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Changes in cerebral oxygen saturation following prone positioning for orthopaedic surgery under general anaesthesia

A prospective observational study

Closhen, Dorothea; Engelhard, Kristin; Dette, Frank; Werner, Christian; Schramm, Patrick

Author Information
European Journal of Anaesthesiology (EJA): June 2015 - Volume 32 - Issue 6 - p 381-386
doi: 10.1097/EJA.0000000000000259
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Abstract

Introduction

For most spinal surgical procedures the anaesthetised patient has to be turned from the supine to the prone position. This procedure necessitates a careful approach, as prone positioning is associated with several potential problems. A decrease in cardiac index is observed primarily due to elevations in intra-abdominal pressure and caval vein compression.1 Injuries to the central nervous system are rare but have severe consequences for the patient. The two relevant mechanisms leading to neuronal injuries are impaired venous drainage from the brain and reduced cerebral perfusion, both of which lead to inadequate cerebral oxygen supply.1 Different positioning devices for body and head are used to try and prevent these complications,1 although these may also affect regional and global haemodynamic parameters. Cases of neurological impairment after prone positioning such as postoperative visual loss have been described.2–4 In addition to direct ocular pressure, one of the most likely causes for this impairment is cerebral hypoperfusion.5 This hypoperfusion may be due to a compromise in global haemodynamic status with a subsequent reduction in cerebral perfusion pressure; this fall in perfusion pressure is due to an increase in intra-cranial pressure secondary to impaired cerebral venous drainage.6

These haemodynamic changes can cause a decrease in cerebral oxygen saturation which can be measured easily and non-invasively, using near-infrared spectroscopy (NIRS). This is a well established technique and can detect cerebral oxygen desaturations during carotid and cardiovascular operations caused by cerebral hypoperfusion and hyperperfusion.7–9 Different NIRS monitors are available: INVOS is a trend monitor that uses two infrared wavelengths to measure the ratio of oxyhaemoglobin to desoxyhaemoglobin (rSO2) and FORE-SIGHT utilises four wavelengths of laser light to calculate absolute oxygen saturation (StO2).

Our hypothesis was that prone positioning would impair cerebral oxygen saturation as measured with two different NIRS monitors in anaesthetised patients undergoing orthopaedic surgery and in awake volunteers.

Methods

The study was approved by the local ethics committee of Rhineland-Palatinate, Germany (approval number: 837.009.10(7018), on 3 March 2010) and written informed consent was obtained from all participants. The presented data are a subset of a previously registered study at clinicaltrials.gov (ID NCT01275898). All patients were recruited and anaesthetised at the Department of Anaesthesiology at the University Medical Centre Mainz, Germany. Patients were identified for inclusion by examination of the planned operating schedule for elective orthopaedic surgery in the prone position and were screened by one of the authors. Exclusion criteria were as follows: age more than 80 and less than 18 years; pre-existing cerebrovascular disease; American Society of Anesthesiologists (ASA) physical status classification IV or V; injury/haematoma on the forehead; intra-cerebral lesions; haemoglobin concentration below 100 g l−1; and pregnancy.

All patients underwent general anaesthesia. About 1 h before induction of general anaesthesia, all patients received oral midazolam 7.5 mg for pre-medication. On arrival in the operating room, ECG, automated arterial blood pressure measurement device and peripheral oximeter (SpO2) were attached. General anaesthesia was induced using intravenous sufentanil 0.3 μg kg−1 followed by propofol 2 mg kg−1 and atracurium 0.5 mg kg−1. Anaesthesia was maintained with 0.7 to 1.0 age-adjusted minimum alveolar anaesthetic concentration of sevoflurane as calculated by the monitoring software (Primus; Draeger, Luebeck, Germany) and repeated injections of sufentanil and atracurium at the discretion of the attending anaesthetist. Pressure-controlled mechanical ventilation with positive end-expiratory pressure (PEEP) of 5 cmH2O, inspiratory oxygen fraction (FIO2) 0.4, was adjusted to maintain an end-tidal carbon dioxide concentration (ETCO2) of 4.7 to 6.0 kPa. The mean arterial blood pressure (MAP) was maintained at more than 60 mmHg on the basis of the institutional clinical standard operating procedures. None of the patients received reversal agents. Fraction of inspired and expired oxygen, ETCO2, end-expiratory sevoflurane, SpO2, automatic arterial blood pressure, body temperature and neuromuscular blockade using train-of-four technology were measured throughout the anaesthesia (Primus and Infinity Delta; Draeger). In the prone position, the patient's head was placed carefully in a cushioned head-positioning device (Disposa-view, Vital Signs Inc., New Jersey, USA) to ensure a straight head and neck position that would enable venous drainage and avoid neck compression. A mirror below the device allowed for continuous monitoring of the nose and eyes. In all the awake volunteers, ECG, non-invasive blood pressure and SpO2 were monitored before, during and after prone positioning.

