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From the Department of Neuroanaesthesia, Institute of Neurological Sciences, Southern General Hospital, Glasgow, United Kingdom.
Address correspondence to: Dr. Colin M. Goutcher, Department of Neuroanaesthesia, Institute of Neurological Sciences, Southern General Hospital, 1345 Govan Road, Glasgow, G51 4TF, United Kingdom. Phone: +44 (0) 141 201 1989; Fax: +44 (0) 141 201 2299; E-mail: c.goutcher{at}ntlworld.com
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Abstract |
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Clinical features: Patient 1 underwent a transmastoid transoccipital excision of a catecholamine-secreting glomus tumour. He exhibited marked hemodynamic instability after handling of the tumour began, which was not controlled by sodium nitroprusside. Improved hemodynamic stability was seen after the patient received magnesium sulfate. Patient 2 also underwent a transmastoid transoccipital excision of a catecholamine-secreting glomus tumour. Magnesium sulfate was commenced prior to tumour handling and continued until the tumour was removed. The patient remained hemodynamically stable. Sodium nitroprusside was not required.
Conclusion: Magnesium sulfate may be useful in preventing or minimizing the blood pressure changes associated with handling during excision of catecholamine-secreting glomus jugulare tumours. It may be of particular benefit in patients where there is significant intracranial extension.
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Introduction |
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TOPAbstractIntroductionCase report 1Case report 2DiscussionReferences |
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Case report 1 |
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TOPAbstractIntroductionCase report 1Case report 2DiscussionReferences |
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Results of a 24-hr urine collection and plasma catecholamines are shown in the Table
. The patient was hypertensive but gave no history suggestive of catecholamine crisis. Blood pressure was 161/68 mmHg supine and 127/84 mmHg standing. Alpha-blockade was achieved with phenoxybenzamine (20 mg three times a day), then beta-blockade with propranolol (40 mg three times a day). These doses were titrated to effect over the eight weeks prior to surgery. Alpha-blockade was judged to be adequate as the patient was normotensive with a minimal postural drop, and asymptomatic (except for tinnitus and facial weakness). Volume status was judged to be normal. Amlodipine was stopped as it would interfere with a metaiodobenzylguanidine (MIBG) scan. This was performed and was consistent with the glomus jugulare tumour being the only source of elevated catecholamines.
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Routine preoperative investigations were unremarkable. The patient had oral premedication consisting of temazepam 30 mg, ranitidine 150 mg and metoclopramide 10 mg. Standard monitoring was applied. A subclavian triple lumen central venous pressure line was inserted under local anesthesia, as was a radial arterial line. Anesthesia was induced and maintained with a target controlled infusion of propofol and a remifentanil infusion. At the same time, an iv infusion of sodium nitroprusside (50 mg/500 mL) was started, initially at 10 mL·hr–1.
The patient was positioned supine, tilted to the right. The initial part of the operation consisted of an extended radical mastoidectomy and superficial parotidectomy with dissection of the facial nerve from the tumour. This took six hours, during which time the patient was stable (Figure 1). The nitroprusside continued at 2 to 5 mL·hr–1.
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). Peaks were controlled with nitroprusside (30–70 mL·hr–1). The operation continued with identification of the lower four cranial nerves. The external jugular vein was divided and followed superiorly. The posterior fossa was entered and the tumour vascular supply identified. During this period blood pressure peaks and troughs were less pronounced. Isoflurane was discontinued and the nitroprusside ran at 0 to 10 mL·hr–1.
As the vagus nerve was being dissected in the jugular fossa, the patient had an asystolic cardiac arrest, presumed to be due to surgical traction on the nerve. Chest compressions were started, 0.6 mg of atropine given and traction on the vagus stopped. An output was obtained after 30 to 40 sec. The remainder of the operation consisted of tying off the venous drainage, piece-meal removal of the tumour and closure. This occurred uneventfully. For most of this period the nitroprusside was off. Fifteen milligrams of morphine were administered before transfer to the neurosurgical ICU.
The patient was sedated overnight with propofol and morphine by infusion and remained ventilated. A low dose norepinephrine infusion was required for six hours to maintain blood pressure. The following day, sedation was reduced and the patient allowed to waken. His trachea was extubated on the second postoperative day.
