Ann Thorac Surg 2006;81:2298-2300
© 2006 The Society of Thoracic Surgeons
Case report
Surgical Approach in Massive Intraoperative Atherosclerotic Embolism
Stefanos Demertzis, MD, PhD
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,
Rafael Trunfio, MD,
Fredi von Rotz, MD,
Francesco Siclari, MD, PhD
Department of Cardiac Surgery, Cardiocentro Ticino, Lugano, Switzerland
Accepted for publication August 22, 2005.
* Address correspondence to Dr Demertzis, Cardiocentro Ticino, via Tesserete 48, Lugano, CH-6900 Switzerland (Email: demertzis{at}cardiocentro.org).
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Abstract
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We describe a case of massive embolization of atherosclerotic material during aortic cannulation and the surgical approach chosen to treat it, that is, retrograde cerebral perfusion and subtotal arch replacement in deep hypothermic circulatory arrest.
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Introduction
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Mobilization of atheromatous material during cardiac surgery is a threatened complication that can cause ischemic brain damage with high postoperative morbidity and mortality. Normally the surgeon is not aware of the complication, embolization is assumed a posteriori (ie, if the patient should present a neurologic deficit or undergo specific diagnostic imaging, or both). In the rare case that atherosclerotic embolism becomes evident in real time, the attempt to invert the flow in the major cerebral arteries can be made, hoping to mobilize eventual emboli.
A 60-year-old man was diagnosed with an aneurysm of the ascending aorta, significant aortic valve regurgitation, and a small atrial septum defect. He was referred for an aortic valve and ascending aorta replacement, as well as closure of an atrial septum defect. Echocardiographically the aortic valve appeared tricuspid but heavily asymmetric. The patient was on warfarin treatment because of a recently developed atrial fibrillation.
After median sternotomy and pericardiotomy, heparin was given intravenously (300 IU/kg) to achieve an activated clotting time of more than 500 seconds. The ascending aorta and the descending aorta were evaluated by means of intraoperative transesophageal echocardiography. Intima was found to be thickened in both; however, intimal thickness was less than 4 mm. By inspection, the proximal ascending aorta appeared diseased (ie, isolated atheromatous yellowish lesions were protruding off the adventitia). The aortic arch at the height of the left carotid artery and both caval veins were prepared. A 24-French arterial cannula (Jostra AG, Hechingen, Germany) was inserted into the aortic arch. It was noticed immediately that atherosclerotic material was pushed with the blood into the cannula. The cannula was flushed and after venous cannulation, extracorporeal circulation was instituted. The anesthesiologist reported the presence of atherosclerotic material in the arterial blood probe drawn from the pressure line in the left radial artery.
Considering a systemic embolism of atherosclerotic material as highly likely, the strategy changed. The patient was cooled down to 18°C nasopharyngeal temperature for aortic arch exploration in circulatory arrest. Myocardial protection was achieved by antegrade and retrograde cold blood cardioplegia.
In circulatory arrest the ascending aorta and aortic arch were inspected; both were found heavily diseased, seeded with numerous ruptured ulcerous lesions containing highly mobile soft atherosclerotic material exposed to the bloodstream (Fig 1). The aortic cannula had obviously hit one of the lesions. Retrograde cerebral perfusion was initiated with the hope to mobilize the embolic material. The venous cannula already in the superior vena cava was connected to the arterial line, and the retrograde cerebral perfusion was performed while keeping the central venous pressure between 20 and 25 mm Hg. Interestingly, loose atherosclerotic particles appeared in the dark blood coming out of the supraaortic vessels. A subtotal arch replacement was performed using a 26-mm gelatine-sealed vascular prosthesis (Vascutek Ltd, Renfrewshire, Scotland, UK). Reperfusion was initiated after cannulation of the arch prosthesis. The aortic root replacement was subsequently performed using a 27-mm composite graft (Carbomedics Inc, Austin TX). The operation was completed performing the prosthesio-prosthetic anastomosis and the ASD closure. The patient was weaned off bypass utilizing the intraaortic balloon pump (IABP) and inotropes because of left ventricular diastolic dysfunction. His ventricular function recovered well, and he could be weaned off the IABP and inotropes 36 hours after surgery. He did not present any sign of either focal or diffuse neurologic injury. The laboratory workup revealed a significant rise of the creatine kinase values that were not followed by the creatine kinase-MB isoenzyme (creatine kinase maximum, 1,777 U/L at 72 hrs with MB 56). Other laboratory values including serum creatinine did not show particularly unusual movements during the same time period. The further clinical recovery was uneventful. A cerebral contrast computed tomographic scan was performed on postoperative day 7 that did not show any subacute cerebral infarction.

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Fig 1. Operative specimen of the proximal aortic arch demonstrating the intimal aortic surface seeded with ulcerating, debris-filled atherosclerotic lesions.
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Comment
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Mobilization of atheromatous material during cardiac surgical procedures is a threatened complication. Release of atherosclerotic material is possible with almost any manipulation of the aorta [1]. If the degree of atherosclerotic disease of the aorta or aortic arch is diagnosed prior to surgery or before surgical manipulation (eg, by means of epi-aortic scanning), then the surgical strategy can be adjusted. In the case described, palpation by the surgeon, as well as transesophageal echocardiography missed the severe atherosclerosis of the ascending aorta, a diagnostic gap well described in the literature. Unfortuantely, epi-aortic scanning was not available. If epi-aortic scanning had been used, the gross atherosclerotic lesions in the ascending aorta would have been recognized and handled well in advance of any aortic manipulation. The only hint to severe atherosclerosis was the visual impression of the ascending aorta. Some unexplained symptoms of our patient could be found in his aortic arch (ie, the patient had reported episodes of optical sensations of short duration in his right or left visual field, or both). Retrospectively these phenomena could be interpreted as sequelae of recurrent microembolism (ie, the atheromatous ascending aorta or aortic arch, or both, are well established sources of cerebral emboli even without any iatrogenic manipulation [2].
Suspecting evolving cerebral embolism during cardiac surgery is a particular situation in which the intraoperative countermeasures of confirmed efficacy and reliability do not exist. Although there is some evidence that flow reversal could attenuate or prevent stroke caused by cerebral embolism [3, 4]. Although this evidence was collected in very different clinical situations, the principle is appealing (ie, the mobilization of the emboli off their wedge position in major branches of the cerebral arteries). The technique of retrograde cerebral perfusion proposed by Ueda and colleagues [5] for cerebral protection during circulatory arrest in aortic surgery was initially introduced for treatment of massive air embolism during cardiopulmonary bypass [6] aiming at the same effect (ie, flow reversion). Although the nutritive effect of retrograde cerebral perfusion is debatable, flow reversal in the main cerebral arteries has been documented [7]. The case described lacks a specific proof of cerebral embolism, as well as the proof of the contribution of retrograde cerebral perfusion in preventing brain injury. The positive neurologic outcome does not necessarily prove the efficacy of the treatment even though this may seem appealing. The aim of this report is to illustrate a potentially helpful strategy when brain damage due to significant intraoperative embolism seems apparently inevitable. The availability of a potentially effective maneuver for reversing suspected cerebral embolism should absolutely not encourage the deviation from the strategy of prevention of cerebral embolism by thorough preoperative and intraoperative diagnostic evaluation of the ascending aorta and aortic arch.
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Acknowledgments
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We thank Bernard Hausen, MD, PhD, for his constructive discussion of this article.
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References
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