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Surgery Critical Care

Surgery Critical Care. PSGS Review Bonaventure Plaza, Greenhills , San Juan 1-2 PM; April 26, 2013. Objectives. To discuss key events and situations that have a major role in the outcome of critical care patient management

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Surgery Critical Care

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  1. Surgery Critical Care PSGS Review Bonaventure Plaza, Greenhills, San Juan 1-2PM; April 26, 2013

  2. Objectives • To discuss key events and situations that have a major role in the outcome of critical care patient management • To discuss areas where targeted goal management plays a major role in achieving positive outcomes in critical care

  3. Discussion Points • Conditions resulting to critical care status • Inflammation state of ICU patient • Optimizing nutrition therapy through: • Early enteral nutrition • Pharmaconutrients • Insulin resistance • Adequate intake • Role of the Nutrition Team

  4. Surgical critical care • Critical illness following surgery or trauma • High risk surgical patients • Shock and hemodynamic compromise • Acute lung injury and ARDS following surgery, trauma, or pancreatitis • Sepsis and severe infections • Trauma evaluation and management • Neurologic emergencies • Post-transplantation • Post-operative complications • Peritonitis, perforated viscus, and abdominal sepsis • Enterocutaneous fistulas • Gastrointestinal hemorrhage • Severe acute pancreatitis • Multisystem organ failure

  5. Shock and hemodynamic compromise Critical illness following surgery or trauma Acute lung injury following surgery or trauma ARDS, complication of acute pancreatitis Sepsis and severe infections Peritonitis, perforated viscus, and abdominal sepsis Enterocutaneous fistulas Inflammation in the critical care state

  6. Shock and hemodynamic compromise

  7. Body compartment percentage of total body fluids: a. 70% b. 60% c. 50% d. 40%

  8. Body composition, all ages

  9. Body compartments in health and disease CARBO + OTHER (1%) PROTEIN (14%) PROTEIN (14%) PROTEIN (12%) PROTEIN (6%) FAT (23%) FAT (15%) FAT (25%) FAT (30%) WATER (72%) WATER (70%) WATER (60%) WATER (55%) OBESE NORMAL STARVATION CRITICAL CARE

  10. Best solution for volume loss repletion: a. Isotonic saline b. Balanced electrolyte solution c. Colloid d. D5LR

  11. Volume and electrolyte changes • Balanced electrolyte solutions • colloid • ECF = loss • Intravascular loss • Interstitial = normal • Electrolytes = normal • Albumin = normal • ECF = loss • Intravascular loss • Interstitial = swollen • Balanced electrolyte solutions • Colloid • Electrolytes = normal • Albumin = low • Hypernatremia • Albumin = normal • ECF = loss/none • Intravascular loss • Cell shrink • D5W • colloid • ECF = loss/none • Intravascular loss • Cell swell • Hypertonic saline (3%SS) • colloid • Hyponatremia • Albumin = low • Avoid D5W • Avoid 0.3% SS Cerebral edema

  12. Crystalloids

  13. Resuscitation: fluids Reference: Zander R, Adams Ha, Boldt J. 2005; 40; 701-719 18

  14. Compute fluids of a 70 kg person • TBF=70kg x 60% = 42L (total body fluid) • ECF=70kg x 20% = 14L (extracellular fluid) • ICF=70kg x 40% = 28L (intracellular fluid) • Total plasma volume = 70kg x 5% = 3.5L • Total blood volume (hct=38) = 5.6L • Total interstitial fluid = 14L – 5.6L = 8.4L

  15. How much is the total blood volume? • How to compute: • Plasma volume is 5% of actual body weight • Weight=70 kg; hematocrit = 38 • Total plasma volume = 5% x 70kg = 3500 ml • Total blood volume = 3500ml x (100/[100-38]) • TBV = 3500 ml x (100/62) = 3500ml x 1.61 • Total blood volume = 5645 ml or 5.6 liters

  16. Body composition and water Human body composition (% of weight): • Water: 60% • ECF (extracellular fluid): 20% • Intravascular fluid • Extravascularinterstital fluid • ICF (intracellular fluid): 40% • Mass: 40% • Lean body mass • Fat mass TBF = ICF + ECF = 42 liters (60% of weight) • ECF = 14 liters • Plasma • Interstitial Fluid • ICF = 28 liters • Computation of usual fluid requirement per day: • 30 ml/kg • or 1.5 to 2.5 L/day

