외과적 영양 (外科的 營養)

Surgical Nutrition

인제대학교 부산백병원
일반외과 · 장기이식센터
이병욱
Department of General Surgery &
Organ Transplantation Center,
Inje University, Pusan Paik Hospital
Byong Wook Lee, M.D.
bwleemd@ijnc.inje.ac.kr potrac@thrunet.com
Inflammatory Response

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Metabolic Response to Injury

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Metabolic Response to Fasting
- Glucose homeostasis

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Metabolic Response to Fasting

60g

120g

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 Gluconeogenesis from 3 carbon presursors
- Cori (lactate) and Alanine Cycle (pyruvate)

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Gluconeogenesis from 3 Carbon precursors
- glutamine, pyruvate

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Metabolic Response to Starvation

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Fat metabolism during Starvation

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Metabolism after Injury

• Sustained activities of
macroendocrine hormones
• Immune cell activation

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Metabolism after Injury
- 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
– Substrate Metabolism

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Interorgan Flux of Nutrients after Injury

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 Metabolism after Injury
- 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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 Metabolism after Injury
- Lipid Metabolism 2

• 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
substrates
 Suppressed by increased uptake and oxidation of free fatty acids
 Suppressed by an associated counter regulatory hormone response
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 Metabolism after Injury
– Carbohydrate Metabolism

• A state of relative insulin resistance

• Net gluconeogenic response due to active control of glucagon with
permissive requirement for cortisol + Proinflammatory mediators
• Reduced glucose oxidation; mediator induced reduction of skeletal
muscle 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
glycogenolysis in response to insulin
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 Metabolism after Injury
– Protein Metabolism

• Net proteolysis
• Skeletal muscle depletion with relative preservation
of visceral tissue
• Extracellular hormonal millieu, proinflammatory
cytokines
• Ubiquitin-dependent proteolytic pathway
upregulated by intracellular oxidative intermediates
and antioxidants
• Greater release of glutamine and alanine than
normal concentration of muscle
• Glutamine; major energy source for lymphoytes,
fibroblasts, and GI tract
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Ubiquitin-ATP dependent Proteolysis

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Severity of Injury and Proteolysis

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 Nutrition 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 Patient
- 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
– 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
– 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
- 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
- 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
synthesis
• Fat overload syndrome
< 2 g/Kg/d for adults
< 4 g/Kg/d for infants

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 Nutritional 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 PNI

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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 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 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
complication rates in posttraumatic situation
– Prevention of bacteria and/or their products from
translocating 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 Substrates
- 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
– 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 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 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 Nutrition
- 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
utilization of endogenous fat secondary to
low plasma insulin level
 Minimize nitrogen breakdown for limited
periods of time
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 Parenteral Nutrition
- 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
- Indications

• Primary Therapy • Supportive therapy

– Efficacy shown – Efficacy shown
 GI-cutaneous fistula  Acute radiation enteritis
 Renal failure  Acute chemotherapy
 Short bowel syndrome toxicity
 Acute burns  Prolonged ileus
 Hepatic Failures  Weight loss preliminary to
– Efficacy not shown major surgery
 Crohn’s disease – Efficacy not shown
 Anorexia nervosa  Before cardiac surgery
 Prolonged respiratory
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support
 Large wound losses
 Complications of Parenteral Nutrition
- Technical

• Placement complications
– Pneumothorax – Sympathetic effusion
– Arterial lacerations – Thoracic duct injury
– Hemothorax – Air embolism
– Mediastinal hematoma – Hydrothorax
– Nerve injury – Catheter embolism

• Late complications
– Erosion of catheter
– Subclavian thrombosis
– Septic thrombosis POTraC 2000
 Complications of Parenteral Nutrition
- 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 Form

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 Complications of Parenteral Nutrition
– Septic Complications

• Catheter Infection
1. Absence of proocol
2. Degree of colonization of the pericatheter skin; > 103
3. G(+) organism from remote site seeding the fibrin
sleeve along catheter; vs G(-) organism
4. Candida from the gut

• Management of patient with suspected catheter sepsis

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Prevention of Catheter Complications

• Catheter Placement

• Nutritional Support teams and Protocols

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Nutritional Protocol

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 Parenteral 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 0-6 mo 6-12 mo School age Adolescent C/N
(g/Kg/d)
2.5-3.0 2.0-2.5 1.75 1.2 150:1

Newborn or Infant
Calories 10-20 Kg > 20 Kg
premature (~ 10Kg)
120 100 100 + 50 100 + 50 + 20
Fat ? 35% of calories (up to 3.5 g/Kg/d)
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Home Hyperalimentation

• Silastic catheters with long

subcutaneous tunnel
• Mean catheter life; 7 years
• Overnight PN
• Septic complications

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 Nutritional 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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