Trigeminocardiac reflex: a unique case of recurrent asystole during bilateral trigeminal sensory root rhizotomy
By Cha, ST, M.D., Eby, JB, M.D., Katzen, JT, M.D., Shahinian, HK, M.D, FACS
The trigeminocardiac reflex is the sudden-onset of dysrhythmia and hypotension during manipulation of any of the branches of the trigeminal nerve. The trigeminal nerve and cardioinhibitory vagus nerve constitute the afferent and efferent pathway in the reflex arc. The trigeminocardiac reflex has been reported to occur during craniofacial surgery, balloon-compression rhizolysis of trigeminal ganglion, and tumor resection in the cerebellopontine angle. In this report we present a unique patient who experienced two unexpected episodes of asystole after transection of the sensory roots of the trigeminal nerve.
The oculocardiac reflex (OCR) is a widely investigated and well-established phenomenon, induced by the stimulation of the ocular and periocular structures innervated by the ophthalmic division of the trigeminal nerve.6 The trigeminocardiac reflex (TCR) is manifested by the sudden development of bradycardia or asystole with arterial hypotension. TCR is thought to occur via stimulation of one or more of the sensory branches of the trigeminal nerve (V1, V2, V3).2, 12 Stimulation of the trigeminal nerve is thought to set off a reflex arc inducing a cardiac depressor response via vagal stimulation. Several procedures have been known to induce the TCR, however, the exact mechanism of TCR remains unclear. Case reports of the TCR during craniofacial surgery support the assumption that stimulation of the trigeminal nerve may play an essential role in the afferent pathway of this reflex arc.18 Percutaneous microcompression of the trigeminal ganglion for trigeminal neuralgia has been shown to induce the cardiovascular depressor response. The noxious effect on the trigeminal nerve during needle insertion and balloon inflation is thought to stimulate the TCR.7 Tumor resection within the cerebellopontine angle stimulating the intracranial portion of the trigeminal nerve has also induced the TCR. 2, 5, 12
Advances in endoscopic and microscopic surgery have allowed surgeons to manipulate the intracranial portion of the trigeminal nerve as it exits the pons, prior to its entry into Meckel's cave. In this report a patient underwent bilateral sectioning of the dorsal sensory root of the trigeminal nerve for intractable, atypical facial pain induced by an intracranial hemangioma. The patient developed TCR evidenced by recurrent asystole (TCR) during each rhizotomy.
A 72-year-old Caucasian male was referred for surgical evaluation of intractable orofacial dyskinesia and bilateral, facial numbness and paresthesia. Over the prior two years, he reported a 10 kg weight loss due to pain with mastication, and subsequent eating difficulties. His past medical and surgical history was significant for ischemic heart disease and four-vessel coronary artery bypass graft. The patient's medication included: Atenolol 50 mg four-times a day, Clonazepam 0.5 mg three-times a day, Lansoprazole 30 mg at bedtime, Sotalol 40 mg twice a day, Aspirin 325 mg tablet once a day, and Irbestartan 160 mg once a day. A preoperative ECG showed bifascicular block and left ventricular hypertrophy with QRS widening. The patient denied tobacco, alcohol, or drug use. CT and MRI studies of the brain and skull base revealed a calcified midline lesion beginning near the sella turcica and extending to the inferior aspect of the clivus. An endoscopic transsphenoidal biopsy confirmed the presence of a calcified hemangioma. Due to the location of the lesion it was believed to be unresectable. However, due to the patients excruciating bilateral facial pain surgical division of bilateral trigeminal nerves was offered for palliation.
