Wankhade Bhushan Sudhakar, Shaikh Wasim Shabbir, Alrais Zeyad Faoor, ElKhouly Adel Elsaid, Salman Ammar Ali
Critical Care Medicine, Rashid Hospital, Dubai Academic Health Corporation, Dubai, ARE.
Cureus. 2024 Jan 24;16(1):e52840. doi: 10.7759/cureus.52840. eCollection 2024 Jan.
Carbon monoxide poisoning (COP) is a common cause of death due to poisoning. After COP, a significant number of patients may develop a distinct type of neurological dysfunction called delayed neurological sequel (DNS). Recently, we came across a disaster of COP cases after a fire in a shared accommodation. The hostel was overcrowded and had a faulty air-conditioning/exhaust system. A total of five patients with loss of consciousness and shock were brought to us. They were diagnosed with acute COP based on their history of exposure to carbon monoxide (CO) and elevated carboxyhemoglobin levels in blood gas measurements. All patients were intubated and mechanically ventilated. Standard intensive care management was given to them, which included oxygenation, sedation, fluid resuscitation, and vasopressors. Their carboxyhemoglobin was rapidly reversed with normobaric oxygen therapy (NBO). Three patients showed good response and neurological recovery after NBO.Unfortunately, two patients developed DNS. DNS is a neuropsychological condition that may have cognitive, psychiatric, vestibulocochlear, motor, sensory, or diffuse demyelinating effects after COP. DNS is diagnosed in patients with a typical history of exposure to CO and a constellation of signs and symptoms. Neuroimaging, specifically magnetic resonance imaging of the brain with gadolinium contrast, is the method of choice for diagnosis. Treatment of DNS after COP begins with anticipation. All patients should receive appropriate oxygen therapy to bring down carboxyhemoglobin as soon as possible. Hyperbaric oxygen therapy (HBO) for the treatment of COP and prevention of DNS is still debatable. In the available medical literature, there are conflicting recommendations regarding the use of HBO in COP/DNS. Moreover, apart from a lack of consensus, there is also a lack of clarity about optimum timing, duration, atmospheric pressure, and number of sessions of HBO in preventing DNS after COP. The development of DNS after COP is not directly responsible for mortality, but recovery sometimes takes a long time, which can contribute to increased morbidity and costs of treatment.
一氧化碳中毒（COP）是中毒致死的常见原因。一氧化碳中毒后，大量患者可能会出现一种独特的神经功能障碍，称为迟发性神经后遗症（DNS）。最近，我们遇到了一起合租公寓火灾后发生的一氧化碳中毒灾难事件。宿舍拥挤不堪，空调/排气系统存在故障。共有五名意识丧失和休克的患者被送到我们这里。根据他们接触一氧化碳（CO）的病史以及血气测量中碳氧血红蛋白水平升高，他们被诊断为急性一氧化碳中毒。所有患者均进行了气管插管并接受机械通气。对他们进行了标准的重症监护管理，包括给氧、镇静、液体复苏和血管加压药。通过常压氧疗（NBO），他们的碳氧血红蛋白迅速恢复正常。三名患者在接受NBO治疗后反应良好，神经功能得以恢复。不幸的是，两名患者出现了DNS。DNS是一种神经心理疾病，在一氧化碳中毒后可能会产生认知、精神、前庭蜗神经、运动、感觉或弥漫性脱髓鞘等影响。DNS在有典型一氧化碳接触史且伴有一系列体征和症状的患者中被诊断出来。神经影像学检查，特别是使用钆对比剂的脑部磁共振成像，是诊断的首选方法。一氧化碳中毒后DNS的治疗首先要做好预期。所有患者都应接受适当的氧疗，以尽快降低碳氧血红蛋白水平。高压氧疗法（HBO）用于治疗一氧化碳中毒和预防DNS仍存在争议。在现有的医学文献中，关于HBO在一氧化碳中毒/迟发性神经后遗症中的使用存在相互矛盾的建议。此外，除了缺乏共识外，对于HBO预防一氧化碳中毒后迟发性神经后遗症的最佳时机、持续时间、大气压和疗程次数也缺乏明确的认识。一氧化碳中毒后迟发性神经后遗症的发生并不直接导致死亡，但恢复有时需要很长时间，这可能会导致发病率增加和治疗成本上升。
