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2.
Crit Care Med ; 49(12): 2042-2057, 2021 12 01.
Article in English | MEDLINE | ID: covidwho-1522362

ABSTRACT

OBJECTIVE: Coronavirus disease 2019 is a heterogeneous disease most frequently causing respiratory tract infection, which can induce respiratory failure and multiple organ dysfunction syndrome in its severe forms. The prevalence of coronavirus disease 2019-related sepsis is still unclear; we aimed to describe this in a systematic review. DATA SOURCES: MEDLINE (PubMed), Cochrane, and Google Scholar databases were searched based on a prespecified protocol (International Prospective Register for Systematic Reviews: CRD42020202018). STUDY SELECTION: Studies reporting on patients with confirmed coronavirus disease 2019 diagnosed with sepsis according to sepsis-3 or according to the presence of infection-related organ dysfunctions necessitating organ support/replacement were included in the analysis. The primary end point was prevalence of coronavirus disease 2019-related sepsis among adults hospitalized in the ICU and the general ward. Among secondary end points were the need for ICU admission among patients initially hospitalized in the general ward and the prevalence of new onset of organ dysfunction in the ICU. Outcomes were expressed as proportions with respective 95% CI. DATA EXTRACTION: Two reviewers independently screened and reviewed existing literature and assessed study quality with the Newcastle-Ottawa Scale and the Methodological index for nonrandomized studies. DATA SYNTHESIS: Of 3,825 articles, 151 were analyzed, only five of which directly reported sepsis prevalence. Noting the high heterogeneity observed, coronavirus disease 2019-related sepsis prevalence was 77.9% (95% CI, 75.9-79.8; I2 = 91%; 57 studies) in the ICU, and 33.3% (95% CI, 30.3-36.4; I2 = 99%; 86 studies) in the general ward. ICU admission was required for 17.7% (95% CI, 12.9-23.6; I2 = 100%) of ward patients. Acute respiratory distress syndrome was the most common organ dysfunction in the ICU (87.5%; 95% CI, 83.3-90.7; I2 = 98%). CONCLUSIONS: The majority of coronavirus disease 2019 patients hospitalized in the ICU meet Sepsis-3 criteria and present infection-associated organ dysfunction. The medical and scientific community should be aware and systematically report viral sepsis for prognostic and treatment implications.


Subject(s)
COVID-19/complications , Hospitalization/statistics & numerical data , Sepsis/etiology , Sepsis/virology , Humans , Intensive Care Units/statistics & numerical data , Multiple Organ Failure/etiology , Patient Admission/statistics & numerical data , SARS-CoV-2 , Sepsis/mortality , Severity of Illness Index
3.
Medicine (Baltimore) ; 100(41): e27400, 2021 Oct 15.
Article in English | MEDLINE | ID: covidwho-1501201

ABSTRACT

ABSTRACT: To depict the clinical characters and prognosis of coronavirus disease 2019 patients who developed multiple organ dysfunction syndrome (MODS).A cohort consisted of 526 patients, which including 109 patients complicated MODS, was retrospectively analyzed to examine the clinical characteristics and risk factors of MODS.Among the 526 novel coronavirus-infected pneumonia patients, 109 patients developed multiple organ failure, the incidence rate was 20.7%. Among all 109 patients with MODS, 81.7% were over 60 years old, and 63.3% were male. The most common symptoms were fever (79.8%), dyspnea (73.4%), and fatigue (55.0%). Compared with patients non-MODS patients, there were 70 cases of MODS patients with one or more underlying diseases (64.2% vs 41.0%, P < .001). Respiratory failure (92.7%), circulatory failure (52.0%), and liver function injury (30.9%) were the most common symptoms within the spectrum of MODS. Invasive ventilator, noninvasive ventilator, and high-flow respiratory support treatment for patients in MODS patients were higher than those in the non-MODS group (P < .001). The antiviral therapy and 2 or more antibacterial drug treatments in MODS patients were higher than those in the non-MODS group (P < .001). The median hospital stay of all patients was 16 days (interquartile range [IQR], 9-26), of which 20 days (IQR, 11.5-30.5) in the MODS patients, which was approximately 4 days longer than that of non-MODS patients. In addition, our data suggested that lymphocyte counts <1.0 ∗ 109/L, Troponin T > 0.014 ng/mL and lower oxygenation index were risk factors for MODS. In the early stage of hospital admission, higher inflammatory indexes and lactic acid concentration were associated with increased risk of death.MODS often leads to poor prognosis in coronavirus disease 2019. Our data suggested the importance of early identification of MODS. We recommend close monitoring and timely supportive therapy for patients with high risks, stopping the disease progression before it was too late.


