Eur J Cardiothorac Surg 1998;14:415-418
© 1998 Elsevier Science NL
Monitoring of regional cerebral oxygenation by near-infrared spectroscopy during continuous retrograde cerebral perfusion for aortic arch surgery1
Hitoshi Ogino,
Yuichi Ueda,
Takaaki Sugita,
Koichi Morioka,
Yutaka Sakakibara,
Keiji Matsubayashi,
Takuya Nomoto
Department of Cardiovascular Surgery, Tenri Hospital, 200 Mishima-cho, Tenri, Nara, 632 Japan
Received 29 December 1997;
received in revised form 25 May 1998;
accepted 27 May 1998.
Corresponding author. Tel.: +81 743 635611; fax: +81 743 625576.
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Abstract
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Objective: To assess the value of monitoring of regional cerebral oxygen saturation (rSO2) during aortic arch surgery using continuous retrograde cerebral perfusion (CRCP) in conjunction with profound hypothermic circulatory arrest (HCA). Methods: The rSO2 of 12 consecutive patients was monitored non-invasively using near-infrared spectroscopy (NIRS) and the data were analyzed statistically. Results: The mean duration of HCA with CRCP was 62±14.1 min. The mean CRCP flow rate was 226±163 ml/min. Surgical outcomes were favorable with only a single hospital death (8.3%). However, the rSO2 decreased gradually in all patients during HCA, even combined with CRCP, and fell to 46±8.7% on average. It did not change so greatly before HCA and returned finally to its initial level at the end of re-warming. Only one patient developed a permanent neurologic deficit; this patient showed the greatest decrease of rSO2 from 56% to 29% after the longest HCA of 88 min. Two parameters, End-rSO2 (the ratio of post- to pre-HCA rSO2) and
-rSO2 (the rate of decrease from pre- to post-HCA rSO2) were obtained since the initial values of rSO2 before surgery differed. There were linear correlations between the CRCP flow rate and each of these two parameters. A multiple regression analysis also revealed a linear equation relating the parameters, which allowed prediction of the safe duration of HCA in different conditions of CRCP and a more favorable adjustment of the CRCP condition in each patient. Conclusions: The study suggests that the combination of HCA and CRCP has a limit of safe duration in spite of its potential usefulness for brain protection, and that rSO2 monitored by NIRS is useful in testing for adequate brain protection. It is hoped that monitoring of rSO2 can facilitate prediction of the safe duration of HCA with CRCP and a more favorable adjustment of CRCP.
Key Words: Regional cerebral oxygen saturation Near-infrared spectroscopy Profound hypothermic circulatory arrest Continuous retrograde cerebral perfusion Aortic arch surgery
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Introduction
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Although profound hypothermic circulatory arrest (HCA) has been routinely used for surgical treatment of aneurysms involving the aortic arch
[1]
[2], there are still major concerns about its safe duration for the brain
[1]
[2]
[3]
[4], even in conjunction with continuous retrograde cerebral perfusion (CRCP). Moreover, the safe duration for HCA may differ between patients or vary in a single patient with conditions such as temperature, CRCF flow rate, CRCP pressure or the anatomy of the vessels. Therefore, for each patient, it is essential to obtain real-time information concerning the safe duration of HCA and adequate conditions for CRCP during a limited period of HCA, generally less than 60 min. For this purpose, regional cerebral oxygen saturation (rSO2)
[5]
[6]
[7]
[8]
[9]
[10] was monitored by means of near-infrared optical spectroscopy (NIRS) during aortic arch surgery using HCA with CRCP. The data obtained were analyzed retrospectively in order to predict the safe duration of HCA and to adjust CRCP parameters including the flow rate and perfusion pressure in different patients.
