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Ann Thorac Surg 2009;88:1264-1268. doi:10.1016/j.athoracsur.2009.06.054
© 2009 The Society of Thoracic Surgeons
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Original Articles: Adult Cardiac

Cardiac Operations in the Presence of Meningioma

Ivan Aleksic, MD, PhDa,*,*, Sebastian-Patrick Sommer, MDa,*, Eva Kottenberg-Assenmacher, MDb, Volkmar Lange, MDa, Christoph Schimmer, MDa, Mehmet Oezkur, MDa, Rainer G. Leyh, MD, PhDa, Armin Gorski, MDa

a Department of Thoracic and Cardiovascular Surgery, Julius-Maximilians-University Würzburg, Würzburg, Germany
b Department of Anesthesiology, University Hospital Essen, University Duisburg-Essen, Essen, Germany

Accepted for publication June 19, 2009.

* Address correspondence to Dr Aleksic, Department of Thoracic and Cardiovascular Surgery, Julius-Maximilians-University, Oberdürrbacher Str 6, 97080, Würzburg Germany (Email: aleksic_i{at}klinik.uni-wuerzburg.de).


   Abstract
Top
 Abstract
Introduction
 Material and Methods
 Results
 Comment
 Footnotes
 References
 
Background: We investigated the effect of concomitant intracranial meningiomas on perioperative and postoperative complications after cardiac operations. Also studied was the intraoperative and perioperative management and long-term outcome of such patients.

Methods: We retrospectively evaluated 16 cardiac surgical patients with intracranial meningiomas between January 1996 and July 2007. Neurologic outcome, incidence of transient neurologic deficits, and long-term follow-up focusing on freedom from any cardiac or neurosurgical intervention were assessed.

Results: Five men and 11 women with a concomitant diagnosis of intracranial meningioma underwent cardiac operations using extracorporeal circulation. One patient received additional edema prophylaxis by intravenous dexamethasone. All patients were discharged home in good physical condition. Data on long-term survival were available on 14 patients, with 12 alive. Postoperatively, 2 patients died from myocardial infarction at 26.8 months and 2 from metastatic colon cancer at 57.9 months. Perioperative neurologic disorders were observed in 2 patients, comprising one stroke after intervention for aortic dissection and one thromboembolic event 2 weeks after biologic mitral valve replacement due to anticoagulation disorders. No meningioma-related adverse event was observed.

Conclusions: The presence of intracranial meningioma does not appear to be a risk factor for patients undergoing cardiac operations. No meningioma-related neurologic sequelae were documented postoperatively. Neurosurgical consultation should be obtained in all patients preoperatively.


   Introduction
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 Abstract
 Introduction
Material and Methods
 Results
 Comment
 Footnotes
 References
 
Meningiomas are the second most common primary intracranial neoplasm. Meningiomas are generally benign lesions (90%) and comprise 18% of all intracranial tumors [1]. They are more commonly identified in older patients, with a peak incidence at age 60 years. They are also more common in women, with a preponderance of 3:2 in the supratentorial compartment but as high as 24:1 [2, 3]. The intracranial incidence is 2 in 100,000 [4]. Because many benign meningiomas do not produce symptoms, the true incidence is likely much higher. Presenting signs and symptoms depend on the size and location of the lesion and include headache, seizure, and neurologic deficits due to local mass effect.

The experience with cardiac operations in the presence of symptomatic meningiomas using cardiopulmonary bypass (CPB) is limited to a few case reports [5–8]. Two reports describe complications after cardiac operations, namely, remitting visual loss after coronary artery bypass grafting (CABG) from a suprasellar meningioma [7] and intratumoral hemorrhage from a posterior fossa meningioma several days after aortic valve replacement due to anticoagulation therapy [8].

CPB may result in cerebral edema and increased blood-brain barrier permeability [9]. Brain tumors themselves may increase intracranial pressure, alter cerebral blood flow, and lead to neovascularization [10]. An additional detrimental effect on edema formation by CPB in meningioma patients is theoretically plausible but has not been ruled out yet.

Larger studies are lacking, as are data on the proper intraoperative and perioperative management and long-term outcome of such patients. We aimed to assess the potential effect of meningiomas on perioperative and long-term neurologic outcome after cardiac operations.


   Material and Methods
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 Abstract
 Introduction
 Material and Methods
Results
 Comment
 Footnotes
 References
 
The local Ethics Committees approved this study in compliance with the Helsinki Declaration. Individual consent from patients who participated in the study was waived because individual patients are not identified.

