Toxicological Information Centre, Department of Occupational Medicine, First Faculty of Medicine, Charles University and General University Hospital, Prague, Czech Republic.
Clinic of Ophthalmology, First Faculty of Medicine, Charles University and General University Hospital, Prague, Czech Republic.
Am J Ophthalmol. 2018 Jul;191:100-115. doi: 10.1016/j.ajo.2018.04.015. Epub 2018 Apr 28.
To study the dynamics and clinical determinants of chronic retinal nerve fiber layer thickness (RNFL) loss after methanol-induced optic neuropathy.
Prospective cohort study.
All patients underwent complete ophthalmic evaluation including spectral-domain optical coherence tomography 3 times during 4 years of observation: 4.9 (±0.6), 25.0 (±0.6), and 49.9 (±0.5) months after discharge.
Eighty-four eyes of 42 survivors of methanol poisoning, mean age (standard deviation) of 45.7 (±4.4) years; and 82 eyes of 41 controls, mean age 44.0 (±4.2) years.
Global and temporal RNFL loss.
Abnormal RNFL thickness was registered in 13 of 42 (31%) survivors of methanol poisoning and chronic axonal loss in 10 of 42 (24%) patients. Significant decrease of global/temporal RNFL thickness during the observation period was found in the study population compared to the controls (P < .001). The risk estimate of chronic global RNFL loss for arterial blood pH < 7.3 at admission was 11.65 (95% confidence interval 1.91-71.12) after adjusting for age and sex. The patients with chronic axonal degeneration demonstrated progressive visual loss in 7 of 10 cases. The patients with abnormal RNFL thickness had magnetic resonance signs of brain damage in 10 of 13 vs 8 of 29 cases with normal RNFL thickness (P = .003). Signs of brain hemorrhages were present in 7 of 13 patients with abnormal RNFL thickness vs 5 of 29 cases with normal RNFL thickness (P = .015).
Methanol-induced optic neuropathy may lead to chronic retinal axonal loss during the following years. Arterial blood pH on admission is the strongest predictor of chronic RNFL thickness decrease. Chronic retinal neurodegeneration is associated with the progressive loss of visual functions and necrotic brain lesions.
研究甲醇中毒性视神经病变后慢性视网膜神经纤维层（RNFL）厚度损失的动力学和临床决定因素。
前瞻性队列研究。
所有患者均接受完整的眼科评估，包括在 4 年的观察期间进行 3 次频域光相干断层扫描：出院后 4.9（±0.6）、25.0（±0.6）和 49.9（±0.5）个月。
42 名甲醇中毒幸存者的 84 只眼，平均年龄（标准差）为 45.7（±4.4）岁；41 名对照者的 82 只眼，平均年龄为 44.0（±4.2）岁。
全局和时间 RNFL 损失。
在 42 名甲醇中毒幸存者中有 13 名（31%）登记了异常的 RNFL 厚度，10 名（24%）患者有慢性轴索丢失。与对照组相比，研究人群在观察期间全局/时间 RNFL 厚度显著下降（P<.001）。在校正年龄和性别后，入院时动脉血 pH <7.3 的慢性全 RNFL 损失的风险估计值为 11.65（95%置信区间 1.91-71.12）。10 例慢性轴索变性患者中有 7 例出现进行性视力丧失。13 例 RNFL 异常患者中有 10 例磁共振检查有脑损伤，而 29 例 RNFL 正常患者中有 8 例（P<.003）。13 例 RNFL 异常患者中有 7 例有脑出血迹象，而 29 例 RNFL 正常患者中有 5 例（P=.015）。
甲醇中毒性视神经病变可能导致随后几年的慢性视网膜轴索丢失。入院时的动脉血 pH 是慢性 RNFL 厚度下降的最强预测因子。慢性视网膜神经退行性变与视觉功能的进行性丧失和坏死性脑病变有关。