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Patients and methods
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In 12 patients with an aortic aneurysm involving the arch, rSO2 was continuously monitored during arch surgery. The mean age was 64±7.6 years old with four females and eight males. Five patients had acute type A aortic dissection and one had a chronic dissecting aneurysm. The other six cases, including two patients with a ruptured aneurysm, had an atherosclerotic aneurysm involving the transverse arch or the distal arch. Replacement with Hemashield woven Dacron grafts (Meadox Medicals, Boston, MA) was carried out using HCA at 18°C with CRCP via the superior vena cava (SVC) as described previously
[3]. The CRCP flow rate was regulated by maintaining the SVC pressure, as measured with a catheter inserted via the right internal jugular vein, at about 15 mmHg. Various surgical procedures were carried out through a median sternotomy replacement of the ascending aorta (asc. Ao) in one case, the asc. Ao to the total arch in five cases, the total arch in two cases, and the distal arch in four cases. Non-invasive NIRS, Invos 3100A (Somanetics, Troy, USA) was employed for simple and real-time determination of rSO2 throughout. Self-adhesive patches containing an infra-red light-emitting diode and two distant sensors (30 mm and 40 mm) were fixed on the left forehead of patients. The rSO2 was calculated from these two sensors and expressed as percent oxygenated hemoglobin (Hb) saturation
[6]
[7]. The data were logged every 5 s and analyzed retrospectively. During surgery, the CRCP conditions were not regulated in order to improve the value of rSO2. Two parameters were studied: the End-rSO2 (the ratio of post- to pre-HCA rSO2) and
-rSO2 (the rate of decrease from pre-HCA to post-HCA rSO2), which were obtained as follows:
 | (1) |
 | (2) |
These are useful, because the initial rSO2 before surgery differed between patients.
Informed consent of this study was obtained pre-operatively from every patient.
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Statistics
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Correlation between the parameters End-rSO2 and
-rSO2 and the intra-operative variables was assessed from the Pearson correlation statistic Multiple regression analysis was also carried out to estimate the end-rSO2 from the individual CRCP conditions. Any P-value less than 0.05 was considered statistically significant.
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Results
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The mean duration of HCA and CRCP was 62±14.1 min (range 3488 min) and 52±13.9 min (range 2673 min) respectively. The mean CRCP flow rate was 226±163 ml/min (range 100400 ml/min). The overall outcomes of surgery were favorable. There was one hospital death (8.3%) from renal failure and permanent neurological deficit. This patient, who had been dependent on renal dialysis following abdominal aortic surgery, underwent emergent replacement of a ruptured arch aneurysm. She fell, post-operatively, into a nearly vegetative state that was revealed in computed tomograph (CT) scans as a serious multiple cerebral infarction including watershed zones. In this patient, the CRCP flow rate was only 100 ml/min even with a slightly higher CRCP pressure of 20 mmHg. Regarding post-operative neurological morbidity, one other patient suffered temporary neurological dysfunction delay of full awakening after emergency total arch replacement for an acute type A aortic dissection.
The rSO2 did not change greatly from the initial value of 61±7.9% (range 5070%) before surgery to the baseline value of 62±8.6% (range 5677%) before the induction of HCA during CPB (
Fig. 1
). However, during HCA, even in conjunction with CRCP, it decreased gradually and eventually fell to an average of 46±8.7% (range 2959%) at the end of HCA (Table 1). In particular, the one patient who had permanent neurological deficit resulting in hospital death showed by far the greatest decrease of rSO2 to 29%, nearly half of its baseline value of 56%, after the longest HCA of 88 min. In all, after re-establishment of CPB following HCA and re-warming, the rSO2 recovered to around 55%, close to the initial value (
Fig. 1).

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Fig. 1. Change of rSO2 (mean±SD). Pre, before cardiopulmonary bypass (CPB); HCA, profound hypothermic circulatory arrest; CRCP, continuous retrograde cerebral perfusion; CPB2, resumed CPB; Post, after the weaning of CPB.
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In the statistical analysis, the CRCP flow rate and its index (the flow rate divided by the body surface area) were correlated with the End-rSO2 as well as
-rSO2, although there was no correlation between the HCA duration and the two parameters (Table 2). In addition, multiple regression analysis revealed a linear equation.
End-rSO2=0.498±0.003xCRCP flow index+0.027xCRCP pressure-0.008xduration of HCA(P=0.016).
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Discussion
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This study suggested that HCA, even in conjunction with CRCP, has a safe limit of brain protection, and that simple and real-time monitoring of rSO2 with NIRS is potentially useful to predict a limit of its cerebral safety and to adjust CRCP conditions adequately.
Svensson et al.
[11] described that HCA over 45 min was associated with a higher risk of stroke, and that HCA over 65 min produced a higher mortality. Ueda et al.
