um.
Research indicates that patients with impaired kidney function, including premature neonates, whoreceive parenteral levels of aluminum at greater than 4 to 5 mcg/kg/day accumulate aluminum at levelsassociated with central nervous system and bone toxicity. Tissue loading may occur at even lower ratesof administration.
Safe and effective use of central venous nutrition requires a knowledge of nutrition as well as clinicalexpertise in recognition and treatment of the complications which can occur. Frequent clinicaleva luation and laboratory determinations are necessary for proper monitoring of central venousnutrition. Laboratory tests should include measurement of blood sugar, electrolyte, and serum proteinconcentrations; kidney and liver function tests; and eva luation of acid-base balance and fluid balance.
Other laboratory tests may be suggested by the patient's condition.
The intravenous administration of these solutions can cause fluid and/or solute overload resulting indilution of serum electrolyte concentrations, overhydration, congested states or pulmonary edema. Therisk of dilutional states is inversely proportional to the solute concentration of the solution infused. Therisk of solute overload causing congested states with peripheral and pulmonary edema is directlyproportional to the concentration of the solution.
Administration of amino acids in the presence of impaired renal function or gastrointestinal bleedingmay augment an already elevated blood urea nitrogen. Patients with azotemia from any cause should not
be infused with amino acids without regard to total nitrogen intake.
Administration of amino acid solutions to a patient with hepatic insufficiency may result in plasma aminoacid imbalances, hyperammonemia, prerenal azotemia, stupor and coma.
Hyperammonemia is of special significance in infants as its occurrence in the syndrome caused bygenetic metabolic defects is sometimes associated, although not necessarily in a causal relationship,with mental retardation. This reaction appears to be dose related and is more likely to develop duringprolonged therapy. It is essential that blood ammonia be measured frequently in infants.
The mechanismsof this reaction are not clearly defined but may involve genetic defects and immature or subclinicallyimpaired liver function.
Conservative doses of amino acids should be given, dictated by the nutritional status of the patient.
Should symptoms of hyperammonemia develop, amino acid administration should be discontinued andthe patient's clinical status reeva luated.
PRECAUTIONS
General
Clinical eva luation and periodic laboratory determinations are necessary to monitor changes in fluid balance, electrolyte concentrations, and acid-base balance during prolonged parenteral therapy orwhenever the condition of the patient warrants such eva luation. Significant deviations from normalconcentrations may require the use of additional electrolyte supplements.
Strongly hypertonic nutrient solutions should be administered through an indwelling intravenous
catheter with the tip located in the superior vena cava.
Care should be taken to avoid circulatory overload, particularly in patients with cardiac insufficiency.
In patients with myocardial infarct, infusion of amino acids should always be accompanied by dextrose,since in anoxia, free fatty acids cannot be utilized by the myocardium, and energy m |
