Dataset Information

Impact of COVID-19 on inpatient clinical emergencies: A single-center experience.

ABSTRACT:

Aim

Determine changes in rapid response team (RRT) activations and describe institutional adaptations made during a surge in hospitalizations for coronavirus disease 2019 (COVID-19).

Methods

Using prospectively collected data, we compared characteristics of RRT calls at our academic hospital from March 7 through May 31, 2020 (COVID-19 era) versus those from January 1 through March 6, 2020 (pre-COVID-19 era). We used negative binomial regression to test differences in RRT activation rates normalized to floor (non-ICU) inpatient census between pre-COVID-19 and COVID-19 eras, including the sub-era of rapid COVID-19 census surge and plateau (March 28 through May 2, 2020).

Results

RRT activations for respiratory distress rose substantially during the rapid COVID-19 surge and plateau (2.38 (95% CI 1.39-3.36) activations per 1000 floor patient-days v. 1.27 (0.82-1.71) during the pre-COVID-19 era; p = 0.02); all-cause RRT rates were not significantly different (5.40 (95% CI 3.94-6.85) v. 4.83 (3.86-5.80) activations per 1000 floor patient-days, respectively; p = 0.52). Throughout the COVID-19 era, respiratory distress accounted for a higher percentage of RRT activations in COVID-19 versus non-COVID-19 patients (57% vs. 28%, respectively; p = 0.001). During the surge, we adapted RRT guidelines to reduce in-room personnel and standardize personal protective equipment based on COVID-19 status and risk to providers, created decision-support pathways for respiratory emergencies that accounted for COVID-19 status uncertainty, and expanded critical care consultative support to floor teams.

Conclusion

Increased frequency and complexity of RRT activations for respiratory distress during the COVID-19 surge prompted the creation of clinical tools and strategies that could be applied to other hospitals.

SUBMITTER: Mitchell OJL

PROVIDER: S-EPMC8096179 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:BackgroundSevere acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is commonly associated with myocardial injury and heart failure. The pathophysiology behind this phenomenon remains unclear, with many diverse and multifaceted hypotheses. To contribute to this understanding, we describe the underlying cardiac findings in fifty patients who died with coronavirus disease 2019 (COVID-19).MethodsIncluded were autopsies performed on patients with a positive SARS-CoV-2 reverse-transcriptase-polymerase-chain reaction test from the index hospitalization. In the case of out-of-hospital death, patients were included if post-mortem testing was positive. Complete autopsies were performed according to a COVID-19 safety protocol, and all patients underwent both macroscopic and microscopic examination. If available, laboratory findings and echocardiograms were reported.ResultsThe median age of the decedents was 63.5 years. The most common comorbidities included hypertension (90.0%), diabetes (56.0%) and obesity (50.0%). Lymphocytic inflammatory infiltrates in the heart were present in eight (16.0%) patients, with focal myocarditis present in two (4.0%) patients. Acute myocardial ischemia was observed in eight (16.0%) patients. The most common findings were myocardial fibrosis (80.0%), hypertrophy (72.0%), and microthrombi (66.0%). The most common causes of death were COVID-19 pneumonia in 18 (36.0%), COVID-19 pneumonia with bacterial superinfection in 12 (24.0%), and COVID-19 pneumonia with pulmonary embolism in 10 (20.0%) patients.ConclusionsCardiovascular comorbidities were prevalent, and pathologic changes associated with hypertensive and atherosclerotic cardiovascular disease were the most common findings. Despite markedly elevated inflammatory markers and cardiac enzymes, few patients exhibited inflammatory infiltrates or necrosis within cardiac myocytes. A unifying pathophysiologic mechanism behind myocardial injury in COVID-19 remains elusive, and additional autopsy studies are needed.