[3], in our unit, introduced CRCP via the SVC as an adjunct to HCA to prolong this cerebral safe limit as well as to prevent air cerebral embolism. This combination has produced favorable outcomes in ninety patients and demonstrated that CRCP can prolong the safe duration of HCA to 80 or 90 min
[3]
[4]; one patient recovered without any neurological morbidity after the longest HCA of 110 min. However, CRCP is a kind of non-physiological perfusion with potential impediments
[3]
[4], so that prolonged HCA, even associated with CRCP, may produce subtle cerebral injury
[3]
[4]
[8]
[9]
[11]. Moreover, the safe duration of HCA may differ between patients or with parameters such as temperature, CRCP flow rate, its pressure, and the anatomy of the vessels. It is essential to assess in real-time the adequacy of cerebral protection and adjustment of CRCP conditions for each patient. Currently, only determination of rSO2 by NIRS is an easily available method to assess the real-time adequacy of cerebral perfusion during complex and time-restricted aortic arch surgery
[8]
[9]. Most attenuation of near-infrared light in human cerebral tissues is due to absorption by deoxyhemoglobin (deoxy-Hb) and oxyhemoglobin (oxy-Hb), so that brain tissue is suitable for determination of rSO2
[5]. The ratio (oxy-Hb/deoxy-Hb) can be converted to the familiar parameter of percent Hb oxygen (O2) saturation
[6]
[7]. In fact, NIRS requires two sensors to distinguish between the shallow tissue (scalp and skull) and the deep one (brain)
[6]
[7]
[11]. Therefore it can indicate real-time rSO2 independently of scalp and skull Hb by the unique advantage of depth resolution
[6]
[7]
[10]
[12].
The initial value of rSO2 before surgery differed individually, which might in turn be caused by the varying conditions of the patients relating to age, anatomy, hemodynamics, and blood oxygenation. However, we could observe the similar pattern of rSO2 variation in the patients. The rSO2 did not change before HCA, even in conjunction with hypotension and hemodilution induced by CPB, although core cooling caused its slight increase due presumably to decrease of cerebral metabolic rate. During HCA, even with CRCP, it decreased unfavorably, which suggested insufficiency of cerebral oxygenation by CRCP. Ausman et al.
[10] demonstrated that a rSO2 of 3035% is critical for cerebral dysfunction. A rSO2 less than 30% can be considered as indicating the onset of cerebral injury; desaturation and O2 delivery may cease, resulting in hypoxia associated with unfavorable anaerobic metabolism. In our results, one patient showed a rSO2 of 29% at the end of HCA, developing critical cerebral dysfunction with multiple cerebral infarction including watershed areas. Another patient underwent a delay in full awakening, although rSO2 remained above 50%. This patient was associated pre-operatively with temporary unconsciousness due to malperfusion of the arch vessels for aortic dissection. Of the ten patients without neurological morbidity, the lowest rSO2 was 35%. However, the patient awaked abruptly 5 h after surgery and her post-operative cognitive function was well preserved in mental state examination. The variation in the lowest value of rSO2 during HCA may be due to differences in the initial value of the rSO2 before surgery. Further examination is required to assess the adequacy of cerebral protection using the actual percentage of rSO2 in different individuals.
The statistical analysis revealed linear correlations between CRCP flow rate and End-rSO2 as well as
-rSO2. Therefore, we propose that a higher CRCP flow rate will produce a more favorable rSO2, resulting in lower neurologic morbidity. However, a higher CRCP pressure above 25 mmHg might induce cerebral edema, as demonstrated experimentally
[13]. In our CRCP protocol, the flow rate was regulated to maintain the SVC pressure at around 15 mmHg. Subsequently, the flow was restricted to 226±163 ml/min. It might be necessary to increase the target CRCP pressure to above 20 mmHg for adequate cerebral perfusion, since the rSO2 decreases during CRCP. We have actually observed temporary recovery of rSO2 in conjunction with increased CRCP flow rate (data was not presented) as Deep et al.
[8] described. A simple equation for prediction of End-rSO2 has been obtained through multiple regression analysis using realistic variables the CRCP flow index, pressure, and HCA duration. If an End-rSO2 of 0.5, a half of the baseline value, shows a critical level of cerebral safety
[10], 125 min will be predicted as a safe limit of HCA for a CRCP flow of 200 ml/min and a CRCP pressure of 15 mmHg. In our experiences
[3], and those of other authors
[4]
[8], a safe limit of HCA with CRCP has been considered to be between 80 and 90 min, which is not so far from the 125 min obtained by this calculation. Therefore, when End-rSO2 is getting close to 0.5, we may have to quit HCA with CRCP by switching to antegrade cerebral perfusion.
