Glutamate-containing parenteral nutrition doubles plasma glutamate: A risk factor in neurosurgical patients with blood-brain barrier damage?
Stover, John F. MD; Kempski, Oliver S. MD, PhD
Critical Care Medicine.
27(10):2252-2256, October 1999.
Objectives: Animal studies have shown that the elevation of plasma glutamate levels increase cerebral edema formation whenever the blood-brain barrier is disturbed. Therefore, changes in plasma glutamate levels as influenced by the administration of a glutamate-containing amino acid solution were investigated in neurosurgical patients.
Design: Prospective, descriptive study.
Setting: Eight-bed neurosurgical intensive care unit in a university hospital.
Patients: Twenty-three neurosurgical patients requiring parenteral nutrition.
Interventions: Parenteral nutrition was begun 24 hrs after craniotomy. Patients receiving a glutamate-containing amino acid solution (3.75 g/L glutamate) were compared with patients infused with a glutamate-free solution.
Measurements and Main Results: Arterial plasma and urine amino acids were analyzed using high-performance liquid chromatography. Administration of a glutamate-containing solution doubled plasma glutamate levels in neurosurgical patients (from 53.3 /- 9.8 [mu]M [preinfusion] to 98.5 /- 18.7 [mu]M [after 4 hrs of infusion]; p < 0.001), whereas no elevation was seen when infusing a glutamate-free solution (from 52.3 /- 7.3 [1 hr of infusion] to 53.6 /- 6.4 [mu]M [4 hrs of infusion]). Upon terminating the glutamate-containing infusion, arterial plasma glutamate levels decreased immediately (from 120 /- 13.2 [mu]M to 81.2 /- 19.5 [mu]M). Glutamate as infused in excess appears to exceed a renal threshold and is eliminated renally.
Conclusions: As shown in animal models, administration of a glutamate-containing amino acid solution significantly increased plasma glutamate levels. Because such an increase in plasma glutamate levels could aggravate cerebral edema formation, glutamate-containing amino acid solutions cannot be recommended for patients with a disturbed blood-brain barrier.
(C) 1999 Lippincott Williams & Wilkins, Inc.