be the first to comment

  • Be the first to like this

Strategizing SIRS in nutrition

  1. 1. Strategizing against Systemic Inflammatory Syndrome Trey Rumph
  2. 2. Objectives <ul><li>Define SIRS and Sepsis, and understand the difference between the two </li></ul><ul><li>Identify those at risk for SIRS or Sepsis </li></ul><ul><li>Understand the general pathophysiology of SIRS </li></ul><ul><li>Understand how organ systems may be affected by SIRS or Sepsis </li></ul><ul><li>Understand how the use of Nutrition can help in the ICU patient population with SIRS or Sepsis </li></ul>
  3. 3. Prevalence <ul><li>Leading cause of death in critically ill patients, claiming approximately 225,000 deaths annually in the US alone </li></ul><ul><li>Associated with a high mortality rate ~40-50%, even with appropriate therapy </li></ul>
  4. 4. Inflammation <ul><li>The Role of inflammation is to contain the site of damage, localize the response and restore tissue function. </li></ul><ul><li>Initiated by microbes or tissue damage </li></ul><ul><li>Dilation of the small blood vessels, causes leakage in those vessels and a pathway for leukocytes to get from the blood stream into the tissue in created  increased blood flow to damaged area. </li></ul><ul><ul><ul><li>Causes the heat and redness associated with inflammation </li></ul></ul></ul><ul><li>Cardinal Signs: </li></ul><ul><li>Redness Swelling Heat Pain </li></ul>
  5. 5. Infection <ul><li>A pathological process involving a sterile or colonized site that becomes over run with a pathogenic paracytic microorganism </li></ul>
  6. 6. SIRS <ul><li>Systemic Inflammatory Response Syndrome </li></ul><ul><ul><li>1+ symptoms </li></ul></ul><ul><ul><li>*Can be observed without the identification of an infection </li></ul></ul>
  7. 7. Sepsis <ul><li>Must meet criteria for Infection + > 2 SIRS criteria </li></ul>
  8. 8. Severe Sepsis <ul><li>Sepsis complicated by organ dysfunction, organ hypoperfusion or hypotension </li></ul>
  9. 9. Septic Shock <ul><li>Persistent arterial hypotension in a septic patient </li></ul><ul><ul><li>Defined: systolic arterial pressure <90 mmHg or a reduction in systolic pressure >40mmHg from baseline </li></ul></ul>
  10. 10. Classification system for Sepsis <ul><li>PIRO System </li></ul><ul><ul><li>P : predisposing conditions </li></ul></ul><ul><ul><li>I : insult, the nature and extent of the </li></ul></ul><ul><ul><li>R : response, the nature and magnitude of the host </li></ul></ul><ul><ul><li>O : organ dysfunction, the degree of concomitant </li></ul></ul><ul><li>this system stratifies patients based on these criteria, but it has not gone through enough clinical trails to be applicable in practice </li></ul>
  11. 11. Pathophysiology of Septic Shock <ul><li>Pathogenic micro-organism </li></ul><ul><li>Body illicit a response to fight off invader </li></ul><ul><ul><li>Neuroendocrine reflexes* </li></ul></ul><ul><ul><li>Inflammatory Response* </li></ul></ul><ul><ul><li>Plasma Protein Cascades </li></ul></ul><ul><ul><ul><li>Complement, Intrinsic and Extrinsic Pathways, Fibrinolytic System </li></ul></ul></ul><ul><ul><li>Innate and Humeral Immunity Response </li></ul></ul><ul><li>The interaction between these different systems is what causes the body microvascular harm  organ/tissue ischemia and multiple organ dysfunction/failure </li></ul>
