외외외 외외 외외외 외외 ( ( 외외외 외외 외외외 외외 ) ) Surgical Nutrition Surgical Nutrition 외외외외외 외외외외외 외외외외 · 외외외외외외 외 외 외 Department of General Surgery & Organ Transplantation Center, Inje University, Pusan Paik Hospital Byong Wook Lee, M.D. [email protected][email protected]
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외과적 영양 ( 外科的 營養 ) Surgical Nutrition 인제대학교 부산백병원 일반외과 · 장기이식센터 이 병 욱 Department of General Surgery & Organ Transplantation
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외과적 영양 외과적 영양 (( 外科的 營養外科的 營養 ))
Surgical NutritionSurgical Nutrition
외과적 영양 외과적 영양 (( 外科的 營養外科的 營養 ))
Surgical NutritionSurgical Nutrition
인제대학교 부산백병원일반외과 · 장기이식센터
이 병 욱Department of General Surgery &
Organ Transplantation Center, Inje University, Pusan Paik Hospital
Metabolic Response to InjuryMetabolic Response to InjuryMetabolic Response to InjuryMetabolic Response to Injury
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Metabolic Response to FastingMetabolic Response to Fasting- Glucose homeostasis- Glucose homeostasis
Metabolic Response to FastingMetabolic Response to Fasting- Glucose homeostasis- Glucose homeostasis
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Metabolic Response to FastingMetabolic Response to FastingMetabolic Response to FastingMetabolic Response to Fasting
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60g
120g
Gluconeogenesis from 3 carbon presursorsGluconeogenesis from 3 carbon presursors- Cori (lactate) and Alanine Cycle (pyruvate)- Cori (lactate) and Alanine Cycle (pyruvate)
Gluconeogenesis from 3 carbon presursorsGluconeogenesis from 3 carbon presursors- Cori (lactate) and Alanine Cycle (pyruvate)- Cori (lactate) and Alanine Cycle (pyruvate)
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Gluconeogenesis from 3 Carbon precursorsGluconeogenesis from 3 Carbon precursors- glutamine, pyruvate- glutamine, pyruvate
Gluconeogenesis from 3 Carbon precursorsGluconeogenesis from 3 Carbon precursors- glutamine, pyruvate- glutamine, pyruvate
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Metabolic Response to StarvationMetabolic Response to StarvationMetabolic Response to StarvationMetabolic Response to Starvation
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Fat metabolism during StarvationFat metabolism during StarvationFat metabolism during StarvationFat metabolism during Starvation
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Metabolism after InjuryMetabolism after InjuryMetabolism after InjuryMetabolism after Injury
• Sustained activities of macroendocrine hormones
• Immune cell activation
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Metabolism after InjuryMetabolism after Injury- Energy Balance- Energy Balance
Metabolism after InjuryMetabolism after Injury- Energy Balance- Energy Balance
• Increase in energy balance directly with severity of injury
• Increased activity of SNS
• energy required for ion pump action to maintain normal transmembrane concentration overcoming increased cell membrane sodium permeability
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Metabolism after Injury Metabolism after Injury – Substrate Metabolism– Substrate Metabolism
Metabolism after Injury Metabolism after Injury – Substrate Metabolism– Substrate Metabolism
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Interorgan Flux of Nutrients after InjuryInterorgan Flux of Nutrients after InjuryInterorgan Flux of Nutrients after InjuryInterorgan Flux of Nutrients after Injury
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Metabolism after InjuryMetabolism after Injury- Lipid Metabolism 1- Lipid Metabolism 1
Metabolism after InjuryMetabolism after Injury- Lipid Metabolism 1- Lipid Metabolism 1
• Free fatty acid; predominant energy source afer injury
• Increased lipolysis by catecholamine, and other stress hormones and reduction in insulin level
• Continuation of net lipolysis during flow phase; oxidation for cardiac and skeletal muscle energy source
• Fatty acid induced inhibition of glcolysis in moderate injury;
not in severe injury, hemorrhage, or sepsis (persistent glycolysis and net proteolysis) Lipoprotein lipase in endothelium Cytokine
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• High concentration of intracellular fatty acids and elevated concentration of glucagon inhibition of fatty acid synthesis
simulate transport of acyl CoA into mitochondria for oxidation and
ketogenesis in liver• Keotgenesis
variable and inversely correlated with severity of injury Decreased after major injury, severe shock and sepsis Suppressed by increases in levels of insulin and other energy substra