  17. Osmolality • Normal cellular function requires normal serum osmolality • Water homeostasis maintains serum osmolality • The contributing factors to serum osmolality are: Na, glucose, and BUN • Sodium is the major contributor (accounts for 90% of extracellular osmolality) • Acute changes in serum osmolality will cause rapid changes in cell volume

  18. How to compute for plasma osmolality Division of glucose and BUN by 18 and 2.8 converts these to mmol/L Na = 140 mmol/L Glucose = 110 mg/dL BUN = 20 mg/dL 2 x [Na] + [glucose]/18 + [BUN]/2.8 Osmolality = Osmolality = (2x140) + (110/18) + (20/2.8) Osmolality = 280 + 6.1 + 7.1 Osmolality = 293.2 mmol/L

  19. Regulation of sodium and water balance

  20. Antidiuretic hormone a. Leads to water retention b. Synthesized by the kidney c. Leads to water loss through the urine d. Stimulated by low plasma sodium level

  21. Anti-diuretic hormone

  22. The post-resuscitation environment Cardiopulmonary arrest Cardio or pulmonary failure Trauma/Injury Shock/hypovolemia ↓oxygenation Microcirculation changes/effects Cellular dysfunction ↑free radicals ↑eicosanoids Acid-base imbalance

  23. The post-resuscitation environment Cardiopulmonary arrest Cardio or pulmonary failure Trauma/Injury Shock/hypovolemia ↓oxygenation Microcirculation changes/effects Cellular dysfunction ↑free radicals ↑eicosanoids Acid-base imbalance ↑ INFLAMMATION

  24. The inflammation environment Monos, macros, lymphos, epithelia in inflammatory state STRESS INJURY Adipose tissue ↑LPL TNF, IL1, IL6 Liver Platelets Endothelium Acute phase response ↑fibrinogen ↓HDL ↑ Aggregability ↑ Adhesion molecules MICROCIRCULATION ENVIRONMENT LPL = lipoprotein lipase; HDL = high-density lipoprotein.

  25. Organ status post-resuscitation • Cardiac status • electrolyte status • neural activity • muscle activity • GUT ISCHEMIA • ↑free radicals • ↑eicosanoids • Accumulation of inflammatory mediators • Cytokines • complement • ↓digestion and absorption • Lung status • gas exchange • mucosal immunity “FIRST HIT”

  26. Organ status post-resuscitation • Cardiac status • electrolyte status • neural activity • muscle activity • GUT ISCHEMIA • ↑free radicals • ↑eicosanoids • Accumulation of inflammatory mediators • Cytokines • complement • ↓digestion and absorption • Lung status • gas exchange • mucosal immunity “FIRST HIT” RESUSCITATION EFFORTS Reperfusion Laparotomy ICU therapies Gut disuse

  27. Organ status post-resuscitation • Cardiac status • electrolyte status • neural activity • muscle activity • GUT ISCHEMIA • ↑free radicals • ↑eicosanoids • Accumulation of inflammatory mediators • Cytokines • complement • ↓digestion and absorption • Lung status • gas exchange • mucosal immunity “FIRST HIT” RESUSCITATION EFFORTS Reperfusion Laparotomy ICU therapies Gut disuse Gut dysfunction Acute Lung Injury Acute Kidney Injury Within 24 hrs “SECOND HIT”

  28. Why? LUNGS GUT • Local inflammatory response: • Pro-inflammatory: • ↓mucosal blood flow • gastric alkalinization • ileus • impaired mucosal defense • Anti-inflammatory: • ↑apoptosis of lymphocytes, • PMN and monocyte deactivation, • shift from Th1 to Th2 phenotype (immuno-suppression) LIVER KIDNEY • Reperfusion → • promotes distribution of pro-inflammatory cytokines to the circulation: • ↑PMN sequestration in target organs • → Liver, lungs, kidney • → MOF (multi organ failure)

  29. Why? • Early isotonic crystalloid resuscitation → • ↑inflammation • ↑edema • promote ileus. • ICU interventions: • Vasopressors = ↓ mucosal perfusion • Stress gastritis prophylaxis = ↑gastric alkalinization • Opiates worsen ileus • Antibiotics ↑bacterial overgrowth • TPN = gut disuse → ↓local gut immunity and ↑systemic CARS. • Laparotomy with bowel manipulation → • ↑gut inflammation • ↑mucosal injury • ileus

  30. Why? • NPO (nothing per os) • TPN (total parenteral nutrition) → • Gut disuse → • ↓local gut immunity → • worsening systemic CARS. • Mechanism: • ↓mucosal blood flow • Epithelial and WBC apoptosis (↑pro-inflammatory status) • ↓mucosal defense to infection • ↓secretoryIgA • ↑bacterial translocation

  31. Immunologic phases of injury ↑inflammation→organ dysfunction ↑immunosuppression→infection→organ dysfunction 24 hours Moore FA. Presidential address: imagination trumps knowledge. Am J Surg 2010: 200: 671-7.

