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Ann Thorac Surg 2009;87:e27-e28. doi:10.1016/j.athoracsur.2008.11.041
© 2009 The Society of Thoracic Surgeons

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Case Reports

Controlled Earlier Reperfusion for Brain Ischemia Caused by Acute Type A Aortic Dissection

Hiroshi Munakata, MD*, Kenji Okada, MD, PhD, Hiroya Kano, MT, Sou Izumi, MD, Yutaka Hino, MD, Masamichi Matsumori, MD, PhD, Yutaka Okita, MD, PhD

Department of Surgery, Division of Cardiovascular Surgery, Kobe University Graduate School of Medicine, Kobe, Japan

Accepted for publication November 17, 2008.

* Address correspondence to Dr Munakata, Department of Surgery, Division of Cardiovascular Surgery Kobe University Graduate School of Medicine, 7-5-2, Kusunoki-cho, Chuo-ku, Kobe, 650-0017, Japan (Email: h-munakata{at}k7.dion.ne.jp).


    Abstract
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 Abstract
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Brain malperfusion caused by acute type A aortic dissection is a life threatening situation that should be relieved as early as possible with minimal reperfusion injury prior to aortic repair. The patient was 72-year-old woman with acute type A aortic dissection. She was referred to us 2.5 hours after onset of chest pain, and she was unconscious with a complete left paralysis. The true lumen of internal carotid artery was severely stenosed. A simple bypass circuit was installed from the femoral artery to the true lumen of the right common carotid artery, which consisted with a roller pump and cold bath for blood cooling. Regional oxygen saturation of the right frontal brain was immediately raised after initiation of the bypass, and she underwent emergency ascending hemi-arch replacement. The postoperative course was complicated with a right brain stroke; however, brain computed tomography and magnetic resonance imaging disclosed minimum brain edema. She was discharged on foot on the 35th postoperative day, and she was walking with a stick after 7 months.


    Introduction
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Emergent surgery of acute aortic dissection remains controversial in patients who have complications with cerebral malperfusion because of its high mortality and cerebral morbidity [1–3]. It is generally accepted that early reperfusion is extremely important to reduce brain ischemic insult, and several techniques have been reported to save brain integrity [4, 5]. However, all of them were applied during the aortic operation, and ischemic insult was continued until the reperfusion of the carotid artery was established.

We reported a preoperative strategy to reduce not only the brain warm ischemia, but also reperfusion injury using a low-flow perfusion and blood tepid cooling system.

A 72-year-old woman complained of sudden onset of the chest and back pain, and manifested a left paralysis with an abrupt onset of consciousness disorder, scoring 12 according to the Glasgow Coma Scale. When she was transported to us, her consciousness level was deteriorated and she was intubated, and she was comatose (7 on the Glasgow Coma Scale). A chest computed tomographic scan showed a Stanford type A acute aortic dissection involving all three arch branches. Duplex ultrasonography showed a scarce blood flow of the right common carotid artery compressed by enlarged false lumen. We considered that the brain ischemia was progressing and should be relieved as early as possible prior to the central aortic operation. The femoral artery and the right common carotid artery were exposed. A simple bypass circuit (Poly-vinyl Prolight 4.5 mm tube [Senko, Tokyo, Japan]) was applied that connected with each of the dialysis catheters (Blood Access UK-Catheter Kit, diameter 2.2 mm [Unitica, Aichi, Japan]) from the femoral artery to the true lumen of the right common carotid artery using a roller pump (HAD 11 [Senko, Tokyo, Japan]). The bypass circuit was cooled in a tepid bath at 30°C (Fig 1). During the procedure, brain oxygenation (rSO2) was monitored by near-infrared spectroscopy (INVOS 4100 [Somanetics, Troy, MI]). Initial rSO2 monitored on the right and left forehead was 17% and 38 %, respectively. A pump flow of 90 mL/min (1.8 mL/kg/min) using the tepid blood cooling system increased the right rSO2 up to 35% with no laterality (Fig 2). Duration of reperfusion system was 2.0 hours. Immediately after stabilizing the brain circulation, she was transferred to the operation room, and an ascending hemi-arch replacement, using selective antegrade cerebral perfusion under deep hypothermia was completed. When selective cerebral perfusion was initiated, the carotid artery perfusion was stopped, and the carotid artery cannula was removed. The postoperative course was uneventful, and she woke up on the first postoperative day. She was extubated the next day. She remained to be hemi-paretic; however, she was able to walk and she was discharged on postoperative day 35. Although serial brain computed tomographic scans and magnetic resonance imaging disclosed multiple strokes in the right cerebral hemisphere, there was a minimum brain edema (Fig 3). At 7 months after the operation, she could walk with a cane.