The patient accepted this option and underwent division of the right trigeminal nerve on January 27, 1999. In the pre-operative holding area the anesthesiologist evaluated and premedicated the patient with 1.5 mg of Midazolam. Anesthesia was induced with 100 mg of Propofol, 150 μg Fentanyl and 12 mg of Atracurium. Intra-operatively the patient had an arterial line, central venous line, blood pressure cuff, 5-lead ECG, as well as end-tidal CO2 detector to monitor his vital signs throughout the surgical procedure. Anesthesia was maintained on a mixture of 0.9-3% Desflurane, with additional divided doses totaling 100μg of Fentanyl and 1.0mg of Dilaudid. The patient was supported with oxygen at 0.4-1 L/min. Prior to the craniotomy, the patient received several divided doses of phenylephrine totaling 500μg for a systolic blood pressure of 80 mm Hg. A retrosigmoid craniotomy was performed. An operating microscope and endoscope were employed to visualize the right trigeminal nerve. The sensory and motor branches were identified and separated with a Teflon pledget placed between the branches. A rhizotomy of the dorsal sensory root of the trigeminal nerve was completed with microscissors. Immediately following sectioning of the nerve, the patient developed a sudden, sustained asystole for 15 seconds, with a concurrent fall in systolic blood pressure from 140 to 80 mm Hg. Surgical manipulation was halted. The patient was administered 150μg of Atropine sulfate and 1.0mg of Epinephrine intravenously. After an additional 15-20 seconds there was a return of a sinus bradycardia, which over the next 15-30 seconds returned to a sinus rhythm with a heart rate of 60-70 bpm and blood pressure to 170 mm Hg. The procedure was resumed and no further complications were experienced. The patient had an uneventful recovery. A post-operative ECG showed normal sinus rhythm with no significant change from the pre-operative ECG.
On February 17, 1999, the patient underwent a left trigeminal rhizotomy through a similar approach. Pre-operatively 2 mg of Midazolam was administered in divided doses. General anesthesia was induced using 120 mg of Propofol, 2 mg of Dilaudid, and 40 mg of Rocuronium. Anesthesia was maintained with a mixture of 2-4% Desflurane and Nitrous oxide at 2-4L/min. The patient supported with oxygen at 0.5-6 L/min. Intra-operatively, the patient received intensive monitoring, as described for the first operation. A left sided retrosigmoid craniotomy was performed. The endoscope was used to identify the motor and sensory branches of the left trigeminal nerve. The dorsal sensory root was isolated and transected using microscissors. Once again, the patient developed abrupt asystole. This episode lasted for 5 seconds and did not result in any change in the patient's blood pressure. Surgery was temporarily halted. Sinus rhythm returned spontaneously without the need for pharmaceutical intervention. After the intracranial rhizotomy was completed, a buccal sulcus incision was made. The anterior wall of the maxilla was degloved, and both infraorbital neurovascular bundles were identified and transected. The procedure was completed without any further episodes of dysrhythmia. The patient's postoperative course was uneventful.
Current theories as to the mechanism of the trigeminocardiac reflex propose that the sensory nerve endings of the trigeminal nerve send neuronal signals via the gasserian ganglion to the sensory nucleus of the trigeminal nerve, forming the afferent pathway of the reflex arc. The afferent pathway continues along the short internuncial fibers in the reticular formation to connect with the efferent pathway in the motor nucleus of the vagus nerve.11 Cardioinhibitory efferent fibers arising from the motor nucleus of the vagus nerve terminate on the myocardium. These vagal stimuli provoke negative chronotropic and inotropic responses. Consequently, the clinical features of the TCR range from sudden-onset of sinus bradycardia, bradycardia terminating asystole, asystole with no preceding bradycardia, arterial hypotension, apnea, and gastric hypermotility. 8
Craniofacial surgery frequently involves osteotomies and soft tissue manipulation of the region innervated by the mandibular (V3), maxillary (V2), and ophthalmic (V1) division of the trigeminal nerve. Several craniofacial procedures have been noted to induce the TCR these include the LeFort I osteotomy, elevation of complex zygomatic fractures, distraction or insufflation of the temporomandibular joint, as well as midface fracture reduction.1-3, 11-13, 15-17, 19 The incidence of reflex bradycardia during craniofacial procedures has been reported to be as high as 1.6%.14
Over the last 20 years, advances in posterior fossa microsurgery have allowed surgeons access to the cerebellopontine angle. Improved visualization and surgical manipulation allow for vascular decompression procedures, tumor removal, and trigeminal nerve sectioning. Using the microscopic retrosigmoid approach, Schaller et al. (1999)18 reported a significant decrease in heart rate and blood pressure during the surgical resection of tumors near the trigeminal nerve within the cerebellopontine angle. The addition of endoscopy to this approach provides improved exposure of the cerebellopontine angle, and permits more accurate manipulation of the intracranial portion of the lower cranial nerves, especially the trigeminal nerve.10
In this case report the trigeminal nerves were approached via a retrosigmoid craniotomy. The endoscope provided excellent visualization of the nerve root, allowing separation of the motor branch and dorsal sensory root of the trigeminal nerve. During each of the procedures there was no indication of any TCR until sectioning of the dorsal sensory root. During the first procedure, transection of the sensory root immediately induced prolonged asystole and hypotension, whereas sectioning of the contralateral nerve during the second operation resulted in a brief episode of asystole.