Unfavorably, there are several limitations to the present study. The methodology using NIRS has some factors influencing rSO2 determination; hemodynamics, temperature, anatomy, oxygenation and so on. The critical level of rSO2 at which cerebral injury would commence has remained unclear, although Ausman
[10] reported it as less than 3035%. This study is so preliminary that the sample size is too small. As far as these inadequacies may result in statistical bias, caution is urged. More clinical experiences are essential. Nevertheless, we regard monitoring of rSO2 as a potentially useful real-time indicator, facilitating the prospect of safe duration of HCA and proper adjustment of CRCP, and encouraging us to continue with a CRCP technique for arch surgery using a slightly higher CRCP flow rate and CRCP pressure than our current protocol.
In conclusion, monitoring of rSO2 with NIRS has proved itself potentially useful for proper brain protection during aortic arch surgery using HCA with CRCP. Further experiences will be able to indicate appropriately safe durations of HCA with CRCP and allow individual, more adequate adjustment of CRCP.
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Footnotes
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Presented at the 11th Annual Meeting of the European Association for Cardio-thoracic Surgery, Copenhagen, Denmark, September 28 October 1, 1997. 
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References
|
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- Griepp R.B., Stinson E.B., Hollingsworth J.F., Buehler D. Prosthetic replacement of the aortic arch. J Thorac Cardiovasc Surg 1975;70:1051-1063.[Abstract]
- Crawford E.S., Saleh S.A., Schuessker J.S. A treatment of aneurysm of the transverse aortic arch. J Thorac Cardiovasc Surg 1979;78:383-393.[Abstract]
- Ueda Y., Miki S., Okita Y., Tahata T., Ogino H., Sakai T., Morioka K., Matsuyama K. Protective effect of continuous retrograde cerebral perfusion on the brain during deep hypothermic systemic circulatory arrest. J Card Surg 1994;9:584-595.[Medline]
- Takamoto S., Matsuda T., Handa M. Simple hypothermic retrograde cerebral perfusion during aortic arch surgery. J Cardiovasc Surg 1992;33:560-567.[Medline]
- Hazeki O., Tamura M. Quantitative analysis of hemoglobin oxygenation state of rat brain in situ by near-infrared spectrophotometry. J Appl Physiol 1988;64:796-802.[Abstract/Free Full Text]
- McCormick P.W., Stewart M., Goeting M.G., Balakrishnan G. Regional cerebrovascular oxygen saturation measured by optical spectroscopy in humans. Stroke 1991;22:596-602.[Abstract/Free Full Text]
- McCormick P.W., Stewart M., Dujovny M., Ausman J.I. Intracerebral penetration of infrared light: technical note. J Neurosurg 1992;76:315-318.[Medline]
- Deeb G.M., Jerkins E., Bolling S.F., Brunsting L.A., Williams D.M., Quint L.E., Deeb N.D. Retrograde cerebral perfusion during hypothermic circulatory arrest reduces neurologic morbidity. J Thorac Cardiovasc Surg 1995;109:259-268.[Abstract/Free Full Text]
- Ganzel B.L., Edmonds H.L., Jr., Pank J.R., Goldsmith L.J. Neurophysiologic monitoring to assure delivery of retrograde cerebral perfusion. J Thorac Cardiovasc Surg 1997;113:748-757.[Abstract/Free Full Text]
- Ausman J.I., McCormick P.W., Stewart M., Lewis G., Dujovny M., Balakrishnan G., Malik G., Ghaly R.F. Cerebral oxygen metabolism during hypothermic circulatory arrest in humans. J Neurosurg 1993;79:810-815.[Medline]
- Svensson L.G., Crawford E.S., Hess K.R., Coselli J.S., Rasskin S., Shenaq S.A., Safi H.J. Deep hypothermic circulatory arrest. Determinants of stroke and early mortality in 656 patients. J Thorac Cardiovasc Surg 1993;106:19-31.[Abstract]
- Hongo K., Kobayashi S., Okudera H., Hokama M., Nakagawa F. Non-invasive cerebral optical spectroscopy: Depth-resolved measurements of cerebral haemodynamics using indocyanine green. Neuro Res 1995;17:89-93.
- Usui A., Oohara K., Liu T.L., Murase M., Tanaka M., Takeuchi E., Abe T. Determination of optimum retrograde cerebral perfusions. J Thorac Cardiovasc Surg 1994;107:300-308.[Abstract/Free Full Text]
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