7 versus 22.1) than patients who never received low-dose corticosteroids. The number of organ dysfunctions (OD) in the low-dose corticosteroids group was 3.9 versus 3.2 in the non-low-dose corticosteroids group.Table 2Patient baseline characteristicsA description of the intensive care therapies that patients selleck received is given in Table Table3.3. Significant differences exist between therapies received in all patients receiving low-dose corticosteroids versus those not receiving low-dose corticosteroids, except for mechanical venous thromboembolism (VTE) prophylaxis. Patients receiving low-dose corticosteroids received more therapeutic organ support and specific severe sepsis therapies, including drotrecogin alfa (activated) (DAA). In general, these differences were most marked in those receiving vasopressors.
Intravenous (IV) fluid resuscitation was given to 94.7% (2,645/2,794) of low-dose corticosteroids patients on vasopressors and 67.7% (174/257) of low-dose corticosteroids patients not receiving vasopressors. Patients receiving low-dose corticosteroids spent longer in ICU than patients not on low-dose corticosteroids (median of 12 versus 8 days; P <0.001), and spent more days on vasopressors (median of 6 versus 3; P <0.001), as shown in Table Table44.Table 3Patient therapiesTable 4Number of days spent in ICU and days on low-dose corticosteroids and vasopressers during ICU stayTable Table55 presents a summary of the mortality data. Hospital mortality with and without low-dose corticosteroids treatment was 60.8% (1,608/2,646) and 49.8% (2,042/4,101; P <0.
001), respectively, in patients receiving vasopressors and 27.4% (66/241) and 23.9% (353/1,475; P = 0.248), respectively, in patients not receiving vasopressors. All patient mortality rates were greater in the low-dose corticosteroids group than in the non-low-dose corticosteroids group at 58.0% (1,674/2,887) versus 43.0% (2,395/5,576; P <0.001).Table 5Hospital mortalityBecause of the noted imbalances in baseline characteristics (greater age, regional use, co-morbidities, disease severity, and requirement for organ support) between those with and without low-dose corticosteroids therapy, mortality results for the two cohorts are not directly comparable. Therefore, multiple logistic regression models were developed utilizing propensity scores and independent mortality risk factors in an attempt to ameliorate the impact of observed differences between the two cohorts in this non-randomized comparison.
Eleven models are presented in Table Table6.6. These models began with one covariate, propensity quintiles (Model 1) based on 12 baseline characteristics (age, seven types of ODs (seven ODs), surgical status, chronic lung disease status, active cancer status, and other chronic disabling condition). Model 3, considered the core model, Anacetrapib includes the propensity score quintiles as well as key covariates used to calculate the propensity quintiles; Age; and seven ODs.
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