Total parenteral nutrition and anesthesia: What are the anesthetist's responsibilities?

JULIANNE HENRY SHEA, CRNA, BSN Ann Arbor, Michigan

Increasingnumbers of patients are presentingfor surgery while receiving TPN therapy. Preoperativenutritional and metabolic assessment reveal valuable information that directs perioperative and immediate postoperative patient care. The infectious consequences may be lethal if TPN lines are violated duringsurgery.

The number of patients coming to the operating room who are receiving total parenteral nutrition (TPN) therapy is increasing rapidly. This has been a gradual, rather than an acute, change in therapy; therefore, most anesthetists have not found it necessary to address comprehensively the specific needs of these patients. TPN is being used perioperatively for several reasons: (1) nutritional deficits are identified earlier, (2) the prognosis following surgical stress is improved when the patient is in a protein anabolic state and (3) more seriously ill patients are requiring surgicial interventions. Certain aspects of preoperatively nutritional/metabolic status affect the perioperative care of the patient. Surgery alone causes a significant metabolic stress response. The anesthetist should review the patient's nutritional status preoperatively and should plan care accordingly.

Preoperative nutritional assessment Nutritionally compromised patients can be placed in one of three categories: (1) chronic nutritional depletion, such as cancer, (2) acute stress, such as trauma and (3) chronic depletion with acute stress, such as cancer and sepsis.1 The patient's nutritional status can be assessed by history, physical examination and objective measures. The type and length of any underlying illnesses prior to surgery indicate potential metabolic aberrations. Examples include hypothyroid and hyperthyroid conditions, cancers requiring immunosuppressive chemotherapy, alcoholism and drug addiction. The presence of fever increases metabolic requirements. In a physical exam, overall muscle bulk should be observed, as well as signs of muscle wasting. A history of rapid weight loss should also be noted. However, normal body weight or obesity are not always reflective of adequate nutritional status. A patient may suffer protein depletion malnutrition (Kwashiorkor) but will still have adequate fat stores. Objective measures of nutritional states include tests that reflect somatic (skeletal muscle) protein as well as visceral proteins (vital organs and their enzymes, serum proteins and immunoglobulins). These tests and normal values are listed in Table I. Anthropometrics include the triceps skin fold indicating fat reserve and mid-arm muscle circum-

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ference reflective of muscle mass and adipose tissue combined. The urinary excretion of creatinine is reduced in malnourished individuals because muscle protein is used for energy. The effects of edema, fluid shifts and acute phase reactions obscure interpretation of protein values once the acute stress of surgery occurs. 3 During the postoperative period, the serum transferrin levels are the most reliable guide to overall nutritional status. TPN may be instituted if the gastrointestinal tract cannot be used to supply nutritional needs. (Table II.) TPN consists of dextrose, lipid, protein, vitamins, minerals and trace elements. Hypertonic dextrose provides necessary calories economically, although the osmolarity of these solutions requires administration via the superior vena cava. Dextrose permits maximum utilization of amino acids and creates a hormonal milieu favoring anabolism by sustaining high insulin concentrations. 4 Lipid emulsions provide essential fatty acids. These emulsions are composed of oils suspended in egg yolk, phospholipids and glycerol. Proteins are supplied by solutions of crystalline amino acids. Deficient nitrogen replacement results in persistent depletion of lean body mass. Excessive nitrogen intake with inadequate caloric intake leads to the utilization of protein for energy. Hepatic deamination of excess amino acids Table I
Measurement of nutritional status Component tested Test weight/height ratio*

results in an elevated BUN, which does not reflect renal dysfunction. 5 Vitamin, mineral and trace element supplements conform to AMA recommendations. Complications The major complications encountered in patients receiving TPN therapy are catheter-related mechanical problems, infections and metabolic abnormalities. Catheter-related complications include pneumothorax, hemothorax, hydrothorax, puncture of the subclavian artery and brachial plexus damage.6 In a report by the Center for Disease Control, based on 2,078 cases from 31 institutions that practiced sound infection control, the septicemia rate averaged 7%. 7 In a study by Ryan and associates, when strict aseptic technique was used in catheter insertion and maintenance, catheter-related sepsis dropped to 3% compared to 20% when breaks in technique were observed. 8 Metabolic complications can be numerous and include excesses or deficiencies of almost any nutrients. (Table III.) Many patients receiving TPN, such as trauma victims and patients in the perioperative and postoperative period, will have impaired use of glucose. This decreased glucose utilization is thought to result from a blunting of endogenous insulin effectiveness because of ele-

Normal value

Severe depletion

Somatic protein

anthropometrics creatinine/height index serum albumin serum transferrin total lymphocytes skin testing

100% 3.5-5.0 g/dl 200-370 mg/dl 1800-2500/mm 3 10-15 mm

70% normal 2.5 g/dl 160 mg/dl 900/mm 3 5 mm induration

Visceral protein

*Normal values for weight/height ratio and creatinine/height index are listed in Appendix I.