Patients
We retrospectively evaluated medical records and operative, perfusion, and anesthesia protocols of all patients with radiologically confirmed intracranial meningioma who underwent cardiac operations in which CPB was used at two institutions from January 1996 until July 2007. Our database showed 16 patients had a prehospital diagnosis of meningioma. Patients who had undergone meningioma operations were excluded. Patients were considered eligible for further study if an intracranial meningioma had been confirmed by preoperative computed tomography or magnetic resonance imaging.

All elective patients with meningiomas and their radiographic studies were seen by a consultant neurosurgeon before cardiac operations were scheduled. If specific measures for edema prevention were deemed necessary, they were recorded and followed strictly. The consultants never determined that intraoperative monitoring of cerebral pressure was necessary. The consultant neurosurgeon recommended 24 mg dexamethasone be given to 1 patient for edema prevention after induction of anesthesia (Fig 1). Emergency operations were required in 3 patients due to Stanford type A aortic dissection and unstable angina, respectively, and no preoperative neurosurgical consultation could be obtained.


Figure 1
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  		Fig 1. Preoperative computed tomography scan shows a frontal falx meningioma, compression of the ventricle by peritumoral edema, and mild midline shift. This patient received antiedematous therapy with dexamethasone after induction of anesthesia.

 
Anesthesia
After premedication with oral flunitrazepam (1 mg), a 5-lead electrocardiography and a pulse oximeter was attached, and a peripheral venous cannula was placed. A radial catheter was inserted under local anesthesia. General anesthesia was induced by midazolam (2 to 5 mg), sufentanil (50 to 100 µg), and etomidate (20 mg), followed by pancuronium (8 mg) or rocuronium (50 mg), according to the anesthetist's preferences.

Anesthesia was maintained with sufentanil and isoflurane (0.6% to 0.8%) end tidal, as required. Moderate hyperventilation (PaCO 2 30 to 35 mm Hg) was established using mainstream capnography. After sternotomy but before CPB was initiated, patients were administered 1 million kallikrein inactivator units (KIU) of aprotinin intravenously and received intravenous heparin (400 U/kg) in preparation for CPB, resulting in activated clotting times exceeding 400 seconds.

After uncomplicated separation from CPB and reversal of heparin by protamine sulfate, additional doses of 500,000 KIU of aprotinin were infused. Activated clotting time was targeted at 100 to 135 seconds postoperatively. Within the first 24 hours, anticoagulation was achieved by continuous administration of low-dose heparin and acetylsalicylic acid started no sooner than 6 hours postoperatively in bypass patients.

Surgical Procedure
All patients underwent median sternotomy. After institution of CPB with a venous two-stage cannula, mild systemic hypothermia of 32°C was instituted. The hematocrit was maintained at 17%. Alpha-stat pH management was used throughout, serum sodium level was kept between 132 to 138 mmol/L, and serum glucose level was controlled with the intermittent administration of small insulin boluses (2 to 5 U). A 40-µm arterial line filter was part of the standard setup of the heart lung-machine in most patients. Alterations of pump prime, such as addition of hypertonic saline or mannitol, were recorded in the pump protocol.

The patients with acute type A aortic dissection were operated on with deep hypothermic circulatory arrest at 18°C. Arrest periods were 23 and 37 minutes, respectively. In addition, topical cooling of the head was used, and thiopental (1 g) and prednisolone (1 g) were given intravenously before circulatory arrest.

Outcome
Outcome data were categorized as number of patients who survived the procedure, number of patients who survived without any neurologic deficit, and number who were discharged after the cardiac operation. All patients were monitored and interviewed by phone by means of a standardized questionnaire focusing on their quality of life after the cardiac procedure, any cardiac reinterventions, and on new symptoms of their meningiomas after the cardiac operation, possible operations for their meningiomas, and freedom from reintervention.


   Results
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 Abstract
 Introduction
 Material and Methods
 Results
Comment
 Footnotes
 References
 
We identified 16 patients (11 women, 5 men) with a prehospital diagnosis of meningioma, comprising 9 falcine meningiomas, 4 convexity meningiomas, and 3 cerebellopontine angle meningiomas. Mean diameter of the tumors was 2.5 cm (range, 1.2 to 6.0 cm). The mean age was 75.4 ± 7.6 years (range, 43 to 84 years) for women vs 71.2 ± 6.9 years (range 66 to 81 years) for men. All men and 6 women underwent CABG, and 5 women were operated on for aortic stenosis and concomitant coronary artery disease (n = 1), mitral valve insufficiency (n = 1), type A aortic dissection (n = 2), and combined coronary artery and mitral valve disease (n = 1). The type of procedure performed is provided in Table 1.