Subject(s)
COVID-19/epidemiology , Multiple Organ Failure/epidemiology , Aged , COVID-19/physiopathology , Comorbidity , Female , Humans , Incidence , Male , Middle Aged , Multiple Organ Failure/etiology , Multiple Organ Failure/physiopathology , Pandemics , Proportional Hazards Models , Retrospective Studies , Risk Factors , SARS-CoV-2
4.
Anaesthesist ; 70(2): 121-126, 2021 Feb.
Article in German | MEDLINE | ID: covidwho-1453674

ABSTRACT

A 59-year-old male patient was admitted to hospital diagnosed with moderate pneumonia associated with COVID-19. Upfront treatment with hydroxychloroquine and azithromycin was started. Due to a clinical deterioration (ARDS, circulatory shock) and greatly increased inflammation markers 6 days after admission, a cytokine storm was suspected and off-label treatment with the IL­6 receptor antagonist tocilizumab was initiated. Subsequently there was a dramatic rise of D­dimers indicating pulmonary intravascular coagulopathy and respiratory insufficiency worsened. After a second dose of tocilizumab was administered severe perimyocarditis with cardiac arrhythmia, hemodynamic instability and ST elevation occurred. Shortly afterwards the patient died due to multiorgan failure. From our experience, exacerbation of COVID-19 following treatment with tocilizumab cannot be ruled out. Randomized controlled studies are necessary to further investigate the efficacy, safety and patient selection criteria for tocilizumab treatment in COVID-19.


Subject(s)
Antibodies, Monoclonal, Humanized/adverse effects , Antibodies, Monoclonal, Humanized/therapeutic use , Antiviral Agents/adverse effects , Antiviral Agents/therapeutic use , Blood Coagulation Disorders/etiology , COVID-19/drug therapy , Cytokine Release Syndrome/drug therapy , Myocarditis/etiology , Receptors, Interleukin-6/antagonists & inhibitors , Fatal Outcome , Humans , Male , Middle Aged , Multiple Organ Failure/etiology , Off-Label Use , Respiratory Distress Syndrome/etiology , Respiratory Insufficiency , Treatment Outcome
5.
Front Immunol ; 12: 729776, 2021.
Article in English | MEDLINE | ID: covidwho-1403478

ABSTRACT

Coronavirus disease 2019 (COVID-19) pandemic is caused by the novel coronavirus that has spread rapidly around the world, leading to high mortality because of multiple organ dysfunction; however, its underlying molecular mechanism is unknown. To determine the molecular mechanism of multiple organ dysfunction, a bioinformatics analysis method based on a time-order gene co-expression network (TO-GCN) was performed. First, gene expression profiles were downloaded from the gene expression omnibus database (GSE161200), and a TO-GCN was constructed using the breadth-first search (BFS) algorithm to infer the pattern of changes in the different organs over time. Second, Gene Ontology enrichment analysis was used to analyze the main biological processes related to COVID-19. The initial gene modules for the immune response of different organs were defined as the research object. The STRING database was used to construct a protein-protein interaction network of immune genes in different organs. The PageRank algorithm was used to identify five hub genes in each organ. Finally, the Comparative Toxicogenomics Database played an important role in exploring the potential compounds that target the hub genes. The results showed that there were two types of biological processes: the body's stress response and cell-mediated immune response involving the lung, trachea, and olfactory bulb (olf) after being infected by COVID-19. However, a unique biological process related to the stress response is the regulation of neuronal signals in the brain. The stress response was heterogeneous among different organs. In the lung, the regulation of DNA morphology, angiogenesis, and mitochondrial-related energy metabolism are specific biological processes related to the stress response. In particular, an effect on tracheal stress response was made by the regulation of protein metabolism and rRNA metabolism-related biological processes, as biological processes. In the olf, the distinctive stress responses consist of neural signal transmission and brain behavior. In addition, myeloid leukocyte activation and myeloid leukocyte-mediated immunity in response to COVID-19 can lead to a cytokine storm. Immune genes such as SRC, RHOA, CD40LG, CSF1, TNFRSF1A, FCER1G, ICAM1, LAT, LCN2, PLAU, CXCL10, ICAM1, CD40, IRF7, and B2M were predicted to be the hub genes in the cytokine storm. Furthermore, we inferred that resveratrol, acetaminophen, dexamethasone, estradiol, statins, curcumin, and other compounds are potential target drugs in the treatment of COVID-19.


