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Alteration in Metabolism in Surgical Patients Energy Metabolism In order to mount a metabolic response to injury the body uses as a fuel glucose, fat and protein How much fuel does the body have? Body Composition Source kg kcal Fat Protein 14 125,000 skeletal muscle other 6 6 24,000 24,000 Glycogen muscle liver free glucose 0.15 0.075 0.02 600 300 80 Body Composition Even though protein is used as a fuel in stress, its depletion is detrimental Body Composition Glycogen - Fuel Fat - Fuel Protein - Structure (use as a fuel should be minimised) Protein & Amino Acid Metabolism Protein 15% body weight - ½ intracellular Enzymes, transport, hormones, immune Fx, muscle It is not usually a food when needed it is converted to glucose Protein & Amino Acid Metabolism Total protein turnover 300g /day Obligatory N loss in urine 12g /day or 80g protein /day Protein & Amino Acid Metabolism Nitrogen Balance N balance = N intake - N out Negative in starvation, injury, severe infection Response to Starvation vs Injury Parameter BMR Mediators Major fuel Ketone production Hepatic ureagenesis Neg N balance Gluconeogenesis Muscle proteolysis Hepatic protein synthesis Starvation Trauma Fat +++ + + + + + ++ +++ Mixed +/+++ +++ +++ +++ +++ Protein & Amino Acid Metabolism If protein is depleted via proteolysis – ability to adapt in stress is compromised protein depletion results in decreased wound healing decreased immune response defective gut-mucosal barrier decreased mobility/ respiratory effort Homeostatic Responses to Stress Designed to maintain homeostasis Same response in controlled or uncontrolled stress Trigger mechanisms: Volume loss Tissue damage Pain Fear Homeostatic Responses to Stress Volume Loss & Tissue Underperfusion Pressure & Stretch receptors activated HR / SV increased ADH / Aldosterone secreted renal and hypothalamic mechanism Need for adequate resuscitation Homeostatic Responses to Stress Tissue Damage Most important trigger Neural pathways from wound reach hypothalamus efferents go to pancreas glucagon insulin efferents to adrenal cortisol, catecolamines Release of cytokines Homeostatic Responses to Stress Pain & Fear Increased levels of catecholamines Fight or flight response Homeostatic Response Elective operation min tissue damage pain/fear managed less hypotension infection rare stress response in controlled Homeostatic Response Trauma major tissue damage pain/fear excessive managed hypotension common infection common Stress response uncontrolled Homeostatic Responses to Stress Triggers Response Volume loss Neurohormonal and Tissue damage Inflammatory arms Pain & Fear Mediators of Stress Response Neurohormonal arm Catecolamines, glucocorticoids, glucagon, ADH, aldosterone Inflammatory arm Cytokines, complement, eicisanoids, PAF Mediators of Stress Response Neurohormonal Arm - Counterregulatory Hormones catecholamines glucagon glycogenolytic, gluconeogenic glucocorticoids?/ACTH maintain circulation, hepatic glycolysis, lipolysis, gluconeogenesis, BMR mobilise muscle protein, gluconeogenesis ADH. Aldosterone Retain water and Na Mediators of Stress Response Inflammatory Arm - Cytokines TNF-alpha, IL-1, IL-2, IL-6, IFN-gamma Local effects - para or autocrine Response to tissue injury Mediators of Stress Response Cytokines In elective surgery confined to wound Trauma/sepsis spill over/ endocrine effect Mediators of Stress Response Cytokines - local effect Promote wound healing Stimulate angiogenesis White cell migration Ingrowth of fibroblasts Localise the wound Mediators of Stress Response Cytokines - spill over Mobilisation of AA, stimulation of acute phase protein synthesis Increase WBC counts/Hypoferremia Fever, subjective discomfort, sleep Mediators of Stress Response Cytokines - severe trauma /sepsis Increased organ vascular permeability Multiple organ dysfunction Hypotension Stress Response The stress just described response may be characterised as a adrenergic corticoid phase When the patient recovers the adrenergic corticoid phase changes to an anabolic phase Stress Response Adrenergic-Corticoid Phase ACTH and cortisol Catecolamines Salt and water