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C: TUBE FEEDINGS
Although oral consumption of nutrients is the easiest approach, this is inadequate in the sick surgical patient, and therefore tube feeding is necessary. Populations such as the major trauma patient, the hypercatabolic critically ill patient or a patient with known malnutrition are candidates. Small feeding tubes, once confirmed to be in proper position, are utilized. Constant infusion is better tolerated than bolus feeding. The initial route and strength (tonicity) of the feedings depend on the length of time the gut has not been used. Mucosal atrophy begins after several days of NPO status, and therefore the absorptive surface is diminished. In addition, deficiencies in mucosal enzymes, such as lactase, may alter the type of solution used initially.

A wide variety of tube feeding solutions are available, with nutrient mixes to meet needs in different clinical disease states. Most are somewhat hyperosmolar, and free water may need to be added to allow for gastrointestinal tolerance. Most also have a Calorie:Nitrogen ratio higher than 150:1. Several high protein solutions now available approach a 100: to 150:1 ratio. Protein supplement can be provided as protein powder to meet protein needs. Solutions are also available for the patient with organ dysfunction, in particular renal and hepatic failure. The rationales behind these nutrient mixes are identical to those described for parenteral feedings. Contraindications to enteral feeding are in most cases relative or temporary rather than absolute. Patients with short bowel, gastrointestinal obstruction, gastrointestinal bleeding, protracted vomiting and diarrhea, fistulas, ileus, or gastrointestinal ischemia will usually not tolerate enteral feeding.


Complications	Complications of Tube Feeding Treatment
Mechanical complications:
Nasopharyngeal irritation	Anesthetics topically
Sinusitis	Decongestants
Mucosal erosions, bleeding	Ice water lavage; remove or reposition tube
Aspiration	Discontinue tube feeding until airway is protected

Gastrointestinal complications:
Cramping, distention	Reduce rate; if patient is lactase deficient, use free solution
Vomiting, diarrhea	Reduce rate and concentration; change formula; give anti-diarrhea drugs

Metabolic complications:
Hyperosmolarity	Add more free water; decrease feeding
Hyperglycemia	Give insulin; reduce carbohydrates
Hepatic encephalopathy	Decrease protein content
Renal failure	Decrease magnesium and phosphate; use essential amino acids
Cardiac failure	Decrease sodium and fluids

D: TOTAL PARENTERAL NUTRITION
Parenteral nutrition is indicated for stressed patients who cannot be nourished enterally and who require nutritional support (catabolic, malnourished). Total parenteral nutrition (TPN) is provided through a sterile access to a central vein, usually the subclavian. Osmolarity of a standard TPN solution exceeds 1000 mOsms and cannot be given by a peripheral venous route. However, this route of delivery is not as safe, or as efficient, as the enteral route. Providing enteral nutrients also fees and maintains the gut and the gut barrier. Parenteral nutrition leads to gut mucosal atrophy and impaired barrier function. Providing some internal nutrients along with parenteral nutrition has the advantage of feeding the gut while the gut dysfunction resolves at which time parenteral nutrition can be switched to the enteral route.

A typical parenteral nutrition fluid is described.

Complications in Parenteral Nutritional Support
Problem	Possible Concerns	Solution
Glucose:
Hyperglycemia, Glycosuria, Osmotic diuresis, hyperosmolar non-ketonic dehydration, Coma	Excessive total dose or rate of infusion of glucose, inadequate endogenous insulin, increased glucorticoids, sepsis Inadequate endogenous insulin response, inadequate exogenous insulin therapy	Reduce amount of glucose infused; Increase insulin; Administer a portion of calories as fat metabolism Give insulin; Reduce glucose input

Fat:
Pyrogenic reaction Altered coagulation Hypertriglyceridemia Impaired liver function	May be due to fat emulsion or to an underlying disease process	Decrease rate of infusion; allow clearance before blood tests Exclude other causes of hepatic dysfunction

Amino Acids:
Hyperchloremic metabolic acidosis	Excessive chloride content of crystalline amino acid solution	Administer sodium and potassium as acetate salts
Prerenal azotemia	Excessive amino acid infusion with inadequate calorie administration	Reduce amino acid intake; increase glucose calories

Electrolyte:
Hypokalemia	Potassium intake inadequate relative to increased requirements for protein anabolism; diuresis	Increase K⁺administration
Hyperkalemia	Excessive potassium administration, especially in metabolic acidosis; renal failure	Decrease K⁺ administration
Hypomagnesemia	Inadequate magnesium administration, relative to increased requirements for protein anabolism and glucose metabolism	Increase Mg⁺ administration
Hypophosphatemia	Inadequate phosphorus administration; redistribution of serum phosphorus into cells, bone, or both	Administer phosphorus (20 mEq potassium dihydrogen phosphate/1000 intravenous calories)
Elevations in SGOT < SGPT < and serum alkaline phosphates levels	Enzyme induction secondary to amino acid imbalance or to excessive deposition of glycogen, fat, or both in liver	Re-evaluate status of patient. Consider alteration in substrate profile

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C: TUBE FEEDINGS