An unusual case of cardiac arrest during deep brain stimulation procedure!

Dear Editor, Deep brain stimulation (DBS) is a highly effective, minimally invasive therapeutic strategy for poorly controlled Parkinson’s disease (PD). Although the American Association of Neurological Surgeons considers DBS a low-risk procedure, with a perioperative mortality rate of <1%,[1] reports of cardiac arrest during DBS due to various reasons have been documented in the literature.[2] We report a case of a patient with poorly controlled PD who experienced an intraoperative cardiac arrest during a DBS procedure. A 62-year-old male diagnosed with PD was scheduled for a DBS procedure under monitored anesthesia care. Detailed informed consent was obtained from the patient. Oxygen was administered through nasal prongs at 2 lt/min. Levetiracetam (1 gm) was administered to the patient. Dexmedetomidine (Dx) infusion was started at 0.2 mcg/kg/min. A sudden drop in SpO2 (from 99% to 70%) was witnessed after 3 min. The Dx infusion was stopped, and the surgical team was informed. Assisted ventilation was provided using a bag and mask. Soon, the patient became unresponsive, and radial pulsations were weak. The Electrocardiogram displayed bradycardia (40/min), followed by asystole. Cardiopulmonary resuscitation (CPR) was started immediately by the neuroanesthesia team. Systemic circulation was restored within 30 s of CPR, and the patient resumed breathing. However, he remained unresponsive and did not follow commands. The pupils were normal in size and reactive to light. No emergency medication was required. The airway was secured with an 8 mm Internal diameter tracheal tube after removing the headgear. Levetiracetam (500 mg) was administered to the patient. A post-procedure computed tomography scan showed unremarkable findings. In the Intensive care unit, echocardiography, troponin T, a Deep vein thrombosis scan, and a chest x ray were performed. The patient regained full consciousness after 2 h, and his trachea was extubated. There are a number of causes that could lead to hemodynamic instability during the DBS procedure.[2] These causes include the trigeminocardaic reflex (TCR), venous air embolism (VAE), and the Bezold–Jarish reflex (BJR). The TCR is activated following irritation of the trigeminal nerve, leading to activation of the vagal motor nucleus.[3] In our case, TCR is unlikely, as there was no surgical stimulation during that phase. The overall incidence of VAE is up to 4.5% during the DBS procedure[4] During electrode placement, patients are mostly in an awake state. Hence, air may get entrained through bone or dural veins, causing VAE. In our case, VAE was ruled out as there was no sudden cough or drop inEnd tidal carbon dioxide O2. In our patient, BJR associated with hypovolemia[5] could be a possible cause of cardiac arrest. A hypovolemic state in the elderly can stimulate the carotid sinus baroreceptors, causing a compensatory increase in heart rate, vasoconstriction, and contractility. Additionally, an empty hypercontractile ventricle can stimulate intramyocardial C fibres, potentially triggering a sudden withdrawal of sympathetic outflow, causing bradycardia and hypotension.[6] Drug (Dx) as a causative factor was ruled out, as the infusion was minimal and administered for a brief period. In conclusion, our case serves as a reminder that adequate fluid replacement and continuous monitoring are essential to avoid cardiac catastrophe in elderly patients with relative hypovolemia undergoing a DBS procedure. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.