Subject(s)
COVID-19/complications , Multiple Organ Failure/genetics , Antiviral Agents/therapeutic use , Brain/metabolism , Brain/virology , COVID-19/drug therapy , COVID-19/genetics , COVID-19/virology , Gene Expression Profiling , Gene Ontology , Humans , Lung/metabolism , Lung/virology , Multiple Organ Failure/drug therapy , Multiple Organ Failure/etiology , Multiple Organ Failure/metabolism , Olfactory Bulb/metabolism , Olfactory Bulb/virology , Protein Interaction Maps , SARS-CoV-2/physiology , Trachea/metabolism , Trachea/virology , Transcriptome
7.
Front Immunol ; 12: 720192, 2021.
Article in English | MEDLINE | ID: covidwho-1378190

ABSTRACT

COVID-19 might lead to multi-organ failure and, in some cases, to death. The COVID-19 severity is associated with a "cytokine storm." Danger-associated molecular patterns (DAMPs) are proinflammatory molecules that can activate pattern recognition receptors, such as toll-like receptors (TLRs). DAMPs and TLRs have not received much attention in COVID-19 but can explain some of the gender-, weight- and age-dependent effects. In females and males, TLRs are differentially expressed, likely contributing to higher COVID-19 severity in males. DAMPs and cytokines associated with COVID-19 mortality are elevated in obese and elderly individuals, which might explain the higher risk for severer COVID-19 in these groups. Adenosine signaling inhibits the TLR/NF-κB pathway and, through this, decreases inflammation and DAMPs' effects. As vaccines will not be effective in all susceptible individuals and as new vaccine-resistant SARS-CoV-2 mutants might develop, it remains mandatory to find means to dampen COVID-19 disease severity, especially in high-risk groups. We propose that the regulation of DAMPs via adenosine signaling enhancement might be an effective way to lower the severity of COVID-19 and prevent multiple organ failure in the absence of severe side effects.


Subject(s)
Alarmins/immunology , COVID-19/physiopathology , Inflammation Mediators/immunology , Adenosine/metabolism , Alarmins/antagonists & inhibitors , Animals , COVID-19/complications , COVID-19/immunology , COVID-19/therapy , Humans , Inflammation/prevention & control , Inflammation Mediators/antagonists & inhibitors , Multiple Organ Failure/etiology , Multiple Organ Failure/prevention & control , Patient Acuity , Signal Transduction , Toll-Like Receptors/antagonists & inhibitors , Toll-Like Receptors/immunology
8.
Sci Rep ; 11(1): 15872, 2021 08 05.
Article in English | MEDLINE | ID: covidwho-1345580

ABSTRACT

COVID-19-associated respiratory failure offers the unprecedented opportunity to evaluate the differential host response to a uniform pathogenic insult. Understanding whether there are distinct subphenotypes of severe COVID-19 may offer insight into its pathophysiology. Sequential Organ Failure Assessment (SOFA) score is an objective and comprehensive measurement that measures dysfunction severity of six organ systems, i.e., cardiovascular, central nervous system, coagulation, liver, renal, and respiration. Our aim was to identify and characterize distinct subphenotypes of COVID-19 critical illness defined by the post-intubation trajectory of SOFA score. Intubated COVID-19 patients at two hospitals in New York city were leveraged as development and validation cohorts. Patients were grouped into mild, intermediate, and severe strata by their baseline post-intubation SOFA. Hierarchical agglomerative clustering was performed within each stratum to detect subphenotypes based on similarities amongst SOFA score trajectories evaluated by Dynamic Time Warping. Distinct worsening and recovering subphenotypes were identified within each stratum, which had distinct 7-day post-intubation SOFA progression trends. Patients in the worsening suphenotypes had a higher mortality than those in the recovering subphenotypes within each stratum (mild stratum, 29.7% vs. 10.3%, p = 0.033; intermediate stratum, 29.3% vs. 8.0%, p = 0.002; severe stratum, 53.7% vs. 22.2%, p < 0.001). Pathophysiologic biomarkers associated with progression were distinct at each stratum, including findings suggestive of inflammation in low baseline severity of illness versus hemophagocytic lymphohistiocytosis in higher baseline severity of illness. The findings suggest that there are clear worsening and recovering subphenotypes of COVID-19 respiratory failure after intubation, which are more predictive of outcomes than baseline severity of illness. Distinct progression biomarkers at differential baseline severity of illness suggests a heterogeneous pathobiology in the progression of COVID-19 respiratory failure.


