Background: Obesity is associated with many cardiopulmonary comorbidities independently associated with worse health outcomes in acute illness, yet the physiological mechanisms potentially making obese patients more susceptible to COVID-19 remain uncertain. Adiposity-derived immunosuppression, increased thrombogenic potential, and predilection towards inflammatory hyperreactivity have all been postulated as potential mediators of this phenomenon. Yet, the most obvious explanation is obese people have reduced respiratory reserve from lower diaphragmatic contractility, smaller airways (making intubation more challenging), and stiffer pulmonary compliance due to greater thoracic wall mass, predisposing them to increased hypoxia and mechanical ventilation requirement. In this study, we explore if obesity has an association with increased length of stay (LOS) or disease severity independent of these weight-associated mechanical factors necessitating increased respiratory support.
Methods: We used the American Heart Association National COVID-19 Registry, a retrospective cohort of adults admitted with COVID-19 to any of over 130 participating U.S. hospitals across 30 states. We included index admissions between March 2020 and April 2021 for participants aged ≥18 years initially hospitalized in non-intensive care to address confounding from immediate mechanical ventilation requirement. To quantify the association between LOS (in days) and BMI category, we applied a multivariable Poisson regression model with identity link and report ß coefficients for difference in LOS with 95% confidence intervals. Multiple imputation was performed for missing data.
Results: 22,915 patients met inclusion criteria. Rising BMI class was associated with younger age and lower presentation with oxygen saturation ≥95% on room air. In the multivariate regression model, overweight and obese patients had a statistically significant dose-dependent relationship between increasing BMI category and decreasing LOS (overweight -0.469 days [95% CI: -0.708 to -0.231, p< 0.01], Class I Obesity -0.480 days [95% CI: -0.733 to -0.226. p< 0.01], Class II Obesity -0.578 days [95% CI: -0.852 to -0.304, p< 0.01]. Table 1). Only Class III Obesity did not follow this trend (-0.0320 days, 95% CI: 0.615 to -0.024, p=0.034) but still represented a reduction in LOS relative to the normal weight category. The same analysis was applied to patients initially admitted to the ICU showing no significant association between BMI and LOS.
Conclusions: Overall, our results do not align with our original hypothesis that increasing BMI is associated with increased LOS. Instead, the inverse was observed once controlling for respiratory compromise (via restriction to non-ICU level care patients and adjustment for respiratory rate, admission oxygenation status, and mechanical ventilation requirement). This suggests that increased hospitalization and ICU level care in this population are due to ventilatory compromise, rather than inflammatory or thrombotic sequelae of increased adiposity. Furthermore, these unexpected (and dose-dependent) findings support the “Obesity Paradox” in non-critical COVID-19, a phenomenon which posits that higher BMI may provide a metabolic reserve for patients to draw upon during acute illness. However, there was no statistically significant relationship for underweight status and LOS.
