Previous Next

Complications

Depression of Serum Folate Concentration

Tennant and colleagues[181] reported acute depression of serum folate concentrations in patients fed preoperatively with parenteral nutrition solutions. Their studies seem to indicate that the amino acid component of the solutions may be at least partially responsible for the fall in serum folate level, as suggested by Krebs and coworkers.[182] Tennant and colleagues[183] cautioned that further investigation may be indicated in patients receiving postoperative parenteral nutrition after anesthesia exposure to nitrous oxide, which may alter serum methionine and folate concentrations.[184] [185]


TABLE 77-7 -- Potential catheter complications of total parenteral nutrition
Infectious Complications Technical Complications
Insertion-site contamination Pneumothorax
  Contamination during insertion Tension pneumothorax
  Contamination during routine care Hemothorax
Catheter contamination Hydrothorax
  Improper technique of catheter insertion Hydromediastinum
  Administration of blood through feeding catheter Cardiac tamponade
  Use of catheter to measure central venous pressure Brachial plexus injury
  Use of catheter to obtain blood samples Horner's syndrome
  Use of catheter to administer medications Phrenic nerve paralysis
  Contaminated solution during preparation of additives Carotid artery injury
  Contaminated tubing through connections Subclavian artery injury
  Three-way stopcocks in system Subclavian hematoma
Secondary contamination Thrombosis, subclavian vein or superior vena cava
  Septicemia, bacterial or fungal Arteriovenous fistula
  Septic emboli Venobronchial fistula
  Osteomyelitis of clavicle Air embolism
  Septic arthritis Catheter embolism
  Endocarditis Thromboembolism

Catheter misplacement

Cardiac perforation

Endocarditis

Thoracic duct laceration

Innominate or subclavian vein laceration
From Dudrick SJ: Parenteral nutrition. In Dudrick SJ, Baue AE, Eiseman B, et al (eds): Manual of Preoperative and Postoperative Care. Philadelphia, WB Saunders, 1983, p 86.

The most common errors are underestimating phosphate needs (40 to 100 mEq/day) and overestimating calcium requirements (3 to 8 mEq/day). The most common abnormality in patients receiving TPN is a mild-to-moderate elevation in results of liver function tests. This may be a result of fatty infiltration of the liver that occurs with excess glucose administration. In a patient who begins with normal indexes of liver function, twofold elevations in serum glutamic oxaloacetate (SGOT) and serum glutamic pyruvate transaminase (SGPT) levels and a progressive mild rise in alkaline phosphatase level are not uncommon. If an increase in bilirubin occurs and SGOT and SGPT levels continue to rise, a cause other than the TPN infusion should be sought. Unfortunately, maintenance or restoration of lean body mass in hypercatabolic patients can be difficult because of the inevitable increased breakdown of muscle protein supplying amino acids for gluconeogenesis. An attempt to induce anabolism by infusing large amounts of carbohydrate increases the metabolic rate, the conversion of carbohydrate into fat, and the rate of DVCO2 ; it does not promote increased protein synthesis, and it results in self-defeating hypermetabolism.[186] Hypercatabolic patients must be given adequate amino acids to achieve nitrogen equilibrium. Patients with persistent negative nitrogen balance should have the ratio of nitrogen to calories increased without increasing nonprotein calories beyond their use capabilities.[153] [186] [187]


