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Page 1: Total aortic arche replacment

CASE REPORT Open Access

Total aortic arch replacement under intermittentpressure-augmented retrograde cerebralperfusionHiroshi Kubota1*, Kunihiko Tonari1, Hidehito Endo1, Hiroshi Tsuchiya1, Hideaki Yoshino2, Kenichi Sudo1

Abstract

Kitahori, Kawata, Takamoto et al. described the effectiveness of a novel protocol for retrograde cerebral perfusionthat included intermittent pressure augmentation for brain protection in a canine model. Based on their report, weapplied this novel technique clinically. Although the duration of circulatory arrest with retrograde cerebral perfu-sion was long, the patient recovered consciousness soon after the operation and had no neurological deficit. Near-infrared oximetry showed recovery of intracranial blood oxygen saturation every time the pressure was augmented.

BackgroundTo prolong the safe limits of conventional retrogradecerebral perfusion (RCP), Kitahori, Kawata, Takamotoet al. assessed a novel protocol, intermittent pressure-augmented retrograde cerebral perfusion (IPA-RCP), ina canine model [1-3]. This new protocol was clinicallyapplied to a 51 year-old-male with a diagnosis of acuteaortic dissection. Near infrared oximetry showed recov-ery of intracranial blood oxygen saturation during thepressure augmentation. Although duration of RCP waslong, the patient recovered consciousness 30 min afterthe operation free of any neurological deficit after totalarch replacement.

Case presentationOn July 24, 2006, a 51 year-old-male with a diagnosis ofacute aortic dissection (DeBakey I, Stanford A) wastransferred to our hospital from a nearby hospital, andemergency operation was performed the same day. Thepericardium was opened through a median sternotomyand a cardiopulmonary bypass was established by can-nulations the inferior and superior venae cavae and theright femoral artery. Circulatory arrest with retrogradecerebral perfusion was commenced when the patient’stympanic temperature reached to 18.0°C. A large longi-tudinal intimal tear was present in the greater curvature

of the aortic arch, and it ended just proximal to the leftsubclavian artery. The aorta was transected between theleft common carotid artery and the left subclavianartery. The aorta was reinforced with two Teflon feltstrips, and a four-branch 24-mm graft was anastomosed.After anastomosis of the left common carotid artery, thegraft was clamped, and antegrade perfusion via a sidebranch and rewarming were started. The brachiocepha-lic artery was then anastomosed and perfused. Finally,the proximal anastomosis was performed, and the aorticclamp was released. Weaning from the cardiopulmonarybypass was achieved smoothly.

Retrograde cerebral perfusionConventional retrograde cerebral perfusion (RCP) with15 mmHg of superior vena cava pressure was performedfirst, and 30 min later, when the anesthesiologist alertthat near-infrared oximetry showed a low value under50%, we converted to the intermittent pressure augmen-ted retrograde cerebral perfusion (IPA-RCP) methodwith superior vena cava pressure increased to 45mmHg. The intervals and durations of the augmenta-tions were irregular, because when the backflow fromthe cervical branch disturbed the anastomosis, the pres-sure decreased expediently. The maximum duration ofaugmentation was limited to 30 sec. The circulatoryarrest time, conventional RCP time, IPA-RCP time were85 min, 30 min, and 55 min, respectively, and a total of10 augmentations were performed. Intracranial regional* Correspondence: [email protected]

1Department of Cardiovascular Surgery, Kyorin University, Tokyo, JapanFull list of author information is available at the end of the article

Kubota et al. Journal of Cardiothoracic Surgery 2010, 5:97http://www.cardiothoracicsurgery.org/content/5/1/97

© 2010 Kubota et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative CommonsAttribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction inany medium, provided the original work is properly cited.

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oxygen saturation (rSO2) was measured with a TOS-96brain oximeter (TOSTEC Co., Ltd. Tokyo, Japan).

ResultsPrior to the anesthesia, the rSO2 was 61% (Left) and60% (Right). At the beginning of the cardiopulmonarybypass, the rSO2 was 55% (Left) and 56% (Right). Atprofound hypothermia, the rSO2 was 64% (Left) and63% (Right), it gradually decreased to 49% (Left) and50% (Right). After commencing the IPA-RCP, the rSO2rose to around 60% at every augmentation, but itdecreased when the augmentation ceased. Just after theresuming antegrade perfusion via a side branch of thegraft, the rSO2 decreased to 40%, then recoveredsmoothly (Figure 1). The rSO2 on the right side recov-ered in a stepwise manner. The patient recovered con-sciousness 30 min after the operation free of anyneurological deficit and the postoperative course wasuneventful.

