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1.
EuropePMC; 2022.
Preprint in English | EuropePMC | ID: ppcovidwho-337699

ABSTRACT

Background: Observational research provides a unique opportunity to learn causal effects when randomized trials are not available, but obtaining the correct estimates hinges on a multitude of design and analysis choices. We illustrate the advantages of modern causal inference methods and compare to standard research practice to estimate the effect of corticosteroids on mortality in hospitalized COVID-19 patients in an observational dataset. We use several large RCTs to benchmark our results. Methods: Our retrospective data source consists of 3,293 COVID-19 patients hospitalized at New York Presbyterian March 1-May 15, 2020. We design our study using the Target Trial Emulation framework. We estimate the effect of an intervention consisting of 6 days of corticosteroids administered at the time of severe hypoxia and contrast with an intervention consisting of no corticosteroids administration. The dataset includes dozens of time-varying confounders. We estimate the causal effects using a doubly robust estimator where the probabilities of treatment, outcome, and censoring are estimated using flexible regressions via super learning. We compare these analyses to standard practice in clinical research, consisting of two main methods: (i) Cox models for an exposure of corticosteroids receipt within various time windows of hypoxia, and (ii) a Cox time-varying model where the exposure is daily administration of corticosteroids starting at the time of hospitalization. Results: The effect in our target trial emulation is qualitatively identical to an RCT benchmark, estimated to reduce 28-day mortality from 32% (95% confidence interval: 31-34) to 23% (21-24). The estimated effect from meta-analyses of RCTs for corticosteroids is an odds ratio of 0.66 (0.53-0.82)(1). Hazard ratios from the Cox models range in size and direction from 0.50 (0.41-0.62) to 1.08 (0.80-1.47) and all study designs suffer from various forms of bias. Conclusion: We demonstrate in a case study that clinical research based on observational data can unveil true causal relations. However, the correctness of these effect estimates requires designing and analyzing the data based on principles which are different from the current standard in clinical research. The widespread communication and adoption of these design and analytical techniques is of high importance for the improvement of clinical research based on observational data.

2.
EuropePMC; 2022.
Preprint in English | EuropePMC | ID: ppcovidwho-336952

ABSTRACT

Background Acute respiratory distress syndrome (ARDS), a life-threatening condition characterized by hypoxemia and poor lung compliance, is associated with high mortality. ARDS induced by COVID-19 has similar clinical presentations and pathological manifestations as non-COVID-19 ARDS. However, COVID-19 ARDS is associated with a more protracted inflammatory respiratory failure compared to traditional ARDS. Therefore, a comprehensive molecular comparison of ARDS of different etiologies groups may pave the way for more specific clinical interventions. Methods and Findings In this study, we compared COVID-19 ARDS (n=43) and bacterial sepsis-induced (non-COVID-19) ARDS (n=24) using multi-omic plasma profiles covering 663 metabolites, 1,051 lipids, and 266 proteins. To address both between- and within-ARDS group variabilities we followed two approaches. First, we identified 706 molecules differently abundant between the two ARDS etiologies, revealing more than 40 biological processes differently regulated between the two groups. From these processes, we assembled a cascade of therapeutically relevant pathways downstream of sphingosine metabolism. The analysis suggests a possible overactivation of arginine metabolism involved in long-term sequelae of ARDS and highlights the potential of JAK inhibitors to improve outcomes in bacterial sepsis-induced ARDS. The second part of our study involved the comparison of the two ARDS groups with respect to clinical manifestations. Using a data-driven multi-omic network, we identified signatures of acute kidney injury (AKI) and thrombocytosis within each ARDS group. The AKI-associated network implicated mitochondrial dysregulation which might lead to post-ARDS renal-sequalae. The thrombocytosis-associated network hinted at a synergy between prothrombotic processes, namely IL-17, MAPK, TNF signaling pathways, and cell adhesion molecules. Thus, we speculate that combination therapy targeting two or more of these processes may ameliorate thrombocytosis-mediated hypercoagulation. Conclusion We present a first comprehensive molecular characterization of differences between two ARDS etiologies – COVID-19 and bacterial sepsis. Further investigation into the identified pathways will lead to a better understanding of the pathophysiological processes, potentially enabling novel therapeutic interventions.

