Anesthetic management of a patient with recurrent shock caused by anaplastic thyroid carcinoma compressing the internal carotid artery: a case report

Abstract

Stimulation of baroreceptors in the carotid sinus may increase vagal activity and decrease sympathetic activity. In rare cases, this can lead to carotid sinus hypersensitivity, which may cause hypotension, bradycardia, or even asystole. An 86-year-old man scheduled for elective thyroid surgery was admitted to the emergency room with repeated episodes of syncope followed by shock. These episodes were suspected to be caused by metastatic lymph nodes compressing the carotid sinus. In the operating room, a video laryngoscope was used for the first laryngoscopy attempt to minimize neck extension. Endotracheal intubation was successful on the first attempt, and the patient remained hemodynamically stable. Excessive neck extension during laryngoscopy and positioning to optimize the surgical field may trigger carotid sinus hypersensitivity. Therefore, measures to minimize neck extension, including use of video laryngoscopy, and careful monitoring during patient positioning are recommended.

INTRODUCTION

Head and neck cancers can cause various complications, including compression of arteries, veins, nerves, and related structures [1]. In rare cases, this may lead to carotid sinus hypersensitivity (CSH), an exaggerated response to stimulation of the carotid sinus baroreceptors located cephalad to the bifurcation of the common carotid artery. Manipulation of the carotid sinus activates the carotid sinus reflex and produces an impulse transmitted via the glossopharyngeal nerve to the medulla oblongata, which may result in hemodynamic alterations such as bradycardia and hypotension [2]. Cardiac arrest caused by CSH during carotid artery surgery and during patient positioning for head and neck surgery has been reported in the literature [3,4]. Therefore, surgeries that may affect the carotid sinus should be performed with caution and carefully monitored by anesthesiologists.

CASE REPORT

The Institutional Review Board of Pusan National University Hospital approved this case report (IRB No. 05-2022-072). Because the patient was deceased at the time of this report and no identifiable personal information was included, the IRB waived the requirement for written informed consent. An 86-year-old man (height, 168 cm; weight, 69.9 kg) scheduled for elective surgery for thyroid cancer was admitted to the emergency room (ER) with shock. During the first episode of shock, a bystander resuscitated him by providing basic life support. However, brain computed tomography, electrocardiography, and laboratory findings were unremarkable, and he was therefore discharged from the ER. Two days later, he returned to the ER with the sudden onset of sweating, dizziness, and nausea. After admission to the general ward, he experienced three episodes of shock accompanied by a sudden decrease in heart rate to below 40 beats per minute and a systolic blood pressure of 60–70 mmHg. He was resuscitated with crystalloid fluid loading and continuous norepinephrine infusion. Consultation with specialists from the otorhinolaryngology, cardiology, and neurology departments suggested that a metastatic lymph node compressing the carotid artery could be the cause of the recurrent shock. Subsequent computed tomography revealed compression of the left carotid artery and thrombosis of the left internal jugular vein (Fig. 1). Nevertheless, the surgical team decided to proceed with the scheduled surgery.

Fig. 1. Preoperative computed tomography of the neck. A metastatic lymph node (white arrow) compresses the left carotid artery (red arrow). (A) Transverse section; (B) sagittal section; (C) coronal section.

Before induction of general anesthesia, a radial arterial cannula was inserted, and standard anesthetic monitoring, including electrocardiography, pulse oximetry, and noninvasive blood pressure measurement, was initiated. Atropine, epinephrine, dopamine, and norepinephrine were prepared in advance, and external defibrillator patches were attached in case the patient developed complications requiring transcutaneous pacing or defibrillation. General anesthesia was induced using propofol (100 mg) and rocuronium (50 mg). The patient was intubated using a video laryngoscope (KoMAC video laryngoscope; KoMAC Co., Ltd., Korea) on the first attempt to minimize excessive neck extension that might trigger CSH. Endotracheal intubation was successful on the first attempt, and the patient remained hemodynamically stable without bradycardia or hypotension during induction of anesthesia. The patient was closely monitored during surgical positioning using electrocardiography and invasive arterial blood pressure measurement. Considering the risk of massive bleeding, a 16-gauge intravenous cannula was inserted into the upper arm vein. Anesthesia was maintained with sevoflurane to keep the bispectral index value between 45 and 55. Analgesia was achieved via continuous intravenous administration of remifentanil (0.025–0.05 mcg/kg/min). During surgery, the heart rate did not change significantly; however, systolic blood pressure fluctuations were relatively large, ranging from 80 to 150 mmHg. Norepinephrine was administered through a peripheral intravenous line (16-gauge, upper arm) as a continuous infusion at a concentration of 83.3 µg/mL, and was initiated and discontinued as needed according to the hemodynamic status of the patient to maintain a mean arterial pressure above 65 mmHg. However, because this study was a retrospective analysis based on medical records, the exact infusion rate was not consistently documented and therefore could not be retrieved. During surgical dissection, the cancer was found to have invaded not only the carotid artery and internal jugular vein, but also the subclavian vein (Fig. 2). After discussion with the vascular surgeon, the attending otolaryngologic surgeon decided not to dissect the subclavian vein or surrounding structures, considering the advanced age of the patient, difficult surgical access, and potential for complications, including excessive bleeding and brachial plexus injury. The patient underwent total thyroidectomy with central neck dissection and left selective neck dissection.

Fig. 2. Intraoperative findings. (A) External view of the left neck mass. (B) Operative field before tumor removal. (C) Preserved left carotid artery (black arrow) and left vagus nerve (white arrow) after tumor excision.