  12. 12. Neuroendocrine reflex <ul><li>The response initiated by recognition of free LPS in the body. </li></ul><ul><ul><li>Fever </li></ul></ul><ul><ul><li>Stimulation of the bone marrow and function of leukocytes </li></ul></ul><ul><ul><li>Catabolism </li></ul></ul><ul><ul><li>Breakdown of muscle proteins </li></ul></ul><ul><ul><li>Rapid increase in production of acute-phase proteins (APP) </li></ul></ul><ul><ul><ul><li>Positive </li></ul></ul></ul><ul><ul><ul><ul><li>(CRP, D-dimer, Coagulation factors, Haptoglobin, Ferritin) </li></ul></ul></ul></ul><ul><ul><ul><li>Negative </li></ul></ul></ul><ul><ul><ul><ul><li>(Albumin, Transferrin, Retinol-binding protein) </li></ul></ul></ul></ul>
  13. 13. Inflammatory Response
  14. 14. Inflammatory Response <ul><li>Hyper-inflammatory state  SIRS “Systemic inflammatory response syndrome” </li></ul><ul><ul><li>If severe can precipitate to Early MOF (multiple organ failure) </li></ul></ul><ul><li>As time proceeds, certain aspects of SIRS begin to down-regulate (to minimize autogenous tissue injury)  CARS “counter anti-inflammatory response syndrome” </li></ul><ul><ul><li>If severe can cause a severe immunosuppressed state </li></ul></ul><ul><ul><ul><li>Lead to infections, local and systemic  Late MOF-associated infections </li></ul></ul></ul>
  15. 15. Liver <ul><li>The liver actively modulates inflammatory processes by filtering, inactivating, and clearing bacteria, bacterial products (e.g., endotoxin), vasoactive substances, and inflammatory mediators. </li></ul><ul><ul><li>A stimulated liver manufactures cytokines, bioactive lipid and Acute phase proteins </li></ul></ul><ul><li>Early Dysfunction (1 st couple of hours) </li></ul><ul><ul><li>Hypoperfusion  “Liver shock” </li></ul></ul><ul><ul><ul><li>Increase in LFTs </li></ul></ul></ul><ul><ul><ul><li>Reversed with adequate treatment </li></ul></ul></ul><ul><li>Late Dysfunction </li></ul><ul><ul><li>Structural and functional injury </li></ul></ul><ul><ul><li>May be accounted to a bacterial, endotoxin, inflammatory mediator spillover that trigger/sustain the MOF </li></ul></ul>
  16. 16. Gastrointestinal Tract <ul><li>Instigator and victim of MOF </li></ul><ul><li>Estimated ~70% of immune system </li></ul><ul><li>Hypoperfusion  decreased function of the intestinal epithelium as a barrier between the enteric flora and portal circulation </li></ul><ul><ul><li>If toxin reaches the portal system then cycle continues, and SIRS response intensifies </li></ul></ul><ul><ul><li>Mesenteric lymph nodes are last line defense to neutralize toxin </li></ul></ul><ul><li>Reperfusion  initiates pro-inflammatory mediators to be made that amplify the early SIRS contributing to MOF </li></ul><ul><li>Bacterial overgrowth and increased release of endotoxin contribute to late sepsis-associated MOF </li></ul>
  17. 17. Gastrointestinal Tract <ul><li>Disuse of the gut </li></ul><ul><ul><li>Leads to ileus formation, colonization of new pathogens in the normally sterile upper gut, and increased mucosal permeability and decreased local gut immunity </li></ul></ul><ul><ul><ul><li>decreased gut immunity  furthers systemic immunosuppression </li></ul></ul></ul><ul><ul><ul><ul><li>Additionally, gut flora disseminate via aspiration or translocation to become pathogenic and cause late infection. </li></ul></ul></ul></ul><ul><li>GI motility is generally decreased following: </li></ul><ul><ul><li>Neurologic injury </li></ul></ul><ul><ul><li>Severe trauma </li></ul></ul>
  18. 18. Gastrointestinal Tract <ul><li>Figure 20.1 “conceptual framework for the role of the gut in late MOF.” </li></ul>
  19. 19. Nutritional Clinical Effects <ul><li>Protein, Carbohydrates and Lipids </li></ul><ul><li>Risks associated with overfeeding </li></ul><ul><li>Clinical Pearls </li></ul>