Subject(s)
COVID-19/diagnosis , Multiple Organ Failure/diagnosis , Aged , COVID-19/complications , COVID-19/physiopathology , Critical Illness , Female , Humans , Male , Middle Aged , Multiple Organ Failure/etiology , Multiple Organ Failure/physiopathology , Organ Dysfunction Scores , Prognosis , SARS-CoV-2/isolation & purification , Severity of Illness Index
9.
Med Intensiva (Engl Ed) ; 45(6): 325-331, 2021.
Article in English | MEDLINE | ID: covidwho-1343315

ABSTRACT

OBJECTIVE: To describe outcomes of critically ill patients with COVID-19, particularly the association of renal replacement therapy to mortality. DESIGN: A single-center prospective observational study was carried out. SETTING: ICU of a tertiary care center. PATIENTS: Consecutive adults with COVID-19 admitted to the ICU. INTERVENTION: Renal replacement therapy. MAIN VARIABLES OF INTEREST: Demographic data, medical history, illness severity, type of oxygen therapy, laboratory data and use of renal replacement therapy to generate a logistic regression model describing independent risk factors for mortality. RESULTS: Of the total of 166 patients, 51% were mechanically ventilated and 26% required renal replacement therapy. The overall hospital mortality rate was 36%, versus 56% for those requiring renal replacement therapy, and 68% for those with both mechanical ventilation and renal replacement therapy. The logistic regression model identified four independent risk factors for mortality: age (adjusted OR 2.8 [95% CI 1.8-4.4] for every 10-year increase), mechanical ventilation (4.2 [1.7-10.6]), need for continuous venovenous hemofiltration (2.3 [1.3-4.0]) and C-reactive protein (1.1 [1.0-1.2] for every 10mg/L increase). CONCLUSIONS: In our cohort, acute kidney injury requiring renal replacement therapy was associated to a high mortality rate similar to that associated to the need for mechanical ventilation, while multiorgan failure necessitating both techniques implied an extremely high mortality risk.


Subject(s)
Acute Kidney Injury/therapy , COVID-19/complications , Critical Illness/therapy , Renal Replacement Therapy , SARS-CoV-2 , Acute Kidney Injury/etiology , Acute Kidney Injury/mortality , Adrenal Cortex Hormones/therapeutic use , Adult , Age Factors , Aged , C-Reactive Protein/analysis , COVID-19/blood , Comorbidity , Continuous Renal Replacement Therapy , Critical Illness/mortality , District of Columbia/epidemiology , Female , Hospital Mortality , Hospitals, University/statistics & numerical data , Humans , Intensive Care Units/statistics & numerical data , Male , Middle Aged , Multiple Organ Failure/etiology , Multiple Organ Failure/mortality , Oxygen Inhalation Therapy/statistics & numerical data , Procedures and Techniques Utilization/statistics & numerical data , Prospective Studies , Renal Replacement Therapy/statistics & numerical data , Respiration, Artificial/statistics & numerical data , Respiratory Distress Syndrome/etiology , Respiratory Distress Syndrome/mortality , Respiratory Distress Syndrome/therapy , Risk Factors , Tertiary Care Centers/statistics & numerical data , Treatment Outcome
10.
Int J Mol Sci ; 22(15)2021 Jul 24.
Article in English | MEDLINE | ID: covidwho-1325681

ABSTRACT

The outbreak of the coronavirus disease 2019 (COVID-19) began at the end of 2019. COVID-19 is caused by infection with the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and patients with COVID-19 may exhibit poor clinical outcomes. Some patients with severe COVID-19 experience cytokine release syndrome (CRS) or a cytokine storm-elevated levels of hyperactivated immune cells-and circulating pro-inflammatory cytokines, including interleukin (IL)-1ß and IL-18. This severe inflammatory response can lead to organ damage/failure and even death. The inflammasome is an intracellular immune complex that is responsible for the secretion of IL-1ß and IL-18 in various human diseases. Recently, there has been a growing number of studies revealing a link between the inflammasome and COVID-19. Therefore, this article summarizes the current literature regarding the inflammasome complex and COVID-19.


