1. Enteral nutrition is preferred over parenteral nutrition for surgical patients who can tolerate enteral feeding as it decreases complications and helps maintain gut function. 2. There are various enteral formula options depending on a patient's needs including standard, immune-enhancing, high calorie/protein, and organ-specific formulas. 3. Enteral access can be achieved through nasogastric/nasojejunal tubes, percutaneous endoscopic gastrostomy, or in some cases parenteral nutrition is required if enteral feeding is not possible. The goal is to meet energy and protein demands to support healing without overfeeding.

1. C
SURGICAL
METABOLISM
Trix M. Asuncion MD.
General Surgery

2. C

3. C

4. C

5. C

6. Majority of surgical patients:
• Well nourished/ Healthy
• Uncomplicated major surgical procedure
• Has sufficient fuel reserve
• Can withstand brief period of catabolic insult and
starvation of 7 days
• Postoperatively:
• Can resume normal oral intake
• Supplemental diet is not needed

7. Surgical patients that needs
nutritional support
• To shorten the postoperative recovery phase and
minimize the number of complications
• Chronically debilitated from their disease or malnutrition.
• Suffered severe trauma, sepsis or surgical complications.

8. Initial hour after Insult:
• Metabolic expenditure of energy
• Urinary nitrogen wasting
• Reprioritization of energy
• Preserve vital organ function
• Support tissue repair

9. DURING FASTING
•Normal healthy adults require ~22-25
kcal/kg per day
•Requirement can be as high as
40kcal/kg in severe stress or burns

10. Provide FUEL BEE (1800kcal)

11. Short fasting (<5 days)
Healthy adult
Muscle protein fats
Storage of carbs in form of glycogen:
300-400g carbs (glycogen)
75-100g stored in the liver
200-250g stored (SM, cardiac, smooth muscle)
Hepatic glycogen will sustain at only 16 hours of
fasting
Most abundant
source energy

12. Healthy adult energy reserve

13. During fasting
•70kg uses 180g glucose/day
Support the metabolism of
1. neurons
2. Leukocytes
3. Erythrocytes
4. Renal medulla

14. What promotes glycogenolysis and
gluconeogenesis?
Glycogenolysis Gluconeogenesis
• Glucagon Glucagon
• Norepinephrine Epinephrine
• Angiotensin II Cortisol
• Vasopressin
Liver and Muscle LIVER

15. Precursor of hepatic
gluconeogenesis
• Lactate
• Glycerol
• Amino acids
• Alanine
• Glutamine
• Glycolysis Skeletal muscle Lactate + Pyruvate
Erythrocytes & leukocytes
Cori Cycle (Liver)
ATP &
NADPH

16. Cori cycle

17. Short-term Fasting
• Lactate - not enough
• Daily protein degradation – 75g/day for a 70kg adult
• Provide AA substrate for gluconeogenesis
• Proteolysis during starvation:
• Decrease insulin
• Increase cortisol
• Increase urinary nitrogen excretion (N- 7 to 10/day up to 30g/day)

18. Prolonged starvation
• Systemic proteolysis
• 20g/day
• Urinary excretion stabilizes:
• 2 to 5 g/day
• ADOPTATION:
• Myocardium
• Renal cortex
• Skeletal muscle
• Brain
• after 2 days-gradually become principal fuel source by
24 days
Uses:
Ketone bodies
Fuel source

19. Prolonged starvation
• Kidney – participate in gluconeogenesis
• Uses Glutamine and Glutamate
• ½ of systemic glucose production

20. Prolonged starvation
Breakdown of
protein and stored
fats
GLUCOSE FUEL

21. Prolonged starvation
• Lipid – in adipose tissue
• Provide 40% or more caloric expenditure
• Energy requirement for basal enzymatic and
muscular function are met
• 160g FFA and glycerol per day
• FFA release is stimulated by
• Insulin level
• Glucagon
• Catecholamine

22. Metabolism after INJURY
• Injury or infection
• neuroendocrine
• immunologic response
Breakdown of
protein and stored
fats
GLUCOSE FUEL

23. Metabolism after INJURY

24. LIPID METABOLISM AFTER INJURY
• Adipose tissue
• Triglycerides
• 50 – 80% energy source after an injury or during critical
illness
• Fat mobilization ( Lipolysis); response to
• Catecholamine
• ACTH
• Thyroid hormone
• Cortisol
• Growth hormone (GH)
• Decrease insulin
Oxidation produce
1g Fat = 9 kcal energy

25. Absorption of
Dietary TAGs
Major source
Hydrolyze TAG – FFA+
Monoglyceride
FFA,
Monoglyceride
absorb
Resynthesize
Esterification
LCT = 12C or>
Shorter FA Directly enter to
portal circulation-liver
carried by albumin

