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Ann Thorac Surg 2008;86:289-291. doi:10.1016/j.athoracsur.2008.01.039
© 2008 The Society of Thoracic Surgeons

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Case Reports

Use of Transcranial Doppler Ultrasound in Endovascular Repair of a Type B Aortic Dissection

Ali Khoynezhad, MD, PhDa,*, Matthew J. Kruse, BSa, Carlos E. Donayre, MDb, Rodney A. White, MDb

a Section of Cardiothoracic Surgery, University of Nebraska Medical Center, Omaha, Nebraska
b Division of Vascular and Endovascular Surgery, Harbor-UCLA Medical Center, Torrance, California

Accepted for publication January 10, 2008.

* Address correspondence to Dr Khoynezhad, Section of Cardiothoracic Surgery, University of Nebraska Medical Center, 982315 Nebraska Medical Center, Omaha, NE 68198-2315 (Email: akhoynezhad{at}unmc.edu).


    Abstract
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 Abstract
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Intraprocedural monitoring with transcranial Doppler ultrasound in thoracic endovascular aortic repair provides critical information regarding the occurrence of cerebral microemboli and adequacy of cerebral blood flow. We present the perioperative course of a patient with complicated Stanford type B aortic dissection undergoing thoracic endovascular aortic repair with continuous intraoperative transcranial Doppler ultrasound monitoring.


    Introduction
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 Abstract
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Postoperative stroke is a dreaded complication after thoracic endovascular aortic repair (TEVAR). The United States multicenter trial with the Gore TAG (W. L. Gore & Associates, Flagstaff, AZ) thoracic endoprosthesis revealed a stroke rate of 4% in both open repair and TEVAR groups [1]. The cause of stroke after endovascular procedures is believed to be embolic. In an autopsy series, catheter-related cerebral embolization in patients undergoing cardiac catheterization was reported in 30% of patients [2]. Recently, transcranial Doppler ultrasound (TCD) has been used to evaluate the embolic effect of guidewires and catheters in the transverse aorta after diagnostic left heart catheterization [3]. In addition to detection of cerebral microemboli in the form of high-intensity transient signals, TCD also provides direct information concerning blood flow that reaches the cerebral circulation by displaying middle cerebral artery (MCA) flow velocity. This case report underscores the use and noninvasiveness of TCD in a patient undergoing TEVAR. Transcranial Doppler ultrasound provided important information changing the intraoperative course and the patient's outcome.

The patient is a 58-year-old man with a history of poorly controlled hypertension and a recent type B aortic dissection. He presented with hypertensive emergency and a new onset of severe left lower extremity claudication, buttock pain, and impotence. Laboratory work revealed blood urea nitrogen and creatinine levels were 22 mg/dL and 1.6 mg/dL, respectively. These were up from normal values on prior admissions. A computed tomographic scan revealed that the dissection flap had propagated into the left common femoral artery since the computed tomographic scan of the prior admission. The left internal iliac artery was now occluded, with the left common and external iliac artery fed by the false lumen. He also had greater than a 1.5 cm increase in the diameter of the proximal descending aorta to 5.2 cm.

The patient was offered TEVAR to treat his new symptoms of renal and peripheral malperfusion, and the rapid aneurysmal dilatation of the proximal descending aorta. Informed consent was obtained, and endovascular exclusion of the false aortic lumen was offered using the Talent endoprosthesis (Medtronic, Inc, Santa Rosa, CA) through a single institution investigational device exemption approved by the Food and Drug Administration. In the endovascular suite, bilateral TCD transducers affixed to the patient's temporal bone windows displayed baseline right and left MCA velocities of 52 cm/second and 69 cm/second, respectively. Left MCA velocity was consistently 15% to 20% higher than right MCA velocity due to the presence of stenosis in the left carotid siphon or terminal left internal carotid artery (Fig 1A). The right common femoral artery was exposed and accessed. The intravascular ultrasound catheter was advanced into the true lumen of the thoracic aorta under fluoroscopic guidance. The proximal dissection entry site was seen to be within 2 cm distal to the left subclavian artery and the true lumen was 3 cm in its largest dimension. There was no evidence of dissection in the aortic arch or brachiocephalic vessels. A 4-French pigtail catheter was introduced in the aortic arch through the right radial artery using a micropuncture set. Angiographic findings concurred with those of intravascular ultrasound and preoperative computed tomography, which revealed a small true lumen (Fig 2A).


Figure 1
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Fig 1. (A) Baseline transcranial Doppler ultrasound (TCD) waveform: the upper tracing is recorded from the left middle cerebral artery (MCA) window, whereas the lower tracing is recorded from the right MCA window. (B) Post-endograft deployment TCD waveform demonstrating drop in left MCA flow. (C) Transcranial Doppler ultrasound waveform after repositioning of the stent graft, revealing return to the preoperative pattern. (NicVue version 2.6.8 software with Companion III TCD system [Nicolet Vascular, Madison, WI]).