Subject(s)
COVID-19/immunology , COVID-19/virology , Inflammasomes/immunology , Inflammasomes/metabolism , SARS-CoV-2/immunology , SARS-CoV-2/metabolism , Adaptive Immunity/immunology , Animals , COVID-19/complications , COVID-19/drug therapy , Cytokine Release Syndrome/drug therapy , Cytokine Release Syndrome/etiology , Cytokine Release Syndrome/immunology , Humans , Multiple Organ Failure/drug therapy , Multiple Organ Failure/etiology , Multiple Organ Failure/immunology
11.
BMJ Case Rep ; 14(1)2021 Jan 29.
Article in English | MEDLINE | ID: covidwho-1314115

ABSTRACT

A 31-year-old G3P2002 with history of two prior caesarean sections presented with influenza-like illness, requiring intubation secondary to acute respiratory distress syndrome. Investigations revealed intrauterine fetal demise at 30-week gestation.She soon deteriorated with sepsis and multiple organs impacted. Risks of the gravid uterus impairing cardiopulmonary function appeared greater than risks of delivery, including that of uterine rupture. Vaginal birth after caesarean was achieved with misoprostol and critical care status rapidly improved.Current guidelines for management of fetal demise in patients with prior hysterotomies are mixed: although the American College of Obstetricians and Gynecologists recommends standard obstetric protocols rather than misoprostol administration for labour augmentation, there is limited published data citing severe maternal morbidity associated with misoprostol use. This case report argues misoprostol-augmented induction of labour can be a reasonable option in a medically complex patient with fetal demise and prior hysterotomies.


Subject(s)
Fetal Death/etiology , Labor, Induced/methods , Labor, Obstetric/drug effects , Misoprostol/administration & dosage , Oxytocics/administration & dosage , Administration, Intravaginal , Adult , Delivery, Obstetric/standards , Female , Humans , Hysterotomy/adverse effects , Intubation, Intratracheal/methods , Misoprostol/pharmacology , Multiple Organ Failure/etiology , Oxytocics/pharmacology , Pregnancy , Pregnancy Complications, Infectious/diagnosis , Pregnancy Trimester, Third , Respiratory Distress Syndrome/complications , Respiratory Distress Syndrome/therapy , Treatment Outcome , Uterine Rupture/prevention & control
12.
J Rehabil Med ; 53(8): jrm00221, 2021 08 07.
Article in English | MEDLINE | ID: covidwho-1243929

ABSTRACT

BACKGROUND: Multiple organ dysfunction syndrome, defined as altered organ function in critically ill patients, is a possible consequence of COVID-19. Investigating the current evidence is therefore crucial in this pandemic, as early rehabilitation could be effective for the functioning of patients with multiple organ failure. This rapid review assesses the effectiveness of rehabilitation interventions in adults with multiple organ dysfunction syndrome. METHODS: A rapid review was conducted including only randomised control trials, published until 30 November 2020. All databases were investigated and the results synthesized narratively, evaluating the risk of bias and quality of evidence in all included studies. RESULTS: A total of 404 records were identified through database searches. After removal of duplicates 346 articles remained. After screening, 3 studies (90 participants) met the inclusion criteria. All studies reported positive effects of neuromuscular electrical stimulation on muscle mass preservation compared with no treatment or standard physio-therapy. CONCLUSION: The lack of evidence on the effectiveness of rehabilitation interventions does not allow any firm conclusion to be drawn. Neuromuscular electrical stimulation might be a possible rehabilitation intervention to prevent muscle volume loss and improve function in patients with multiple organ dysfunction syndrome. However, further studies are needed to support these preliminary findings.


Subject(s)
COVID-19 , Critical Illness , Multiple Organ Failure/rehabilitation , Adult , Humans , Multiple Organ Failure/etiology , Pandemics , Randomized Controlled Trials as Topic , SARS-CoV-2
13.
Lancet Respir Med ; 9(6): 622-642, 2021 06.
Article in English | MEDLINE | ID: covidwho-1219780

ABSTRACT

The zoonotic SARS-CoV-2 virus that causes COVID-19 continues to spread worldwide, with devastating consequences. While the medical community has gained insight into the epidemiology of COVID-19, important questions remain about the clinical complexities and underlying mechanisms of disease phenotypes. Severe COVID-19 most commonly involves respiratory manifestations, although other systems are also affected, and acute disease is often followed by protracted complications. Such complex manifestations suggest that SARS-CoV-2 dysregulates the host response, triggering wide-ranging immuno-inflammatory, thrombotic, and parenchymal derangements. We review the intricacies of COVID-19 pathophysiology, its various phenotypes, and the anti-SARS-CoV-2 host response at the humoral and cellular levels. Some similarities exist between COVID-19 and respiratory failure of other origins, but evidence for many distinctive mechanistic features indicates that COVID-19 constitutes a new disease entity, with emerging data suggesting involvement of an endotheliopathy-centred pathophysiology. Further research, combining basic and clinical studies, is needed to advance understanding of pathophysiological mechanisms and to characterise immuno-inflammatory derangements across the range of phenotypes to enable optimum care for patients with COVID-19.


