脑干出血患者气管切开拔管后持续性难治性高碳酸血症：一例病例报告

文献信息

中文摘要

背景： 在脑干损伤患者的气管切开拔管决策中，临床医生通常关注气道通畅性、吞咽功能和整体呼吸状态。然而，部分患者即使解剖气道通畅性已恢复，仍可能因中枢通气驱动受损及其他伴随因素而在拔管后面临慢性低通气风险。
病例介绍： 一名老年男性脑干出血患者于2024年1月切除肉芽组织后接受拔管，当时无即刻并发症。随访期间，他出现持续性二氧化碳（CO₂）潴留，并在随后19个月内因高碳酸血症性呼吸衰竭再入院9次，动脉血二氧化碳分压峰值达172 mmHg。尽管反复接受药物治疗和无创通气，仍未实现长期通气稳定，遂于2025年8月再次行气管切开术。
结论： 本病例提示，脑干损伤患者拔管后可能经历一个延长的代偿期——该患者慢性代偿性高碳酸血症在临床上被良好耐受达19个月——之后才出现迟发的、由事件触发的失代偿。随访期间进行的FEES证实双侧声带麻痹伴严重误吸（穿透-误吸量表7级），这比单纯中枢驱动受损更能直接解释反复肺炎和进行性通气负荷增加。拔管前PaCO₂正常，证实拔管时中枢通气驱动充足；慢性代偿性高碳酸血症本身并非再次置管的指征。有必要对通气稳定性进行纵向评估，且该临床过程很可能是多因素的。每位脑干损伤患者——而不仅是那些有明确吞咽困难记录者——都应考虑在拔管前行FEES或柔性喉镜检查，并且拔管后CO₂监测应针对那些结果会改变管理的高危患者。

英文摘要

BACKGROUND: In tracheostomy decannulation decisions for patients with brainstem injury, clinicians typically focus on airway patency, swallowing, and overall respiratory status. However, some patients may remain at risk of chronic hypoventilation after decannulation because of impaired central ventilatory drive and other concomitant factors, even when anatomical airway patency has been restored.
CASE PRESENTATION: An elderly male with brainstem hemorrhage underwent decannulation after excision of granulation tissue in January 2024, with no immediate complications. During follow-up, he developed persistent carbon dioxide (CO₂) retention and was readmitted nine times for hypercapnic respiratory failure over the subsequent 19 months, with a peak arterial partial pressure of carbon dioxide of 172 mmHg. Despite repeated medical therapy and noninvasive ventilation, long-term ventilatory stability was not achieved, and a repeat tracheostomy was performed in August 2025.
CONCLUSIONS: This case suggests that decannulation in brainstem-injury patients can be followed by a prolonged compensated phase-chronic compensated hypercapnia was clinically well tolerated for 19 months in this patient-before late, event-triggered decompensation. FEES performed during follow-up confirmed bilateral vocal cord paralysis with severe (penetration-aspiration scale level 7) aspiration, identifying a more direct mechanism for recurrent pneumonia and progressive ventilatory load than central drive impairment alone. The pre-decannulation PaCO₂ was normal, confirming that central ventilatory drive was sufficient at the time of decannulation; chronic compensated hypercapnia is not, in itself, an indication for recannulation. Longitudinal assessment of ventilatory stability is warranted, and the clinical course was likely multifactorial. Pre-decannulation FEES or flexible laryngoscopy should be considered in every brainstem-injury patient-not only those with documented dysphagia-and post-decannulation CO₂ monitoring should be targeted to selected high-risk patients in whom the results would alter management.