False Hyperchloremia During Anesthesia in 2 Patients Treated With Potassium Bromide for Refractory Epilepsy
Potassium bromide (KBr) was once a main antiepileptic and has been withdrawn from clinical use because of serious side effects, although its effectiveness for refractory epilepsy was recently reevaluated.1 Because it is rarely used, there is scant information about anesthetic management of patients treated with KBr. Herein, we present 2 cases of anesthetic management of refractory epileptic patients treated with KBr.
Case 1: A 15-year-old girl diagnosed with West syndrome and Lennox-Gastaut syndrome, and treated with antiepileptics including KBr (2.5 g/d) was scheduled for a callostomy. Our preoperative evaluation showed an increased level of chloride (Cl−) (131 mmol/L; BioMajesty JCA-BM2250, Jeol), which markedly increased (231 mmol/L; ABL620, Radiometer) following induction of general anesthesia. Other electrolytes were within normal ranges, while the vital signs and the surgical field were normal. We initially suspected an overdose of KBr, which was later shown to be unlikely, as a blood sample sent to the central clinical laboratory revealed a Cl− level of 104 mmol/L (DimensionARX, Siemens). Thus, the operation was continued as planned and the anesthetic course was uneventful. Thereafter, the serum Br− concentration was 18.8 mmol/L.
Case 2: An 8-year-old boy diagnosed with Dravent syndrome and treated with antiepileptics, including KBr (2.1 g/d), was scheduled for a callostomy. Preoperative Cl was 126 mmol/L, whereas that level was 235 mmol/L at the time of skin incision and 215 mmol/L at 4 hours after the incision. Surgery and anesthesia were performed uneventfully.
Following this case, we tested the properties of 3 types of Cl− electrodes (BioMajesty, ABL620, DimensionARX) in response to KBr added to Ringer’s lactate solution (Fig. 1). This test showed that the indicated levels of Cl− were increased by KBr in a dose-dependent manner, whereas their magnitude differed among the electrodes.
Bromism was once a well-known disorder but is now rare, as bromide was discontinued from clinical use as an anticonvulsant or sedative. However, it continues to be used as a stabilizing agent. Among anesthetic agents, bromide-containing drugs include halothane, neostigmine, scopolamine, and rocuronium.2 In the present cases, the amount of bromide (<10 mg/d) given as an anesthetic (rocuronium bromide) was <1% of that of KBr (>2 g/d), and the perioperative bromism was thought to be mainly due to KBr. False hyperchloremia has also been used as an indicator of bromism.2 However, the magnitude of false hyperchloremia differs among electrodes. Thus, estimation of Br− level from Cl− level is possible only under limited conditions. Notably, in the perioperative period, blood tests can be performed in a variety of locations (eg, another institution, outpatient clinic, operating room, ward), resulting in various Cl− levels that can cause confusion. Moreover, in neurosurgical anesthesia cases, where electrolyte and acid-base disorders may occur during surgery, electrode interference conveys a certain risk for anesthetic management. In conclusion, in patients with refractory epilepsy, administration of KBr and false hyperchloremia should be taken into account. During the perioperative period, we recommend using the same electrolytes analyzer for blood chemistry analysis. This will eliminate confusion due to differences in results among devices and will allow detection of an electrolyte disorder caused by neurosurgery.