3.
J Palliat Care ; : 8258597221098130, 2022 May 03.
Article in English | MEDLINE | ID: covidwho-1820047

ABSTRACT

OUTCOMES: Morbidity and mortality are higher in older adults with COVID-19, but their decisions about aggressive care, severity of disease, and outcomes during the first surge in New York City are not well characterized. We sought to determine if the oldest patients chose intubation and comfort care at different rates compared to younger geriatric patients. We also studied outcomes among patients admitted with severe disease and those who chose aggressive versus comfort care. METHODS: This retrospective analysis used electronic health record data from patients 65 years and older at two medical centers in New York City admitted between 3/5/2020 and 5/15/2020. The primary outcome was comfort care orders, and secondary outcomes included death, palliative care consultation, goals of care discussion, code status, and ventilator weaning. RESULTS: Of the 854 patients, 214 were in the oldest old (OO, age > = 85) group, 269 middle old (MO, age 75-84), and 371 young old (YO, age 65-74). Among those with serious disease, the OO were more likely to choose comfort care (45% vs. 21% MO and 6.8% YO), less likely to be intubated (17% vs. 37% MO and 44% YO), more likely to have a palliative care consult, more likely to be DNR/DNI on admission (60% vs. 17% MO and 9.3%% YO), and more likely to die during admission (65% vs. 42% MO and 21% YO) (all p-values < 0.001). Of all 216 intubated patients, 78% of the OO died, versus 66% of the MO and 36% of the YO (p = <0.001). CONCLUSIONS: Adults 85 and above admitted with COVID-19 were more likely to forego intubation and die with comfort-based care. Irrespective of intubation choice, patients 85 and older had a markedly poorer prognosis than other cohorts over 65.

4.
J Crit Care ; 70: 154045, 2022 08.
Article in English | MEDLINE | ID: covidwho-1814672

ABSTRACT

PURPOSE: Prolonged observation could avoid invasive mechanical ventilation (IMV) and related risks in patients with Covid-19 acute respiratory failure (ARF) compared to initiating early IMV. We aimed to determine the association between ARF management strategy and in-hospital mortality. MATERIALS AND METHODS: Patients in the Weill Cornell Covid-19 registry who developed ARF between March 5 - March 25, 2020 were exposed to an early IMV strategy; between March 26 - April 1, 2020 to an intermediate strategy; and after April 2 to prolonged observation. Cox proportional hazards regression was used to model in-hospital mortality and test an interaction between ARF management strategy and modified sequential organ failure assessment (mSOFA). RESULTS: Among 632 patients with ARF, 24% of patients in the early IMV strategy died versus 28% in prolonged observation. At lower mSOFA, prolonged observation was associated with lower mortality compared to early IMV (at mSOFA = 0, HR 0.16 [95% CI 0.04-0.57]). Mortality risk increased in the prolonged observation strategy group with each point increase in mSOFA score (HR 1.29 [95% CI 1.10-1.51], p = 0.002). CONCLUSION: In Covid-19 ARF, prolonged observation was associated with a mortality benefit at lower mSOFA scores, and increased mortality at higher mSOFA scores compared to early IMV.


Subject(s)
COVID-19 , Respiratory Distress Syndrome , Respiratory Insufficiency , COVID-19/therapy , Hospital Mortality , Humans , Organ Dysfunction Scores , Respiration, Artificial , Respiratory Insufficiency/therapy
5.
Am J Pathol ; 2022 Apr 22.
Article in English | MEDLINE | ID: covidwho-1800217

ABSTRACT

Vascular injury is a well-established, disease-modifying factor in acute respiratory distress syndrome (ARDS) pathogenesis. Recently, coronavirus disease 2019 (COVID-19)-induced injury to the vascular compartment has been linked to complement activation, microvascular thrombosis, and dysregulated immune responses. We sought to assess whether aberrant vascular activation in this prothrombotic context was associated with the induction of necroptotic vascular cell death. To achieve this, proteomic analysis was performed on blood samples from COVID-19 subjects at distinct time points during ARDS pathogenesis (hospitalized at risk, N = 59; ARDS, N = 31; and recovery, N = 12). Assessment of circulating endothelial markers in the at-risk cohort revealed a signature of low vascular protein abundance that tracked with low platelet levels and increased mortality. This signature was replicated in the ARDS cohort and correlated with increased plasma angiopoietin 2 levels. COVID-19 ARDS lung autopsy immunostaining confirmed a link between vascular injury (angiopoietin 2) and platelet-rich microthrombi (CD61) and induction of necrotic cell death (phosphorylated mixed lineage kinase domain-like). Among recovery subjects, the vascular signature identified patients with poor functional outcomes. Taken together, this vascular injury signature was associated with low platelet levels and increased mortality and could be used to identify ARDS patients most likely to benefit from vascular targeted therapies.