 

Figure 2
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Fig 2. (A) Pre-deployment angiogram. (B) Post-deployment angiogram: normal angiographic findings of an unrestricted common carotid artery orifice after endograft deployment in landing zone II can be deceptive; transcranial Doppler ultrasound confirmed that flow to the middle cerebral artery was in fact impeded.

 
Using adenosine-induced cardiac arrest, the stent graft was deployed just distal to the left common carotid artery orifice to achieve an adequate proximal landing zone and effective exclusion of the false lumen. At this point, the TCD data indicated a high-intensity transient signal, as well as a sudden decrease of approximately 20% in the mean velocity of the left MCA. In contrast to baseline and pre-deployment values, the left MCA velocity waveform became evenly matched with that of the right MCA velocity (Fig 1B). A post-deployment intravascular ultrasound examination revealed no interference of the left carotid artery by the endograft. Aortography confirmed correct placement of the endograft and effective exclusion of the dissection entry tear, demonstrating normal flow to the innominate and left carotid arteries with negligible opacification of the false lumen in the abdominal aorta (Fig 2B). However, given the timing and persistence of this drop in left MCA velocity, a partial coverage of left internal carotid artery was diagnosed. A compliant balloon was advanced into the mid-portion of the endograft and was inflated to the diameter of the graft; the endograft was then pulled slightly more distally. Subsequently, the left MCA velocity returned to the baseline pattern of 15% to 20% higher than the right MCA velocity (Fig 1C). Repeat intravascular ultrasound examination confirmed luminal apposition of the stent graft, complete coverage of the primary entry site, as well as acute enlargement and increased pulsatility of the true lumen. After removal of the endovascular devices and repair of access sites, a femoral-femoral bypass was performed because the perfusion status of the left lower extremity had not significantly improved. The patient was hydrated postoperatively. Subsequent hospital course was without complications. He was discharged home on postoperative day 4.


    Comment
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 Abstract
 Introduction
 Comment
 References
 
Given the new symptoms of peripheral and renal malperfusion and aneurysmal growth of the descending thoracic aorta, exclusion of the false aortic lumen by TEVAR offered an effective and less invasive option for this complicated type B aortic dissection. In this case, intraoperative monitoring with transcranial Doppler ultrasound apprised the surgeon of a critical procedural detail, a partially covered left common carotid artery that was missed by intravascular ultrasound and angiography. Transcranial Doppler ultrasound detected a moderate decrease in the patient's left MCA mean velocity for several minutes immediately after endograft deployment, caused by marginalized blood supply to the left middle cerebral artery and carrying ominous future implications if the position of the endograft had not been adjusted. Furthermore, an unrestricted flow pattern to the left common carotid artery is crucial in this patient because it also supplies the left subclavian artery due to the position of the stent graft.

Intraoperative monitoring with TCD has shown to have clinical implications and to benefit patients undergoing open repair of type A aortic dissection [4]. Careful attention should be given to TCD data during portions of the operation likely to affect the cerebral circulation, either by changes in blood flow or the number of high-intensity transient signals. The significance of cerebral microemboli detected as high-intensity transient signals by TCD is found in their association with cognitive impairment [5]. As postoperative stroke seems to be a perpetual risk of thoracic aortic interventions, TCD monitoring is poised to become a more widespread tool in analyzing the cause of stroke in these procedures.


    References
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 Abstract
 Introduction
 Comment
 References
 

  1. Makaroun MS, Dillavou ED, Kee ST, et al. Endovascular treatment of thoracic aortic aneurysms: results of the phase II multicenter trial of the GORE TAG thoracic endoprosthesis J Vasc Surg 2005;41:1-9.[Medline]
  2. Ramirez G, O'Neill Jr WM, Lambert R, Bloomer HA. Cholesterol embolization: a complication of angiography Arch Intern Med 1978;138:1430-1432.[Abstract/Free Full Text]
  3. Braekken SK, Endresen K, Russell D, Brucher R, Kjekshus J. Influence of guidewire and catheter type on the frequency of cerebral microembolic signals during left heart catheterization Am J Cardiol 1998;82:632-637.[Medline]
  4. Estrera A, Garami Z, Miller 3rd CC, et al. Cerebral monitoring with transcranial Doppler ultrasonography improves neurologic outcome during repairs of acute type A aortic dissection J Thorac Cardiovasc Surg 2005;129:277-285.[Abstract/Free Full Text]
  5. Russel D. Cerebral microemboli and cognitive impairment J Neurol Science 2002;203–204:211-214.



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[Abstract] [Full Text] [PDF]


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