Abstracts

Hyponatremia in Pediatric Patients Undergoing Intracranial Monitoring and Epilepsy Surgery for Intractable Partial Seizures

Abstract number : 2.293
Submission category : 9. Surgery
Year : 2010
Submission ID : 12887
Source : www.aesnet.org
Presentation date : 12/3/2010 12:00:00 AM
Published date : Dec 2, 2010, 06:00 AM

Authors :
Amy McGregor, S. Fulton, D. Clarke, F. Perkins, F. Boop, S. Einhaus and J. Wheless

Rationale: Hyponatremia is a known complication of intracranial surgery. The goal of this study was to describe risk factors for hyponatremia in pediatric patients undergoing intracranial monitoring (phase II) and epilepsy surgery (phase III) for partial seizures. Methods: The charts of pediatric epilepsy patients who underwent intracranial monitoring followed by epilepsy surgery for intractable partial seizures were analyzed. Patients who developed hyponatremia in the peri-operative period were identified, and their records were reviewed. Results: Of 61 pediatric patients who underwent intracranial monitoring and epilepsy surgery (phases II and III) for partial seizures in a 4.5 year period, 33 (54%) patients developed hyponatremia (Na ? 134) during the hospitalization despite normal sodium at admission. In 9 (27%) of these patients the lowest sodium measured was 134. However, 10 patients (30%) had a sodium nadir less than or equal to 130. Of these 10 patients, seven (70%) were on oxcarbazepine. Eight (80%) of the 10 patients had surgery involving the left hemisphere, and nine (90%) had resection of the temporal and/or occipital lobes. Sodium replacement was performed in 3 patients (ages 7-18); two of the patients had severe hyponatremia (sodium <125), and the third s lowest value was 128. The patient with the lowest nadir (120) had a history of glioma status past resection and radiation, meningococcal meningitis, and hypopituitarism. All 3 of the patients who underwent sodium replacement experienced hyponatremia with both phases II and III, with lower sodium values following resection. One patient underwent left temporal lobectomy, one underwent a left occipital resection, and one underwent a left temporal-occipital resection. All three patients were taking oxcarbazepine in addition to a second anti-epileptic drug (zonisamide or levetiracetam). The patient whose sodium nadir was 128 was maintained on oxcarbazepine, and the other two were changed to another anti-epileptic medication. One of these patients resumed oxcarbazepine following discharge. Conclusions: Hyponatremia is common in the setting of intracranial electrode placement and epilepsy surgery, occurring in more than half of the patients. Most of the time, it resolves without intervention. This study suggests that oxcarbazepine may be a risk factor for hyponatremia in the peri-operative period. Also, resection of the left temporal and/or occipital lobe(s) appeared to be a risk factor. Further studies are needed to clarify the role of oxcarbazepine and whether the hemisphere or lobe of resection affect risk.
Surgery