Subject(s)
COVID-19 , Multiple Organ Failure , SARS-CoV-2/pathogenicity , COVID-19/immunology , COVID-19/physiopathology , Endothelium/physiopathology , Humans , Immunity , Multiple Organ Failure/etiology , Multiple Organ Failure/physiopathology , Patient Acuity , Severity of Illness Index
14.
Medicine (Baltimore) ; 100(15): e25255, 2021 Apr 16.
Article in English | MEDLINE | ID: covidwho-1180670

ABSTRACT

RATIONALE: Fibrinolysis shutdown associated with severe thrombotic complications is a recently recognized syndrome that was previously seldom investigated in patients with severe severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. It presents a unique therapeutic dilemma, as anticoagulation with heparin alone is insufficient to address the imbalance in fibrinolysis. And while the use of fibrinolytic agents could limit the disease severity, it is often associated with bleeding complications. There is a need for biomarkers that will guide the timely stratification of patients into those who may benefit from both anticoagulant and fibrinolytic therapies. PATIENT CONCERNS: All 3 patients presented with shortness of breath along with comorbidities predisposing them to severe SARS-CoV-2 infection. One patient (Patient 3) also suffered from bilateral deep venous thrombosis. DIAGNOSES: All 3 patients tested positive for SARS-CoV-2 RNA by reverse transcription polymerase chain reaction (RT-PCR) and were eventually diagnosed with respiratory failure necessitating intubation. INTERVENTIONS: All 3 patients required mechanical ventilation support, 2 of which also required renal replacement therapy. All 3 patients were also placed on anticoagulation therapy. OUTCOMES: In Patients 1 and 2, the initial D-dimer levels of 0.97 µg/ml fibrinogen equivalent units (FEU) and 0.83 µg/ml FEU were only slightly elevated (normal <0.50 µg/ml FEU). They developed rising D-dimer levels to a peak of 13.21 µg/ml FEU and >20.0 µg/ml FEU, respectively, which dropped to 1.34 µg/ml FEU 8 days later in Patient 1 and to 2.94 µg/ml on hospital day 13 in Patient 2. In Patient 3, the D-dimer level on admission was found to be elevated to >20.00 µg/ml FEU together with imaging evidence of thrombosis. And although he received therapeutic heparin infusion, he still developed pulmonary embolism (PE) and his D-dimer level declined to 5.91 µg/ml FEU. Despite "improvement" in their D-dimer levels, all 3 patients succumbed to multi-system organ failure. On postmortem examination, numerous arterial and venous thromboses of varying ages, many consisting primarily of fibrin, were identified in the lungs of all patients. LESSONS: High D-dimer levels, with subsequent downtrend correlating with clinical deterioration, seems to be an indicator of fibrinolysis suppression. These findings can help form a hypothesis, as larger cohorts are necessary to demonstrate their reproducibility.


Subject(s)
Anticoagulants/therapeutic use , COVID-19 , Fibrin Fibrinogen Degradation Products/analysis , Multiple Organ Failure , Thrombolytic Therapy/methods , Autopsy/methods , COVID-19/blood , COVID-19/complications , COVID-19/physiopathology , COVID-19/therapy , Clinical Deterioration , Female , Fibrinolysis , Humans , Male , Middle Aged , Multiple Organ Failure/blood , Multiple Organ Failure/diagnosis , Multiple Organ Failure/etiology , Predictive Value of Tests , Prognosis , Renal Replacement Therapy/methods , Respiration, Artificial/methods , SARS-CoV-2/isolation & purification , Severity of Illness Index , Venous Thrombosis/blood , Venous Thrombosis/complications , Venous Thrombosis/diagnosis
16.
Sci Rep ; 11(1): 7163, 2021 03 30.
Article in English | MEDLINE | ID: covidwho-1159799