ConclusionsRCP by augmentation of CVP to 15 to 20 mmHg is rou-tinely used in our institute for the additional brain pro-tection during deep hypothermic circulatory arrestbecause much evidence has been accumulated to sug-gest an increased risk of perfusion-induced brain injuryassociated with RCP, especially when continuously highRCP pressures are used [4]. However, there is a safetylimit of the deep hypothermic circulatory arrest duration

because it cannot open all intracranial vessels but par-tially. To overcome this drawback, Kitahori, Kawata,Takamoto et al. developed a new intermittent pressureaugmentation method in which CVP is intermittentlyincreased to 45 mmHg [1-3]. They used a canine model,and showed that the retinal vessels were effectivelydilated at an augmented pressure of 45 mm Hg (arteries,107% + 3% of control veins, 114% + 3% of control),whereas when antegrade selective cerebral perfusion wasused, the retinal vessels were smaller than the corre-sponding preoperative vessels. They concluded that theintermittent pressure augmentation allows an adequateblood supply without injuring the brain and providesadequate neuroprotection equivalent to that provided byantegrade cerebral perfusion. In the canine model, theyadministered the RCP through the maxillary vein toovercome the drawbacks of jugular vein valves to reachdirectly the cranial veins. In the majority of humans, asde Brux et al. described, the jugular vein had competentvalves and it is hypothesized that the RCP gains thebrain through a collateral network of veins (azygos,intercostal, medullary and vertebral veins). The useful-ness of higher perfusion pressure could be either to dis-tend the valves or more probably to increase thepressure in the collateral vein network to improve cere-bral oxygenation [5]. Thus, the clinical effectiveness ofthe IPA-RCP through a cannulae inserted to the SVC isunknown field. We examined the effect of the IPA-RCPby measuring rSO2 which represents the brain blood

Figure 1 rSO2 during deep hypothermic circulatory arrest. L: left rSO2, R: right rSO2. Initial 30 min of conventional retrograde cerebralperfusion (RCP), rSO2 gradually declined. When intermittent-pressure-augmented (45 mmHg) retrograde cerebral perfusion (IPA-RCP) wasinduced, rSO2 rose. The maximum duration of pressure augmentation was limited to 30 sec. A total of 10 augmentations at irregular intervalswere tried. A. Start of deep hypothermic circulatory arrest and conventional RCP. B. Start of IPA-RCP. C. Final dip: Start of the antegrade perfusionto the left common carotid artery, and the left subclavian artery via graft branch. D. Start of antegrade perfusion via the brachiocephalic artery.

Kubota et al. Journal of Cardiothoracic Surgery 2010, 5:97http://www.cardiothoracicsurgery.org/content/5/1/97

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perfusion. Although only the anterior part of the brainrSO2 is assessed by a TOS-96 brain oximeter, becausemost attenuation of near-infrared light in human cere-bral tissues is due to absorption by deoxyhemoglobinand oxyhemoglobin, brain tissue is suitable for determi-nation of rSO2. Only determination of rSO2 is an easilyavailable method to assess the real-time adequacy ofcerebral perfusion during deep hypothermic time-restricted aortic arch surgery [6].At first, we planned to perform the operation on our

patient using conventional RCP. However, because therSO2 declined to 49%, the duration of circulatory arresttime was expected to exceed 60 min due to the fragileaortic wall to reinforce and deep distal anastomosis, weapplied the intermittent pressure augmentation techni-que for the first time. According to the original report,the central venous pressure was controlled at 15 mmHg and it was augmented to 45 mm Hg quickly andthen decreased again to the baseline level of 15 mmHgas soon as it reached 45 mm Hg every 30 seconds.However, the same protocol is difficult to apply clini-cally because backflow from the three arch vesselsincreased and disturbed the anastomosis when CVP wasaugmented. CVP was decreased to 15 mmHg expedi-ently. Although the optimal duration of pressure aug-mentation during deep hypothermic circulatory arrest inclinical settings is unknown, to prevent the brain edema,the maximum duration of pressure augmentation thatwe set was 30 sec.Along with every pressure augmentation, rSO2

showed immediate recovery up to 60% and it decreasedwhen the augmentation ceased. The essential effect ofIPA-RCP may not only be a temporary increase in rSO2but elevation of the declining curve during RCP. Ourpreliminary randomized comparative study in clinicalaortic arch replacement cases of IPA-RCP (n = 10) andstandard RCP (n = 10) showed that the interval fromthe end of the operation to full awakeness of the IPA-RCP group was 85 ± 64 min. in contrast with 310 ± 282min. in RCP group (p < 0.05) accompanying with therSO2 decline ratio 60 min after the initiation of theIPA-RCP group was 13.1 ± 3.7% in contrast with 24.5 ±13.1% in RCP group (p < 0.05). There was no significantdifference of the used amount of the anesthetic agent. Itmay support the “bottom raising effect” of this newprotocol.Just after the resumption of antegrade perfusion, the