2912

TABLE 77-8 -- Potential metabolic complications of total parenteral nutrition
Complications Etiology
Glucose Metabolism
Hyperglycemic glycosuria, osmotic diuresis, nonketotic hyperosmolar dehydration, and coma Excessive total dose or rate of infusion of dextrose; inadequate endogenous insulin; glucocorticoids; sepsis
Ketoacidosis of diabetes mellitus Inadequate endogenous insulin response; inadequate exogenous insulin therapy
Postinfusion (rebound) hypoglycemia Persistence of endogenous insulin production secondary to prolonged stimulation of islet cells by high-carbohydrate infusion
Respiratory acidosis with hypercarbia Excessive dextrose administration
Amino Acid Metabolism
Hyperchloremic metabolic acidosis Excessive chloride and monohydrochloride content of crystalline amino acid solutions
Serum amino acid imbalance Unphysiologic amino acid profile of the nutrient solution; different amino acid use with various disorders
Hyperammonemia Excessive ammonia in protein hydrolysate solutions: deficiencies of arginine, ornithine, aspartic acid, and/or glutamic acid in crystalline amino acid solutions; primary hepatic disorder
Prerenal azotemia Excessive total dose or rate of infusion of protein hydrolysate or amino acid solutions
Lipid Metabolism
Hyperlipidemia Excessive total dose or rate of administration of fat emulsion
Hyperamylasemia Lipoid pancreatitis
Hyperbilirubinemia Excessive dose or rate of administration of fat emulsion
Hypoxia Interstitial lipoid pneumonitis with alveolar-capillary block
Serum deficiencies of phospholipid linoleic and arachidonic acids; serum elevations of 5.8.11-eicosatrienoic acid Inadequate essential fatty acid administration; inadequate vitamin E administration
Calcium and Phosphorus Metabolism
Hypophosphatemia Decreased erythrocyte 2,3-diphosphoglycerate Inadequate phosphorus administration; redistribution of serum phosphorus into cells and/or bone
Increased affinity of hemoglobin for oxygen
Aberrations of erythrocyte intermediary metabolites
Hypocalcemia Inadequate calcium administration; reciprocal response to phosphorus repletion without simultaneous calcium infusion; hypoalbuminemia
Hypercalcemia Excessive calcium administration with or without high doses of albumin; excessive vitamin D administration
Vitamin D deficiency; hypervitaminosis D Inadequate or excessive vitamin D administration
Miscellaneous Complications
Hypokalemia Inadequate potassium intake relative to increased requirements for protein anabolism: diuresis
Hyperkalemia Excessive potassium administration, especially in metabolic acidosis, renal decompensation
Hypomagnesemia Inadequate magnesium administration relative to increased requirements for protein anabolism and glucose metabolism
Hypermagnesemia Excessive magnesium administration; renal decompensation
Anemia Iron deficiency; folic acid deficiency; vitamin B12 deficiency; copper deficiency; other deficiencies
Bleeding Vitamin K deficiency
Hypervitaminosis A Excessive vitamin A administration
Elevations in SGOT, SGPT, and serum alkaline phosphatase Enzyme induction caused by amino acid imbalance; excessive glycogen and/or fat deposition in the liver
Cholestatic hepatitis Decreased water content of bile; amino acid and/or fatty acid imbalance
From Dudrick SJ: Parenteral nutrition. In Dudrick SJ, Baue AE, Eiseman B, et al (eds): Manual of Preoperative and Postoperative Care. Philadelphia, WB Saunders, 1983, p 86.


2913
Respiratory Complications of Nutrition Support and Relative Starvation

In 1976, Doekel and coworkers[188] reported that normal volunteers fed 400 kcal/day of carbohydrate orally for 10 days experienced a decrease in ventilatory response to hypoxia, a measure of respiratory drive (see Fig. 77-10 ). Weissman and associates[189] observed that 7 days of infusion of 400 kcal/day of 5% dextrose resulted in a reduced mean inspiratory flow, another measure of neuromuscular drive.

Arora and Rochester[190] found that chronically ill, nutritionally depleted patients had significant reductions in respiratory muscle strength, as measured by maximal inspiratory and expiratory pressures; endurance, as measured by maximal voluntary ventilation; and vital capacity. High-protein nutritional support improves respiratory muscle strength and ventilatory drive.[152] [191]

Excessive glucose administration leads to an increase in minute ventilation that is proportional to an increase in DVCO2 caused by oxidation of carbohydrate (RQ = 1) or lipogenesis (RQ = 8).[192] Infusion of glucose as a sole energy source can lead to increased respiratory work because ventilation increases in response to added CO2 .

In summary, Weismann and Askanazi[192] recommended that nonprotein calories be administered as 50% carbohydrate and 50% lipid. They recommended this balanced supply of energy sources for patients with poor respiratory function and for those who are septic and hypermetabolic. This approach leads to less DVCO2 than occurs with methods supplying 100% of the nonprotein calories as glucose. The combined substrate technique causes less increase in energy expenditure and norepinephrine secretion in the septic and hypermetabolic patient[193] and prevents essential fatty acid deficiency.[150] Later work suggests that using glucose-based formula but reducing the total calories to that which the patient is actually consuming reduces the complications of overfeeding and hyperlipidemia. Essential fatty acids must be replaced with 500 mL of lipid three times per week. Hyperglycemia should be aggressively treated with insulin to improve outcomes. Long-term propofol infusions provide significant lipid calories, and nutritional support must be adjusted.[194]

Hypoglycemia

The most common cause of hypoglycemia is a slowing or a cessation of infusion. The increased secretion of insulin that accompanies TPN when suddenly unopposed by exogenous glucose results in hypoglycemia. For this reason, TPN solutions should never be abruptly discontinued in the operating room without being replaced with a concentrated glucose solution, such as 10% dextrose solution.