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  		Table 1 Demographic Data for Patients With Meningioma
 
Emergency operations were required in 3 patients, 2 with type A aortic dissection and 1 with unstable angina due to coronary artery disease. All other patients underwent elective procedures. One patient was operated on twice. She required reoperation 2 years after primary CABG due to new onset of significant aortic valve stenosis.

All patients survived their operations and were discharged home in good general condition. Data on long-term survival and physical abilities were available from 14 of 16 patients at time of investigation. Two patients were lost to follow-up. No death certificates were archived with the census office. Of the 14 patients, 12 were alive and in good health, with a mean postoperative survival of 31 ± 28 months (range, 3.7 to 88.9 months; Fig 2).


Figure 2
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  		Fig 2. Kaplan-Meier curve shows survival analysis after cardiac operation in 16 patients with meningioma.

 
Perioperative neurologic disorders were observed in 2 women. A stroke was documented in 1 patient during a Bentall-de Bono procedure for treatment of type A aortic dissection. The other patient sustained a thromboembolic event 2 weeks after biologic mitral valve replacement due to anticoagulation disorders. In both patients the neurologic disorders were completely reversible within a few months. The first patient was still alive at the time of the survey at 88.9 months postoperatively. The second died from metastatic colonic cancer at 57.9 months but was free from neurologic or cardiac disorders at that time. A third patient was found to have mild transient perioperative perturbation but was completely adequate at the time of discharge. This patient is alive without any adverse neurologic events 24.2 months after CABG. During long-term follow-up, another female patient died from myocardial infarction at 26.8 months.

The mean survival time of all patients was 42.7 ± 22.3 months. All surviving patients are currently under intermittent medical follow-up by a physician or cardiologist.

All patients reported postoperative improvement in their New York Heart Association functional class from 2.8 ± 0.7 to 1.7 ± 0.5. Cardiac reintervention (coronary angioplasty) due to recurrent coronary artery disease was necessary in 2 women. None of our patients reported new neurologic symptoms that could be related to their meningiomas. No patients required an operation for meningioma.


   Comment
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 Abstract
 Introduction
 Material and Methods
 Results
 Comment
Footnotes
 References
 
Neurologic complications account for significant postoperative morbidity and mortality after cardiac operations. The incidence of perioperative strokes in prospective studies is 1.5% to 5.2% [11, 12]. A much larger proportion of patients will have subtle, mostly subclinical changes in neurocognitive function detectable by decreasing test scores only [13]. Short-term cognitive decline is reported in 30% to 80% of patients undergoing CABG with CPB [14].

Paralleling the increasingly older patients referred for cardiac procedures, one must anticipate that the incidence of patients with concomitant cerebral meningioma is growing. The effect of cerebral meningiomas on outcome in patients undergoing cardiac procedures has not been extensively evaluated. The potential relevance of meningiomas is highlighted by a recent case report from Karizu and coworkers [15]. They described a 75-year-old woman who was found to have delayed hemiplegia 2 days after mitral valve replacement. Magnetic resonance imaging showed she had a meningioma with severe perifocal edema. After neurosurgical removal of the tumor, the patient recovered completely.

Some authors have considered meningiomas as a possible risk factor in cardiac operations and advocated altered regimens for cerebral protection [5, 6]. Data on this issue are scarce. All recommendations are based on case reports. Given the low overall incidence of meningiomas in the overall population, we found a rather high number of patients with meningiomas in our database. The assumption that some of these patients had been denied operations by other cardiac surgery units because of their meningioma could not be confirmed from the records and from interviews with the surviving patients. It supports our opinion that we operate on more elderly patients with meningioma than we actually know. In fact, all of our patients were known to have a meningioma because of imaging studies that are not routinely performed in all elderly patients. Therefore, it is possible that more meningiomas would be detected if more cerebral imaging studies were done before cardiac procedures.