retention Insulin and glucagon (via epinephrine) circulatory adjustment metabolic response if prolonged Aldosterone and ADH mobilises proteingluconeogenesis gluconeogenesis Cytokines confined to wound Stress Response Adrenergic - corticoid phase Remains until insult corrected Hypermetabolism-BMR increases 10-15% in elective operation 25% in long bone fracture 200% in 50% burn Stress Response Adrenergic - corticoid phase Altered Glucose Metab Normal/low insulin and insulin resistance persisting hyperglycaemia injured tissue uses glucose Stress Response ADRENERGIC - CORTICOID PHASE Altered protein metabolism Extensive muscle protein release extensive urine N loss reduced by feeding Altered fat metabolism Accelerated lipolysis via hormone sensitive lipase Ketosis blunted Stress Response ANABOLIC PHASE gluconeogenesis catecolamines aldosterone and ADH insulin and glucagon Salt and water loss protein anabolism cytokines reduction Elective Operations Adrenergic corticoid phase period of catabolism lasts 1-3 days Anabolic phase starts D3-D6 positive N balance protein synthesis recovery of lean mass Nutritional Support for Elective Operations Because the adrenergic-corticoid phase is short in elective, uncomplicated surgery – Fluid therapy with 5% dextrose is enough for up to 5-7 days Nutritional Support for Severe Stress The adrenergic-corticoid phase is prolonged in severe injury Malnourished patients Infected patients Nutritional therapy is needed Stress Responses The response is affected Malnutrition Age Gender Infection Consequences of Malnutrition Metabolic response needs increased energy expenditure If intake < expenditure - protein/fat mass lost Loss of 15% BW interacts with disease process to compromise immune response - sepsis, MOF poor wound healing edema due to albumin reduced mobility, respiratory muscle strength & vital capacity pneumonia altered GI function/breached mucosal barrier Normal Post Op Drip Energy provided as dextrose 1 L of D5W - 50g or 170 kcal Typical post op patient gets 500 kcal/d enough to stimulate pancreatic insulin not enough to support a severe stress reaction Need for nutritional support to match energy expenditure if stress is prolonged Metabolic Response to Trauma / Severe Surgical Stress Unfed trauma patients rapidly use their protein and fat stores resulting in increased susceptibility to effects of haemorrhage, operations and infection resulting in organ system failure, sepsis and death Malnourished patients are at greater risk Determinants of Host Responses to Surgical Stress Age Fat mass increase with age Loss of muscle mass Loss of strength with immobility Decreased sensitivity to perturbations Decreased effectiveness to maintain homeostasis Determinants of Host Responses to Surgical Stress Gender Lean body mass less in females N loss more pronounced in muscular males Determinants of Host Responses to Surgical Stress Invasive Infection May complicate any operation / injury Results in increases metabolic rate fever, hyperventilation, etc Nutritional depletion synergystic Metabolic Response to Trauma / Severe Surgical Stress Cuthbertson described in 1930 the Ebb or shock phase Flow phase Cuthbertson Ebb Flow not described Modern unresuscitated adrenergic-corticoid anabolic Metabolic Response to Trauma / Severe Surgical Stress Cuthbertson Ebb or shock phase 12-24 hours BP, CO, Temp, O2 consumption due to haemorrhage, hypoperfusion, lactic acidosis Flow phase (adrenergic - corticoid) hypermetabolism, CO, Urine N loss, altered glucose, tissue catabolism similar to elective surgery but greater Questions ? A 64 year old 70 kg man comes for a gastrectomy. Prior to operation he had been eating poorly for 4 weeks. On the 7th POD after Billroth II gastrectomy he was drowsy and febrile. There was green fluid coming from his drain. Describe the metabolic responses this patient has. What are the confounding factors that may complicate his recovery? Coming soon to a Lecture Theatre near you – Nutritional Support In a severely injured patient the priorities are: - resuscitation - wound care Nutritional support usually after 48 hrs The next lecture will cover all aspects of nutrition Questions