Acute Physiology and Chronic Health Evaluation II Score as a Predictor of Hospital Mortality in Patients of Coronavirus Disease 2019

Zou, Xiaojing; Li, Shusheng; Fang, Minghao; Hu, Ming; Bian, Yi; Ling, Jianmin; Yu, Shanshan; Liang, Jing; Li, Donghui; Huang, Jiao

doi:10.1097/ccm.0000000000004411

Cited by 197 publications

(209 citation statements)

References 24 publications

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“…The co-expression of ACE2 and TMPRSS2 was reported in type 1 pneumocytes [195], alveolar macrophages [9,192], lymphocytes [9], smooth muscle cells and enterocytes in the gastrointestinal tract [9,195], vessel smooth muscle cells [9], cardiomyocytes [9,192], hepatocytes [169], kidney cells [87], proximal tubule cells [114], and neurons [112], all of which are in line with the common clinical symptoms of COVID-19 [15,19,61,151,166,183,191,197]. Single-cell RNA profiling revealed that male gender, advanced age, and smoking habit can increase the co-expression of ACE2 and TMPRESS2 Viral components are recognized by the MyD88 pathway in the endosome, leading to the releases of IL-6 and NFκB from immune cells including macrophages, monocytes, and dendrites.…”

Section: The Mechanisms Underlying Sars-cov-2 Infectionsupporting

confidence: 53%

“…As noted above, the lungs are the organ most vulnerable to SARS-CoV-2, and importantly, respiratory failure associated with ARDS is the leading cause of death in individuals with COVID-19, contributing to 86% of the deaths [132]. In the severe or critical cases in intensive care units (ICUs), 53-95% of the patients developed ARDS [2,183,197]. Among those, 2-11% of the patients with ARDS required extracorporeal membrane oxygenation support, and the survival rate of those patients was quite low [61,166,183,191].…”

Section: Multi-organ Dysfunction/failure Respiratory Failure/ardsmentioning

confidence: 99%

“…Numerous studies revealed that acute cardiac injury was also a common complication of COVID-19 [2,19,50,61,138,139,166,183,191,197] and was associated with poor outcomes among severe COVID-19 patients [50,138,139]. It has been proposed that this might be due to the development of heart failure [138,191] and lethal arrhythmias [50].…”

Section: Myocardial Injurymentioning

confidence: 99%

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Inflammation Triggered by SARS-CoV-2 and ACE2 Augment Drives Multiple Organ Failure of Severe COVID-19: Molecular Mechanisms and Implications

et al. 2020

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The widespread occurrence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has led to a pandemic of coronavirus disease 2019 (COVID-19). The S spike protein of SARS-CoV-2 binds with angiotensin-converting enzyme 2 (ACE2) as a functional “receptor” and then enters into host cells to replicate and damage host cells and organs. ACE2 plays a pivotal role in the inflammation, and its downregulation may aggravate COVID-19 via the renin-angiotensin system, including by promoting pathological changes in lung injury and involving inflammatory responses. Severe patients of COVID-19 often develop acute respiratory distress syndrome and multiple organ dysfunction/failure with high mortality that may be closely related to the hyper-proinflammatory status called the “cytokine storm.” Massive cytokines including interleukin-6, nuclear factor kappa B (NFκB), and tumor necrosis factor alpha (TNFα) released from SARS-CoV-2-infected macrophages and monocytes lead inflammation-derived injurious cascades causing multi-organ injury/failure. This review summarizes the current evidence and understanding of the underlying mechanisms of SARS-CoV-2, ACE2 and inflammation co-mediated multi-organ injury or failure in COVID-19 patients.

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Section: The Mechanisms Underlying Sars-cov-2 Infectionsupporting

confidence: 53%

Section: Multi-organ Dysfunction/failure Respiratory Failure/ardsmentioning

confidence: 99%

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Inflammation Triggered by SARS-CoV-2 and ACE2 Augment Drives Multiple Organ Failure of Severe COVID-19: Molecular Mechanisms and Implications

et al. 2020

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“…In our study, both neutrophils and lymphocytes were shown to have excellent predictive ability to identify severe COVID-19 disease, which was in agreement with the typical progress of virus infection. Another important nding in our study was related to platelet levels, a lower level of platelet was identi ed as an independent risk factor for severe COVID-19, which was in consistent with the study published by Zhe Zhu et.al [8]. As we know, platelets are small (2-4 µm in diameter) anucleated cells derived from megakaryocytes in bone marrow, and are responsible for maintaining the integrity of the vasculature.…”