26. LIPID metabolism
• Hepatocytes:
• Use FA as fuel source during stress
• Synthesize phospholipids or triglyceride (Fed state)
• Systemic tissue: (Muscle, Heart)
• Use Chylomicron and triglyceride as fuel
• Lipolysis is Mediated by TNF( during stress and injury)

27. Period of energy DEMAND
• Lipolysis and FA oxidation
• Mediate by hormonal influences such as:
• Catecholamine
• ACTH
• Thyroid hormones
• Growth hormone
• Glucagon

28. Fat
mobilizatio
n in
adipose
tissue
Hydrolyze TAG=
FFA+gycerol
ALBUMIN + FFA to tissues

29. Carnitine
shuttle

30. • LCTs (Long-chain Triglyceride)
• Need carnitine shuttle to be transported to mitochondria
• MCTs (Medium-chain triglyceride)
• 6-12 carbons
• Readily cross the mitochondria
• Exclusive use associated with higher metabolic demands, toxicity
and essential fatty acid deficiency

31. • TCA (Tricarboxylic Acid cycle)
• 1 acetyl-CoA molecule =
• 12 ATP
• Carbon dioxide (CO2)
• Water (H2O)
• Excess Acetyl-CoA
• Precursor of ketogenesis

32. KETOGENESIS
• Carbohydrate depletion Acetyl-CoA
TCA cycle
lipolysis
carbohydrate
KETOSIS- Hepatic ketone production exceeds
extrahepatic utilization
HAPATIC KETOGENESIS
Ketogenesis rate = inversely related
severity of the injury

33. CARBOHYDRATE METABOLISM
• Carbohydrate digestion Small Intestine
Complex carbs
pancreatic enzyme
Intestinal enzyme
Disaccharides
1. Sucrase
2. lactase
3. Maltase
Intestinal Brush border
Simple Hexose
1. Glucose
2. Galactose
3. fructose
Readily absorb
Intestinal mucosa
Na-pump active
transport
Facilitated
diffusion

34. CARBOHYDRATE METABOLISM
• Refers to the utilization of glucose
• Oxidation of 1g CARBS= 4 kcal
• Parenteral = 3.4kcal/g of dextrose
Starvation:
Glucose production Expense Protein(Skeletal Muscle)
Primary Goal : Minimize muscle wasting
Glucose 50g/d will reduce ketosis
Sepsis & severe trauma exogenous glucose
administration = never suppress AA degradation to
gluconeogenesis

35. Glucose
metabolism
Cells

36. Excess glucose (overfeeding)
carbon dioxide production
immune response
Infection risk
Glucosuria
Thermogenesis
lipogenesis
Hyperglycemia
Mimics DM

37. Injury and severe infection
• Hypermetabolic state
• Peripheral glucose intolerance
• Gluconeogenesis – liver (Lactate & pyruvate)
• Increase splanchnic glucose production
• 50-60% in sepsis
• 50-100% in burn
• Hepatic gluconeogenesis (alanine &Glutamine)
• Nervous system
• Wounds
• erythrocytes
Cannot be suppress by
giving exogenous
glucose
Provide fuel

38. GLUCOSE TRANSPORT &
SIGNALING
• Hydrophobic cell membrane – impermeable to
hydrophilic glucose molecules
• 2 classes of glucose membrane transporter
1. GLUT (glucose transporter)
• Facilitated diffusion transport of glucose down a concentration
gradient
2. SGLT (Na glucose transporter)
• transports glucose molecules against concentration gradient by
active transport

40. GLUT SGLT
GLUT 1
– transporter in human
erythrocytes
- Part of the endothelium in the
BBB (BRAIN)
SGLT 1
- Prevalent on brush borders of the small
intestine enterocytes
- Primarily mediates the active uptake of
luminal glucose
- Enhances gut retention of water through
osmotic absorption
GLUT 2
- major glucose transporter in
Hepatocytes
- Important in glucose uptake and
and release
GLUT 3
- Neuronal tissues
SGLT 1 and 2
- Associated with glucose reabsorption at
proximal renal tubules
GLUT 4
- Primary glucose transporter of
insulin-sensitive tissues
- Implications in insulin resistant
DM
GLUT 5
- Fructose transporters
Adipose tissue, skeletal muscle &
cardiac muscle

41. PROTEIN & AA METABOLISM
• Average protein intake: 80-120 g/day
• 1 g protein = 4 kcal energy
• 6 g protein = 1 g nitrogen
• Urinary nitrogen excretion
• Excess of 30g/g = 1.5 lean body mass lost
• Injured individual who does not received nutrition for 10
days  15% lean body mass lost
• Excessive lean body mass lost of 25-30% DEATH