Unlike OCR which has undergone extensive investigation6, the exact mechanism of TCR is still unclear.2, 5, 12 This case demonstrates an isolated central induction mechanism for the TCR. This finding supports the assumption that the main sensory branch of the trigeminal nerve is the major, if not the exclusive modulating afferent pathway of the TCR.
Several factors have been postulated to predispose patients to TCR based on cases of the OCR.6 These factors include hypercapnea, hypoxemia, light anesthesia, children with high resting vagal tone, narcotics such as Sufentanil and Alfentanil, and pre-operative beta-blockers and calcium channel blockers. 11, 20
However, the nature of stimulus is the most important risk factor to inducing the TCR. During craniofacial surgery, abrupt and sustained traction is more reflexogenic than smooth and gentle traction.6 From our experience, gentle intracranial manipulation of the trigeminal nerve does not provide such a noxious stimuli as to provoke the TCR.9 However, as depicted in this report surgical division of the trigeminal nerve can induce a sudden and severe occurrence of the TCR. Other potent stimuli can induce the TCR. These include needle insertion, balloon inflation of the trigeminal ganglion, and tumor resection within the cerebellopontine angle. 4, 18
If dysrhythmia and hypotension develop during trigeminal rhyzotomy, the surgeon must cease all manipulation of the nerve to prevent any further noxious stimuli. Reports have shown that removal of the triggering factor can abolish the reflex phenomenon without further treatment.11, 15, 19 The anesthesiologist must be aware of predisposing factors and be prepared to intervene with medication as necessary. Intravenous injection of Atropine or Glycopyrrolate is recommend to treat the cardioinhibitory vagal effect and regain normal sinus rhythm. 1-3, 11-13, 15, 16, 19 Once normal sinus rhythm and the blood pressure and oxygenation are maintained the surgery may once again proceed. Most reported cases of TCR reveal that the procedures were completed uneventfully following the administration of intravenous anticholinergic medication.1, 3, 8, 14, 15, 21 This is appears to be effective in preventing additional episodes of dysrythmia. 6, 15, 18 Local anesthetic infiltration or block of the nerves can be considered in anticipation of invasive trigeminal nerve stimulation or controlled hypotension.5
However, the surgeon must continue the operation with a gentle and less reflexogenic maneuver. A detailed, anatomical knowledge of the neurovascular anatomy of the craniofacial area enables the surgeon to gently manipulate the craniofacial skeleton and prevent TCR. Anticipating possible injury to the dorsal sensory root of the trigeminal nerve during surgery within the cerebellopontine angle and posterior fossa must be considered in advance. A noninvasive and temporary pacemaker should be prepared for patients with known cardiac risk. 7, 18
In short, the surgeon and the anesthesiologist must always be aware of the potential for the TCR, and must both be prepared surgically and pharmacologically to treat the possible life-threatening consequences during surgery.
We believe this unique case of bilateral trigeminocardiac reflex induced by the isolated sectioning of the intracranial dorsal sensory roots of both trigeminal nerves; provides clear evidence of the central role of the trigeminal nerve as the afferent pathway of the reflex arc.
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