Regional cerebral oxygen saturation (rSO2) was assessed continuously using the INVOS cerebral oximeter (Somanetics, Troy, Michigan, USA) and cerebral tissue oxygen saturation (StO2) was assessed with FORE-SIGHT cerebral oximeter (Cas Medical Systems Inc, Branfort, Connecticut, USA). Before induction of anaesthesia the sensors of each oximeter were positioned according to the manufacturer's instructions on the right and the left forehead in the frontotemporal position. Allocation of INVOS and FORE-SIGHT sensors to the right or left side was assigned in an alternate randomisation fashion.

A clinically relevant change in cerebral oxygen saturation was defined as either a decrease to levels to less than 50% or a change of more than 5%.10 Measurement of cerebral oxygenation started after induction of general anaesthesia and steady state FIO2 at 0.4 and was maintained throughout the anaesthesia. Measurement in the supine position was defined as baseline, followed by the measurement period during prone position. At the end of surgery and return to the supine position an averaged measurement period of 10 min was followed. A decrease in cerebral oxygenation of more than 20% or a fall in the absolute level to less than 50% was managed according to a pre-defined protocol which included checking head positioning, ventilation, blood loss and treatment of hypotension. For awake volunteers, the trial consisted of 10 min in the supine position (baseline) followed by 10 min in the prone position and then finally 10 min in the supine position.

Physiological data are expressed as the mean ± standard deviation. Power analysis was performed with software R (www.r-project.org) for pairwise comparison of cerebral oxygenation, revealing a minimum sample size of 29 patients with a clinically relevant delta of 5, an estimated standard deviation of 9, a significance level of 0.05 and a power of 0.9 using an one-sided paired t-test. Based on this calculation it was planned to include 40 patients to compensate for any dropouts.

The primary endpoint of the study was the time-course of cerebral oxygenation with adjustment for potentially influencing factors. Linear mixed models were applied to account for correlation within patients. Because of the absence of a gold standard measurement of cerebral oxygen saturation, no Bland-Altman plot was performed but rather linear mixed models were applied to compare both oximeters. A P value less than 0.05 was considered statistically significant (SPSS version 22, SPSS Inc., Chicago, Illinois, USA).

Results

Forty patients undergoing orthopaedic surgery in the prone position were enrolled between May 2010 and February 2011. Four of these patients were excluded as surgical intervention was not performed and one patient was excluded due to a malfunction of the FORE-SIGHT monitor. In total 35 patients were analysed. Thirty patients underwent spinal disc surgery, two upper arm surgery, one kyphoplasty and one lumbar osteosynthesis material removal. Thirty-five volunteers were also enrolled between January and February 2011. The data for both cohorts are shown in Table 1.

Table 1
Table 1:
Personal data of participants

Cerebral oxygen saturation measured with INVOS (rSO2) was 75 ± 8% at baseline and decreased transiently to 72 ± 8% after turning the patient to the prone position. During the prone positioning rSO2 increased with a slope of 0.0324% per minute [95% CI 0.0231 to 0.0417; P < 0.01 mixed model without adjustment], but did not exceed the previously defined clinically relevant limit of 5% (Fig. 1, Table 2). Adjusting rSO2 for SpO2, MAP and ETCO2 the slope was 0.0321% per minute (95% CI 0.0227 to 0.0415; P < 0.01) and, therefore, independent of the tested cofactors.

Fig. 1
Fig. 1:
Cerebral oxygen saturation measured with INVOS (rSO2) and with FORE-SIGHT (StO2) during prone positioning in anaesthetised patients. Data are mean ± standard deviation. Arrows indicate the start and the end of prone positioning.
Table 2
Table 2:
Physiological parameters of the patients at different time points

Cerebral oxygen saturation measured using FORE-SIGHT (StO2) was 74 ± 5% at baseline and decreased transiently to 72 ± 4% after turning the patient to the prone position. During the prone positioning StO2 then slightly increased with a slope of 0.0324% per minute (95% CI 0.0254 to 0.0393; P < 0.01) but did not reach the previous defined clinically relevant change of 5% (Fig. 1, Table 2). After adjustment for SpO2, MAP, ETCO2 the slope was significant with 0.0314% per minute (95% CI 0.0245 to 0.0383; P < 0.01) and, therefore, independent of the tested cofactors.

Further variables like MAP, heart rate, ETCO2, end-tidal sevoflurane and SpO2 showed no relevant fluctuations over the measurement period (Table 2).