42. PROTEIN & AA METABOLISM
• After injury
• Mediated by glucocorticoid
• Increase urinary nitrogen excretion and negative
nitrogen balance (CHON Catabolism)
• Protein catabolism- gluconeogenesis
• Mainly in skeletal muscle (Preserve Liver & Kidney)
• Excretion of intracellular elements
• Creatinine
• Sulfur
• Phosphorus
• Potassium
• magnesium
Rapid Utilization of this elements
Indicative of HEALING during
recovery
After injury- peak 7Days
Persist – 3to 7 weeks
Response to:
1. Tissue hypoxia
2. Acidosis
3. Insulin resistance
4. Elevated glucocorticoid

43. Effect of injury severity on nitrogen
wasting

44. C
NUTRITION IN
SURGICAL
PATIENT

45. C
WHAT IS YOUR
GOAL?

46. Prevent or reverse the catabolic effects
of disease or injury

47. GOALS
(1) meet the energy requirements for metabolism
(2) meet the substrate requirements for protein
synthesis

48. First goal: Estimation of
energy requirements
1. Physical examination
• Muscle
• Adipose tissue
• Organ dysfunction
• Skin
• Hair
• Neuromuscular function
2. Anthropometric data
• Weight change
• Skinfold thickness
• Arm circumference muscle area
3. Biochemical
determination
• Creatinine
• Albumin level
• Prealbumin
• TLC
• Transferrin

49. SURGICAL NUTRITION
• Estimate of energy requirements:
basal energy expenditure (BEE) using the Harris-
Benedict equation
Estimate: 30kcal/kg/day will adequately meet the requirements in most
post surgical patient

50. 2nd goal: meet substrate
requirement for CHON synthesis
Nonprotein-calorie:nitrogen ratio = 150:1
Evidence= 80:1 to 100:1 benefit healing
Vitamins and minerals: ensure that adequate
replacement is available in diet or by
supplementation.
Essential fatty acid supplementation: patients with
depletion of adipose tissue

51. Overfeeding
• Result from overestimation of caloric needs
• Contribute to clinical deterioration
1. Increase in oxygen consumption
2. Increase carbon dioxide production
3. Prolonged ventilatory support
4. Fatty liver
5. Hyperglycemia
6. Decrease immune response
7. Increase infection risk

52. ENTERAL NUTRITION
• Rationale:
1. low cost
2. Decrease intestinal mucosal atrophy
3. Less infection (Vascular access complication)
4. Consequence of GI tract disuse
• IgA production
• Cytokine production
• Bacterial overgrowth
• Altered mucosal defense
Enteral over Parenteral
feeding

53. Indication for Enteral feeding
• Hemodynamically stable
• Functional GI tract
• Early enteral feeding (24-48 hours) ICU stay
• Preoperative patient with protein caloric
malnutrition
10 days partial starvation: in patient undergoing
elective surgery (IV dextrose only)

54. Initiation of feeding
• Patient must have adequate urine output
• Presence of bowel sound and flatus or passage of stool are
not absolute.
• < 200ml in 4-6hours gastric residual
• Low output enterocutaneous fistula (<500ml/day)
• Enteral feeding: short bowel syndrome, clinical
malabsorption( necessary calories, essential minerals &
vitamins= parenteral)
• Trophic feeding= no additional benefits
Gastroparesis= feeding should be distal to pylorus

55. Feeding formula consideration
1. GI-tolerance promoting
2. Anti-inflammatory
3. Immune modulating
4. Organ supportive
5. Standard enteral nutrition
Each physician must use his or her own clinical
judgment = what best formula for the patients need

56. Factors that influence the
choice of formula
1. Extent of organ dysfunction
2. Nutrients needed to restore optimal
function and healing
3. Cost
There are no conclusive data to
recommend one category of product
over the other

57. Immunonutrients
• Glutamine- Nonessential AA
• Most abundant
• 2/3 of the free intracellular AA pool
• 75% within skeletal muscle
• Synthesize in SM and Lung
• Major fuel in enterocytes, immunocytes
• Precursor of glutathione
During stress= peripheral glutamine are rapidly depleted and
AA use primarily for fuel source toward the visceral organs and
tumor

58. •Arginine
• Nonessential AA
• Immunoenhancing property
• Wound-healing benefits
• Led net nitrogen retention and protein synthesis
Omega-3 PUFA, Omega-6 PUFA
• Reduces proinflammatory response from prostaglandin
production

59. ENTERAL FORMULAS
LOW RESIDUE ISOTONIC
• Provide a caloric density of 1 kcal/mL
• Approx. 1500-1800 ml
• Nonprotein-calorie: nitrogen ratio: 150:1
• Standard or first-line formulas for stable patients
with intact gastrointestinal tract

