PDF(Pubmed)
Abstract：
The COVID-19 pandemic has created a major alteration in the medical literature including the sepsis discussion. From the outset of the pandemic, various reports have indicated that although there are some unique features pertinent to COVID-19, many of its acute manifestations are similar to sepsis caused by other pathogens. As a consequence, the old definitions now require consideration of this new etiologic agent, namely SARS-CoV-2. Although the pathogenesis of COVID-19 has not been fully explained, the data obtained so far in hospitalized patients has revealed that serum cytokine and chemokine levels are high in severe COVID-19 patients, similar to those found with sepsis. COVID-19 may involve multiple organ systems. In addition to the lungs, the virus has been isolated from blood, urine, faeces, liver, and gallbladder. Results from autopsy series in COVID-19 patients have demonstrated a wide range of findings, including vascular involvement, congestion, consolidation, and hemorrhage as well as diffuse alveolar damage in lung tissue consistent with acute respiratory distress syndrome (ARDS). The presence of viral cytopathic-like changes, infiltration of inflammatory cells (mononuclear cells and macrophages), and viral particles in histopathological samples are considered a consequence of both direct viral infection and immune hyperactivation. Thromboembolism and hyper-coagulopathy are other components in the pathogenesis of severe COVID-19. Although the pathogenesis of hypercoagulability is not fully understood, it has been pointed out that all three components of Virchow’s triad (endothelial injury, stasis, and hypercoagulable state) play a major role in contributing to clot formation in severe COVID-19 infection. In severe COVID-19 cases, laboratory parameters such as hematological findings, coagulation tests, liver function tests, D-dimer, ferritin, and acute phase reactants such as CRP show marked alterations, which are suggestive of a cytokine storm. Another key element of COVID-19 pathogenesis in severe cases is its similarity or association with hemophagocytic lymphohistiocytosis (HLH). SARS-CoV-2 induced cytokine storm has significant clinical and laboratory findings overlapping with HLH. Viral sepsis has some similarities but also some differences when compared to bacterial sepsis. In bacterial sepsis, systemic inflammation affecting multiple organs is more dominant than in COVID-19 sepsis. While bacterial sepsis causes an early and sudden onset clinical deterioration, viral diseases may exhibit a relatively late onset and chronic course. Consideration of severe COVID-19 disease as a sepsis syndrome has relevance and may assist in terms of determining treatments that will modulate the immune response, limit intrinsic damage to tissue and organs, and potentially improve outcome.
摘要：
COVID-19大流行在包括败血症讨论在内的医学文献中造成了重大变化。从大流行开始，各种报道表明,尽管与COVID-19有一些独特的特征,但其许多急性表现与其他病原体引起的脓毒症相似.因此,旧的定义现在需要考虑这种新的病原体，即SARS-CoV-2。尽管COVID-19的发病机制尚未得到充分解释，迄今为止在住院患者中获得的数据显示，重症COVID-19患者的血清细胞因子和趋化因子水平很高，与败血症相似。COVID-19可能涉及多个器官系统。除了肺,病毒已经从血液中分离出来,尿液,粪便,肝脏,和胆囊。COVID-19患者的尸检系列结果显示了广泛的发现，包括血管受累,拥塞，合并，与急性呼吸窘迫综合征（ARDS）一致的肺组织出血以及弥漫性肺泡损伤。病毒细胞病变样变化的存在，炎症细胞（单核细胞和巨噬细胞）的浸润，和组织病理学样品中的病毒颗粒被认为是直接病毒感染和免疫过度活化的结果。血栓栓塞和超凝病变是严重COVID-19发病机制的其他组成部分。尽管尚未完全了解高凝的发病机理，有人指出，Virchow三合会的所有三个组成部分（内皮损伤，stasis,和高凝状态）在导致严重COVID-19感染的血凝块形成中起主要作用。在严重的COVID-19病例中，实验室参数，如血液学结果，凝血试验,肝功能检查,D-二聚体,铁蛋白,和急性期反应物如CRP显示明显的变化，这暗示了细胞因子风暴。严重病例中COVID-19发病机制的另一个关键因素是其与噬血细胞性淋巴组织细胞增多症（HLH）的相似性或相关性。SARS-CoV-2诱导的细胞因子风暴具有与HLH重叠的重要临床和实验室发现。与细菌性败血症相比，病毒性败血症有一些相似之处，但也有一些差异。在细菌性败血症中，影响多器官的全身性炎症比COVID-19脓毒症更占优势。虽然细菌性败血症导致早期和突然发作的临床恶化，病毒性疾病可能表现为相对迟发和慢性病程。将严重的COVID-19疾病视为脓毒症综合征具有相关性，可能有助于确定调节免疫反应的治疗方法，限制组织和器官的内在损伤，并有可能改善结果。
