Metabolic Changes and Nutritional Management of Surgical Patients

1. Metabolic Changes and Nutritional Management of Surgical Patients James Taclin C. Banez, MD, FPSGS, FPCS

2. 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

3. Surgical Patients that Needs Nutritional Support • To shorten the postoperative recovery phase and minimize the number of complications: • Chronically debilitated from their diseases or malnutrition. • Suffered severe trauma, sepsis or surgical complications

4. Metabolic Changes in Surgical Patients • Metabolic events brought about by STIMULI: • Injury • Starvation • Metabolic response is directed to restore: • Homeostasis • Repair

5. HYPOGLYCEMIA – is primary stimulus Hormonal Changes: increase cortisol, catecholamines, glucagon, growth hormones Primary gluconeogenic precursors by the liver & kidney: a. lactate b. glycerol c. amino acid (alanine & glutamine) Metabolic Response to Starvation

6. Proteolysis increase due to increase CORTISOL ------> inc. urinary nitrogen first 4 days of starvation (8-12g/day = 6.25g of muscle/g of nitrogen).

7. Protein catabolism for gluconeogenesis primarily comes from SKELETAL muscle, but in pure starvation other organs are involved • In liver. CHON loss is selective; spare enzymes for gluconeogenesis and lipolysis. • In pancreas and GIT, enzymes for digestion and protein for regeneration of epithelium is involved -> PARADOXICAL FOOD INTOLERANCE

8. Rapid proteolysis of body CHON cannot proceed at 75 g/day for long, or else patient will die immediately RANDLE EFFECT. • decrease urinary excretion of nitrogen 2 – 4 gm/day due to keto-adaptation of the brain • decrease protein degeneration and major source of energy is FAT (90%)

9. Metabolism of Injured Patient PHASES: • Catabolic phase(Ebb, Adrenergic-Corticoid): • immediately following surgery or trauma • characterized w/ hyperglycemia, increase secretion of urinary nitrogen beyond the level of starvation • caused by increase glucagon, glucocorticoid, catecholamines and decrease insulin • tries to restore circulatory volume and tissue perfusion

10. Metabolism of Injured Patient PHASES: • Early anabolic phase (flow, corticoid-withdrawal): • tissue perfusion has been restored, may last for days to months depending on: • severity of injury • previous health • medical intervention • sharp decline in nitrogen excretion • nitrogen balance is positive (4g/day) indicating synthesis of CHON and there is a rapid and progressive gain in weight and muscular strength

11. Metabolism of Injured Patient PHASES: • Late anabolic phase: • several months after injury • occurs once volume deficit have been restored • slower re-accumulation of CHON • re-accumulation of body fat

12. Metabolism of Injured Patient Carbohydrate Metabolism in Injured Patient: Hyperglycemia = proportional to the severity of injury • Importance: • Homeostatic significance • Ready source of energy to the brain • Adequate delivery

13. Metabolism of Injured Patient Carbohydrate Metabolism: Hyperglycemia: • Caused by: • Increased catecholamine (primarily), cortisol, glucagon, GH, vasopressin, angiotensin II, somatostatin and decrease insulin. • Gluconeogenesis in liver and kidney and impaired peripheral uptake of glucose

14. Metabolism of Injured Patient Carbohydrate Metabolism: Hyperglycemia: • Insulin resistance: • During the Ebb phase there is reduction in beta cell sensitivity to glucose due to Catecholamine, somatostatin and reduced pancreatic blood flow • Resistance to exogenous administration on insulin in both EBB and early FLOW phases • In middle and late Flow phase, beta cell sensitivity return to normal and it’s level is higher, but hyperglycemia persist because of continuous gluconeogenesis

15. Metabolism of Injured Patient Carbohydrate Metabolism: • Glucose metabolism in wounded tissue: • Increase glucose uptake and lactate production because of anaerobic glycolysis due to local tissue hypoxia • (+) insulin insensitivity

16. Metabolism of Injured Patient Lipid metabolism: • primary source of energy • Best stimulus for hormone-sensitive lipase is CATECHOLAMINE • RANDLE EFFECT is not present

17. Metabolism of Injured Patient Protein Metabolism: • Nitrogen urine excretion 30-50g/day due to proteolysis; 20% utilized for energy (calories) the rest for gluconeogenesis by liver and kidney (cortisol, glucagon, catecholamine). • Primary source of protein is the skeletal muscle and the visceral organs are spared.