tes Suppressed by increased uptake and oxidation of free fatty acids Suppressed by an associated counter regulatory hormone response
Metabolism after InjuryMetabolism after Injury- Lipid Metabolism 2- Lipid Metabolism 2
Metabolism after InjuryMetabolism after Injury- Lipid Metabolism 2- Lipid Metabolism 2
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Metabolism after Injury Metabolism after Injury – Carbohydrate Metabolism– Carbohydrate Metabolism
Metabolism after Injury Metabolism after Injury – Carbohydrate Metabolism– Carbohydrate Metabolism
• A state of relative insulin resistance• Net gluconeogenic response due to active control of glucagon with permi
ssive requirement for cortisol + Proinflammatory mediators• Reduced glucose oxidation; mediator induced reduction of skeletal muscl
e pyruvate dehydrogenase activity shunting of 3-carbon skeleton to liver
• Increased hepatic gluconeogenesis Hyperglycemia energy source of nervous system, wound, RBC, WBC
• Wound; increase in glucose uptake associated with an increased in activity of
phosphoructokinase dereased insulin sensitivity and failed glucose uptake and glycogenol
ysis in response to insulin
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• Net proteolysis• Skeletal muscle depletion with relative preservation of
• Estimate changes in body nutritional composition to predict risk for surgery
• Evaluation of nutritional system; measurement of functional lean body mass (muscular, respiratory, cardiac, hepatic, renal, immunologic and host defense function)
• Prognostic Nutritional Index (PNI)
– = 158- 16.6 alb – 0.78 TSF – 0.20 TFN – 5.8 DH
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Bases of PNIBases of PNIBases of PNIBases of PNI
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Malnourished Patients at Risk Malnourished Patients at Risk Malnourished Patients at Risk Malnourished Patients at Risk
• Recent weight loss > 10% body weight and/or body weight 80-85% ideal body weight
• Serum albumin in a stable, hydrated patient < 3.0 g/dl
• Anergy to injected skin recall antigens
• True transferrin < 200 mg/dl
• History of functional impairment
• Significant deficits in hand dynamometry or muscle response to nerve stimulation
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Indication for Nutritional SupportIndication for Nutritional SupportIndication for Nutritional SupportIndication for Nutritional Support
• Premorbid state
• Nuritional status
• Age
• Duration of starvation
• Degree of anticipated insult
• Likelihood of resuming normal intake soon
• Weight loss of 15%
• Serum albumin level < 3.0 g/d
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Route of Administration- Enteral routeRoute of Administration- Enteral routeRoute of Administration- Enteral routeRoute of Administration- Enteral route
• More physiologic• Costs less• Protects and improves hepatic function• Mimics normal ingress of nutrients to liver• Maintains gut mucosal integrity• early gut feedings resulting in lower mortality and septic compl
ication rates in posttraumatic situation– Prevention of bacteria and/or their products from translocat
ing the gut mucosa releasig catecholamines and other counter regulatory stimuli, preventing hypercatabolism
– Increased substrate supply to the liver improved hepatic acute phase protein synthesis
• Goals of Nutritional Support Use the gut if possible Administer at least 20% of caloric and protein requirement by gut
• Smalllest possible nasgastric tube, tip at the duodenum• Constant infusion except at bed time, head up 30• For gastric feeding, first osmolality and then volume,
reversed for jejunal feeding• Complications
Malposition and/or aspiration Diarrhea, dehydration, hyperglycemia and ions Pneumaosis intestinalis with perforation Hyperosmolar nonketotic coma perforation
Parenteral Nutrition for Pediatric PatientsParenteral Nutrition for Pediatric PatientsParenteral Nutrition for Pediatric PatientsParenteral Nutrition for Pediatric Patients
• More rapid growth• High proportion of viscera with little fat or muscle• Incompletely developed enzyme system• Liable to heat loss
• Nutritional Requirements in Pediatric Patients
Protein
(g/Kg/d)
0-6 mo 6-12 mo School age Adolescent C/N
2.5-3.0 2.0-2.5 1.75 1.2 150:1
CaloriesNewborn or premature
Infant
(~ 10Kg)10-20 Kg > 20 Kg
120 100 100 + 50 100 + 50 + 20
Fat ? 35% of calories (up to 3.5 g/Kg/d)POTraC 2000POTraC 2000POTraC 2000POTraC 2000
Home HyperalimentationHome HyperalimentationHome HyperalimentationHome Hyperalimentation
• Silastic catheters with long subcutaneous tunnel