The majority of severe complications following spinal surgery are related to dural injury and intracranial hypotension [6]. The incidence of dural injury during spinal surgery has been reported as 5.5 to 10.1% [5, 7]. Dural injuries can cause intracranial hemorrhage [8, 9] and even stroke and death [10]. Seizure is the one of the manifestation of intracranial events [1,2,3,4]. In the previous reports, seizure appeared a few hours or days after the surgeries. However, seizure appeared during emergence from anesthesia in our patient, probably because larger dose of CSF spilled over from a subarachnoid space during surgery. When intraoperative dural injury is recognized, it is immediately repaired, preventing the subsequent development of postoperative intracranial hypotension. However, if the dural injury is not obvious during surgery like as our patient, the resultant CSF leakage can consequently lead to severe intracranial hypotension. Furthermore, the drainage tube can contribute to intracranial hypotension [7].
In retrospect, the actual onset time was thought when the drainage tube was opened and started suction. Seizure was masked by ongoing anesthesia and muscle relaxation; we recognized the seizure just after discontinuing anesthetics and reversal of the muscle relaxant. Regrettably, BIS was not monitored. If it had been monitored, abnormal spike waves might have been captured from the onset of the seizure. Although seizure activity might have damaged the central nerve system for a few minutes, it was fortunate that any neurologic sequelae had not been left. In order to detect earlier sign of intracranial hypotension that can lead to SAH and other catastrophic events, we should have knowledge of surgical procedures and their related potentially life-threatening adverse intracranial events even in common spinal cases. In addition, careful vigilance of patients and potentially useful BIS monitor are crucial. Brain CT and/or MRI are decisive to confirm intracranial hypotension and hemorrhage.
While the exact relation between intracranial hypotension and SAH is unclear in this patient, it has been postulated that extensive CSF loss can lead to a downward displacement of the brain and stretching/compromise of the bridging veins [11, 12]. In addition, an increased pressure gradient between venous blood and CSF can contribute to SAH [11, 12].
It is possible that the patient’s seizure stopped when the natural production of CSF resolved her intracranial hypotension. This is supported by the finding that plasma concentrations of valproic acid and levetiracetam had not reached therapeutic levels by postoperative day 2, and the patient’s headache disappeared on postoperative day 3. Headaches due to CSF leak are usually benign and 80% resolve within 5 days [12,13,14].
Symptomatic seizure after spinal anesthesia [15, 16], combined spinal-epidual anesthesia [17], and accidental dural puncture during epidural anesthesia [18, 19] have previously been reported. In these cases, intracranial hemorrhage after spinal and epidural anesthesia led to seizure. The pathophysiological mechanisms causing intracranial hypotension after spinal and epidural anesthesia are likely to be the same as those caused by spinal surgeries.
In the case of seizure during emergence from general anesthesia, we had to diagnose the cause of seizure immediately and manage it correctly. Causes of seizure following general anesthesia include epilepsy, hyponatremia, hypocalcemia, hypoglycemia, hyperglycemia, uremia, hepatic encephalopathy, local anesthetic toxicity, intracranial lesions, antibiotic solution used to irrigate the wound, and foreign matter in the CSF cavity. Our patient had no history of epilepsy. Arterial blood gas analysis, blood tests, and electroencephalography were normal. Initial brain imaging was unremarkable. Also, no antibiotic solution was used to irrigate the wound before wound closure. Hence, intracranial hypotension was not initially considered as a cause of her seizure.