ABSTRACT

The spread of virus via the blood stream has been suggested to contribute to extra-pulmonary organ failure in Coronavirus disease 2019 (COVID-19). We assessed SARS-CoV-2 RNAemia (RNAemia) and the association between RNAemia and inflammation, organ failure and mortality in critically ill COVID-19 patients. We included all patients with PCR verified COVID-19 and consent admitted to ICU. SARS-CoV-2 RNA copies above 1000/ml measured by PCR in plasma was defined as RNAemia and used as surrogate for viremia. In this cohort of 92 patients 59 (64%) were invasively ventilated. RNAemia was found in 31 patients (34%). Hypertension and corticosteroid treatment was more common in patients with RNAemia. Extra-pulmonary organ failure biomarkers and the extent of organ failure were similar in patients with and without RNAemia, but the former group had more renal replacement therapy and higher mortality (26 vs 16%; 35 vs 16%, respectively, p = 0.04). RNAemia was not an independent predictor of death at 30 days after adjustment for age. SARS-CoV2 RNA copies in plasma is a common finding in ICU patients with COVID-19. Although viremia was not associated with extra pulmonary organ failure it was more common in patients who did not survive to 30 days after ICU admission.Trial registration: ClinicalTrials NCT04316884.


Subject(s)
COVID-19/etiology , COVID-19/mortality , Viremia/etiology , Aged , Biomarkers/blood , COVID-19/therapy , Comorbidity , Critical Illness , Female , Humans , Hypertension/epidemiology , Hypertension/etiology , Interleukin-6/blood , Male , Middle Aged , Multiple Organ Failure/etiology , Multiple Organ Failure/virology , Prospective Studies , RNA, Viral/blood , Renal Replacement Therapy , Respiration, Artificial , Sweden/epidemiology , Viremia/mortality , Viremia/therapy
18.
Sci Rep ; 11(1): 5975, 2021 03 16.
Article in English | MEDLINE | ID: covidwho-1137818

ABSTRACT

Since the emergence of SARS-CoV-2, numerous studies have been attempting to determine biomarkers, which could rapidly and efficiently predict COVID-19 severity, however there is lack of consensus on a specific one. This retrospective cohort study is a comprehensive analysis of the initial symptoms, comorbidities and laboratory evaluation of patients, diagnosed with COVID-19 in Huoshenshan Hospital, Wuhan, from 4th February to 12th March, 2020. Based on the data collected from 63 severely ill patients from the onset of symptoms till the full recovery or demise, we found not only age (average 70) but also blood indicators as significant risk factors associated with multiple organ failure. The blood indices of all patients showed hepatic, renal, cardiac and hematopoietic dysfunction with imbalanced coagulatory biomarkers. We noticed that the levels of LDH (85%, P < .001), HBDH (76%, P < .001) and CRP (65%, P < .001) were significantly elevated in deceased patients, indicating hepatic impairment. Similarly, increased CK (15%, P = .002), Cre (37%, P = 0.102) and CysC (74%, P = 0.384) indicated renal damage. Cardiac injury was obvious from the significantly elevated level of Myoglobin (52%, P < .01), Troponin-I (65%, P = 0.273) and BNP (50%, P = .787). SARS-CoV-2 disturbs the hemolymphatic system as WBC# (73%, P = .002) and NEUT# (78%, P < .001) were significantly elevated in deceased patients. Likewise, the level of D-dimer (80%, P < .171), PT (87%, P = .031) and TT (57%, P = .053) was elevated, indicating coagulatory imbalances. We identified myoglobin and CRP as specific risk factors related to mortality and highly correlated to organ failure in COVID-19 disease.


Subject(s)
C-Reactive Protein/analysis , COVID-19/pathology , Myoglobin/analysis , Aged , Aged, 80 and over , Biomarkers/blood , COVID-19/complications , COVID-19/mortality , COVID-19/virology , Comorbidity , Female , Humans , Male , Middle Aged , Multiple Organ Failure/etiology , Retrospective Studies , Risk Factors , SARS-CoV-2/isolation & purification , Severity of Illness Index , Survival Analysis , Thorax/diagnostic imaging , Tomography, X-Ray Computed , Troponin I/blood
19.
Scand J Gastroenterol ; 56(5): 585-587, 2021 05.
Article in English | MEDLINE | ID: covidwho-1132187