  20. 20. TPN Formulation <ul><li>Protein Aminosyn 15% </li></ul><ul><ul><li>GOAL: attenuate the loss of lean body mass (high protein) </li></ul></ul><ul><ul><ul><li>Normal </li></ul></ul></ul><ul><ul><ul><ul><li>1.2 – 2.0 g/kg (ABW)  BMI <30 </li></ul></ul></ul></ul><ul><ul><ul><li>Obese </li></ul></ul></ul><ul><ul><ul><ul><li>> 2.0 g/kg (IBW)  BMI 30-40 </li></ul></ul></ul></ul><ul><ul><ul><ul><li>> 2.5 g/kg (IBW)  BMI > 40 </li></ul></ul></ul></ul><ul><ul><li>During Stress  </li></ul></ul><ul><ul><ul><li>the body is in an increased metabolic state and more proteolysis is occurring, use nutrition to attenuate damage incurred by supplying enough protein to maintain the nitrogen balance. </li></ul></ul></ul>
  21. 21. TPN Formulation <ul><li>Carbohydrates Dextrose 70% </li></ul><ul><ul><li>GOAL: reduce excess glucose </li></ul></ul><ul><ul><ul><li>Patients are in a catabolic state and experience glucose intolerance </li></ul></ul></ul><ul><ul><li>During Stress  </li></ul></ul><ul><ul><ul><li>hepatic glucose production is double the normal rates during stressed state, and the provision of glucose at a rate of 4mg/kg/min is only able to suppress 50% of the endogenous glucose production. </li></ul></ul></ul>
  22. 22. TPN Formulation <ul><li>Lipids Liposyn 20%/30% </li></ul><ul><ul><li>GOAL: limit serum FFA </li></ul></ul><ul><ul><li>During Stress  </li></ul></ul><ul><ul><ul><li>Insulin secretion is inhibited </li></ul></ul></ul><ul><ul><ul><li>Lipolysis is activated </li></ul></ul></ul><ul><ul><ul><li>Hepatic clearance of FFA increases </li></ul></ul></ul><ul><ul><ul><li>Increased production of hepatic TG </li></ul></ul></ul><ul><ul><ul><li>Increased hepatic TG leads to accumulation in the liver  “fatty liver” </li></ul></ul></ul>
  23. 23. Summary
  24. 24. Consequences Overfeeding <ul><li>Protein </li></ul><ul><ul><li>Impair kidney function due to the following: </li></ul></ul><ul><ul><ul><li>Uremia </li></ul></ul></ul><ul><ul><ul><li>Hypertonic dehydration </li></ul></ul></ul><ul><ul><ul><li>Metabolic acidosis </li></ul></ul></ul><ul><li>Carbs </li></ul><ul><ul><li>Fatty Liver, mechanical ventilation </li></ul></ul><ul><ul><ul><li>Hyperglycemia </li></ul></ul></ul><ul><ul><ul><li>Hypercapnia </li></ul></ul></ul><ul><li>Fats </li></ul><ul><ul><li>Fatty Liver </li></ul></ul><ul><ul><ul><li>Hypertriglyceridemia </li></ul></ul></ul><ul><ul><ul><li>Fat overload syndrome </li></ul></ul></ul>
  25. 25. <ul><li>During a stress response the patient will have increase glucose circulation along with FFA mobilization  increased metabolic activity (ICU patients) </li></ul><ul><li>Important to realize is that this therapy does not prevent catabolism it merely minimizes the amount of damage that could possibly incur in the patient without proper nutrition </li></ul>
  26. 26. Clinical Pearls <ul><li>Tight Glycemic control (BG < 150) </li></ul><ul><ul><li>No more than 3.0mg/kg/min </li></ul></ul><ul><ul><li>Patients become insulin intolerant </li></ul></ul><ul><li>Limit Lipids </li></ul><ul><ul><li>Due to increased FFA during sepsis limit lipids to < 20% of NP </li></ul></ul><ul><li>Ample Protein on board </li></ul><ul><ul><li>To help prevent proteolysis we add between 1.2-2.5g/kg, depending on the BMI of the patient </li></ul></ul>
  27. 27. Questions??? <ul><li>“ The microorganisms…turn out…to be rather more like bystanders. It is our response to their presence that makes the disease. Our arsenals for fighting off bacteria are so powerful…that we are more in danger from them than the invaders.” </li></ul><ul><li>-Lewis Thomas </li></ul>Germs NEJM 1972;287:553-5
  28. 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

×