60. ISOTONIC W/ FIBER
• Reduce diarrhea (delay intestinal transit time)
• Contain soluble and insoluble fiber (most often soy-
based
IMMUNE-ENHANCING
• Contains: glutamine, omega-3 fatty acids, Arginine and
nucleotides
No additional benefit for critically ill except for burn
and trauma patients that are already stabilize

61. CALORIE-DENSE
• Calorie-dense (greater caloric value for the same
volume)
• Suitable for patient requiring fluid restriction
• Provide 1.5-2.0 kcal/ml, suitable for patients
requiring fluid restriction
• Have higher osmolality than standard formulas and
are suitable for intragastric feedings

62. HIGH PROTEIN
• Available in isotonic and non-isotonic mixtures and
proposed for critically ill or trauma patients with high
protein requirements
• 80-120:1 nonprotein-calorie:nitrogen ratio

63. ELEMENTAL
• Contain predigested nutrients and provide proteins
in the form of small peptides, limited complex
carbohydrates, minimal fat content
• Easily absorbed
• Trace elements limits its long-term use
• Used mostly in patient with malabsorption, gut
impairment, and pancreatitis

64. RENAL-FAILURE FORMULA
Lower concentration of K,P, Mg
Contains essential amino acids
Lack vitamins and trace elements
PULMONARY FAILURE FORMULA
Fat content increased to 50% or total calories to reduce
CO2 production
HEPATIC FAILURE FORMULA
50% of proteins and branched chain amino acids (reduce
aromatic amino acids)
Goal is to reduce aromatic AA levels

65. OPTIONS

66. OPTIONS FOR ENTERAL
FEEDING ACCESS
A. Nasogastric tube
Short-term use only
aspiration risks
nasopharyngeal trauma
frequent dislodgment

67. B. Nasoduodenal/nasojejunal
tube
Short-term use
lower aspiration risks in jejunum
placement challenges (radiographic
assistance often necessary)

68. C. PERCUTANEOUS ENDOSCOPIC
GASTROSTOMY (PEG)
Endoscopy skills required
may be used for gastric decompression or bolus
bolus feeds
aspiration risks
can last 12–24 months
slightly higher complication rates with
placement and site leaks

71. D. SURGICAL GASTROSTOMY
Requires general anesthesia and small
laparotomy
procedure may allow placement of extended
duodenal/jejunal feeding ports
laparoscopic placement possible

72. E.FLUOROSCOPIC GASTROSTOMY
Blind placement using needle and T-
prongs to anchor to stomach;
can thread smaller catheter through
gastrostomy into duodenum/jejunum
under fluoroscopy

73. F. PEG-JEJUNAL TUBE
two-stage procedure with PEG
placement, followed by fluoroscopic
conversion with jejunal feeding tube
through PEG

74. G. DIRECT PERCUTANEOUS ENDOSCOPIC
JEJUNOSTOMY (DPEJ)
Direct endoscopic tube placement with
enteroscope
placement challenges
greater injury risks

75. H. SURGICAL JEJUNOSTOMY
Commonly carried out during
laparotomy
general anesthesia

76. I. FLUOROSCOPIC
JEJUNOSTOMY
–
Difficult approach with injury risks
not commonly done

77. PARENTERAL NUTRITION
• Continuous infusion of a hyperosmolar solution
containing carbohydrates, proteins, fat and other
necessary nutrients through an indwelling catheter
inserted into the superior vena cava
• To obtain the maximum benefit, the calorie:protein
ratio must be adequate (at least 100 to 150 kcal/g
nitrogen) and both carbohydrates and proteins must
be infused simultaneously

78. PARENTERAL NUTRITION
• Rationale:
(1)Malnutrition
(2)Sepsis
(3)Seriously ill patients for
whom GIT feeding is
not possible
(4)For supplemental
nutrition when there’s
inadequate oral intake

79. CENTRAL
PARENTERAL
NUTRITION
PERIPHERAL
PARENTERAL
NUTRITION
Central vein Peripheral vein
Dextrose content of the
solution is high (15% to
25%)
Reduced levels of dextrose (5%
to 10%) and protein (3%)
macronutrients and
micronutrients
Amount of Macronutrients
and micronutrients.
Appropriate for severe
malnutrition
*used when central routes not
available
*only used for less than 2 wks

80. COMPLICATIONS OF
PARENTERAL NUTRITION
Sepsis
Hyperglycemia
Overfeeding
Hepatic steatosis
Cholestasis and gallstones
Intestinal atrophy and decrease immunity

81. THANK
YOU !!!

82. “Students, you do not
study to pass the test. You
study to prepare for the
day when you are the only
thing between a patient
and the grave”
Mark Ried