6.
Ann Neurol ; 91(6): 740-755, 2022 06.
Article in English | MEDLINE | ID: covidwho-1729093

ABSTRACT

OBJECTIVE: The purpose of this study was to estimate the time to recovery of command-following and associations between hypoxemia with time to recovery of command-following. METHODS: In this multicenter, retrospective, cohort study during the initial surge of the United States' pandemic (March-July 2020) we estimate the time from intubation to recovery of command-following, using Kaplan Meier cumulative-incidence curves and Cox proportional hazard models. Patients were included if they were admitted to 1 of 3 hospitals because of severe coronavirus disease 2019 (COVID-19), required endotracheal intubation for at least 7 days, and experienced impairment of consciousness (Glasgow Coma Scale motor score <6). RESULTS: Five hundred seventy-one patients of the 795 patients recovered command-following. The median time to recovery of command-following was 30 days (95% confidence interval [CI] = 27-32 days). Median time to recovery of command-following increased by 16 days for patients with at least one episode of an arterial partial pressure of oxygen (PaO2 ) value ≤55 mmHg (p < 0.001), and 25% recovered ≥10 days after cessation of mechanical ventilation. The time to recovery of command-following  was associated with hypoxemia (PaO2 ≤55 mmHg hazard ratio [HR] = 0.56, 95% CI = 0.46-0.68; PaO2 ≤70 HR = 0.88, 95% CI = 0.85-0.91), and each additional day of hypoxemia decreased the likelihood of recovery, accounting for confounders including sedation. These findings were confirmed among patients without any imagining evidence of structural brain injury (n = 199), and in a non-overlapping second surge cohort (N = 427, October 2020 to April 2021). INTERPRETATION: Survivors of severe COVID-19 commonly recover consciousness weeks after cessation of mechanical ventilation. Long recovery periods are associated with more severe hypoxemia. This relationship is not explained by sedation or brain injury identified on clinical imaging and should inform decisions about life-sustaining therapies. ANN NEUROL 2022;91:740-755.


Subject(s)
Brain Injuries , COVID-19 , Brain Injuries/complications , COVID-19/complications , Cohort Studies , Humans , Hypoxia , Retrospective Studies , Unconsciousness/complications
7.
EuropePMC; 2020.
Preprint in English | EuropePMC | ID: ppcovidwho-311326

ABSTRACT

Increasing evidence has shown that Coronavirus disease 19 (COVID-19) severity is driven by a dysregulated immunologic response. We aimed to assess the differences in inflammatory cytokines in COVID-19 patients compared to contemporaneously hospitalized controls and then analyze the relationship between these cytokines and the development of Acute Respiratory Distress Syndrome (ARDS), Acute Kidney Injury (AKI) and mortality. In this cohort study of hospitalized patients, done between March third, 2020 and April first, 2020 at a quaternary referral center in New York City we included adult hospitalized patients with COVID-19 and negative controls. Serum specimens were obtained on the first, second, and third hospital day and cytokines were measured by Luminex. Autopsies of nine cohort patients were examined. We identified 90 COVID-19 patients and 51 controls. Analysis of 48 inflammatory cytokines revealed upregulation of macrophage induced chemokines, T-cell related interleukines and stromal cell producing cytokines in COVID-19 patients compared to the controls. Moreover, distinctive cytokine signatures predicted the development of ARDS, AKI and mortality in COVID-19 patients. Specifically, macrophage-associated cytokines predicted ARDS , T cell immunity related cytokines predicted AKI and mortality was was associated with cytokines of activated immune pathways, of which IL-13 was universally correlated with ARDS, AKI and mortality. Histopathological examination of the autopsies showed diffuse alveolar damage with significant mononuclear inflammatory cell infiltration. Additionally, the kidneys demonstrated glomerular sclerosis, tubulointerstitial lymphocyte infiltration and cortical and medullary atrophy. These patterns of cytokine expression offer insight into the pathogenesis of COVID-19 disease, its severity, and subsequent lung and kidney injury suggesting more targeted treatment strategies.

