Accidental Epidural Injection of Rocuronium in a Pediatric Patient: A Case Report and Literature Review

Accidental administration of non-epidural drugs into the epidural or subarachnoid spaces may be associated with unexpected pain, morbidity, adverse effects, increased level of care, prolonged hospital stay, and mortality. We describe a 12-month-old admitted for secondary-stage hypospadias reconstruction. General anesthesia was induced with sevofiurane and a peripheral catheter was placed. Instead of ropivacaine, rocuronium (80 mg; 6.3 mg/kg) was injected into the epidural space by the caudal route. Surgery was uneventful and was completed 160 minutes after rocuronium was given. The patient exhibited paralysis with 1 of 4 twitches to the train-of-four with some posttetanic potentiation at the end of surgery. He was transferred to the pediatric intensive care unit for supportive ventilation and recovery. He did not experience oxygen desaturation or hypoventilation between the time of rocuronium administration and intubation. He was hemodynamically stable, without respiratory insufficiency, and his neurologic exam was normal, without motor or sensorial block. The patient was discharged home on the morning of the first postoperative day. Clinical examination 1 week after surgery revealed no lasting sequelae from the error.

Developmental upregulation of presynaptic NCKX underlies the decrease of mitochondria-dependent posttetanic potentiation at the rat calyx of Held synapse

The sensitivity of posttetanic potentiation (PTP) to high-frequency stimulation (HFS) steeply decays during the first 2 postnatal weeks. We investigated the underlying mechanisms for the developmental change of PTP induced by HFS (100 Hz, 2 s) at postnatal days 4–6 and 9–11 at the rat calyx of Held synapse. Low-concentration tetraphenylphosphonium (2 μM), an inhibitor of mitochondrial Na+/Ca2+ exchanger, suppressed the amount of posttetanic residual Ca2+ and PTP to a larger extent at the immature calyx synapse, indicating a developmental reduction of mitochondrial contribution to PTP. The higher amount of mitochondrial Ca2+ uptake during HFS and consequent posttetanic residual Ca2+ at the immature calyx of Held was associated with higher peak of HFS-induced Ca2+ transients, most likely because the mitochondrial Ca2+ uptake during HFS was supralinearly dependent on the presynaptic resting Ca2+ level. Probing into the contribution of Na+/Ca2+ exchangers to Ca2+ clearance, we found a specific upregulation of the K+-dependent Na+/Ca2+ exchanger (NCKX) activity in the mature calyx of Held. We conclude that the upregulation of NCKX limits the Ca2+ buildup and inhibits mitochondrial Ca2+ uptake during HFS, which in turn results in the reduction of posttetanic residual Ca2+ and PTP at the mature calyx of Held synapse.