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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
Byong Wook Lee, [email protected] [email protected]
InflammatoryInflammatory ResponseResponseInflammatoryInflammatory ResponseResponse
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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
visceral tissue• Extracellular hormonal millieu, proinflammatory cytok
ines• Ubiquitin-dependent proteolytic pathway upregulated b
y intracellular oxidative intermediates and antioxidants• Greater release of glutamine and alanine than normal c
oncentration of muscle• Glutamine; major energy source for lymphoytes, fibrob
lasts, and GI tract
Metabolism after Injury Metabolism after Injury – Protein Metabolism– Protein Metabolism
Metabolism after Injury Metabolism after Injury – Protein Metabolism– Protein Metabolism
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Ubiquitin-ATP dependent ProteolysisUbiquitin-ATP dependent ProteolysisUbiquitin-ATP dependent ProteolysisUbiquitin-ATP dependent Proteolysis
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Severity of Injury and ProteolysisSeverity of Injury and ProteolysisSeverity of Injury and ProteolysisSeverity of Injury and Proteolysis
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Nutrition in the Surgical PatientsNutrition in the Surgical PatientsNutrition in the Surgical PatientsNutrition in the Surgical Patients
• Obligatory increases in energy expenditure and nitrogen excretion
• Post-injury metabolic environment precluding efficient oxidation of fat and ketone production
continued erosion of protein pools
critical organ failure
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Nutritional Supprot of the Surgical PatientNutritional Supprot of the Surgical Patient- Protein- Protein
Nutritional Supprot of the Surgical PatientNutritional Supprot of the Surgical Patient- Protein- Protein
• Requirement
– Average normal requirement; 0.8 g/Kg/d
– Essential amino acids
– On parenteral nutrition, 200-250 nitrogen/Kg/d
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Nutritional Support of the Surgical Patient Nutritional Support of the Surgical Patient – Calories– Calories
Nutritional Support of the Surgical Patient Nutritional Support of the Surgical Patient – Calories– Calories
• Caloric Sources– Amino acids 15% (BCAA 6-7%)– Fat 70-75%– Carbohydraes 10-15%
• Calorie-Nitrogen Ratio
– Normal ratio for protein synthesis; 100-150:1– Changes in different disease states;
100:1 for sepsis, 400:1 for uremia
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Nutritional Support of the Surgical Patient Nutritional Support of the Surgical Patient – Energy Requirement– Energy Requirement
Nutritional Support of the Surgical Patient Nutritional Support of the Surgical Patient – Energy Requirement– Energy Requirement
• BEE
=66.5 + 13.7 x weight (Kg) + 5.0 x height (cm) – 6.8 x age (yr.) [male]
= 655.1 + 9.56 x wt + 1.85 x ht – 4.68 x age [female]
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Nutritional Support of the Surgical Patient Nutritional Support of the Surgical Patient - Carbohydrates- Carbohydrates
Nutritional Support of the Surgical Patient Nutritional Support of the Surgical Patient - Carbohydrates- Carbohydrates
• Supplement calories without elevating glucose concentration
• Lipid supplementation; replacing glucose as energy source
• lipid not efficient in severe sepsis
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Nutritional Support of the Surgical Patient Nutritional Support of the Surgical Patient - Fat- Fat
Nutritional Support of the Surgical Patient Nutritional Support of the Surgical Patient - Fat- Fat
• Caroric source• Source of essential fatty acids providing precursors of PG’s
– Modifying inflammatory and immunologic response• 25% of nonprotein calories as fat; optimal for hepatic protein s
ynthesis• Fat overload syndrome
< 2 g/Kg/d for adults < 4 g/Kg/d for infants
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Nutritional AssessmentNutritional AssessmentNutritional AssessmentNutritional Assessment
• 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
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Enterocyte-specific Nutritional SubstratesEnterocyte-specific Nutritional Substrates- Glutamine- Glutamine
Enterocyte-specific Nutritional SubstratesEnterocyte-specific Nutritional Substrates- Glutamine- Glutamine
• Conditionally essential amino acid
• 40% of available glutamine taken up by gut from general circulation
• Addition of 2% glutamine to parenteral nutrition maintains jejunal or ileal mucosal thickness, protein content and DNA
• Prevention or healing of chemotherapeutic or radiation toxicity
• Regrowth after massive small bowel resection
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Enterocyte-specific Nutrients Enterocyte-specific Nutrients – Short Chain Fatty Acids– Short Chain Fatty Acids
Enterocyte-specific Nutrients Enterocyte-specific Nutrients – Short Chain Fatty Acids– Short Chain Fatty Acids
• Acetoacetate (10%), propionic acid (50%), butyrate (80%)
• Produced by fermentation of soluble pectin by colonic bacteria
• Disruption of colonic mucosa in deficient state
• BHBA
– wall thickening and increased protein content of ileum and colon
– 70% of energy supply to colonic mucosa