The patient developed a cerebrospinal fluid leak resulting in a collection under his skin flap, and later necrosis of the posterior part of the wound. This leak required an extended period of spinal drainage which delayed his discharge for three weeks. The necrotic part of the wound granulated over time and did not require further intervention. He went home off all medication except bendroflumethiazide. He continues to have a left sided facial palsy.
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Case report 2 |
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. He gave a history of right sided pulsatile tinnitus and hearing loss. An MRI scan showed a right sided glomus jugulare tumour with destruction of the right petrous temporal bone, eroding posteromedially to reach dura over the right cerebellar hemisphere with slight displacement of the anterior aspect of the cerebellar hemisphere and erosion anteriorly to the right carotid canal. Blood pressure was normal (140/80 mmHg) with no suggestion of catecholamine crises. An MIBG scan was consistent with the glomus jugulare tumour being the only source of elevated catecholamines. Alpha-blockade was achieved with phenoxybenzamine (10 mg daily), then beta-blockade with atenolol (10 mg daily) over four weeks prior to surgery. Although low, these doses were judged to be adequate as the patient was normotensive with no postural drop, and asymptomatic (except for tinnitus). Volume status was judged to be normal.
A transmastoid, transoccipital excision of the tumour was again planned as a combined procedure involving neurosurgery and otolaryngology. Four days before the scheduled operation date, particle embolization of the tumour was performed (under local anesthetic).
A preoperative electrocardiogram showed right bundle branch block with left anterior fascicle block, otherwise preoperative assessment was unremarkable. The patient had oral premedication consisting of lorazepam 2 mg, ranitidine 150 mg and metoclopramide 10 mg. Standard monitoring was applied. A radial arterial line was inserted under local anesthesia. Anesthesia was induced and maintained with a target controlled infusion of propofol and an alfentanil infusion. A femoral central venous pressure line and a lumbar spinal drain were inserted after induction.
The patient was positioned supine, tilted to the left. The initial part of the operation consisted of an extended radical mastoidectomy and superficial parotidectomy with dissection of the facial nerve from the tumour. This took eight hours, during which time the patient was stable (Figure 2). After this time, the surgeon indicated he was getting close to the tumour. The patient was given 16 mmol (4 g) of magnesium sulfate over 20 min, followed by an infusion of 4 mmol·hr–1 (1 g·hr–1) for the remainder of the case, until the tumour was removed. We chose to change the regimen from that previously used following a review of the published literature. The dose chosen was based on published advice2 and had the advantage of allowing us to continue the infusion for as long as required. The patient remained hemodynamically stable with only minor increases in blood pressure (Figure 2). These were controlled with low dose isoflurane; nitroprusside was not required. Serum magnesium was 1.59 mmol·L–1 and 1.61 mmol·L–1 during the continued infusion.
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The patient was transferred to the ICU, sedated overnight with propofol and morphine by infusion and kept ventilated. A low dose norepinephrine infusion was required for six hours to maintain blood pressure. The following day, sedation was reduced and the patient allowed to waken. His trachea was extubated late on the first postoperative day.
The patient was discharged home off all medication. He continues to have a right sided facial weakness.
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Discussion |
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TOPAbstractIntroductionCase report 1Case report 2DiscussionReferences |
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Our case reports are the first to describe the management of a catecholamine-secreting glomus jugulare tumour with intracranial extension using magnesium sulfate to control blood pressure. Magnesium sulfate has previously been suggested for use in the manage-ment of pheochromocytoma2,7 including the rapid preparation of a patient who could not be adequately 
-blocked.8 A potential criticism of our two cases concerns the degree of -blockade. This was judged to be adequate in both patients as they were normotensive with minimal postural changes and had no symptoms related to catecholamine excess. Their volume status was normal. In addition, when Patient 1 became hemodynamically unstable phentolamine had no effect, and both patients required norepinephrine infusions to maintain blood pressure after tumour excision.
The management of patients where there is intra-cranial involvement introduces another difficulty. The principles of neuroanesthesia – maintaining adequate cerebral perfusion while ensuring optimum intracranial operative conditions, mean that the anesthetic technique must be geared towards hemodynamical stability, arguably more so than in pheochromocytoma or in cases without intracranial involvement. Magnesium may be of more benefit in patients with glomus tumours than those with pheochromocytoma. The more established methods for controlling blood pressure (e.g., nitroprusside) react to changes which have already happened. Our reports suggest magnesium may be useful in preventing or minimizing the blood pressure changes in the first place. This may result in improved hemodynamic stability with the associated benefit for cerebral perfusion.
