Renal Replacement Therapy (Dec 2018)

Sleep apnea syndrome caused lowering of cerebral oxygenation in a hemodialysis patient: a case report and literature review

  • Kiyonori Ito,
  • Susumu Ookawara,
  • Mariko Fueki,
  • Sojiro Imai,
  • Takashi Hattori,
  • Satoshi Kiryu,
  • Yukari Sugai,
  • Noriko Wada,
  • Mitsutoshi Shindo,
  • Yasushi Ohnishi,
  • Noriaki Iino,
  • Kaoru Tabei,
  • Yoshiyuki Morishita

DOI
https://doi.org/10.1186/s41100-018-0194-3
Journal volume & issue
Vol. 4, no. 1
pp. 1 – 5

Abstract

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Abstract Background Sleep apnea syndrome (SAS) is a sleep disturbance, which is frequently comorbid in dialysis patients. SAS induces hypoxia, and therefore, systemic and cerebral oxygenation would be low. Near-infrared spectroscopy (NIRS) has recently been used to measure regional saturation of oxygen (rSO2), as a marker of tissue oxygenation. Although cerebral rSO2 was measured in patients in various clinical settings, few reports have previously shown the associations of changes in cerebral rSO2 and systemic oxygenation using measurement of peripheral arterial oxygen saturation (SpO2) in patients undergoing hemodialysis (HD) with SAS. We herein report a first HD case with SAS-induced reduction in cerebral oxygenation during sleep. Case presentation A 74-year-old woman underwent HD therapy for 1 month, because of advanced CKD caused by hypertension and obesity. In addition, she was diagnosed with obstructive sleep apnea with polysomnography about 4 years prior. Her apnea-hypopnea index (AHI) was 77.5 per hour, and therefore, continuous positive airway pressure (CPAP) was started. Thereafter, her AHI was improved to 3 to 6 per hour. However, she discontinued CPAP therapy at HD initiation. Since her oxygenation without CPAP would deteriorate, we evaluated her SpO2 and cerebral rSO2 by NIRS monitoring during sleep. We confirmed the deterioration in cerebral rSO2 according to the SpO2 decrease, and furthermore, the improvement in cerebral rSO2 was apparently delayed even after the improvement in her SpO2. The patient’s cerebral oxygenation under CPAP therapy could not be evaluated because she refused to receive CPAP therapy after HD initiation. Therefore, as a comparison, we evaluated a 69-year-old male HD patient without SAS and found that in contrast to a patient with SAS, his SpO2 and cerebral rSO2 were maintained throughout sleep. Conclusion We observed deterioration in cerebral oxygenation during sleep in addition to a decrease in systemic oxygenation in a patient with SAS undergoing HD. Real-time cerebral NIRS monitoring during sleep might be a useful method for detection of SAS.

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