Hypophosphatemia parenteral nutrition

Hypophosphatemia is associated with chronic alcoholism, parenteral nutrition with inadequate phosphate supplementation, chronic ingestion of antacids, diabetic ketoacidosis, and prolonged hyperventilation. 

Since chronic renal insufficiency is frequently complicated by rises in serum potassium, phosphate, and magnesium, parenteral nutrition solutions used to treat malnourished patients with chronic renal insufficiency are usually prepared with little supplementation of these cations. Four patients with chronic renal insufficiency developed significant hypophosphatemia 3-5 days after starting parenteral nutrition. Other electrolyte abnormalities included hypomagnesaemia (n = 1) and hypokalemia (n — 3) (50). Hypophosphatemia may be the most significant of the electroljde risks in this clinical setting, and the electrolytes of such patients should be monitored closely when nutritional support is begun. 

Druml W, Kleinberger G. Hypophosphatemia in patients with chronic renal failure during total parenteral nutrition. J Parenter Enteral Nutr 1999 23(l) 45-6. 

Phosphate occurs extensively in the body and is involved in many physiological processes since it is the principal anion of intracellular fluid. Most foods contain adequate amounts of phosphate, making hypophosphatemia (phosphate deficiency) virtually unknown except for certain disease states or in patients receiving total parenteral nutrition. Treatment is usually by the oral administration of up to 100 mmol of phosphate daily. 

The goals of therapy are the reversal of signs and symptoms of hypophosphatemia, normalization of serum phosphorus concentrations, and management of underlying conditions. Awareness of the clinical situations in which hypophosphatemia may be anticipated (alcoholism, diabetic ketoacidosis, and parenteral nutrition) is of vital importance in preventing iatrogenic hypophosphatemia. The routine addition of phosphorus in concentrations of 12 to 15 mmol/L to intra-... 

The most frequent abnormality of mineral metabolism seen in patients receiving total parenteral nutrition is hypophosphatemia. Predominantly, this abnormality occurs during the anabolic state. 

Hyperphosphatemia during the course of total parenteral nutrition is uncommon. When it occurs, it usually signifies an excessive intake of phosphate—assuming, of course, that the patient is not azotemic. Similarly, hypercalcemia occurs with excessive calcium intake but may also occur if excessive Vitamin D is added. In infants, hypercalcemia consistently accompanies hypophosphatemia (due to an inadequate phosphate content of the infusate) this situation occurs even in the absence of a concurrent intake of calcium (Heird, W. C., in press). 

Hypocalcemia, even in the absence of the calcium intake, is uncommon in patients receiving total parenteral nutrition except, of course, under unusual circumstances. One such circumstance is correction of hypophosphatemia by administration of a large amount of exogenous phosphate in the absence of a supplementary calcium intake, In this situation, calcium may fall rapidly and tetany may result. 

Mineral metabolism Refeeding hypophosphatemia is a risk during parenteral nutrition. In 70 patients with refeeding hypophosphatemia who were matched with controls the independent susceptibility factors were significant malnutrition a dose of less than 12 mmol of total phosphate during the first day and an initial rate of infusion of more than 70% of calculated requirements [62. Increasing amounts of non-lipid phosphate in the first day s regimen were protective. 

---