Data_Sheet_1_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.

氧中毒被定义为急性中枢神经系统（central nervous system, CNS）、急性肺及慢性肺氧中毒。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。

本研究回顾了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日期间与作者通信的两类患者资料：一类是存在既往确诊为急性中枢神经系统氧中毒的体征和/或症状的患者，另一类是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的患者。急性病例定义为接受≤5次高压氧治疗后发病者，慢性病例则为接受>5次高压氧治疗后发病者。慢性病例进一步按氧分压分为1.5 ATA、>1.5 ATA及<1.5 ATA三组。计算症状发作时的氧累积暴露剂量，单位为大气压-小时（atmosphere-hours, AHs）。

本研究共纳入7例急性病例，平均氧累积暴露剂量为4.0±2.7 AHs，另纳入52例慢性病例：其中31例属于1.5 ATA组（平均116±106 AHs）、12例属于>1.5 ATA组（103±74 AHs）、9例属于<1.5 ATA组（114±116 AHs）。再发暴露的平均剂量分别为81±55、67±49及22±17 AHs，出现3次及以上发作的病例对应的平均暴露剂量分别为25±18、83±7.5及5.4±6.0 AHs。多数病例的症状可逆转。成人与儿童患者之间无显著统计学差异（p=0.72）。症状出现后3个月内接受急性干预的病例，其对氧暴露的敏感性显著高于延迟干预病例，发病时的氧累积暴露剂量分别为21.1±8.8 AHs与123±102 AHs（p=0.035）。外部来源报告了1例因急性氧暴露死亡的病例、2例因慢性氧暴露死亡的病例，以及1例因慢性氧中毒被收治入院的患者。此外本研究还发现了氧中毒戒断综合征。

本研究在低于2.0绝对大气压的条件下，发现了慢性神经系统疾病患者接受高压氧治疗后引发的急性及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 AHs，但个体间差异较大。成人与儿童患者之间无显著统计学差异，但亚急性干预病例的敏感阈值低于慢性干预病例。早期识别该病症可实现症状逆转，且有助于合理设定高压氧治疗的给药剂量。若忽视该病症并继续进行高压氧治疗，则会导致永久性致残甚至死亡。