Metabolism in the Surgical patient

1. Surgical Metabolism
Hamzeh Halawani M.D.
American University of Beirut

2. Overview
• Metabolism during fasting
• Metabolism after injury
• Basic biochemical aspects of Protein,
Carbohydrate and fat absorption and
utilization.
• Nutrition in surgical patients
• Enteral feeding
• Parental feeding

3. Body Fuel Reserve in a 70 kg man

4. Metabolism during Fasting
• Basal metabolic needs at rest and fasting is
approximately 22-25 Kcal/kg/d
• Main source of fuel during short term fasting
( <5 days) are muscle protein and fat
• Liver Glycogen (75-100g) stores are depleted
within hours (<16h)
• 200-250 g of Glycogen are stored within
skeletal muscle, cardiac and smooth muscle
cells. Lack glucose-6-phosphatase

5. Obligate
glycotic cells
Precursors for hepatic glucneogenesis

7. • Significant amount of protein must be
degraded daily (75 g/d for 70kg adult)
• Urinary nitrogen excretion increase to 30g or
more each day (normally 7-10 g)
• In prolonged starvation, systemic proteolysis
is reduced to 20 g/d and urinary nitrogen
excretion to 2-5 g/d due to adaptation of vital
organs to use ketone bodies as primary fuel.

8. Prolonged Starvation
• The kidney participate in gluconeogensis by the
use of glutamine and glutamate. Account for one
half of systemic glucose production.
• Energy requirement for basal enzymatic and
muscular function like gluconeogensis, neural
transmission, and cardiac output are met by
mobilization of TG from adipose tissue. (160g)
• By reduction of insulin level, and by increase in
glucagon and catecholamine.
• Ketone bodies spare glucose utilization by
inhibiting pyruvate dehydrogenase

10. Metabolism after Injury
• Directly proportional to the severity of insult.
• Mediated by sympathetic activation and
catecholamine release.

13. Lipid metabolism after injury
• Adipose stores are the predominant energy
source during critical illness and after injury,
50-80%.
• Influenced by various hormones
(catecholamines, ACTH, Thyroid, cortisol,
glucagon, GH, and reduction in insulin level)
• Oxidation of 1 g of fat = 9 Kcal

14. Lipid absorption
• Pancreatic lipase + phospholipase hydrolyze
TG into FFA + monoglyceride.
Long
Chain TG
MCT + SCT ->
Portal circulation
by albumin carrier

15. Lipolysis and Fatty Acid Oxidation

16. • FFA absorbed by cells conjugate with acyl-CoA
within cytoplasm.
• Carnitine shuttle for transport of FFA from outer
mitochondrial membrane to inner.
• MCT bypass Carnitine shuttle
• Within the mitochondria, fatty acyl-CoA
undergoes Beta Oxidation which produce acetyl-
CoA.
• Each acetyl-CoA enters TCA cycle undergoes
oxidation to produce 12 ATP.

18. • Excess acetyl – CoA serves a precursor for
ketogenesis.
• Unlike glucose metabolism, FA requires less O2
and produce less CO2.
• Respiratory Quotient (RQ) = CO2 produced/O2
• RQ = 0.7  greater FA oxidation
• RQ = 1  greater carbohydrate oxidation,
overfeeding. Resulting in glucosuria,
thermogenesis, and conversion to fat. Along with
elevation of Co2 production which may affect
respiratory function.
• RQ = 0.85  equal amount

19. Ketogenesis
• Carbohydrate depletion slows the entry of Acetyl-CoA
into TCA cycle secondary to depleted TCA
intermediates and enzyme activity.
• Increased lipolysis and reduced systemic carbohydrate
availability during starvation divert excess acetyl – CoA
toward Ketogenesis.
• A number of extra hepatic tissue, but not the liver
utilizes ketones for fuel
• Ketosis represents a state in which hepatic ketone
production exceeds extrahepatic ketone utilization.
• The rate of ketogenesis appears to be inversely related
to the severity of injury.

20. Carbohydrate Metabolism
• Glucose and Galactose are primarily absorbed by
energy dependant active transporter coupled to
sodium pump.
• Fructose absorption by concentration dependant
facilitated diffusion.
• Neither Galactose nor Fructose evokes insulin.
• The oxidation of 1g Carb = 4 Kcal
• In starvation, glucose production occurs at the expense
of protein stores.
• Injury and sever infection s induce a peripheral glucose
intolerance ( gluconeogenesis, reduced pyruvate
dehydrogenase, catecholamines, glucagon,
glucocoricoid ,,,etc )

21. Glucose Transport and Signaling
• Two classes of membrane glucose transporter
• GLUT : facilitated diffusion (down
concentration gradient)
• SGLT : Sodium glucose secondary active
transporter (against concentration gradient)

22. GLUT 2 is bidrectional, important for rapid export of glucose from gluconeogensis
GLUT 4 is insulin responsive: adipose tissue and skeletal muscles
GLUT 5 : fructose transporter

23. SGLT
• Active transporter against concentration
• SGLT 1: brush borders of small intestine
enterocytes
• SGLT 1 and 2 : glucose reabsorption at
proximal renal tubules