Pre-defined treatment thresholds of NIRS (decrease in cerebral oxygenation more than 20% or decrease below in absolute level <50%) were not reached in any patient. The pre-defined threshold of MAP (<60 mmHg) was reached and treated in nine patients with a fluid bolus of 500 ml hydroxyethyl starch 130/0.4/6%, in two patients with 1000 ml of hydroxyethyl starch 130/0.4/6% and in 30 patients with one or more boluses of phenylephrine (0.1 to 0.6 mg in total).

Cerebral oxygen saturation in awake volunteers at baseline was 75 ± 8% using INVOS and 70 ± 3% using FORE-SIGHT, with no initial changes after prone positioning. Cerebral oxygenation showed a significant increase over time during the prone position period with a slope of 0.171% per minute (95% CI 0.078 to 0.263; P < 0.01) using INVOS and 0.082% per minute (95% CI 0.006 to 0.158; P = 0.04) using FORE-SIGHT, without changes over the previously defined clinical relevant limit of 5% (Fig. 2, Table 3). After adjustment for MAP and SpO2 the slope changed to 0.179% per minute (95% CI 0.086 to 0.273; P < 0.01) using INVOS and 0.096% per minute (95% CI 0.019 to 0.172; P = 0.02) using FORE-SIGHT and the increase was independent of measured cofactors.

Fig. 2
Fig. 2:
Cerebral oxygen saturation measured with INVOS (rSO2) and with FORE-SIGHT (StO2) during prone positioning in healthy volunteers. Data are mean ± standard deviation. Arrows indicate the start and the end of prone positioning.
Table 3
Table 3:
Physiological parameters of volunteers at different time points

Comparison of paired rSO2 and StO2 measurements in patients and volunteers (Fig. 3) showed a good correlation with a slope of 0.68 ± 0.05 (95% CI 0.57 to 0.78; P < 0.01). No skin irritation or other adverse events using either NIRS sensor were observed.

Fig. 3
Fig. 3:
Comparison of both cerebral oximeters INVOS (rSO2) and FORE-SIGHT (StO2). Values are from measurement of healthy volunteers and patients.

Discussion

Patients undergoing general anaesthesia in the prone position showed a slight increase in cerebral oxygen saturation as measured by two different monitors. However, this increase was less than 5% and is of limited clinical relevance. Surprisingly this small increase was also detected in awake volunteers. The results of the present study, therefore, demonstrate the absence of impairment in cerebral oxygen saturations in the prone position.

Our results are in accord with those obtained by Fuchs et al.11 who measured rSO2 in 14 healthy volunteers and in 48 patients undergoing lumbar discectomy and demonstrated a non-significant decrease in rSO2 during the first 5 min after prone positioning in both groups. The observation period in this previous study may have been too short to detect the small increase in rSO2 observed in the present study. The underlying mechanisms responsible for the small increase in rSO2 observed with both NIRS devices can only be speculative. Potential influencing factors like MAP, heart rate, ETCO2, FiO2, end-tidal sevoflurane and SpO2 were constant throughout the investigation period and did not influence the slope after adjusting the regression analysis for the above-mentioned parameters. A relevant factor influencing cerebral oxygen saturation is the arterial partial pressure of oxygen (PaO2). However, one of the major limitations of the present study is the lack of measurement of this parameter because of the invasive nature of the arterial line. Thus, we can only hypothesise that in patients undergoing general anaesthesia, the observed increase in cerebral oxygen saturation may be an effect of slow recruitment of pulmonary atelectasis in the prone position with subsequent increase in PaO2. The induction of general anaesthesia with administration of muscle relaxant leads to a loss in lung volume, particularly when the airways are kept at atmospheric pressure with no PEEP. Consequently, a decrease in functional residual capacity will result from atelectasis formation which may reach up to 20% of the lung even in uneventful anaesthesia.12,13 This atelectasis formation was mainly treated after tracheal intubation with controlled ventilation and PEEP, but during positioning a disconnection of the tracheal tube to prepare the patient's head was necessary. This may explain the observed initial decrease in rSO2/StO2 after positioning. The subsequent increase in cerebral oxygen saturation may have been caused by recruiting atelectatic lung in the dorsal (non-dependent) areas more than formation of atelectasis in the ventral (dependent) areas due to the prone positioning.14 This recruitment may have led to an increase in PaO2 and an elevation in cerebral oxygen saturation.