Magnesium sulfate appears to inhibit the release of catecholamines from both the adrenal medulla and peripheral adrenergic nerve terminals. It may also block catecholamine receptors directly2,9 and may have an action on vascular smooth muscle as increased concentrations of extracellular magnesium cause vasodilatation and attenuate agonist induced vasoconstriction.10 Magnesium may have additional benefits in patients, such as those in this report, where there is significant intracranial involvement. It acts as an N-methyl-D-aspartate antagonist9 and has been shown to be neuroprotective in experimental models of brain injury11,12 and spinal cord injury,13 although to date clinical studies have failed to demonstrate any benefit. Magnesium does not appear to have any detrimental effects on cerebral blood flow in healthy volunteers.14 It has also been shown to reduce the pressor response to laryngoscopy.15
Because of the low incidence of catecholamine-secreting glomus jugulare tumours, randomized controlled trials using magnesium sulfate are not feasible. Our report suggests that magnesium sulfate may have a useful role both prophylactically in patients who are well -blocked, and as a rescue drug where other treatments are ineffective.
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Footnotes |
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References |
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2 James MF, Huddle KR, Owen AD, van der Veen BW. Use of magnesium sulphate in the anesthetic management of pheochromocytoma in pregnancy. Can J Anaesth 1988; 35: 178–82.
3 Ghani GA, Sung YF, Per-Lee JH. Glomus jugulare tumors – origin, pathology and anesthetic considerations. Anesth Analg 1983; 62: 686–91.
4 Newland MC, Hurlbert BJ. Chemodectoma diagnosed by hypertension and tachycardia during anesthesia. Anesth Analg 1980; 59: 388–90.
5 Kremer R, Michel RP, Posner B, Wang NS, Lafond GP, Crawhall JC. Case report: catecholamine-secreting paraganglioma of glomus jugulare region. Am J Med Sci 1989; 297: 46–8.[Medline]
6 Trusso RA. Anesthesia for excision of a glomus jugulare tumor: report of a case. J Am Osteopath Assoc 1978; 77: 386–9.[Medline]
7 James MF. Use of magnesium sulphate in the anaesthetic management of phaeochromocytoma: a review of 17 anaesthetics. Br J Anaesth 1989; 62: 616–23.
8 Poopalalingam R, Chin EY. Rapid preparation of a patient with pheochromocytoma with labetolol and magnesium sulfate. Can J Anesth 2001; 48: 876–80.
9 Fawcett WJ, Haxby EJ, Male DA. Magnesium: physiology and pharmacology. Br J Anaesth 1999; 83: 302–20.
10 Laurant P, Touyz RM. Physiological and pathophysiological role of magnesium in the cardiovascular system: implications in hypertension. J Hypertens 2000; 18: 1177–91.[Medline]
11 Saris NE, Mervaala E, Karppanen H, Khawaja JA, Lewenstam A. Magnesium. An update on physiological, clinical and analytical aspects. Clin Chim Acta 2000; 294: 1–26.[Medline]
12 Marinov MB, Harbaugh KS, Hoopes PJ, Pikus HJ, Harbaugh RE. Neuroprotective effects of preischemia intraarterial magnesium sulfate in reversible focal cerebral ischemia. J Neurosurg 1996; 85: 117–24.[Medline]
13 Suzer T, Coskun E, Islekel H, Tahta K. Neuroprotective effect of magnesium on lipid peroxidation and axonal function after experimental spinal cord injury. Spinal Cord 1999; 37: 480–4.[Medline]
14 Sherman R, Armory P, Moody P, Hope T, Mahajan RP. Effects of magnesium sulphate on cerebral haemodynamics in healthy volunteers: a transcranial Doppler study. Br J Anaesth 2003; 91: 273–5.
15 Dube L, Granry JC. The therapeutic use of magnesium in anesthesiology, intensive care and emergency medicine: a review. Can J Anesth 2003; 50: 732–46.
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