TPN discontinuation and metabolic derangements

TPN is usually slowed prior to anethesia primarily to avoid complications from excessive (hyperosmolarity) or rapid decrease (hypoglycemia) in infusion rates in the busy operating area. That said, because abrupt discontinuation may lead to severe hypoglycemia, TPN must be turned down gradually.

According to Miller, Dr. Michael F. Roizen has adopted the following: " Infusion of TPN or enteral nutrition is reduced the night before surgery and a 5% or 10% dextrose solution is substituted preoperatively. If serum glucose, phosphate, and potassium concentrations measured preoperatively are abnormal, they are restored to whithin normal limits. Strict asepsis is maintained. Conversely, one should continue infusing the TPN solution by using a pump system or enteral nutrition while strictly maintaining its normal rate and asepsis, administering all fluids through a different IV site and performing a rapid sequence intubation (for those who received enteral nutrition)."

The most common abnormality in patients receiving TPN is elevated serum hepatic transaminases levels. Serum glutamic oxaloacetic transaminase (SGOT) and serum glutamic pyruvate transaminase (SGPT) are frequently increased to two times normal levels; in addition alkaline phosphatase may be mildly elevated. More profound rises in alkaline phosphatase, accompanied by elevated bilirubin levels, may indicate a cholestatic jaundice, which may be the result of lipid emulsion administration. This condition may be managed by either diminishing the amount of lipid administered to approximately 1 g/kg/day or placing the patient on enteral nutrition.

Glucose loading, as occurs during administration of TPN results in intracellular glucose movement. As TPN is instituted, glucose transport and oxidative phosphorylation acutely increase, resulting in increase demand for intracellular phosphate to support the formation of ATP. This risk of hypophosphatemia is one of the reasons why parenteral regimens are advanced slowly for the first few days. That said, refeeding syndrome is primarily the result of hypophosphatemia and can lead to impaired myocardial contractility and cardiovascular collapse as well as respioratory failure, rhabdomyolysis, seizures, delirium and death.

In addition, hypophosphatemia and hypercalcemia are frequently seen in patients on TPN because phosphate requirements (40 to 100 mEq/day) are usually underestimated while calcium requirements (3 to 8 mEq/day) are overestimated.