Figure 1
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Fig 1. A simple bypass circuit was established from the femoral artery to the true lumen of the right common carotid artery in the emergency room. (F = false lumen of aortic dissection; Rt CCA = right common carotid artery; Rt FA = right femoral artery; T = true lumen of aortic dissection.)

 

Figure 2
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Fig 2. Serial change of rSO2 during the procedure. (CPB = cardiopulmonary bypass; CRS = cerebral reperfusion system; rSO2 = brain oxygenation; SCP = selective cerebral perfusion.)

 

Figure 3
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Fig 3. Serial brain computed tomographic (CT) scans and magnetic resonance imaging (MRI) showed large right cerebral infarctions; however, brain edema was minimized. (POD = postoperative day.)

 

    Comment
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 Comment
 References
 
Brain malperfusion caused by acute type A aortic dissection is one of many tragedies and usually manifests as a transient or permanent ischemic neurologic deficit. Ongoing brain ischemia caused by the carotid artery dissection with cessation of the blood flow should be relieved as early as possible, not only to prevent brain ischemia, but also to alleviate the reperfusion injury of the brain, which eventually ensues as irreversible brain edema.

In the majority of cases, aortic repair in the operation theater has been selected to solve this problem. However, several hours are required to obtain the normal brain blood flow through true lumen of the carotid artery, and this strategy is usually too late to achieve satisfactory outcome of the brain. A few successful maneuvers to reduce the brain damage has been reported [4, 5]; but there was not a single report to demonstrate that the ongoing brain warm ischemic insult was relieved preoperatively.

We have developed a simple bypass circuit to save the brain prior to the aortic repair in the emergency room. The brain-saving system was based on two concepts. One was to accomplish the earlier reperfusion when the patient was recognized to have a serious ongoing brain ischemia. In the present case, we could reperfuse the right common carotid artery within a 3-hour onset of neurologic symptom, and the brain oxygenation (rSO2) increased dramatically soon after common carotid artery reperfusion. Another concept is to minimize the reperfusion injury. The optimal reperfusion flow and blood temperature remained unclear. It is believed that higher flow reperfusion causes more brain edema; on the other hand, lower flow results in the lack of brain perfusion [6]. In the present case, the reperfusion flow of 1.8 mL/kg/min was determined according to the recovery of near-infrared spectroscopy. We retrospectively investigated that the reperfusion flow was satisfactory since the right brain oxygenation (rSO2) raised up to 35% with no laterality and a minimum brain edema documented by serial computed tomographic scans and magnetic resonance imaging. The optimal reperfusion flow at tepid blood temperature (30°C) was set at between half and one third the normal common carotid artery flow of 4 to 6 mL/kg/min under normothermia (36°C to 37°C).

Further investigation is mandatory to pursue the optimal blood flow or temperature, but we believe that our simple brain-saving system that was applied prior to aortic repair has a great advantage to reduce brain warm ischemia-reperfusion injury cause by complicated acute aortic dissection.


    References
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 Abstract
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 Comment
 References
 

  1. Geirsson A, Szeto WY, Pochettino A, et al. Significance of malperfusion syndromes prior to contemporary surgical repair for acute type A dissection: outcomes and need for additional revascularizations Eur J Cardiothorac Surg 2007;32:255-262.[Abstract/Free Full Text]
  2. Sinatra R, Melina G, Pulitani I, Fiorani B, Ruvolo G, Marino B. Emergency operation for acute type A aortic dissection: neurologic complications and early mortality Ann Thorac Surg 2001;71:33-38.[Abstract/Free Full Text]
  3. Tanaka H, Okada K, Yamashita T, Morimoto Y, Kawanishi Y, Okita Y. Surgical results of acute aortic dissection complicated with cerebral malperfusion Ann Thorac Surg 2005;80:72-76.[Abstract/Free Full Text]
  4. Sakaguchi G, Komiya T, Tamura N, et al. Cerebral malperfusion in acute type A dissection: direct innominate artery cannulation J Thorac Cardiovasc Surg 2005;129:1190-1191.[Free Full Text]
  5. Urbanski PP. Carotid artery cannulation in acute aortic dissection with malperfusion J Thorac Cardiovasc Surg 2006;131:1398-1399.[Free Full Text]
  6. Chalmers J. Blood pressure in acute stroke: in search of evidence J Hypertens 2005;23:277-278.[Medline]



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