Ahuja, V

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SAJAA 2007;13(6) • Nov/Dec                              33 ■ Case ReportSAJAA 2007; 13(6): 33-35Trigeminocardiac reflex unresponsive toatropine during microvascular decompressionof trigeminal nerve root: A potentially lethalcomplication of a simple surgeryINTRODUCTIONMicrovascular decompression (MVD) of trigeminal nerve rootentry zone is a well described technique in the treatment oftrigeminal neuralgia. It is considered safe and is reported tohave a high level of effectiveness.1 Trigeminocardiac reflex(TCR), a reflex consisting of bradycardia, hypotension, apnoeaand gastric hypermotility is reported to occur, during craniofacialsurgery,2,3 cerebellopontine angle surgery,4 percutaneous microdecompression of trigeminal ganglion5,6 and MVD for trigeminalneuralgia.7 We describe a case of TCR during MVD in a patienton chronic amitryptyline and carbamazepine therapy presentingas bradycardia followed by cardiac arrest nonresponsive toatropine, adrenaline and dopamine. This was successfully treatedwith isoprenaline and noradrenaline.CASE REPORTA 55 year old (height 168 cm, weight 70 kilogram) male, whowas a chronic smoker, was scheduled for MVD of the trigeminalnerve for facial pain. The patient had been refractory to medicaltreatment with oral carbamazepine 400 mg twice daily and oralamitryptyline 25 mg once daily, for the previous two years. Hispast history was unremarkable except that he was diagnosedas being hypertensive during the pre-anaesthetic checkup. Thiswas controlled on oral amlodipine 5 mg and oral atenolol 50mg once daily, for 10 days. The patient did not have anycardiovascular symptoms. He had a complete cataract in theright eye. Pre-operative blood haematology and biochemistrywere within normal limits. Electrocardiography (ECG) showedleft axis deviation, a heart rate of 84/min, regular, with a PRinterval of 144 ms, without any evidence of heart block. ChestX-ray demonstrated emphysematous changes, andechocardiography revealed an ejection fraction of 55%, noregional wall motion abnormality, and normal systolic anddiastolic function. Magnetic resonance imaging of the brain wasreported as normal.The patient was premeditated with diazepam 10 mg and ranitidine150 mg orally at bedtime, and two hours prior to surgery.Amlodipine is a calcium channel blocker and is normallycontinued until the morning of surgery. It does not contributeto bradycardia, as one of the side-effects of calcium channelblockers is tachycardia. Anaesthesia was induced with propofol1.5 mg/kg and morphine150 g/kg intravenously. Ecuronium 7mg was administered intravenously to facilitate tracheal intubation.The trachea was intubated with an 8.5 mm internal diameter(ID) cuffed tube. The right radial artery was cannulated afterinduction. Monitoring included invasive arterial blood pressure(IABP), oxygen saturation (SpO2), ECG, end tidal carbon dioxide(EtCO2), and temperature. Anaesthesia was maintained with 67%N2O and 33% oxygen, propofol infusion and intermittentvecuronium. The patient was preloaded with one litre of normalsaline. His position was changed from supine to right lateraldecubitus. The intra-operative period of one hour was uneventful,and the arterial blood gas (ABG) that was done as part of themonitoring was within normal limits. Towards the end of surgery,when the surgeon was introducing the Teflon sponge betweenthe trigeminal nerve root and the superior cerebellar artery, thepatient developed sudden bradycardia. The heart rate (HR)decreased from 60 to 30/min (a 50% decrease) and the IABPdecreased from 130/90 (103) to 60/40 (46) mmHg (57% decrease).The surgeon was requested to stop the surgery. Propofol andN2O were discontinued, and the patient was ventilated with100% oxygen. Atropine 0.6 mg was administered and a further1.2 mg repeated without any response. The patient was givenadrenaline 10 mcg intravenously, cardiac massage was commenced,and dopamine was started at 10 g/kg/min. The patientsimultaneously developed prolonged A-V conduction, followedby broad complexes and ventricular tachycardia. Defibrillationwith 200J, 300J and 300J was attempted, followed bycardiopulmonary resuscitation. Intravenous adrenaline 1 mg wasadministered via the peripheral vein, and defibrillation wasrepeated. The patient developed A-V junctional bradycardia andhypotension which responded to the intravenous infusion ofisoprenaline 4 g/min, and noradrenaline 4 g/min, and revertedto sinus rhythm. An ABG performed immediately after resuscitationshowed a pH of 6.92, PaO2 of 453 mmHg, PaCO2 of 45 mmHg,HCO3 = 9, BE = -22, SpO2 = 99%. The serum potassium (K+) was4.5 meq/l. Sodium bicarbonate 230 meq was administeredintravenously. There was no acidosis prior to the event. Theduration of the cardiac arrest was 5 minutes, and the ABG