Complications of Intravenous Fat Emulsions

Extended TPN using lipid emulsions may injure the bilirubin-transfer mechanism in the liver and lead to progressive cholestasis. This is usually a benign, readily reversible state, but continued TPN without a change in the constituents can cause liver injury with hepatocyte necrosis and periportal fibrous changes. In a study by Allardyce,[195] patients with a high lipid intake had significant elevations of the serum bilirubin and alkaline phosphate levels at the completion of parenteral nutrition. Cholestatic jaundice is associated with administration of lipid emulsion in a dose of 3 g/kg/day in patients fed intravenously for more than 3 weeks. The condition improves, with a return of liver function to normal, when the dose of lipid emulsion is reduced or when intravenous feeding is discontinued. Lipid emulsion may be limited to 1 g/kg/day, and liver function may be evaluated twice weekly. It appears that the dose of lipid emulsion should be reduced if a progressive rise in serum alkaline phosphatase level occurs. Early use of intravenous fat emulsion in trauma patients is associated with increased septic complications compared with glucose-based intravenous feedings.[162] [196]

Disorders of Water Metabolism

Bistrian and colleagues[134] pointed out that the tendency to retain water is characteristic of many of the disease states for which TPN is employed, including postoperative states, shock resuscitation, congestive heart failure, oliguric renal failure, hepatic insufficiency, and severe malnutrition. The antinatriuresis that results from the hyperinsulinemia seen with glucose-based TPN can lead to serious water overload in a brief period. This can be minimized or avoided by matching total fluid losses plus 5 dL, by limiting sodium intakes to less than 40 mEq of sodium beyond loss replacement, and by limiting insulin response by the use of a mixed-fuel system.

Enteral Nutrition

Many patients who are candidates for enteral feeding are at increased risk for aspiration because of mechanical ventilatory support or altered consciousness. Trauma patients with pulmonary injuries such as contusions, aspiration at the scene, hemopneumothorax, or acute respiratory distress syndrome (ARDS) are at even greater risk of pulmonary aspiration of gastric contents. Advances in the field of tube feeding have made early enteral nutrition a valuable tool in initiating nutrition therapy through a feeding tube in the proximal jejunum. A feeding algorithm was developed by the American Society for Parenteral and Enteral Nutrition to assist in selecting the type and route of administration of nutritional support ( Fig. 77-22 ). Enteral nutrition may possess several advantages over parenteral nutrition for postoperative or post-trauma patients. In patients with a functional gastrointestinal tract, enteral feeding assists in maintaining a thicker gut barrier by nourishing the enterocytes at the local level, which protects the host from bacterial translocation from gut lumen to the blood. Jejunal tube feeding has advantages over gastric tube feeding, including faster metabolic recovery, less vomiting, and less risk of regurgitation and aspiration.

Enteral nutrition can be started at a rate of 10 to 40 mL/hour and increased by 20 mL every 8 hours to reach target rates over a period of 24 to 48 hours. Standard tube-feeding solutions provide 1 kcal/mL, whereas concentrated formulas provide 1.5 to 2 kcal/mL and contain a standard mix of vitamins and minerals that meet recommended daily allowance when 1700 to 2000 mL of solution are provided. Supplements such as glutathione, vitamin E, and β-carotene are important for providing food antioxidants. Additional supplements are needed


2914


Figure 77-22 Clinical decision algorithm governing assessments for route of nutrition support in adults. GI, gastrointestinal; PN, parenteral nutrition. (Data from Aspen Board of Directors: Clinical Pathways and Algorithms for Delivery of Parenteral and Enteral Nutrition Support in Adults. Silver Spring, MD, American Society for Parenteral and Enteral Nutrition, 1998.)

for preserving gut mucosa. Approximately 10% of the caloric requirements should be satisfied by so-called colonic food (i.e., prebiotics), and more than 10 g of fiber per day is recommended. Protein administration is prescribed at the same rate as with TPN: 1.5 to 2.0 g of protein/kg/day. Protein module is added to the formula to reach the protein goals.

Previous Next