18. Metabolism of Injured Patient Protein Metabolism: • Ketoadaptation is inhibited ----> gluconeogenesis persist ---> proteolysis persist (INTERLEUKIN I). • The degree and duration (-) nitrogen balance is related to severity of injury. The net CHON catabolism depends on the age, sex andphysical condition of the patient (> in young, healthy and male) • (-) nitrogen balance can be reduced by high caloric nitrogen supplement

19. Traumatized Man

20. Injury of any type is associated with: • Immobilization • Starvation • Repair • the first two are associated with reduction in energy requirement. While the third is associated w/ increase energy requirement • The amount of energy produced in injured pt. is not optimum, to supply necessary energy for the repair due to: • reduced or absent nutritional intake • significant reduction of energy charge and ATP content during shock, hypoxia, sepsis, ischemia and wound - anaerobic metabolism

21. REE (Resting energy expenditure) by Harris and Benedict: (MEN)66.47 + 13.75 (W) + 5.0 (H) – 6.76 (A) = Kcal/day (Female)65.51 + 9.56 (W) + 1.85 (H) – 4.68 (A) = Kcal/day Fever: increase resting energy expenditure of approximately 7% for each degree of F of fever.

23. Nutritional Support Fundamental goal of nutritional support: • To meet the energy requirement for metabolic processes • To maintain a normal core body temperature • For tissue repair

24. Nutritional Support Indication of nutritional support: • Pre-morbid state • Age of the patient • Duration of starvation • Degree of the insult • Likelihood of resuming normal intake within finite period

25. Nutritional Support Determination of Lean Body Mass: • Displacement • Exchange of labeled ions (radioactive K+) • Neutron activation analysis • Total body counter • Nuclear magnetic resonance • Clinical history and physical examination • History of weight loss, anorexia and disease process that interfered with intake • Anthropometric data (skin fold thickness , arm circumference measurement, thenar eminence) • Biochemical determination (TP, albumin, globulin, liver profile, kidney function test)

26. Route of Administration: • ENTERAL ROUTE • PARENTERAL ROUTE (TPN) • COMBINATION

27. ENTERAL • Advantages: • more physiological (liver not bypassed) • lesser cardiac work • safer and more efficient • better tolerated by the patient • more economical

28. ENTERAL Route: • Naso-enteric tube feeding(blended food – Casseinates and whole protein formulas) • Naso-esophageal or NGT / NJT. • Gastrostomy tube (blended food) • Stamm (sero-lined) – temporary • Glassman (mucous-lined) – permanent • Percutaneous endoscopic gastrostomy • Jejunostomy tube (elemental diet) • Roue-en-y - permanent • Witzel - permanent • Endoscopic

31. ENTERAL • Hyperosmolar solution are better tolerated by the stomach: • Gastric feeding – increase osmolality first then the volume • Small bowel – volume first is increase then osmolality • Precautions to be observe to prevent reflux/aspiration: • 30 degree angle • Conscious • Stop feeding at 11 pm • Use French 10 and after administration of food clean the tube • Prolonged used render the cardia incompetent and sometimes caused stricture

32. Complication of Enteral Feeding • Malposition of the catheter (pharynx/trachea): • Inadvertently moved • Reinsert ideally w/ fluoroscopic guidance • Aspiration due to: • Overloading • Supine position / unconscious • Change in gastric motility • Solute overloading --> diarrhea, dehydration, electrolyte imbalance (hypokalemia, hypomagnesemia), hyperglycemia (hyperosmolar, nonketotic coma) • Avoided by gradual increase in the osmolality of the fluid • Perforation (rare)

33. Parenteral Nutrition Components: • CHON: • Mixture of single amino acid of synthetic origin, largely produced from “intelligent bacteria” cultures • CHO: • Provides calories; hypertonic dextrose • Fat emulsion: • 10 or 20% emulsion of soy or safflower oil emulsions, usually emulsified and stabilized with egg phosphatides and lecithin