samplewas taken after sinus rhythm was restored. At that time hypotensionwas still present, and this could have led to the metabolic acidosis. Subsequent ABG showed the following: pH = 7.05, PaO2 = 174mmHg, PaCO2 = 40 mmHg, HCO3 = 16, BE = -14, SapO2 = 98.4%,Ahuja VDepartment of Anaesthesia and Intensive care, Pgimer, Chandigarh, IndiaCorrespondence to: Dr Vanita Ahuja, e mail: vanitaanupam@yahoo.co.inCase Report■ 34 SAJAA 2007;13(6) • Nov/DecK+ 4.5 meq/l. Sodium bicarbonate 150 meq was repeatedintravenously. The post resuscitation Glasgow Coma Scale (GCS)was E1V_M1. The left pupil was dilated and was not reacting tolight. The patient’s temperature was 36 degree Celsius, IABPwas 86/44(58) mmHg and HR was 130/min. The right internaljugular vein was cannulated and surgery was completed. Postoperative CT scan of the head showed a normal study. The ECGshowed sinus tachycardia and chest X-ray confirmed the correctplacement of the central line. After four hours, the troponin Ttest was negative, GCS improved to E2V_M6, the left pupil wasnormal in size and reacting to light. The IABP was 110/70(83)mmHg, HR 120/min, the ABG was normal and CVP was 12mmHg.Isoprenaline infusion was stopped. After twelve hours the GCSwas E4V_M6, IABP was 116/70(85) mmHg, HR 106/min, ABGwas normal, CVP was 11 mmHg and urine output was 100 ml/hr.The infusion of noradrenaline was stopped and infusion dopaminewas reduced to 5 g/kg/min. After twenty fours hours, the patient’sGCS was E4V_M6 with no neurological deficit, IABP was 130/86(100) mmHg, HR was 94/min and hence his trachea was exubated.The patient had complete relief of his facial pain and did notrequire antihypertensive therapy for the control of blood pressure.DISCUSSIONTCR is defined as a decrease in mean arterial blood pressureand heart rate of more than 20% of the base line values beforethe stimulus, coinciding with the manipulation of the trigeminalnerve.7 The trigeminal nerve and the vagus nerve constitute theafferent and efferent pathways in the reflex arc8 (Figure1).Interruption of the surgical manoeuver immediately followingTCR is considered sufficient for heart rate and blood pressureto return to normal without the necessity of adding cholinergicmedication, in most cases.3 This reflex has been discussedfrequently in ophthalmology, as well as during maxillofacialsurgery, but less attention has been paid to it, especially duringthe surgical manipulation of the trigeminal ganglion and root.The occurrence of significant autonomic changes duringpercutaneous compression of the trigeminal ganglion has beenreported.6,9 The incidence of TCR during MVD for trigeminalneuralgia under a standardised anaesthetic protocol is reportedas 18% (5/28 patients) in only one retrospective study.7 In thisstudy, TCR reverted back to normal after cessation of the stimulusand administration of atropine, leading to the cessation of thereflex during the remainder of the procedure. Recurrent asystoledue to TCR after the transaction of the sensory root of thetrigeminal nerve for palliation of intractable trigeminal pain hasbeen reported in a 72 year male. This responded to the intravenousadministration of 150 g atropine and 1.0 mg of epinephrine.8Several factors are known to increase the risk of recurrence ofTCR i.e. light plane of anaesthesia, hypercapnia, hypoxaemiaand the nature of the stimulus (strong and long). These factorswere ruled out in the case under review. Long term therapyPONS TNRCompressed byblood vesselsTGGGMain sensorynucleus ofVth nerveMotor nucleusof vagusnerveCardiac depressorresponseAfferentEfferentTNR = Trigeminal Nerve RootTG = Trigeminal GanglionV1 = Ophthalmic NerveV2 = Maxillary NerveV3 = Mandibular NerveGG = Gasserian GanglionIF = Internuncial FibresFigure 1: The trigeminocardiac reflex pathwayV1V2V3IFSAJAA 2007;13(6) • Nov/Dec                              35 ■ Case Reportwith drugs i.e. chronic calcium channel blocker, beta-blockerand carbamazepine may predispose the patient to this reflex.7The strongest association (80%) has been reported betweenchronic carbamazepine therapy and TCR.7 In the case underreview, chronic carbamazepine therapy   probably predisposedthe patient to TCR.In the differential diagnosis of the intra-operative bradycardiaand hypotension, several possibilities were considered.Hypovolaemia was ruled out, as the patient had received aninfusion of one litre of fluid and intra-operative blood loss wasminimal. Electrolyte imbalance was excluded, as an ABG doneprior to the event was within normal limits. The bradycardiaand hypotension that occurred were not preceded by eitherhypoxia or hypercarbia. Myocardial ischaemia was ruled out,as the post-operative ECG showed sinus tachycardia and thetroponin T test was negative. A special note to exclude venousair embolism needs to be mentioned, as there was no