After surgery, neuromuscular blockade was reversed using sugammadex (Bridion^®; Merck and Co., USA) 200 mg. He was successfully and smoothly extubated and transferred to the post-anesthesia care unit, and subsequently to the general ward. In this case, norepinephrine was initiated in response to intraoperative hemodynamic instability; however, owing to the retrospective nature of the study, detailed information regarding infusion rates and the exact timing of discontinuation was unavailable. Nevertheless, the maintenance of systolic blood pressure above 130 mmHg from the end of surgery through the post-anesthesia care unit stay without vasopressor support is clinically relevant, suggesting resolution of reflex-mediated hemodynamic instability after surgical completion.

The patient did not experience further episodes of syncope or shock. He underwent fasting therapy and conservative treatment for postoperative chyle leakage. He was discharged 28 days after surgery without any adverse effects.

DISCUSSION

The carotid sinus contains numerous baroreceptors that respond to stretching of the arterial wall adjacent to the sinus. Stimulation of these baroreceptors can cause increased vagal activity and decreased sympathetic activity, a phenomenon known as CSH [5]. These effects can result in bradycardia, profound hypotension, and even asystole. CSH represents a likely cause of syncope and falls, particularly in older patients, as the incidence of CSH increases with age [6]. The patient in this case was elderly and had metastatic lymph nodes adjacent to the carotid sinus bifurcation. Thus, the repeated episodes of shock were assumed to be related to CSH.

The patient was receiving calcium channel blockers for hypertension and alpha-adrenergic blockers for benign prostatic hyperplasia, and these medications could have caused orthostatic hypotension leading to dizziness, pre-syncope, and syncope [7]. In patients with CSH, chronic vasodilator therapy does not have a direct effect on carotid sinus reflexivity; however, delayed recovery of blood pressure may indirectly potentiate the severity of clinical manifestations. The persistence of hypotension for some time after carotid sinus massage suggests that vasodilators impair compensatory mechanisms [8].

Head and neck surgeries, such as thyroidectomy, tonsillectomy, and carotid endarterectomy, often necessitate hyperextension of the neck to optimize the surgical field. Numerous cases of cardiac arrest have been reported during patient positioning for such head and neck surgeries [2,3,4]. In one case of robotic-assisted total thyroidectomy, the neck was hyperextended, and the left arm was elevated and stretched to facilitate endoscope passage. During manipulation near the carotid bifurcation, sudden cardiac arrest with asystole occurred without preceding events such as bradycardia or hypotension. The anesthesiologist immediately requested cessation of surgical manipulation and administered intravenous atropine (0.5 mg), after which the electrocardiogram returned to sinus rhythm within a short period [9]. Atropine has been reported to eliminate the cardioinhibitory response to diagnostic massage in patients with cardioinhibitory carotid sinus syndrome. However, persistent asystole lasting dozens of seconds without response to atropine has also been reported. In that case, after successful induction of anesthesia and positioning for thyroidectomy, a roll was placed under the shoulders and the head was lowered. A few seconds later, the heart rate decreased and asystole developed despite administration of atropine (1 mg). Cardiopulmonary resuscitation was initiated immediately. Neck extension was suspected as the triggering factor, and spontaneous circulation was restored immediately after the neck was returned to a neutral position [10]. Therefore, when bradycardia likely caused by CSH occurs during surgery, surgeons should promptly consider returning the neck to a neutral position if neck extension is present.

During induction of general anesthesia, some patients require excessive neck extension to ensure adequate visibility during direct laryngoscopy, and lifting of the laryngeal structures with the laryngoscope may sometimes be necessary. These actions may provoke CSH in vulnerable patients. Cardiac arrest during direct laryngoscopy has been reported previously [11,12]. Two pathophysiological mechanisms have been proposed to explain this phenomenon: CSH and direct vagal stimulation. Glossopharyngeal sensory nerve fibers are distributed in the pharynx, and the internal branches of the superior laryngeal nerves are distributed on the laryngeal surface. In one reported case, placement of the laryngoscope on the laryngeal surface of the epiglottis without significant tension did not trigger bradycardia, whereas significant tension during suspension laryngoscopy induced bradycardia regardless of epiglottic contact [13]. These findings are consistent with the characteristics of CSH [14]. We anticipated that minimizing neck extension during laryngoscopy would reduce the risk of CSH and associated complications. Therefore, patients undergoing laryngoscopy and surgical positioning should be carefully monitored using electrocardiography and invasive arterial blood pressure measurement. Moreover, because cardiac pacing is considered a treatment option for CSH with recurrent syncope, external defibrillator patches should be attached in advance for use during events requiring transcutaneous pacing or defibrillation, as in this case [2,15,16].

Surgeries that may affect the carotid sinus require careful approach and monitoring by anesthesiologists. Invasive arterial blood pressure monitoring, electrocardiography, adequate intravenous access, preparation of vasopressors, and transcutaneous pacing represent reasonable steps in the perioperative care of vulnerable patients in whom CSH may be triggered. Excessive neck extension during laryngoscopy, suspension during intubation for induction of anesthesia, and positioning to optimize the surgical field may also contribute to the occurrence of CSH. Therefore, measures to minimize neck extension, such as use of video laryngoscopy, should be actively employed to reduce the incidence of CSH. In addition, close communication and shared awareness with the surgical team are essential for prompt management of hemodynamic instability potentially caused by carotid sinus stimulation.