8.
Crit Care Explor ; 3(12): e0589, 2021 Dec.
Article in English | MEDLINE | ID: covidwho-1608099

ABSTRACT

OBJECTIVES: This report aims to characterize the kinetics of serum albumin in critically ill patients with coronavirus disease 2019 compared with critically ill patients with sepsis-induced acute respiratory distress syndrome. DESIGN: Retrospective analysis. SETTING: We analyzed two critically ill cohorts, one with coronavirus disease 2019 and another with sepsis-induced acute respiratory distress syndrome, treated in the New York Presbyterian Hospital-Weill Cornell Medical Center. PATIENTS: Adult patients in the coronavirus disease 2019 cohort, diagnosed through reverse transcriptase-polymerase chain reaction assays performed on nasopharyngeal swabs, were admitted from March 3, 2020, to July 10, 2020. Adult patients in the sepsis-induced acute respiratory distress syndrome cohort, defined by Sepsis III criteria receipt of invasive mechanical ventilation and a Pao2/Fio2 ratio less than 300 were admitted from December 12, 2006, to February 26, 2019. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: We evaluated serial serum albumin levels within 30 days after ICU admission in each cohort. We then examined the albumin progression trajectories, aligned at ICU admission time to test the relationship at a similar point in disease progression, in survivors and nonsurvivors. Albumin trajectory in all critically ill coronavirus disease 2019 patients show two distinct phases: phase I (deterioration) showing rapid albumin loss and phase II (recovery) showing albumin stabilization or improvement. Meanwhile, albumin recovery predicted clinical improvement in critical coronavirus disease 2019. In addition, we found a deterioration and recovery trends in survivors in the sepsis-induced acute respiratory distress syndrome cohort but did not find such two-phase trend in nonsurvivors. CONCLUSIONS: The changes in albumin associated with coronavirus disease 2019 associated respiratory failure are transient compared with sepsis-associated acute respiratory distress syndrome and highlight the potential for recovery following a protracted course of severe coronavirus disease 2019.

9.
Ann Am Thorac Soc ; 2021 Dec 22.
Article in English | MEDLINE | ID: covidwho-1599188

ABSTRACT

RATIONALE: The coronavirus disease 2019 (COVID-19) pandemic has led to a dramatic increase in the number of survivors of critical illness. These survivors are at increased risk of physical, psychological, and cognitive impairments known collectively as Post-Intensive Care Syndrome (PICS). Little is known about the prevalence of PICS in COVID-19 survivors. OBJECTIVES: To report the prevalence of physical, psychological, and cognitive impairment among COVID-19 intensive care unit (ICU) survivors receiving follow-up care in an ICU recovery clinic, to assess for associations between PICS and ICU-related factors, and to compare the cohort of ICU survivors who attended post-ICU clinic to a cohort of ICU survivors who did not. METHODS: We performed a retrospective cohort study of COVID-19 ICU survivors admitted from March to May 2020 who were subsequently seen in a post-ICU recovery clinic in New York City. We abstracted medical chart data on available clinical screening instruments for physical, psychological, and cognitive impairment. Associations between these outcomes and care-related variables were tested. Baseline characteristics and in-hospital treatments of the post-ICU clinic cohort were compared to COVID-19 ICU survivors from the same institution who were not seen in post-ICU clinic. RESULTS: 87 COVID-19 ICU survivors were seen in our post-ICU recovery clinic. The median age was 62 years and 74% were male. The median length of hospitalization was 51 days and the median length of ICU stay was 22 days. At the post-ICU follow-up visit, 29%, 21%, and 13% of patients reported clinically significant levels of depressive symptoms, anxiety, and post-traumatic stress disorder symptoms, respectively. 25% had cognitive impairment. The overall prevalence of PICS was 90%. There were no associations between length of ICU stay, delirium, exposure to benzodiazepines, steroids, or systemic paralytics with positive screens for physical, psychological, or cognitive impairment. Baseline characteristics and ICU-related factors were similar in the cohort of COVID-19 ICU survivors who attended ICU recovery clinic and those who did not. CONCLUSION: PICS is common in COVID-19 survivors. We did not find any association with length of ICU stay, the use of benzodiazepines, steroids, or paralytics.