tachycardia,right ventricular strain pattern, decrease in EtCO2 or hypoxia atthe time of the event.Patients on chronic tricyclic antidepressant therapy (TCA) showdecreased sensitivity to atropine.10 Since their adrenergic receptorsare either desensitised or their catecholamines are depleted,only direct acting sympathomimetics are effective in suchpatients.11 Noradrenaline has been successfully used to managecirculatory shock, whilst dopamine was ineffective in a patienton chronic TCA therapy.12 The short term infusion of 0.005 -0.008 g/kg/min of isoprenaline is reported to improve atrialfunction after cardioversion.13 In the case under review, bradycardiaand hypotension towards the end of surgery most probablyoccurred due to TCR, which was precipitated by chroniccarbamazepine therapy, and did not respond to atropine anddopamine, probably because of chronic amitryptyline therapy.Junctional bradycardia and hypotension after defibrillationsuccessfully responded to the infusion of isoprenaline andnorepinephrine in the case under review. The isoprenalineimproved the atrial function and noradrenaline corrected thehypotension. However, the effect of adrenaline and dopaminein the successful resuscitation cannot be completely excludedfor the following reasons: delivery via a peripheral vein duringCPR may be inadequate; the ability of adrenaline to displace _blockers from occupied receptors, increasing susceptibility tothe subsequent administration of other _ stimulant drugs shouldnot be overlooked. However, patients on chronic antidepressantsrespond to the blood pressure effects of direct-actingsympathomimetics, ranging from two to three times greater forphenylephrine, four to eight times greater for norepinephrineand two to four times greater for epinephrine.12CONCLUSIONSSince patients with trigeminal neuralgia are frequently on chroniccarbamazepine and antidepressant therapy, the predispositionof such patients to TCR, which is unresponsive to atropine anddopamine, should be kept in mind. TCR during manipulationof the trigeminal ganglion and root is usually self-limiting.However, at times, complications like cardiac arrest non-responsiveto the usual resuscitation measures may occur, leading tosignificant morbidity.REFERENCES:1. Li ST, PanQ, Liu N. Trigeminal Neuralgia: What are the important factors forgood operative outcome with microvascular decompression. Surg Neurol2004;62:400-405.2. Stott DG. Reflex bradycardia in facial surgery. Br J Plast Surg 1989;42:595-597.3. Lang S, Lanigan DT, Van der wal M. Trigemino cardiac reflex: maxillary andmandibular variants of oculocardiac reflexes. Can J Anaesth 1991;38:757-760.4. Schaller B, Probst R, Strebel S. Trigemino cardiac reflex during surgery inceribello pontine angle. J Neurosurg 1999;90:215-220.5. Brown JA, Preul MC. Trigeminal depressor response during percutaneousmicrodecompression of trigeminal ganglion for trigeminal neuralgia. Neurosurg1988;23:745-48.6. Brown JA, Preul MC. Percutaneous trigeminal ganglion compression forTrigeminal neuralgia: Experience in 22 patients and review of literature. JNeurosurg 1989;70:900-9047. Schaller B. Trigemino cardiac reflex during microvascular trigeminaldecompression in case of trigeminal neuralgia. J Neurosurg Anaesthesiol2005;17:45-48.8.  Cha ST, Eby JB, Katzen JT. Trigemino cardiac reflex: A unique case of recurrentasystole during bilateral trigeminal sensory root rhizotomy. J of cranio-maxillofacial surgery 2002;30:108-111.9.  Spaziante R, Cappabianca P, Peca C. Subarachnoid haemorrhage and normalpressure hydrocephalus: Fatal complication of percutaneous microcompressionof the gasserian ganglion. Neurosurg 1988;22:148-50.10.  Hansen D, Syben R, Breckwoldt J. Perioperative cardiovascular reactions andthe noradrenaline plasma level in patients on chronic   antidepressantmedication. Anesthetist 1993;42:376-82.11.  Stoelting RK. Drug used for psychopharmacologic therapy. Pharmacologyand physiology in anaesthesia practice.  Philadephia JB Lippincott, 1999:360-4.12.  Sprung J, Schoenwald PK, Levy P: Treating intraoperative hypotension in apatient on long term tricyclic antidepressants; a case of aborted aortic surgery.Anesthesiology 1997;86:990-992.13.  Date T, Takahashi A, Iesaka Y. Effect of low dose isoproterenol infusion onleft atrial appendage function soon after cardioversion of chronic atrialtachyarrythmias. Int J Cardiology 2002:84:59-67.

Trigeminocardiac reflex unresponsive to atropine during microvascular decompression of trigeminal nerve root: A potentially lethal complication of a simple surgery

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Trigeminocardiac reflex unresponsive to atropine during microvascular decompression of trigeminal nerve root: A potentially lethal complication of a simple surgery

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