ABSTRACT

BACKGROUND: A relation between coronavirus disease 2019 (COVID-19) and acute pancreatitis has been suggested. However, the incidence and clinical relevance of this relation remain unclear. OBJECTIVE: We aimed to investigate the incidence, severity and clinical impact of acute pancreatitis in patients with COVID-19. METHODS: This is a cross-sectional study of a prospective, observational cohort concerning all COVID-19 patients admitted to two Dutch university hospitals between 4 March 2020 and 26 May 2020. Primary outcome was acute pancreatitis potentially related to COVD-19 infection. Acute pancreatitis was defined according to the revised Atlanta Classification. Potential relation with COVID-19 was defined as the absence of a clear aetiology of acute pancreatitis. RESULTS: Among 433 patients with COVID-19, five (1.2%) had potentially related acute pancreatitis according to the revised Atlanta Classification. These five patients suffered from severe COVID-19 infection; all had (multiple) organ failure and 60% died. None of the patients developed necrotizing pancreatitis. Moreover, development of acute pancreatitis did not lead to major treatment consequences. CONCLUSIONS: In contrast with previous research, our study demonstrated that COVID-19 related acute pancreatitis is rare and of little clinical impact. It is therefore debatable if acute pancreatitis in COVID-19 patients requires specific screening. We hypothesize that acute pancreatitis occurs in patients with severe illness due to COVID-19 infection as a result of transient hypoperfusion and pancreatic ischemia, not as a direct result of the virus.


Subject(s)
COVID-19 , Multiple Organ Failure , Pancreas , Pancreatitis , COVID-19/epidemiology , COVID-19/physiopathology , COVID-19/therapy , Cross-Sectional Studies , Female , Humans , Incidence , Intensive Care Units/statistics & numerical data , Ischemia/etiology , Ischemia/physiopathology , Length of Stay/statistics & numerical data , Male , Middle Aged , Multiple Organ Failure/diagnosis , Multiple Organ Failure/etiology , Multiple Organ Failure/physiopathology , Netherlands/epidemiology , Outcome and Process Assessment, Health Care , Pancreas/blood supply , Pancreas/physiopathology , Pancreatitis/diagnosis , Pancreatitis/epidemiology , Pancreatitis/etiology , Pancreatitis/physiopathology , Severity of Illness Index
20.
Int Immunopharmacol ; 97: 107569, 2021 Aug.
Article in English | MEDLINE | ID: covidwho-1129044

ABSTRACT

BACKGROUND: To investigate the prognostic value of a novel immune-inflammatory index, the interleukin-6-to-lymphocyte ratio (IL-6/LY), with the clinical outcomes of severe coronavirus disease 2019 (COVID-19) cases. METHODS: A cohort study of COVID-19 patients in Tongji Hospital, from January 2020 to February 2020, was evaluated. Kaplan-Meier method and the log-rank test was performed to analyze survival data. Univariate and multivariate analyses were performed with COX proportional hazard regression model. The primary and secondary outcomes were in-hospital mortality and multiple organ dysfunction syndrome (MODS), respectively. RESULTS: Total 320 adult patients were enrolled in our analyses. Patients were divided into low IL-6/LY group and high IL-6/LY group based on the cutoff value with 2.50. The Kaplan-Meier survival curves showed that high-value group (IL-6/LY ≥ 2.50) had a greater risk of poor prognosis (P < 0.001, respectively). Multivariate analysis indicated that IL-6/LY was the independent risk predictor for in-hospital mortality (hazard ratio [HR], 3.404; 95% confidence interval [CI], 1.090-10.633, P = 0.035) and MODS development (HR, 4.143; 95%CI, 1.321-12.986, P = 0.015). Meanwhile, IL-6/LY was positively correlated with the MuLBSTA score (r = 0.137, P = 0.031), suggesting that IL-6/LY was associated with long-term mortality (90-day). Furthermore, kinetic analysis revealed that the dynamic changes of inflammatory immune indexes were related to the severity of the disease. CONCLUSIONS: The elevated IL-6/LY was related with the increased risk of poor prognosis. Not only that, IL-6/LY could be used for risk stratification and early clinical identification of high-risk patients.


Subject(s)
COVID-19/blood , Interleukin-6/blood , Lymphocytes/immunology , COVID-19/complications , COVID-19/mortality , Cohort Studies , Female , Hospital Mortality , Humans , Kaplan-Meier Estimate , Male , Middle Aged , Multiple Organ Failure/blood , Multiple Organ Failure/etiology , Multivariate Analysis , Prognosis , Proportional Hazards Models , Risk Factors , Severity of Illness Index
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