重症SARS-CoV-2肺炎后长期肺泡-毛细血管弥散损伤。

IF 4.3
Annals of medicine Pub Date : 2025-12-01 Epub Date: 2025-03-28 DOI:10.1080/07853890.2025.2483383
Laura Pini, Jordan Giordani, Guido Levi, Michele Guerini, Simone Piva, Elena Peli, Manuela Violini, Stefano Piras, Yehia El Masri, Alessandro Pini, Dina Visca, Deodato Assanelli, Maria Lorenza Muiesan, Nicola Latronico, Claudio Tantucci
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引用次数: 0

摘要

背景:持续的呼吸道症状和气体交换障碍在COVID-19肺炎康复患者中很常见。肺一氧化碳弥散量(DLCO)和一氧化碳传递系数(KCO)不能充分区分肺泡膜功能障碍和血管异常。本研究旨在研究重症监护后既往SARS-CoV-2肺炎患者持续弥散损伤和DLCO降低的特征。方法:出院后,患者进行肺活量测定、DLCO测量和每6个月进行6分钟步行测试。如果DLCO在18-24个月时仍然受损,则联合评估肺一氧化氮弥散能力(DLNO)和DLCO,以区分肺泡-毛细血管膜(DmCO)和肺毛细血管血容量(Vc)的改变。结果:在20例持续DLCO降低的患者中,3例为阻塞性通气模式,6例为限制性通气模式,12例为低KCO。在限制性情况下,KCO减少,但仍在正常范围内,没有补偿。所有患者DLNO/DLCO比值均超过预测值113.5%。DmCO损伤7例,Vc降低16例。结论:两种DLCO决定因素均受影响,以血管损害为主。大多数患者存在Vc降低,其平均值低于正常值的下限,而DmCO受影响较小,通常正常。DLNO/DLCO比值的升高表明,持续的DLCO降低主要是由延长的肺毛细血管循环功能障碍驱动的,而不是肺泡膜的改变,这突出了血管成分是长期损伤的主要部位。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Long-term alveolar-capillary diffusion impairments after severe SARS-CoV-2 pneumonia.

Long-term alveolar-capillary diffusion impairments after severe SARS-CoV-2 pneumonia.

Background: Persistent respiratory symptoms and impaired gas exchange are common in patients recovering from COVID-19 pneumonia. The Lung Diffusing Capacity for Carbon Monoxide (DLCO) and Carbon Monoxide Transfer Coefficient (KCO) do not adequately distinguish alveolar membrane dysfunction from vascular abnormalities. This study aimed to characterize persistent diffusion impairment in post-ICU patients with prior SARS-CoV-2 pneumonia and reduced DLCO.

Methods: After hospital discharge, patients underwent spirometry, DLCO measurement, and a 6-minute walking test every six months. If DLCO remained impaired at 18-24 months, a combined Lung Diffusing Capacity for Nitric Oxide (DLNO) and DLCO assessment was performed to differentiate alveolar-capillary membrane (DmCO) and pulmonary capillary blood volume (Vc) alterations.

Results: Among 20 patients with persistent DLCO reduction, 3 had an obstructive ventilatory pattern, 6 had restriction, and 12 had low KCO. In restrictive cases, KCO was reduced but remained within normal limits without compensation. The DLNO/DLCO ratio exceeded 113.5% predicted in all patients. DmCO was impaired in 7 patients, while Vc was reduced in 16.

Conclusion: Both DLCO determinants were affected, with vascular impairment predominating. Vc reduction was present in most patients, with mean values below the lower limit of normality, whereas DmCO was less affected and often normal. The elevated DLNO/DLCO ratio suggests that persistent DLCO reduction is primarily driven by prolonged pulmonary capillary circulation dysfunction rather than alveolar membrane alterations, highlighting the vascular component as the primary site of long-term impairment.

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