34. Parenteral Nutrition Indications: • Principal indication is found in seriously ill patients suffering from Malnutrition, Sepsis,severe surgical or accidentaltrauma when the use of the Gastrointestinal tract for feeding is not possible. • Can be supplemental in patients with inadequate oral intake

35. Parenteral Nutrition As Primary Therapy: • TPN influence the disease process: • GIT fistula • Renal failure (ATN) • Short Bowel Syndrome • Acute Burn (severe trauma) • Hepatic failure • With normal bowel length but with malabsorption syndrome due to SPRUE, enzymatic or pancreatic insufficiency, Ulcerative colitis, regional enteritis • Anorexia nervosa

36. Parenteral Nutrition As Supportive Therapy: • Nutritional support can be achieved but alteration in the disease process have not been established. • New born GIT anomalies (TIF, gastrochisis, omphalocele) • Alimentary tract obstruction (achalasia, stricture, carcinoma, pyloric obstruction) • Acute radiation enteritis • Acute chemotherapy toxicity • Prolonged ileus • Prolonged respiratory support • Large wound losses

39. Parenteral Nutrition Contraindication of TPN: • Lack of specific goal for severe metabolic management (inevitable dying). • Cardiovascular instability / severe metabolic derangement. • Feasible GIT feeding • Patient with good nutritional status • Infants with less than 3cm of small bowel • Irreversible decerebrate (dehumanized)

40. Route of TPN: Central hyperalimentation Subclavian vein Internal jugular vein Femoral vein Gauge 16, 8-12 inches radio-opaque catheter end at SVC Checked position w/ x-ray Parenteral Nutrition

41. Parenteral Nutrition Complication of TPN: • Technical complication: • Early: - related to catheter insertion • Pneumothorax • Arterial laceration • Hemothorax • Mediastinal hematoma • Nerve injury to the brachial plexus • Hydrothorax • Air embolism • Catheter embolism

42. Parenteral Nutrition Complication of TPN: • Technical complication: • Late: • Erosion of the catheter to the bronchus or right atrium • Thrombosis: • Upper arm swelling and pain at the base of the neck • Streptokinase / heparin ---> coumadin • Septic thrombosis: • Antibiotic therapy • Fogarty catheter embolectomy • Excision of the subclavian vein and superior venacava

43. Parenteral Nutrition Complication of TPN: • Metabolic complication: • Inadequate administration of certain nutrient • Trace metal deficiency: • Zinc deficiency: • perioral pustular rash • darkening of the skin creases • neuritis • Copper deficiency: • microcytic anemia

44. Parenteral Nutrition Complication of TPN: • Metabolic complication: • Inadequate administration of certain nutrient: • Essential Fatty Acid deficiency: • Dry flaky skin w/ small reddish papules and alopecia • Disorder of Glucose metabolism: • Hypoglycemia – unexpected slowing of the glucose infusion / excessive insulin administration

45. Parenteral Nutrition Complication of TPN: • Metabolic complication: • Disorder of Glucose metabolism: • Hyperglycemia – most dangerous metabolism complication in TPN • Due to rapid infusion (60 ml/hr the increase of 20ml/hr every 24-48 hrs) • DM (Hyperosmolar nonketotic coma) due to osmotic diuresis ---> dehydration, fever, obtundation and coma ---> death. • Tx: insulin 200 units/day and administration of large dextrose free hypo=osmolar solution (0.45% NSS w/ K+).

46. Parenteral Nutrition Complication of TPN: • Metabolic complication: • Liver function derangement: • Adnormalities in SGOT / SGPT / Alk. PO4 • Fatty infiltrate of liver ----> fat emulsion

47. Parenteral Nutrition Complication of TPN: • Septic complication: • Catheter infection: • most lethal complication of TPN • Bacterial / fungal (candida) • Site of entry of the organism ---> site of catheter • Symptom: - sudden spike of fever • Management: • Change TPN bottle, tubes and filter – culture / investigate for presence of pneumonia, UTI, wound infection, etc. • If fever persist after 8 hrs. ---> removed catheter and culture the tip of the tube.

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