Table II
Indications for TPN therapy Efficacy proven Fistulas Short bowel syndrome Burns Acute renal failure Efficacy putative Regional ileitis Acute pancreatitis Perioperative support Cancer therapy Hepatic failure Efficacy unknown

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vated levels of circulating catecholamines and a marked decrease in the insulin's capacity to suppress muscle proteolysis and, therefore, its failure to inhibit gluconeogenesis. 9 An excessive dose of glucose may result in hyperglycemia, glycosuria, osmotic diuresis and, possibly, hyperosmolar nonketotic coma. A more recently recognized group of complications are related to carbohydrate excess. When dextrose is infused at a level greater than 2.5 mg/kg/min, the excess glucose reaching the liver is synthesized to fat. Lipogenesis produces large amounts of CO2. The total body respiratory quotient (CO 2 production to 02 consumption ratio) may increase as high as 1.1 to 1.4 (normal is 0.8). High CO 2 levels may lead to respiratory failure or difficulty in discontinuing mechanical ventilation. 10 Preoperative evaluation The anesthetist should determine preoperatively whether the patient is malnourished and anticipate potential anesthetic problems. Specifically, the forced vital capacity (FVC) should be assessed in malnourished patients to indicate whether the patient can recover from mechanical ventilation and expectorate secretions effectively. An FVC less than 50 ml/kg in the absence of lung disease indicates respiratory muscle wasting. Hypoalbuminemia reflects a decreased oncotic pressure which alters fluid replacement therapy. Hypoalbuminemia also indicates a depletion of visceral proteins such as surfactant and pseudocholinesterase. 1 If the patient is receiving TPN through a central line, the chest x-ray must be reviewed. Abnormalities in glucose homeostasis should Table III
Metabolic complications of TPN

Glucose
Hyperosmolar nonketotic coma Hypoglycemia
Amino acids Hyperammonemia Azotemia Hyperchloremic acidosis Calcium-phosphorus Hypercalcemia Hypophosphatemia

be identified preoperatively. Surgical stress promotes glucose intolerance; therefore, proper control should be ascertained preoperatively. 12 Hypercarbia, excessive minute ventilation and a history of mechanical ventilator dependency are evidence of excessive CO 2 production associated with TPN therapy.13 Hepatic function should be reviewed since patients receiving TPN may have elevated liver function tests indicating increased metabolic work in the liver. In patients without pre-existing hepatic disease, the liver enzymes return to normal within one week of stopping TPN therapy. A prothrombin time should be checked preoperatively, since many pharmacies include heparin in TPN to prevent catheter-clotting. During surgery TPN may be continued at the preoperative administration rate. Stress induced glucose intolerance may develop and should be closely monitored. TPN also may be weaned 12 to 24 hours prior to surgery, taking care to avoid rebound hypoglycemia associated with rapid weaning or abrupt cessation. 14 In restarting TPN during the recovery phase, when dextrose utilization is high, hypophosphatemia can be a serious complication. Hypophosphatemia probably results from an extravascular to intravascular shift of phosphate. A serum phosphate of less than 1 mg/dl leads to paresthesias, muscle weakness and confusion. Also associated with hypophosphatemia is a reduction in 2, 3 diphosphoglyceric acid (DPG) which results in an increased affinity of hemoglobin for oxygen making less oxygen available to peripheral tissues.15 Some investigators speculate that maintenance of intraoperative lipid therapy during anesthesia may affect the MAC of inhalational agents. Halogenated agents are lipid soluble. Lipids such as intralipid may act as a sink, altering halogenated anesthetic absorption.', Perioperative management When a patient arrives for surgery with a TPN infusion, the TPN line should be maintained as a closed system throughout the procedure. Stopcocks should not be added, blood should not be withdrawn, and drugs should not be administered via this line. Blood should not be given with TPN since dextrose hemolyzes blood. The TPN administration rate should remain continuous throughout the procedure. TPN should not be used as a fluid bolus, and the total amount of TPN administered perioperatively should be included in fluid totals at the end of the procedure. Blood glucose and serum K should be checked every one to two hours, depending on

Essential fatty acid deficiency Liver abnormalities

Trace element deficiencies

Vitamin toxicity (vitamins A, D)

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initial results. Hypophosphatemia, hypermagnesemia and hypocalcemia increase sensitivity to nondepolarizing muscle relaxants; therefore, dosages should be adjusted accordingly. Glucose intolerance is thought to be associated more frequently with halothane than with the other inhalational
agents. Extubation is predicted in part by the pa-

tient's preoperative nutritional assessment indicating respiratory reserve as well as by the length and extent of the surgical procedure. 17

Summary Increasing numbers of patients are presenting for surgery while receiving TPN therapy. Preoperative nutritional and metabolic assesment reveal valuable information that directs perioperative and immediate postoperative management. The consequences indeed may be lethal if TPN lines are violated during surgery. The patient receiving TPN therapy is truly a challenge to the anesthetist.