To prevent cerebral edema, Grigore and colleagues [6] changed their anesthetic management by using moderate hyperventilation with a target PaCO 2 of 30 to 35 mm Hg, giving 4 mg of dexamethasone intravenously immediately after institution of CPB and another 4 mg after cessation of CPB, and by addition of hypertonic saline to the pump prime. We have not used dexamethasone routinely because all elective patients were seen by neurosurgeons preoperatively. In all patients, we followed their instructions, and only 1 patient received dexamethasone. Two of the three emergency operations were for type A aortic dissection with circulatory arrest and both patients received 1 g of prednisolone as part of our routine cerebral protection in case of deep hypothermic circulatory arrest.

Tashiro and colleagues [5] performed off-pump CABG (OPCAB) in a patient with a brain tumor to avoid cerebral complications. In 11 patients who underwent isolated CABG in our cohort, OPCAB could have been an option. However, the operations in 10 of these 11 patients occurred during an era when OPCAB was performed only occasionally and reimbursement issues were not definitively settled for off-pump procedures.

CPB may result in cerebral edema due to decreased plasma osmolarity and increased blood-brain barrier permeability [9]. The increased production of antidiuretic hormone encountered after operations with CPB decreases plasma osmolarity and contributes to cerebral swelling [16]. In a lamb model, Cavaglia and colleagues [17] found detrimental effects of CPB on the blood-brain barrier by increased inducible transcription factor gene expression, namely the protooncogene c-fos (cellular-feline osteogenic sarcoma) and increased leakage of fluorescent albumin from blood vessels.

Methods to reduce brain edema with cardiopulmonary bypass include the maintenance of normal osmolarity by adding hypertonic saline as described by Grigore and colleagues [6]. Maintenance of normal serum sodium levels is closely correlated with cerebral swelling in animal models [18]. Other important measures for the reduction of cerebral edema include stringent perfusion pressure management, avoiding periods of hyperperfusion and hypoperfusion, and avoidance of hyperglycemia and hyperthermia as stated in the American College of Cardiology/American Heart Association practice guidelines [19].

Optimizing management protocols and implementation of evidence-based guidelines has a major effect on the incidence of neurologic morbidity after cardiac operations. Suojaranta-Ylinen and colleagues [20] reported a decrease in neurologic complications from 6.7% to 2.7% (p < 0.01) and a corresponding decrease in intensive care unit mortality from 3.8% to 2.0% (p < 0.01).

Brain tumors may increase intracranial pressure, alter cerebral blood flow, and lead to neovascularization by vessels that lack normal blood-brain barrier characteristics [10]. Meningiomas, in particular, produce vascular endothelial growth factor (VEGF), a potent stimulator for angiogenesis and peritumoral edema [21]. Peritumoral edema has an incidence of 40% to 78% in meningioma patients [22]. Furthermore, vascular endothelial growth factor messenger RNA isoforms 121 and 165 are significantly up-regulated in meningioma patients treated with partial preoperative embolization [23].

On the other hand, embolization is a significant complication by itself during cardiac operations [11, 12]; perhaps this could trigger increased edema formation in meningiomas due to higher expression of the above-mentioned VEGF isoforms. In addition, patients aged 61 to 70 with meningioma have more peritumoral brain edema than younger patients as calculated by the mean edema index [24].

This study has several limitations. First, this is a retrospective analysis of a rather small patient cohort. Second, the retrospective nature precluded a more systematic approach to thorough neuropsychologic assessment before and after the operation to evaluate any possible impairment. In addition, only few patients received preoperative and postoperative cerebral imaging to determine any changes of the meningiomas like progression of peritumoral edema. Future studies with such patients should incorporate neuropsychologic testing and preoperative and postoperative neuroradiologic imaging. Current imaging techniques, such as diffusion-weighted magnetic resonance imaging have to be used for such studies.

That no meningioma-related complications were observed and the long-term outcome of our patients was favorable indicates that the presence of cerebral meningioma is not necessarily a risk factor for cardiac operations. Further studies with larger patient cohorts might elucidate the influence of meningioma on neurologic complications after cardiac operations and should evaluate the role of a standard corticosteroid-based edema prophylaxis.

Because the judgment about the tumor's potential for significant edema formation and complications is beyond the scope of cardiac surgeons, we advocate the consultation by a neurologist or neurosurgeon apart from applying established techniques for the prevention of cerebral edema as stated in our current practice guidelines.


   Footnotes
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 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Footnotes
References
 
* Both authors contributed equally to this work. Back


   References
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 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Footnotes
 References
 

  1. Rachlin J, Rosenblum M. Etiology and biology of meningiomasIn: Al-Mefty O, editor. Pathology of tumours of the nervous system. Baltimore: Williams and Wilkins; 1991. pp. 22-37.
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