12.
Cell Metab ; 33(11): 2174-2188.e5, 2021 11 02.
Article in English | MEDLINE | ID: covidwho-1446535

ABSTRACT

Individuals infected with SARS-CoV-2 who also display hyperglycemia suffer from longer hospital stays, higher risk of developing acute respiratory distress syndrome (ARDS), and increased mortality. Nevertheless, the pathophysiological mechanism of hyperglycemia in COVID-19 remains poorly characterized. Here, we show that hyperglycemia is similarly prevalent among patients with ARDS independent of COVID-19 status. Yet among patients with ARDS and COVID-19, insulin resistance is the prevalent cause of hyperglycemia, independent of glucocorticoid treatment, which is unlike patients with ARDS but without COVID-19, where pancreatic beta cell failure predominates. A screen of glucoregulatory hormones revealed lower levels of adiponectin in patients with COVID-19. Hamsters infected with SARS-CoV-2 demonstrated a strong antiviral gene expression program in the adipose tissue and diminished expression of adiponectin. Moreover, we show that SARS-CoV-2 can infect adipocytes. Together these data suggest that SARS-CoV-2 may trigger adipose tissue dysfunction to drive insulin resistance and adverse outcomes in acute COVID-19.

13.
BMJ Open Respir Res ; 8(1)2021 08.
Article in English | MEDLINE | ID: covidwho-1367445

ABSTRACT

PURPOSE: To evaluate the association between body mass index (BMI) and clinical outcomes other than death in patients hospitalised and intubated with COVID-19. METHODS: This is a single-centre cohort study of adults with COVID-19 admitted to New York Presbyterian Hospital-Weill Cornell Medicine from 3 March 2020 through 15 May 2020. Baseline and outcome variables, as well as lab and ventilatory parameters, were generated for the admitted and intubated cohorts after stratifying by BMI category. Linear regression models were used for continuous, and logistic regression models were used for categorical outcomes. RESULTS: The study included 1337 admitted patients with a subset of 407 intubated patients. Among admitted patients, hospital length of stay (LOS) and home discharge was not significantly different across BMI categories independent of demographic characteristics and comorbidities. In the intubated cohort, there was no difference in in-hospital events and treatments, including renal replacement therapy, neuromuscular blockade and prone positioning. Ventilatory ratio was higher with increasing BMI on days 1, 3 and 7. There was no significant difference in ventilator free days (VFD) at 28 or 60 days, need for tracheostomy, hospital LOS, and discharge disposition based on BMI in the intubated cohort after adjustment. CONCLUSIONS: In our COVID-19 population, there was no association between obesity and morbidity outcomes, such as hospital LOS, home discharge or VFD. Further research is needed to clarify the mechanisms underlying the reported effects of BMI on outcomes, which may be population dependent.


Subject(s)
Body Mass Index , COVID-19 , Morbidity , Adult , COVID-19/diagnosis , Cohort Studies , Hospitalization , Humans , New York City
14.
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
15.
Sci Rep ; 11(1): 12606, 2021 06 15.
Article in English | MEDLINE | ID: covidwho-1270673

ABSTRACT

Increasing evidence has shown that Coronavirus disease 19 (COVID-19) severity is driven by a dysregulated immunologic response. We aimed to assess the differences in inflammatory cytokines in COVID-19 patients compared to contemporaneously hospitalized controls and then analyze the relationship between these cytokines and the development of Acute Respiratory Distress Syndrome (ARDS), Acute Kidney Injury (AKI) and mortality. In this cohort study of hospitalized patients, done between March third, 2020 and April first, 2020 at a quaternary referral center in New York City we included adult hospitalized patients with COVID-19 and negative controls. Serum specimens were obtained on the first, second, and third hospital day and cytokines were measured by Luminex. Autopsies of nine cohort patients were examined. We identified 90 COVID-19 patients and 51 controls. Analysis of 48 inflammatory cytokines revealed upregulation of macrophage induced chemokines, T-cell related interleukines and stromal cell producing cytokines in COVID-19 patients compared to the controls. Moreover, distinctive cytokine signatures predicted the development of ARDS, AKI and mortality in COVID-19 patients. Specifically, macrophage-associated cytokines predicted ARDS, T cell immunity related cytokines predicted AKI and mortality was associated with cytokines of activated immune pathways, of which IL-13 was universally correlated with ARDS, AKI and mortality. Histopathological examination of the autopsies showed diffuse alveolar damage with significant mononuclear inflammatory cell infiltration. Additionally, the kidneys demonstrated glomerular sclerosis, tubulointerstitial lymphocyte infiltration and cortical and medullary atrophy. These patterns of cytokine expression offer insight into the pathogenesis of COVID-19 disease, its severity, and subsequent lung and kidney injury suggesting more targeted treatment strategies.


