We experienced a HD patient with SAS who showed a decrease in cerebral oxygenation in addition to a decrease in systemic oxygenation during sleep. In general, a decrease in systemic oxygenation would induce the deterioration of tissue oxygenation, including the brain. However, thus far, few reports have directly examined changes in cerebral oxygenation during sleep. Therefore, this case is a first report about nocturnal real-time monitoring of cerebral rSO2 in a HD patient with SAS.
Sleep disorders, including SAS, are known as long-term complications in dialysis patients [1, 2]. Nocturnal hypoxia was associated with a poor prognosis for cardiovascular events [9], and patients with ischemic stroke have a high risk of obstructive sleep apnea, with lowest overnight SpO2 values < 80% in more than half of observed patients [10]. Furthermore, in the clinical setting of HD therapy, cognitive impairment is common in patients undergoing HD and the pathogenesis of cognitive impairment would be associated with hemodynamic factors including changes in BP or anemia [11]. In particular, both intradialytic hypotension and anemia reportedly induced the deterioration of cerebral oxygenation [12, 13]. In addition, the decrease in cerebral oxygen supply was associated with neuronal death, and hypoxia promoted the formation of amyloid ß peptide in experimental studies [14, 15]. Therefore, systemic oxygenation should be maintained to prevent worsening of cerebral oxygenation, which would be associated with the deterioration of cognitive function, in patients with SAS.
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The measurement of cerebral rSO2 by NIRS has recently been performed in various clinical settings, including cardiovascular surgery, pediatrics, and dialysis [3,4,5,6,7,8, 16,17,18]. We therefore, reviewed the literature for reports of cerebral rSO2 values in dialysis patients (Table 1). Cerebral rSO2 values in HD patients were lower than healthy control or non-dialysis patients [3, 8, 19,20,21] and were lower than peritoneal dialysis patients [22]. Therefore, the presence of renal dysfunction or dialysis therapeutic modality might influence the status of cerebral oxygenation. Furthermore, longer HD therapy itself might cause hypoxia of the brain because HD duration was negatively associated with cerebral rSO2 [3, 19]. Regarding the association between cerebral rSO2 and clinical parameters in maintenance HD patients, various factors, i.e., serum albumin, pH, Hb, and blood pressure, were related to cerebral rSO2 [3, 13, 23]. Based on these previous reports, it would be important to maintain the nutritional status, and control Hb level and blood pressure in the clinical setting of HD therapy. On the other hand, it was also reported that there are little changes in cerebral rSO2 during HD in spite of Hb increase induced by ultrafiltration in patients undergoing HD without intradialytic hypotension [6, 13, 20, 24]. However, thus far, there are few reports regarding the association between changes in systemic oxygenation and those in cerebral oxygenation in HD patients with or without SAS. Recently, evaluation of cerebral rSO2 was reported to be useful for detection of SAS in addition to that using a pulse oximeter in children [18]. This report described that cerebral NIRS monitoring could detect SAS even in patients in whom SAS was ruled out with polysomnography, and AHI determined using cerebral rSO2 had higher sensitivity for the detection of SAS compared with that using SpO2 [18]. In HD patients with SAS, we noticed that a decrease in cerebral rSO2 was observed more frequently than a decrease in SpO2, and this result might be consistent with a previous report [18]. On the other hand, the HD patient without SAS in this study showed little changes in SpO2 and cerebral rSO2 during sleep. Therefore, in addition to the usefulness of polysomnography evaluation as a standard method for diagnosing SAS, cerebral rSO2 measurement using NIRS might play an important role in the diagnosis of SAS in HD patients.
Furthermore, the improvement in cerebral rSO2 was apparently delayed even after the improvement in SpO2 level (Fig. 1a). Although it is difficult to accurately state the mechanism of this phenomenon, we suspected two reasons regarding the difference between systemic and cerebral oxygenation improvement. First, NIRS monitoring was reported to have higher sensitivity for detecting SAS [18]. Therefore, the delay in cerebral oxygenation improvement might have the possibility to reflect the deep tissue oxygenation status, which was different from superficial arterial oxygenation status as shown in SpO2 monitoring. Second, NIRS monitoring would mainly help observe venous oxygenation status (70-80%), against capillary (5%), or arterial blood (20-25%) [25]. On the other hand, SpO2 monitoring could observe in the arterial blood oxygenation status. Brain cell would need the uptake of steady amount of oxygen into the cell according to the changes in oxygen supply in various conditions. In situations of decreased oxygen supply to brain such as severe anemia or hypoxic condition in SAS, cerebral rSO2 would be low, which reflected the decrease of oxygen supply and the increase of oxygen extraction into the brain cell [13]. When hypoxic status in SAS transiently disappears during sleep, arterial oxygenation will be immediately improved, which lead to the SpO2 increase. However, changes in oxygen extraction into brain cell might not be immediately normalized in response to the sudden increase of oxygen supply. As a result, there will be a lag time between the improvement in cerebral oxygenation and that of systemic oxygenation during sleep in this SAS patient. However, the mechanism of this phenomenon is yet not to be accurately clarified, and therefore, further studies are needed.
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The use of CPAP improves systemic hypoxia in patients with SAS, and patients with OSA may have better outcomes under CPAP therapy through a decrease in the rate of recurrent myocardial infarction [26]. According to her prior medical records, the patient’s AHI became relatively low under CPAP therapy compared to that without CPAP. Therefore, CPAP therapy would be effective in the prevention of systemic hypoxia during non-HD periods. Based on this result, cerebral oxygenation could be improved by CPAP therapy in patients with SAS in addition to the improvement of systemic oxygenation. However, further studies are needed to confirm the association between improvement in cerebral oxygenation and CPAP therapy in patients with SAS because we were unable to observe these associations in this study.
In conclusion, we observed cerebral oxygenation deterioration during sleep in addition to a decrease in systemic oxygenation in a patient undergoing HD with SAS. Furthermore, cerebral NIRS monitoring during sleep might be a useful method for the detection of SAS.
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