炎症、血栓形成和破坏:创伤和 SARS-CoV-2 引起的 ARDS 的三头地狱犬。
Inflammation, Thrombosis, and Destruction: The Three-Headed Cerberus of Trauma- and SARS-CoV-2-Induced ARDS.
机构信息
Institute of Clinical and Experimental Trauma-Immunology, University Hospital Ulm, Ulm, Germany.
出版信息
Front Immunol. 2020 Sep 25;11:584514. doi: 10.3389/fimmu.2020.584514. eCollection 2020.
Physical trauma can be considered an unrecognized "pandemic" because it can occur anywhere and affect anyone and represents a global burden. Following severe tissue trauma, patients frequently develop acute lung injury (ALI) and/or acute respiratory distress syndrome (ARDS) despite modern surgical and intensive care concepts. The underlying complex pathophysiology of life-threatening ALI/ARDS has been intensively studied in experimental and clinical settings. However, currently, the coronavirus family has become the focus of ALI/ARDS research because it represents an emerging global public health threat. The clinical presentation of the infection is highly heterogeneous, varying from a lack of symptoms to multiple organ dysfunction and mortality. In a particular subset of patients, the primary infection progresses rapidly to ALI and ARDS. The pathophysiological mechanisms triggering and driving severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-induced ALI/ARDS are still poorly understood. Although it is also generally unknown whether insights from trauma-induced ARDS may be readily translated to SARS-CoV-2-associated ARDS, it was still recommended to treat coronavirus-positive patients with ALI/ARDS with standard protocols for ALI/ARDS. However, this strategy was questioned by clinical scientists, because it was documented that some severely hypoxic SARS-CoV-2-infected patients exhibited a normal respiratory system compliance, a phenomenon rarely observed in ARDS patients with another underlying etiology. Therefore, coronavirus-induced ARDS was defined as a specific ARDS phenotype, which accordingly requires an adjusted therapeutic approach. These suggestions reflect previous attempts of classifying ARDS into different phenotypes that might overall facilitate ARDS diagnosis and treatment. Based on the clinical data from ARDS patients, two major phenotypes have been proposed: hyper- and hypo-inflammatory. Here, we provide a comparative review of the pathophysiological pathway of trauma-/hemorrhagic shock-induced ARDS and coronavirus-induced ARDS, with an emphasis on the crucial key points in the pathogenesis of both these ARDS forms. Therefore, the manifold available data on trauma-/hemorrhagic shock-induced ARDS may help to better understand coronavirus-induced ARDS.
身体创伤可被视为一种未被识别的“大流行”,因为它可能发生在任何地方,影响任何人,代表着全球的负担。在严重的组织创伤后,尽管采用了现代外科和重症监护概念,患者仍经常发生急性肺损伤(ALI)和/或急性呼吸窘迫综合征(ARDS)。在实验和临床环境中,已对危及生命的 ALI/ARDS 的复杂潜在病理生理学进行了深入研究。然而,目前冠状病毒家族已成为 ALI/ARDS 研究的焦点,因为它代表着新兴的全球公共卫生威胁。感染的临床表现高度异质,从无症状到多器官功能障碍和死亡不等。在特定的患者亚群中,原发性感染迅速进展为 ALI 和 ARDS。触发和驱动严重急性呼吸综合征冠状病毒 2(SARS-CoV-2)引起的 ALI/ARDS 的病理生理机制仍知之甚少。尽管一般也不知道创伤性 ARDS 的见解是否可以轻易转化为 SARS-CoV-2 相关的 ARDS,但仍建议用 ALI/ARDS 的标准方案治疗冠状病毒阳性的 ALI/ARDS 患者。然而,这种策略受到临床科学家的质疑,因为有记录表明,一些严重低氧血症的 SARS-CoV-2 感染患者表现出正常的呼吸系统顺应性,这种现象在另一种基础病因的 ARDS 患者中很少见。因此,冠状病毒引起的 ARDS 被定义为一种特定的 ARDS 表型,因此需要调整治疗方法。这些建议反映了先前尝试将 ARDS 分为不同的表型,总体上可能有助于 ARDS 的诊断和治疗。基于 ARDS 患者的临床数据,提出了两种主要的表型:高和低炎症。在这里,我们对创伤/失血性休克引起的 ARDS 和冠状病毒引起的 ARDS 的病理生理途径进行了比较性综述,重点介绍了这两种 ARDS 形式发病机制中的关键要点。因此,创伤/失血性休克引起的 ARDS 的大量现有数据可能有助于更好地理解冠状病毒引起的 ARDS。