Subject(s)
COVID-19/mortality , COVID-19/physiopathology , Cytokines/blood , Acute Kidney Injury/blood , Acute Kidney Injury/pathology , Acute Kidney Injury/virology , Aged , COVID-19/blood , COVID-19/therapy , Case-Control Studies , Cytokine Release Syndrome/virology , Female , Hospitals , Humans , Lung/pathology , Lung/virology , Male , Middle Aged , New York City , Respiration, Artificial , Respiratory Distress Syndrome/blood , Respiratory Distress Syndrome/virology , Treatment Outcome
16.
J Biomed Inform ; 118: 103794, 2021 06.
Article in English | MEDLINE | ID: covidwho-1209791

ABSTRACT

From early March through mid-May 2020, the COVID-19 pandemic overwhelmed hospitals in New York City. In anticipation of ventilator shortages and limited ICU bed capacity, hospital operations prioritized the development of prognostic tools to predict clinical deterioration. However, early experience from frontline physicians observed that some patients developed unanticipated deterioration after having relatively stable periods, attesting to the uncertainty of clinical trajectories among hospitalized patients with COVID-19. Prediction tools that incorporate clinical variables at one time-point, usually on hospital presentation, are suboptimal for patients with dynamic changes and evolving clinical trajectories. Therefore, our study team developed a machine-learning algorithm to predict clinical deterioration among hospitalized COVID-19 patients by extracting clinically meaningful features from complex longitudinal laboratory and vital sign values during the early period of hospitalization with an emphasis on informative missing-ness. To incorporate the evolution of the disease and clinical practice over the course of the pandemic, we utilized a time-dependent cross-validation strategy for model development. Finally, we validated our prediction model on an external validation cohort of COVID-19 patients served in a demographically distinct population from the training cohort. The main finding of our study is the identification of risk profiles of early, late and no clinical deterioration during the course of hospitalization. While risk prediction models that include simple predictors at ED presentation and clinical judgement are able to identify any deterioration vs. no deterioration, our methodology is able to isolate a particular risk group that remain stable initially but deteriorate at a later stage of the course of hospitalization. We demonstrate the superior predictive performance with the utilization of laboratory and vital sign data during the early period of hospitalization compared to the utilization of data at presentation alone. Our results will allow efficient hospital resource allocation and will motivate research in understanding the late deterioration risk group.


Subject(s)
COVID-19/diagnosis , Clinical Deterioration , Computer Simulation , Aged , Female , Hospitalization , Hospitals , Humans , Male , New York City , Pandemics , ROC Curve , Retrospective Studies , Risk Assessment
17.
J Biomed Inform ; 118: 103789, 2021 06.
Article in English | MEDLINE | ID: covidwho-1188720

ABSTRACT

Patients treated in an intensive care unit (ICU) are critically ill and require life-sustaining organ failure support. Existing critical care data resources are limited to a select number of institutions, contain only ICU data, and do not enable the study of local changes in care patterns. To address these limitations, we developed the Critical carE Database for Advanced Research (CEDAR), a method for automating extraction and transformation of data from an electronic health record (EHR) system. Compared to an existing gold standard of manually collected data at our institution, CEDAR was statistically similar in most measures, including patient demographics and sepsis-related organ failure assessment (SOFA) scores. Additionally, CEDAR automated data extraction obviated the need for manual collection of 550 variables. Critically, during the spring 2020 COVID-19 surge in New York City, a modified version of CEDAR supported pandemic response efforts, including clinical operations and research. Other academic medical centers may find value in using the CEDAR method to automate data extraction from EHR systems to support ICU activities.


Subject(s)
COVID-19 , Databases, Factual , Electronic Health Records , Intensive Care Units , Aged , Aged, 80 and over , Critical Care , Critical Illness , Female , Humans , Male , Middle Aged , New York City
18.
Signif (Oxf) ; 18(1): 40-43, 2021 Feb.
Article in English | MEDLINE | ID: covidwho-1061644

ABSTRACT

Katherine Hoffman is a biostatistician in the pulmonary and critical care team of a New York City hospital, who found herself part of the Covid-19 response when the outbreak first hit in March 2020. This is her story.

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