In awake volunteers an observation period of only 10 min in prone position also revealed an increase in cerebral oxygen saturation. Similar underlying mechanisms can be considered in this cohort. Observation with computed tomography scans in healthy volunteers in the supine position has shown dorsal pulmonary atelectasis.13,15 Prone positioning may also recruit dorsal atelectasis in healthy volunteers and, thereby, improve oxygen delivery to the brain and increase cerebral oxygen saturation.14

In the present study the head positioning was inline and the neck was free of compression to optimise cerebral venous drainage. Lateral head rotation leads to a decrease in cerebral blood flow velocity and to a decline of cerebral oxygen saturation measured with NIRS.16,17

In contrast to the irrelevant changes in rSO2 observed in the prone position, other perioperative positioning challenges may have different effects. Authors have demonstrated that Trendelenburg positioning with the head tilted down over a long surgical period did not affect cerebral oxygen saturation.18,19 In contrast, by positioning the anaesthetised patient head up in beach chair position, the oxygen saturation of the brain decreased by about 10%. This suggests the need for close haemodynamic and cerebral monitoring to avoid further deterioration of the cerebral oxygen saturation when this position is used.20

The two NIRS monitors use different measurement techniques. No gold standard for the non-invasive measurement of cerebral oxygenation exists and, therefore, the comparison of both monitors was of secondary interest. The INVOS cerebral oximeter represents a trend monitor that uses two infrared wavelengths (730 and 810 nm) to provide the ratio of oxyhaemoglobin to deoxyhaemoglobin. FORE-SIGHT is a cerebral oximeter that uses four wavelengths (690, 778, 800 and 850 nm) of laser light to calculate absolute regional cerebral oxygen saturation values. The absolute values and the observed changes of the values of both monitors were comparable in the present study but FORE-SIGHT showed a smaller fluctuation with lower standard deviations. In patients undergoing off-pump coronary bypass surgery, differences between both monitors were found, with higher values and smaller fluctuations in FORE-SIGHT derived data.21 Additionally, different time delays in changes of rSO2 and StO2 in response to changes in mean arterial blood pressure were detected in the latter study. In the present study the smaller fluctuations in FORE-SIGHT were demonstrated, but the mean values obtained from both monitors were comparable. The differing time delays of cerebral oxygen saturation readings in response to changes in arterial blood pressure were, however, not observed. This can be explained by the absence of rapid and large changes in MAP and that we undertook the measurements over a longer time scale.

The present study has several limitations. First, an inherent weakness of the NIRS technology is the potential for contamination of the signal with extracranial tissue oxygenation. Therefore, changes in values may not exactly reflect alterations in cerebral oxygenation.22 This is well defined and already integrated in the calculation of the oxygen saturation values. Furthermore, NIRS does not differentiate between arterial and venous blood. Changing body position affects arterial and venous pressure and alters the venous/arterial ratio. Alterations in NIRS value may, therefore, be due to changes in blood distribution rather than a change in cerebral oxygen saturation.23 Second, there were differences in baseline characteristics between the surgical patients and the control group. Awake volunteers were younger and healthier than patients undergoing surgery. Despite these differences and the absence of general anaesthesia in the volunteer group, the findings in both groups are surprisingly similar. Relevant influencing factors of cerebral oxygenation are haemoglobin concentration and PaO2. Both were not measured in the present study because this would have made an invasive arterial line necessary which was not clinically indicated in these patients. However, it can be assumed that both parameters did not change meaningfully during the time of measurement. The haemoglobin concentration is altered by fluid administration and/or by blood loss. The blood loss in all patients was very low and the amount of intravenous fluid administered was modest and should not have influenced the haemoglobin concentration. In addition a decrease in haemoglobin concentration during the operation period should have led to a decrease in cerebral oxygenation which was not observed. Third, the anaesthesiologist was not blinded to the NIRS measurement which has the potential to introduce bias. However, the pre-defined thresholds in cerebral oxygen saturation were not reached by any of the patients and the FIO2, as the most relevant influencing factor, was constant at 0.4 throughout the measurement. The anaesthesiologist carefully maintained the MAP thresholds independent of the NIRS values. Thus, the unblinded nature of the study should not have influenced the presented results.

Cerebral oxygen saturation increases very slowly during the prone positioning of healthy volunteers and anaesthetised patients undergoing orthopaedic surgery. This small increase did not reach clinical relevance. Therefore, prone positioning with inline positioning of the head and avoidance of neck compression can be regarded as safe, in terms of the maintenance of cerebral oxygen saturation.

Acknowledgements relating to this article

Assistance with the study: the authors thank Herbert Günter for data acquisition and Prof. Berres for statistical support.

Financial support and sponsorship: this work was supported by the Department of Anaesthesiology, University Medical Centre Mainz, Germany.

Conflicts of interest: none.

Presentations: preliminary data for this study were presented as a poster presentation at the Annual meeting of the American Society of Anesthesiologists (ASA, 18 October 2011) and the Meeting of the Society for Neuroscience in Anesthesiology and Critical Care (SNACC, 14 October 2011).

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