  32. Inflammation and organ failure in the ICU Tissue inflammation, Early organ failure (MOF) and Death SIRS TNF, IL-1, IL-6, IL-12, IFN, IL-3 PRO days weeks Inflammatory balance ANTI IL-10, IL-4, IL-1ra, Monocyte HLA-DR suppression Immunosuppression Delayed MOF and death 2nd Infections CARS Insult (trauma, sepsis) Griffiths, R. “Specialized nutrition support in the critically ill: For whom and when? Clinical Nutrition: Early Intervention; Nestle Nutrition Workshop Series

  33. insulin resistance

  34. Insulin resistance Stress/Injury WBC, endothelium ↑cytokines ↓enteral nutrition Liver: ↑glycogenolysis ↑gluconeogenesis ↑catecholamines ↑glucagon Adrenals ↑cortisol HYPERGLYCEMIA ↑energy requirements → malnutrition ↑inflammatory environment → SIRS ↑susceptibility to infection → sepsis ↑coagulable state of microcirculation → DIC

  35. Blood glucose and mortality Hyperglycemia related mortality in critically ill patients varies with admission diagnosis. Falciglia M et al. Crit Care Med 2009; 37(12): 3001-9.

  36. Insulin resistance Stress/Injury WBC, endothelium ↑cytokines ↓enteral nutrition Liver: ↑glycogenolysis ↑gluconeogenesis ↑catecholamines ↑glucagon Adrenals ↑cortisol HYPERGLYCEMIA Managed By: Glucose control (insulin – tight or pragmatic) Early enteral feeding (effect of incretins, GLP-1 on glucagon/insulin)

  37. 100 100 Intensive treatment 96 96 Intensive treatment 92 92 Conventional treatment In-Hospital Survival (%) Survival in the ICU (%) 88 88 Conventional treatment 84 84 0 40 80 120 160 0 65 130 195 260 Days after admission Days after admission Strict glucose control with insulin Van den Berghe, G et al. Intensive insulin therapy in critically ill patients. NEJM 2001; 345:1359-1367

  38. early enteral nutrition

  39. “ NPO until further orders”

  40. Early enteral nutrition • Mechanics: • Once vital signs are stable START Gastric/small bowel feeding • 10-15 ml/hr enteral pump • Gastric residual protocol • Pharmaconutrition: • Fish oils • Glutamine • Arginine • Antioxidants • Intraluminal nutrients reverse shock-induced mucosal hypoperfusion • Sustains mucosal cell quality and function • Mucosal immunity sustained • Reverse impaired intestinal transit • ↓ileus mediated bacterial translocation • Reverses CARS Window of opportunity = 24 to 48 hrs • Requires protocols of feeding and gastric residual volume decision • Needs calorie and protein counting practice • Strict fluid balance

  41. Early enteral nutrition

  42. Feeding pathways Can the GIT be used? “Inability to use the GIT” Yes No “inadequate intake” Parenteral nutrition Oral Tube feed < 75% intake Short term Long term More than 3-4 weeks Central PN Peripheral PN Yes No NGT A.S.P.E.N. Board of Directors. Guidelines for the use of parenteral and enteral nutrition in adult and pediatric patients, III: nutritional assessment – adults. J ParenterEnteralNutr 2002; 26 (1 suppl): 9SA-12SA. Gastrostomy Nasoduodenal or nasojejunal Jejunostomy

  43. Parenteral nutrition • COMPOSITION • Carbohydrates • Lipids • LCT (structural) • MCT (energy) • Fish Oils (immuno-modulation) • Protein • BCAA • Glutamine • Vitamins/Trace elements • Antioxidants • Sustains cellular metabolism and functions (MACRO & MICRONUTRIENTS) • Sustains mucosal cell quality and function (=GLUTAMINE) • Mucosal immunity sustained (GLUTAMINE & FISH OILS) • Reverses CARS (FISH OILS, GLUTAMINE, ANTIOXIDANTS) • Requires protocols for access, feeding patterns, delivery • Needs calorie and protein counting practice • Strict fluid balance • MAY BE TOTAL PARENTERAL OR SUPPLEMENTAL PARENTERAL NUTRITION

  44. MCT vs. LCT

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