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|LETTERS TO EDITOR
|Year : 2018 | Volume
| Issue : 1 | Page : 237-238
Ictal bradycardia: A missed etiology for intraoperative bradycardia
Unnikrishnan Prathapadas, Smita Vimala, Karen Ruby Lionel, Ajay Prasad Hrishi
Division of Neuroanesthesia, Department of Anesthesiology, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum, Kerala, India
|Date of Web Publication||11-Jan-2018|
Dr. Ajay Prasad Hrishi
Division of Neuroanesthesia, Department of Anesthesiology, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum - 695 011, Kerala
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Prathapadas U, Vimala S, Lionel KR, Hrishi AP. Ictal bradycardia: A missed etiology for intraoperative bradycardia. Neurol India 2018;66:237-8
Intraoperative bradycardia and asystole is one of the most dreaded anesthetic emergencies. We report a case of intraoperative bradycardia and brief asystole, which was in fact an ictal bradycardia as visualized on the intraoperative electroencephalogram (ECoG) recordings. The search of literature proved that there are no reported cases of intraoperative ictal bradycardia being suspected as a cause for intraoperative bradycardia. By convention, anesthesiologists consider seizures as an etiology in intraoperative tachycardia scenarios. Thus, the authors intend to create an awareness about this rare phenomenon that remains undiagnosed and may lead to life-threatening events in the intraoperative period.
A 30-year old male patient had refractory complex partial seizures from childhood and was diagnosed to be having mesial temporal sclerosis of the right temporal lobe. He was admitted for a right anterior temporal lobectomy and hippocampectomy, and underwent standard induction of anesthesia with routine monitoring. After positioning the patient for surgery in supine position, as the surgical team was draping the surgical site, there was a sudden slowing of heart rate (HR) from 76 beats per minute (bpm) to 30 bpm during which injection atropine 0.01 mg/kg was administered. There was no response to atropine, and as the repeat dose was given, the heart rate further slowed down rapidly resulting in a brief period of asystole lasting for less than 30 s, wherein chest compressions were initiated as part of cardiopulmonary resuscitation. This resulted in sinus rhythm with the HR slowly raising to 60 bpm within a min. This episode lasted for approximately 2–3 min during which there was no fall in oximetry (SpO2) nor end-tidal carbon dioxide (EtCO2). Following this episode, the patient remained hemodynamically stable. After discussion with the surgical team and the patients' relatives, it was decided to proceed with surgery. The patient remained hemodynamically stable during the craniotomy and dural opening. As an intraoperative electrocorticography (ECoG) monitoring of the temporal lobe was instituted to guide the surgical resection, there was a transient drop in the HR to 25 bpm. Concomitantly, the electrophysiologist reported an ictal activity on the ECoG and immediately injection thiopentone 100 mg was administered, resulting in cessation of the electrographic seizures with simultaneous termination of bradycardia with the HR settling back to the baseline of 64 bpm. The etiology of the episode of bradycardia and asystole following induction could have been possibly due to a seizure discharge, which did not manifest clinically because the patient had received muscle relaxants as a part of the routine anesthetic regimen. Hence, we concluded that this could be a case of “ictal bradycardia.”
Changes in the cardiac rhythm are common during clinical seizures as well as nonconvulsive seizures. Majority of studies report tachycardia as the most commonly occurring rhythm abnormality seen in more than 70% of temporal lobe seizures., Ictal bradycardia has been reported in 6% of patients with complex partial seizures., The ictal bradycardia syndrome is known to occur in patients with established epilepsy, when epileptiform discharges disrupt the normal cardiac rhythm, leading to a decrease in HR of more than 10 bpm below the baseline. Majority of patients with ictal bradycardia have temporal lobe seizures. It is believed that abnormal neuronal activity during a seizure can affect central autonomic regulatory centers in the brain, leading to cardiac rhythm changes. There are no reported cases of intraoperative ictal bradycardia and asystole, which is attributed to the fact that these events have been missed because intraoperative ECoG monitoring is not routinely in place.
Neuroanesthesiologists should be aware of “ictal bradycardia,” which could be misdiagnosed as one of the routine neurogenic causes of bradycardia-like vagal/trigeminal stimulation as they have an identical presentation. The possibility of “ictal bradycardia” should also be considered as a cause of the intraoperative bradycardia scenarios, especially in patients with a history of temporal lobe seizures. Ictal bradycardia usually will be abrupt, causing a transient slowing of HR in the absence of vagal or trigeminal stimulation. The response to anticholinergics such as atropine will be absent or sluggish. The bradycardia will respond to antiepileptic therapy or to anesthetics with an antiepileptic effect such as thiopentone sodium/midazolam or cold saline irrigation of the exposed cerebral cortex. It is important to identify ictal bradycardia as a potential harbinger of lethal rhythms, such as asystole, as this may lead to a sudden unexpected death in patients with epilepsy presenting for surgery.
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