Section: Discussionsupporting

confidence: 91%

Clinical Value of Blood Markers to Assess the Severity of Coronavirus Disease 2019

Xiao

Zhong

et al. 2020

Preprint

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Background: Severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2) is threatening the world with the symptoms of seasonal influenza. This study was conducted to investigate the patient characteristics and clinical value of blood markers to assess the severity of coronavirus disease 2019 (COVID-19). Methods: 187 patients, diagnosed with COVID-19 (non-severe and severe cases) and admitted to hospital between January 27th and March 8th of 2020, were enrolled in the present study. Results: A higher proportion of clinical symptoms, including cough, expectoration, myalgia and fatigue were observed in non-severe group. Significant increased level of WBC count, neutrophils, CRP, IL-6 and IL-8 were noted in severe group. The level of neutrophils, CRP, IL-6 and IL-8 were significantly increased, while platelet was remarkely decreased in the severe group. The risk model based on lymphocyte, IL-6, IL-8, CRP and platelet had the highest area under the receiver operator characteristic curve (AUROC). The baseline of IL-6, IL-8 and CRP was positively correlated with other parameters except lymphocyte, hemoglobin and platelet. While the baseline of platelet was negatively correlated with other parameters except lymphocyte and hemoglobin. Additionally, there was no connection between severity of COVID-19 and cultures of blood, sputum and catheter secretion. Conclusions: The present study suggested that IL-6, IL-8, CRP and platelet played a critical role in deterioration of COVID-19 with potential value for monitoring the severity of COVID-19.

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“…In our study, there was no association between comorbidities and clinical outcome. Another investigation reported that in COVID-19 ICU patients, APACHE II and SOFA scores were independent outcome predictors [ 23 ]. A retrospective, observational study of 85 fatal cases reported that the most common causes of death in COVID-19 ICU patients are respiratory failure (46.9%), septic shock (19.8%), multiple organ failure (16%), and cardiac arrest (8.6%).…”

Section: Discussionmentioning

confidence: 99%

Lactate Kinetics Reflect Organ Dysfunction and Are Associated with Adverse Outcomes in Intensive Care Unit Patients with COVID-19 Pneumonia: Preliminary Results from a GREEK Single-Centre Study

et al. 2020

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Coronavirus disease-19 (COVID-19) continues to be a health threat worldwide. Increased blood lactate is common in intensive care unit (ICU) patients; however, its association with outcomes in ICU COVID-19 patients remains currently unexplored. In this retrospective, observational study we assessed whether lactate is associated with outcomes in COVID-19 patients. Blood lactate was measured on ICU admission and thereafter daily up to day 14 in 45 patients with confirmed COVID-19 pneumonia. Acute physiology and chronic health evaluation (APACHE II) was calculated on ICU admission, and sequential organ failure assessment (SOFA) score was assessed on admission and every second day. The cohort was divided into survivors and non-survivors based on 28-day ICU mortality (24.4%). Cox regression analysis revealed that maximum lactate on admission was independently related to 28-day ICU mortality with time in the presence of APACHE II (RR = 2.45, p = 0.008). Lactate’s area under the curve for detecting 28-day ICU mortality was 0.77 (p = 0.008). Mixed model analysis showed that mean daily lactate levels were higher in non-survivors (p < 0.0001); the model applied on SOFA scores showed a similar time pattern. Thus, initial blood lactate was an independent outcome predictor in COVID-19 ICU patients. The time course of lactate mirrors organ dysfunction and is associated with poor clinical outcomes.

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Acute Physiology and Chronic Health Evaluation II Score as a Predictor of Hospital Mortality in Patients of Coronavirus Disease 2019

Cited by 197 publications

References 24 publications

Inflammation Triggered by SARS-CoV-2 and ACE2 Augment Drives Multiple Organ Failure of Severe COVID-19: Molecular Mechanisms and Implications

Inflammation Triggered by SARS-CoV-2 and ACE2 Augment Drives Multiple Organ Failure of Severe COVID-19: Molecular Mechanisms and Implications

Clinical Value of Blood Markers to Assess the Severity of Coronavirus Disease 2019

Lactate Kinetics Reflect Organ Dysfunction and Are Associated with Adverse Outcomes in Intensive Care Unit Patients with COVID-19 Pneumonia: Preliminary Results from a GREEK Single-Centre Study

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