Data_Sheet_2_Acute and chronic central nervous system oxidative stress/toxicity during hyperbaric oxygen treatment of subacute and chronic neurological conditions.pdf

IntroductionOxygen toxicity has been defined as acute central nervous system (CNS), acute pulmonary, and chronic pulmonary oxygen toxicity. This study identifies acute and chronic CNS oxygen toxicity under 2.0 atmospheres absolute (ATA) pressure of oxygen. Methods: The authors’ medical records from September 29, 1989 to January 20, 2023 and correspondence to the authors (9/1994 to 1/20.2023) from patients with signs and/or symptoms historically identified as acute CNS oxygen toxicity and those with neurological deterioration receiving hyperbaric oxygen for neurological conditions were reviewed. Acute cases were those occurring with ≤5 HBOTs and chronic cases >5 HBOTs. Chronic cases were separated into those at 1.5 ATA, > 1.5 ATA, or < 1.5 ATA oxygen. Cumulative dose of oxygen in atmosphere-hours (AHs) was calculated at symptom onset.
ResultsSeven acute cases, average 4.0 ± 2.7 AHs, and 52 chronic cases were identified: 31 at 1.5 ATA (average 116 ± 106 AHs), 12 at >1.5 ATA (103 ± 74 AHs), and 9 at <1.5 ATA (114 ± 116 AHs). Second episodes occurred at 81 ± 55, 67 ± 49, and 22 ± 17 AHs, and three or more episodes at 25 ± 18, 83 ± 7.5, and 5.4 ± 6.0 AHs, respectively. Most cases were reversible. There was no difference between adults and children (p = 0.72). Acute intervention in cases (<3 months) was more sensitive than delayed intervention (21.1 ± 8.8 vs. 123 ± 102 AHs, p = 0.035). Outside sources reported one acute and two chronic exposure deaths and one patient institutionalized due to chronic oxygen toxicity. A withdrawal syndrome was also identified.
ConclusionHyperbaric oxygen therapy-generated acute and chronic cases of CNS oxygen toxicity in chronic neurological conditions were identified at <2.0 ATA. Chronic CNS oxygen toxicity is idiosyncratic, unpredictable, and occurred at an average threshold of 103–116 AHs with wide variability. There was no difference between adults and children, but subacute cases were more sensitive than chronic intervention cases. When identified early it was reversible and an important aid in proper dosing of HBOT. If ignored permanent morbidity and mortality resulted with continued HBOT.

引言：氧中毒被定义为急性中枢神经系统（Central Nervous System, CNS）、急性肺脏及慢性肺脏氧中毒。本研究聚焦于2.0绝对大气压（Atmospheres Absolute, ATA）下的急性与慢性中枢神经系统氧中毒。
方法：回顾性分析1989年9月29日至2023年1月20日的作者方医疗记录，以及1994年9月至2023年1月20日期间，存在既往确诊急性中枢神经系统氧中毒症状/体征的患者，与因神经系统疾病接受高压氧治疗（Hyperbaric Oxygen Therapy, HBOT）后出现神经功能恶化患者的医患往来资料。急性病例定义为接受≤5次高压氧治疗后发病者，慢性病例定义为接受>5次高压氧治疗后发病者。慢性病例进一步按氧分压分为1.5ATA、>1.5ATA及<1.5ATA三组。于症状发作时计算氧暴露的累积剂量，单位为大气压-小时（atmosphere-hours, AHs）。
结果：共纳入7例急性病例，平均氧暴露剂量为4.0±2.7大气压-小时，另纳入52例慢性病例：其中31例属于1.5ATA组（平均116±106大气压-小时）、12例属于>1.5ATA组（103±74大气压-小时）、9例属于<1.5ATA组（114±116大气压-小时）。二次发作患者的平均氧暴露剂量分别为81±55、67±49及22±17大气压-小时，三次及以上发作患者的平均氧暴露剂量分别为25±18、83±7.5及5.4±6.0大气压-小时。多数病例的症状可实现逆转。成人与儿童患者无显著统计学差异（p=0.72）。发病后<3个月接受早期干预的急性病例比延迟干预病例更为敏感（21.1±8.8 vs 123±102大气压-小时，p=0.035）。外部来源报告1例急性暴露死亡病例、2例慢性暴露死亡病例，另有1例因慢性氧中毒被收治入院的患者。本研究还观察到戒断综合征。
结论：本研究在<2.0ATA的压力条件下，确认了慢性神经系统疾病患者接受高压氧治疗后发生的急性与慢性中枢神经系统氧中毒病例。慢性中枢神经系统氧中毒具有个体特异性、难以预测，平均发病阈值为103~116大气压-小时，但个体差异较大。成人与儿童患者无显著统计学差异，但亚急性病例比慢性干预病例更为敏感。早期识别该病症可实现症状逆转，这对合理制定高压氧治疗剂量具有重要指导意义。若忽视该病症并持续进行高压氧治疗，则会导致永久性发病甚至死亡。