Hutchings Sam D, Watchorn James, Trovato Francesca, Napoli Salvatore, Mujib Salma F, Hopkins Philip, McPhail Mark
Department of Inflammation Biology, School of Immunology and Microbial Sciences, Faculty of Life Sciences and Medicine, King's College London, London, UK.
Department of Military Anaesthesia and Critical Care, Royal Centre for Defence Medicine, London, UK.
Shock. 2021 Jun 1;55(6):752-758. doi: 10.1097/SHK.0000000000001672.
Critically ill patients with COVID-19 infection frequently exhibit a hyperinflammatory response and develop organ failures; however, the underlying mechanisms are unclear. We investigated the microcirculatory, endothelial, and inflammatory responses in critically ill COVID-19 patients and compared them to a group of patients with septic shock in a prospective observational case control study. Thirty critically ill patients with COVID-19 were compared to 33 patients with septic shock.Measurements of sublingual microcirculatory flow using Incident Dark Field video-microscopy and serial measurements of IL-6 and Syndecan-1 levels were performed. COVID-19 patients had significantly less vasoactive drug requirement and lower plasma lactate than those with septic shock. Microcirculatory flow was significantly worse in septic patients than those with COVID-19 (MFI 2.6 vs 2.9 p 0.02, PPV 88 vs 97% P < 0.001). IL-6 was higher in patients with septic shock than COVID-19 (1653 vs 253 pg/mL, P 0.03). IL-6 levels in COVID 19 patients were not elevated compared to healthy controls except on the day of ICU admission. Syndecan-1 levels were not different between the two pathological groups. Compared to patients with undifferentiated septic shock an overt shock state with tissue hypoperfusion does not appear typical of COVID-19 infection. There was no evidence of significant sublingual microcirculatory impairment, widespread endothelial injury or marked inflammatory cytokine release in this group of critically ill COVID-19 patients.
新型冠状病毒肺炎（COVID-19）感染的重症患者常表现出高炎症反应并发生器官功能衰竭；然而，其潜在机制尚不清楚。在一项前瞻性观察性病例对照研究中，我们调查了COVID-19重症患者的微循环、内皮细胞和炎症反应，并将其与一组感染性休克患者进行比较。将30例COVID-19重症患者与33例感染性休克患者进行比较。使用入射暗场视频显微镜测量舌下微循环血流，并对白细胞介素-6（IL-6）和 Syndecan-1水平进行连续测量。与感染性休克患者相比，COVID-19患者对血管活性药物的需求量显著减少，血浆乳酸水平更低。感染性休克患者的微循环血流明显比COVID-19患者差（微血管血流灌注指数[MFI] 2.6对2.9，P = 0.02；灌注良好血管比例[PPV] 88%对97%，P<0.001）。感染性休克患者的IL-6水平高于COVID-19患者（1653对253 pg/mL，P = 0.03）。除重症监护病房（ICU）入院当天外，COVID-19患者的IL-6水平与健康对照相比并未升高。两个病理组之间的Syndecan-1水平没有差异。与未分化感染性休克患者相比，明显的休克状态伴组织灌注不足在COVID-19感染中似乎并不典型。在这组COVID-19重症患者中，没有证据表明存在明显的舌下微循环障碍、广泛的内皮损伤或显著的炎症细胞因子释放。
