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Critical Care Metabolic demand for inflammation, sepsis, surgery, trauma, wounds, organ failure increase stress factor by 1.3 With intubation, sedation.

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Presentation on theme: "Critical Care Metabolic demand for inflammation, sepsis, surgery, trauma, wounds, organ failure increase stress factor by 1.3 With intubation, sedation."— Presentation transcript:

1 Critical Care Metabolic demand for inflammation, sepsis, surgery, trauma, wounds, organ failure increase stress factor by 1.3 With intubation, sedation patients are at risk for acute malnutrition and catabolism Body utilizes endogenous energy stores which deplete muscle mass, immune response, endocrine function Glycogenolysis, breakdown of glycogen or stored hepatic glucose which provides energy for <3hrs Gluconeogenesis, production of glucose by the liver by utilizing non-glucose substrates like TAGs and AAs

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4 Critical Care Lipolysis, breakdown of adipose tissue with FAs oxidation for slow steady energy demands Ketosis, when glucose stores are depleted and FAs remain in circulation the liver produces ketone bodies for survival Body utilizes endogenous energy stores which deplete muscle mass, immune response, endocrine function The uses transporters specific for glucose, to triage vital organs for when energy stores are depleted The brain NEEDS glucose as regulated by the brain-blood barrier, making it the priority for glycogen stores

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9 Critical Care The heart, liver, kidneys can function with FAs or ketone bodies but utilization of these requires increased energy As starvation continues, organs begin to shut down to preserve energy, catabolism occurs, and output decreases Hypermetabolism, when demand exceeds supply with increases BMR, negative nitrogen balance, and higher O2 demand Catecholamines like glucagon and cortisol counter regulate starvation by increasing available energy stores Aldosterone and ADH, increase to limit excretion of AAs or electrolytes and fluids

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12 Critical Care Markers for starvation ARE NOT albumin, pre-albumin, and CRP but rather indicators of clinical status A patient can be adequately nourishes and have low lab values or be malnourished and have acceptable labs C-reactive Protein is an inflammatory maker which typically indicates catabolic response Critical care typically holds nutrition for 24-48hrs to stabilize a patient, BUT then >48hrs EARLY NUTRITION is vital Heavy sedation, narcotics, and IVFs can complicate peristalsis, GI function, and electrolyte balance

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14 Critical Care Use of NGT/OGT is ideal, checking GRV every 4hrs with a decrease in rate at 250ml, or HOLD at 500ml Early feeding, even 10ml/hr reduces risk for gut ischemia, paralytic Ileus, acidosis, tissue necrosis NO EN with severe hypotension, perforated bowel, high dose pressors, esophageal strictures Burns require the >energy and fluid, tissue damage and shock can utilize >5000 KCALS, 200gm PRO

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16 Critical Care PARKLAND formula for fluids is 4 x KG x %BS = mL/24hrs, then total mL/2/8hrs, with the remaining mL/16hrs Man 85kg, with 20% burns, 4 x 85 x 20% = 6800ml, then 6800ml/2 = 3400ml, 3400ml/8hrs is 435ml/hr, 3400ml/16 = 213ml/hr Specific EN formula for increased protein demand for burn patients typically providing 25% of total KCALS Protein needs for ICU patients are 1.2-2gm/KG, or disease specific, with Obese at using IBW OFTEN sedation or hydration can limit EN rate, causing chronic protein deficiency and need for elemental protein supplements

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18 Critical Care Sedation can affect EN rate given propofol is a lipid emulsion providing 1.1 KCALS/mL, or 40mL/hr = 1065 KCALS of total fat Remember, IVFS D10W, D5W provide KCALS from CHO which need to be considered in total energy In general, ICU patients have higher KCAL demand with stress factors at 1.3 or 130% of REE That said, permissive under-feeding is often indicated depending on clinical status of the patient Without nutrition ICU patients can lose 2% of total muscle mass in 24hrs, develop third spacing, and cardiac arrest

19 Critical Care With intubated patients DO NOT over-feed, reduce respiratory function, risk for aspiration Total KCALS are often less with intubation given ventilators fully support active breathing In contrast COPD patients NOT INTUBATED have extreme KCAL demand at > 1.3 stress factor Pulmonary specific EN formulas HAVE NOT been shown to reduce mortality or improve respiration

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22 Critical Care In COPD, high CHO intake increases CO2 output which MAY cause acidosis, SOB, and acute respiratory distress Fiber containing EN formulas SHOULD NOT be used with ICU patients on pressors, ventilation, heavy sedation LOW residue, KCAL dense formulas are ideal to prevent gastric distention, bloating, and high GRV ICU patients should ALWAYS receive EN via continuous infusion, NOT BOLUS feeding

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24 Critical Care EN recommendations should advance to GOAL slowly to prevent refeeding syndrome, after starvation Excessive metabolic activity in refeeding, causes electrolyte derangement with <labs for P, Mg, K EN formulas should start at 25% of patients KCALS/KG, then advance by 25% every 12-24hrs REMEMBER fluids are a vital nutrient that should always be considered in ANY nutrition assessment


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