Appendix I
Ideal weight and urinary creatinine for height* Men Total mg creatinine/ 24 hours (medium frame) 1288 1325 1359 1386 1426 1467 1513 1555 1596 1642 1691 1739 1785 1831 1891 Women Total mg creatinine/ 24 hours (medium frame) 830 851 875 900 925 949 977 1006 1044 1076 1109 1141 1174 1206

Height 5' 5' 5' 5' 5' 5' 5' 5' 2" 3" 4" 5" 6" 7" 8" 9"

Small frame 128-134 130-136 132-138 134-140 136-142 138-145 140-148 142-151 144-154 146-157 149-160 152-164 155-168 158-172 162-176

Medium frame 131-141 133-143 135-145 137-148 139-151 142-154 145-157 148-160 151-163 154-166 157-170 160-174 164-178 167-182 171-187

Large frame 138-150 140-153 142-156 144-160 146-164 149-168 152-172 155-176 158-180 161-184 164-188 168-192 172-197 176-202 181-207

Height 4' 10" 4' 11" 5' 0" 5' 1" 5' 2" 5' 3" 5' 4" 5' 5" 5' 6" 5' 7" 5' 8" 5' 9" 5' 10" 5' 11"

Small frame 102-111 103-113 104-115 106-118 108-121 111-124 114-127 117-130 120-133 123-136 126-139 129-142 132-145 135-148

Medium frame 109-121 111-123 113-126 115-129 118-132 121-135 124-138 127-141 130-144 133-147 136-150 139-153 142-156 145-159

Large frame 118-131 120-134 122-137 125-140 128-143 131-147 134-151 137-155 140-159 143-163 146-167 149-170 152-173 155-176

5' 10" 5' 11" 6' 0" 6' 1" 6' 2" 6' 3" 6' 4"

*Weights at ages 25-59 based on lowest mortality. Source of basic data: 1979 Build Study, Society of Actuaries and Association of Life Insurance Medical Directors of America, 1980. Reproduced with permission.

REFERENCES
(1) Gladen RN. 1983. Nutrition and the surgical patient. The anesthesiologists' responsibility. ASA 34th Annual Refresher Course Lectures, Atlanta, pp. 110-116. (2) Allardyce DB. 1978. Total parenteral nutrition. The Canadian Journal of Surgery. 21:6 pp. 495-500. (3) Meakens JL, Pietsch JB, Bubenick 0., et al. 1977. Delayed hypersensitivity: Indicator of acquired failure of defenses in sepsis and trauma. Ann. of Surgery. 186:2341. (4) Allardyce DB. 1978. Total parenteral nutrition. The Canadian Journal of Surgery. 21:6, pp. 495-500. (5) Gladen RN. 1983. Nutrition and the surgical patient. The anesthesiologists' responsibility. ASA 34th Annual Refresher Course Lectures, Atlanta, pp. 110-116. (6) Fleming RC, McGill DB, Hoffman HN and Nelson RA. 1976. Total parenteral nutrition. Mayo Clinic Proceedings. 51, pp. 187-200. (7) Goldman DA, Maki DG. 1973. Infection control in total parenteral nutrition. JAMA. 223:1360-1364. (8) Ryan JA, Abel RM, Abbott WM, et al. 1973. Septicemia and total parenteral nutrition: Distinguishing catheter-related from other septic episodes. N. Eng J Med. 290:757-761. (9) Fleming RC, McGill DB, Hoffman HN, Nelson RA. 1976. Total parenteral nutrition. Mayo Clinic Proceedings. 51, pp. 187-200. (10) Gladen RN. 1983. Nutrition and the surgical patient. The anesthesiologists' responsibility. ASA 34th Annual Refresher Course Lectures, Atlanta, pp. 110-116. (11) Gladen RN. 1983. Nutrition and the surgical patient. The anesthesiologists' responsibility. ASA 34th Annual Refresher Course Lectures, Atlanta, pp. 110-116. (12) Dudrick SJ, MacFadyen BV, Van Buren CT, et al. 1972. Parenteral hyperalimentation: Metabolic problems and solutions. Ann Surg. 176:259-264 (13) Gladen RN. 1983. Nutrition and the surgical patient. The anesthesiologists' responsibility. ASA 34th Annual Refresher Course Lectures, Atlanta, pp. 110-116.

Journal of the American Association of Nurse Anesthetists

(14) Gladen RN. 1983. Nutrition and the surgical patient. The anesthesiologists' responsibility. ASA 34th Annual Refresher Course Lectures. Atlanta, 110-116. (15) Fleming RC, McGill DB, Hoffman HN, and Nelson RA. 1976. Total parenteral nutrition. Mayo Clinic Proceedings. 51, pp. 187-200.

(16) Rudo M. Personal communication. (17) Gladen RN. 1985. Nutrition and the surgical patient. The anesthesiologists' responsibility. ASA 34th Annual Refresher Course Lectures, Atlanta, pp 110-116.

AUTHOR
Julianne Henry Shea, CRNA, BSN is a 1978 graduate of the University of Michigan School of Nursing. After working several years in various intensive care units in Detroit and Boston, she entered the University of Michigan Program of Nurse Anesthesia. Shortly after her graduation in 1982, she moved to London, England, obtained a British Nursing license and worked as an anesthetic research nurse on the research team directed by Professor J. P. Payne of the Royal College of Surgeons of England. Currently, she is the assistant chief nurse anesthetist at the University of Michigan Hospitals, Ann Arbor, Michigan.

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