24. Protein and Amino Acid Metabolism
• 1 g of protein = 4 Kcal
• Every 6 g of protein yields 1 g of nitrogen
• After injury it provides substrates for
gluconeogensis and for acute phase protein
synthesis
• Skeletal muscles are preferentially depleted

26. Nutrition in the Surgical Patient
• Goal:
– Prevent or reverse the catabolic effect of disease
or injury
– Improvement in clinical outcome and restoration
of function
– Core temperature maintenance
– Enough energy for tissue repair

27. Estimation of Energy Requirement
• Harris-Benedict equation, 1918
• Estimation of Basal Energy Expenditure (BEE)
– Men = 66.4730 + (13.7516 x weight in kg) + (5.0033 x
height in cm) – (6.7550 x age in years)
– Women = 655.0955 + (9.5634 x weight in kg) +
(1.8496 x height in cm) – (4.6756 x age in years)
• After trauma or sepsis, adding non protein
calories is needed to meet the demand, 1.2-2 X
than the calculated BEE.
• Provision of 30 Kcal/kg/d is adequate in most
post surgical patients

29. Overfeeding
• Result from overestimation, for ex. Using
actual weight for fluid overload and obese
critically ill patient.
• Use pre-injury weight or adjusted lean body
weight.
• Indirect calorimetry can be used as well.
• Overfeeding increase oxygen consumption,
increase Co2 production, prolong the need for
ventilation, fatty liver, suppress WBC,
hyperglycemia and increased risk for
infections

30. Enteral Nutrition
• Lower cost
• No vascular access complication
• Reduce intestinal atrophy
• Reduce infectious complication

31. Enteral Formulas
• Low-Residue isotonic formula
– 1Kcal/mL , no fiber, leave minimum residue ,
standard formula for intact GI tract. Contains
electrolytes, carbohydrates, fat, protein, vitamins.
• Isotonic formula with fiber
– Soluble and insoluble fiber, soy based. Delay
intestinal transit time, reduce the incident of
diarrhea
• Immune enhancing formula
– Enhanced with glutamine, arginine, branched
chain AA, Omega 3- FA, nucleotides and beta –
carotene. High cost

32. Enteral Formulas, cont
• Calorie Dense formula
– Greater calorie value for same volume. Higher
osmolality, 1.5-2 Kcal/mL
• High Protein formula
– Non protein calorie:nitrogen 80:1 and 120:1
• Elemental formula
– Predigested nutrient , small peptides protein
– Easy for absorpion, lack vitamins and trace
elements. Used in malabsorption, gut impairment
and pancreatitis . High cost

33. Enteral Formulas, cont
• Renal- failure formula
– Lower concentration of K, P, Mg. contains
essential AA. 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 are branched chain AA (reduce
aromatic AA)

34. Disadvantages:
-Clogging and kinking
-Inadvertent displacement or removal of the tube
-Nasopharyngeal complications
-Short term , if more than 30 days percutaneous access should be done

35. Most common indication for PEG : impaired swallowing, proximal obstruction, major facial
trauma, passive gastric decompression..etc
Relative C/I : ascites, coagulopathy, gastric varices, gastric cancer.
Complications of PEG (up to 3%of patients) : wound infection, Necrotizing fascitis, peritonitis,
aspiration, leak, dislodgment, bowel perforation, enteric fistula , and bleeding.

36. Relative Contraindication : sever edema of intestinal wall, radiation
enteritis, IBD, ascites, sever immunodeficiency , and bowl ischemia
Pneumatosis intestinalis and small bowl necrosis are infrequent but
significant problems in patients receiving jejunal tube feeding, contributing
factors: hyperosmolarity of enteral solution, bacterial overgrowth,
fermentation, and accumulation of metabolic breakdown productions.
Common pathophysiology: bowel distention and reduction in bowl wall
perfusion.
Risk factors: cardiogenic and circulatory shock , vasopressors use, DM ,
COPD

37. Parental Nutrition
• Provides dextrose, AA, Fat, vitamins, trace
elements via large diameter vein.
• PPN is used for short duration < 2 weeks
• Monitor for electrolytes , volume, acid-base,
septic complication and weight.
• Intravenous access method needed:
– 16-gauge percutaneous catheter
– Tunneled port
– PICC

38. Indications

39. Complication of TPN
• Technical complications
– Sepsis , secondary to contamination of the central line.
Less likely due to contamination of TPN solution.
– Pneumothorax, hyemothorax, hydrothorax, subclavian
artery injury, thoracic duct injury, cardiac arrhythmia, air
embolism, catheter embolism and cardiac perforation.
• Metabolic complications
– Hyperglycemia, overfeeding,hepatic steatosis, chlestasis
and formation of GBS. Raise in LFT
• Intestinal atrophy
– Lack of enteral feeding cause intestinal atrophy,
diminished villous height, bacterial overgrowth, reduced
lymphoid tissue size, decrease IgA.

40. Nutrition induced inflammatory
modulation
• Mode of nutritional supplement influence
stress induced inflammatory response
• Parental feeding demonstrate heightened
response to pro inflamottory stimuli such as
endotoxin.
• Enteral nutrients may act as agonists for
endogenous neuroendocrine anti-
inflammatory pathway.

41. Any questions ?