– Stimulation of ketogenesis, increased ATP generation, lipolysis, absorption of sodium and potassium
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Principles of Eneral FeedingPrinciples of Eneral FeedingPrinciples of Eneral FeedingPrinciples of Eneral Feeding
• Stmach;principal defense against an enteral osmotic load
• Duodenum; calcium,iron and other metal absorption
• Small bowel: principal area for nutreint absorption
• Terminal ileum; enterohepaic circulation
• Bile and pancreatic juice; fat and protein absorption
• Immunologic functions of the gut• largest immunoogic organ in the body; GALT, secretory Ig’s
• Secretion of mucin
• Gut mucosal barrier function
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Practical Enteral FeedingPractical Enteral FeedingPractical Enteral FeedingPractical Enteral Feeding
• 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
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Parenteral NutritionParenteral Nutrition- Peripheral Hyperalimentation- Peripheral Hyperalimentation
Parenteral NutritionParenteral Nutrition- Peripheral Hyperalimentation- Peripheral Hyperalimentation
• Without protocol
• Lipid system;
10-20% of caloric need as fat emulsion
+ 5% dextrose and amino acids
• Hypocaloric amino acids and 5% dextrose or glycerol solution Dextrose free amino acids by allowing utiliz
ation of endogenous fat secondary to low plasma insulin level
Minimize nitrogen breakdown for limited periods of time
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Parenteral NutritionParenteral Nutrition- Central Approach- Central Approach
Parenteral NutritionParenteral Nutrition- Central Approach- Central Approach
• Silastic or Teflon-coated catheters
• Percutaneous or open
• Temporal or permanent
• Enforced protocol for TPN
• Nutritional requirements
– 250 mg nitrogen/Kg/d
– 35 Kcal/Kg/d
– 20-25% of nonprotein calories as fat
– Adequate vitamin and trace minerals
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Parenteral Nutrition Parenteral Nutrition - Indications- Indications
Parenteral Nutrition Parenteral Nutrition - Indications- Indications
• Primary Therapy
– Efficacy shownGI-cutaneous fistulaRenal failureShort bowel syndromeAcute burnsHepatic Failures
– Efficacy not shownCrohn’s diseaseAnorexia nervosa
• Supportive therapy
– Efficacy shownAcute radiation enteritisAcute chemotherapy toxici
tyProlonged ileusWeight loss preliminary to
major surgery
– Efficacy not shownBefore cardiac surgeryProlonged respiratory supp
ortLarge wound losses
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Complications of Parenteral NutritionComplications of Parenteral Nutrition- Technical- Technical
Complications of Parenteral NutritionComplications of Parenteral Nutrition- Technical- Technical
• Placement complications
– Pneumothorax
– Arterial lacerations
– Hemothorax
– Mediastinal hematoma
– Nerve injury
• Late complications
– Erosion of catheter
– Subclavian thrombosis
– Septic thrombosis
– Sympathetic effusion
– Thoracic duct injury
– Air embolism
– Hydrothorax
– Catheter embolism
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Complications of Parenteral Nutrition Complications of Parenteral Nutrition - Metabolic Complications- Metabolic Complications
Complications of Parenteral Nutrition Complications of Parenteral Nutrition - Metabolic Complications- Metabolic Complications
• Plasma electrolyte abnormalities
• Trace mineral deficiency
– zinc, copper, chromium, selenium
• Essential fatty acid deficiency
• Disorders of glucose metabolism
– Hypoglycemia
– Hyperglycemia
– Diabetic patient; hyperosmolar nonketotic coma
– Liver function derangements
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Parenteral Nutrition Order FormParenteral Nutrition Order FormParenteral Nutrition Order FormParenteral Nutrition Order Form
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Complications of Parenteral NutritionComplications of Parenteral Nutrition – Septic Complications – Septic Complications
Complications of Parenteral NutritionComplications of Parenteral Nutrition – Septic Complications – Septic Complications
• Catheter Infection1. Absence of proocol2. Degree of colonization of the pericatheter skin; > 103
3. G(+) organism from remote site seeding the fibrin sleeve along catheter; vs G(-) organism4. Candida from the gut
• Management of patient with suspected catheter sepsis
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Prevention of Catheter ComplicationsPrevention of Catheter ComplicationsPrevention of Catheter ComplicationsPrevention of Catheter Complications
• Catheter Placement
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• Nutritional Support teams and Protocols
Nutritional ProtocolNutritional ProtocolNutritional ProtocolNutritional Protocol
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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
• Mean catheter life; 7 years
• Overnight PN
• Septic complications
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Nutritional PharmacologyNutritional PharmacologyNutritional PharmacologyNutritional Pharmacology
• Nutritional support to change either the milieu or the pathophysiology of a disease process to affect outcome
Arginine Glutamine Nucleotides Omega 3-fatty acids Ketone bodies
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