Abstract
Abstract Disclosure: J. Rebernigg: None. K. Baez: None. N. Torres Rivera: None. B. Contreras: None. S. Yenari: None. K. Hamad: None. W. Wiese-Rometsch: None. V. Farhangi: None. •While certain endocrinopathies are known to increase dysglycemia in critically ill patients with sepsis or COVID-19, the impact on glycemic dysregulation in the presence of concomitant diagnoses is unclear.•We aimed to characterize glycemic variability among sepsis patients with vs without extant obesity (Obes) and/or diabetes (DM) undergoing intensive care with vs without lab confirmed SARS-CoV-2 infection (CoV-2+). •Clinicodemographic and administrative data including ICD-10-based Elixhauser comorbidity categories were extracted under IRB exemption from electronic medical records between March 14, 2020 and July 31, 2022.•Baseline serum glucose (SG) was assayed from initial blood sample in ED when patients were tested for CoV-2+.•Mean, median, minimum and maximum SG were computed to characterize longitudinal glycemic patterns.•Univariate and multivariate regression analyses computed Youden Index estimating mortality thresholds for glycemic parameters controlling for significant (p<.05) confounders including comorbidities, treatment known to affect SG, sepsis severity and pathway to ICU. •Continuous data summarized with median [IQR] was compared using Kruskal Wallis test. •Discrete data summarized as proportions were compared with chi-square test.•P-values for intergroup contrasts were Bonferroni corrected (p<.0125). •Among 2650 consecutively discharged sepsis patients with at least two SG assays were segmented into Control (1323, 49%), DM (473, 18%), Obes (418, 16%) and ObesDM (436, 17%) with similar (p>.0125) demographics including 62% males and 38% females aged 71 [60,79] years distributed across Whites (85%), Blacks (7%) and other races (8%).•Intergroup results are similarly sequenced and intragroup sequenced CoV-2+ vs not.•Insulin was given to Control (68 vs 56%, p<.05), DM (94 vs 96%, ns), Obes (83 v 66%, p<.001), ObesDM (99 vs 98%, ns).•Intragroup corticosteroids were given to Control (91 vs 48%, p<.0001), DM (89 vs 48%, p<.0001), Obes (97 vs 65%, p<.001), and ObesDM (95 vs 56%), p<.001).•Intergroup distribution of comorbidities included HTN (63%, 83%, 75%, 87%), iron deficiency anemia (47%, 48%, 47%, 54%), neurological disease (47%, 46%, 51%, 49%), heart failure (30%, 42%, 35%, 44%), renal failure (22%, 44%, 28%, 41%), coagulation disease (37%, 33%, 37%, 30%) and chronic pulmonary disease (25%, 23%, 27%, 32%).•Relative longitudinal impact of CoV-2+ is best represented by differential (p<.001) prevalence [n assays] of visit median glucose >131 mg/dL across Control (44% [14] vs 27% [20]), DM (82% [19] vs 66% [14], Obes (55% [29] vs 25% [19]) and ObesDM (84% [31] vs 67% [18]).•Varied mortality includes Control (49 vs 26%), DM (59 vs 23%), Obes (77 vs 22%) and ObesDM (68 vs 19%).•In conclusion, critically ill sepsis patients with DM and/or obesity comorbid with COVID-19 infection variously amplifies glycemic dysregulation and susceptibility to death. Presentation: Thursday, June 15, 2023
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