rSO2 decreased to 40%, but then recovered smoothly.We named this phenomenon the “final dip”. When weuse RCP, the final dip always appears just after theresumption of antegrade perfusion. This phenomenonmay represent wash out of deoxygenated blood thatremained and did not circulate in the brain despite theperformance of retrograde cerebral perfusion. The

stepwise recovery of the rSO2 of the right side maymean that the resumption of antegrade perfusion via theleft arch branches was insufficient to wash out theremaining blood in our patient. In conclusion, this novelprotocol may have some advantages over conventionalRCP. Because it is difficult to verify the efficacy of IPA-RCP by quantitative analysis, accumulation and analysisof data e.g. measurement of the concentration of Tauproteins in the CSF, comparison of the pre- and post-operative cognitive function, measurement of the dia-meters of the retinal vessels during IPA-RCP maydemonstrate the advantages of this new method of brainprotection [7].

AcknowledgementsWe would like to gratefully acknowledge the outstanding original idea ofthe IPA-RCP protocol, laboratory investigation, and cooperation given to usby all the cardiac surgeons at the Mitsui Memorial Hospital: S Takamaoto, TMiyairi, Columbia University Medical Center: H Takayama, and TokyoUniversity Hospital: M Kawata, T Taketani, K Kitahori, K Nawata, T Morota, NMotomura, M Ono.

Author details1Department of Cardiovascular Surgery, Kyorin University, Tokyo, Japan.2Department of Cardiology, Kyorin University, Tokyo, Japan.

Authors’ contributionsHK, KT, HE, HT conceived of the study, and participated in its design andcoordination. HY and SK participated in the sequence alignment. All authorsread and approved the final manuscript.

Competing interestsThe authors declare that they have no competing interests.

Received: 7 June 2010 Accepted: 2 November 2010Published: 2 November 2010

References1. Kitahori K, Takamoto S, Takayama H, Suematsu Y, Ono M, Motomura N,

Morota T, Takeuchi K: A novel protocol of retrograde cerebral perfusionwith intermittent pressure augmentation for brain protection. J ThoracCardiovasc Surg 2005, 130:363-370.

2. Kawata M, Takamoto S, Kitahori K, Tsukihara H, Morota T, Ono M,Motomura N, Murakami A, Suematsu Y: Intermittent pressureaugmentation during retrograde cerebral perfusion under moderatehypothermia provides adequate neuroprotection: An experimentalstudy. J Thorac Cardiovasc Surg 2006, 132:80-88.

3. Kawata M, Sekino M, Takamoto S, Ueno S, Yamaguchi S, Kitahori K,Tsukihara H, Suematsu Y, Ono M, Motomura N, Morota T, Murakami A:Retrograde cerebral perfusion with intermittent pressure augmentationprovides adequate neuroprotection: diffusion- and perfusion-weightedmagnetic resonance imaging study in an experimental canine model. JThorac Cardiovasc Surg 2006, 134:933-40.

4. Usui A, Oohara K, Liu TL, Murase M, Tanaka M, Takeuchi E, Abe T:Determination of optimum retrograde cerebral perfusion conditions. JThorac Cardiovasc Surg 1994, 107:300-8.

5. De Brux JL, Subayi JP, Pegis JD, Pillet J: Retrograde cerebral perfusion:anatomic study of the distribution of blood to the brain. Ann Thorac Surg1995, 60:1294-8.

6. Ogino H, Ueda Y, Sugita T, Morioka K, Sakakibara Y, Matsubayashi K,Nomoto T: Monitoring of regional cerebral oxygenation by near-infraredspectroscopy during continuous retrograde cerebral perfusion for aorticsurgery. Eur J Cardiothorac Surg 1998, 14:415-8.

7. Kubota H, Takamoto S, Yoshino H, Kitahori K, Kawata M, Tonari K, Endo H,Tsuchiya H, Inaba Y, Takahashi Y, Sudo K: Clinical Application of

Kubota et al. Journal of Cardiothoracic Surgery 2010, 5:97http://www.cardiothoracicsurgery.org/content/5/1/97

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Intermittent Pressure-Augmented Retrograde Cerebral Perfusion. AnnThorac Surg 2010, 90:1340-3.

doi:10.1186/1749-8090-5-97Cite this article as: Kubota et al.: Total aortic arch replacement underintermittent pressure-augmented retrograde cerebral perfusion. Journalof Cardiothoracic Surgery 2010 5:97.

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