000 04681nam a22005537a 4500
008 210607s20212021 xxu||||| |||| 00| 0 eng d
022 _a0020-1324
024 _a10.4187/respcare.08599 [doi]
024 _arespcare.08599 [pii]
040 _aOvid MEDLINE(R)
099 _a33906956
245 _aAnalysis of Noninvasive Ventilation in Subjects With Sepsis and Acute Respiratory Failure.
251 _aRespiratory Care. 66(7):1063-1073, 2021 Jul.
252 _aRespir Care. 66(7):1063-1073, 2021 Jul.
252 _zRespir Care. 2021 Apr 27
253 _aRespiratory care
260 _c2021
260 _fFY2022
265 _saheadofprint
265 _sppublish
266 _d2021-06-07
268 _aRespiratory Care. 2021 Apr 27
269 _fFY2021
520 _aBACKGROUND: Acute respiratory failure is among the sequelae of complications that can develop in response to severe sepsis. Research into sepsis-related respiratory failure has focused on ARDS and invasive mechanical ventilation. We studied the factors associated with success and failure of noninvasive ventilation (NIV) in the treatment of sepsis-related acute respiratory failure.
520 _aCONCLUSIONS: NIV failure in sepsis-related acute respiratory failure was independently predicted by patient acuity, first systolic blood pressure after sepsis alert, initial FIO2 settings on NIV, fluid resuscitation, and signs of volume overload. However, only NIV failure independently predicted death in this cohort of subjects. Copyright (c) 2021 by Daedalus Enterprises.
520 _aMETHODS: This retrospective study included 136 subjects with a diagnosis of acute respiratory failure and intrapulmonary or extrapulmonary sepsis who were placed on NIV. Subjects were divided into 2 groups based on the need for intubation from NIV: NIV failure (n = 70) and NIV success (n = 66). Demographic, clinical, and outcome data were collected and compared between groups, with the development of multivariate models to predict NIV failure and mortality.
520 _aRESULTS: The overall NIV failure rate in subjects with a diagnosis of sepsis was 51%. There were no between-group differences in demographic or baseline characteristics. However, there were significant differences in clinical variables, with higher SOFA scores (NIV failure: 6.4 [+/- 3.0] vs NIV success: 4.9 [+/- 2.1]; P = .002), 2nd lactate levels (NIV failure: 2.6 [1.7 - 4.3] vs NIV success: 1.9 [1.4 - 2.6] mmol/L; P = .007), and initial NIV FIO2 settings (NIV failure: 0.50 [0.40 - 0.70] vs NIV failure: 0.40 [0.35 - 0.50]; P = .003) in subjects who failed NIV. There were also more subjects in the NIV failure group who had a lactate >= 4 mmol/L prior to NIV start compared to those who succeeded on NIV (33% vs 15%, P = .02). At NIV start, subjects in the NIV failure group had lower mean arterial pressure (85 mm Hg [IQR 74-96] vs 91.7 mm Hg [IQR 78-108], P = .042) and Glasgow coma scale scores (14 [IQR 13-15] vs 15 [IQR 14-15], P < .002), while fewer subjects in the NIV failure group received a fluid bolus in the 24 h prior to NIV start (33% vs 53%, P = .02) or had signs of volume overload (36% vs 64%, P < .001). Multivariate analysis indicated that age (odds ratio 1.05 [95% CI 1.01-1.09], P = .02), SOFA score (odds ratio 1.49 [95% CI 1.15-1.94], P = .002), first systolic blood pressure (odds ratio 0.97 [95% CI 0.95-0.99], P = .02), signs of volume overload (odds ratio 0.23 [95% CI 0.07-0.68], P = .008], fluids prior to NIV (odds ratio 0.08 [95% CI 0.02-0.31], P < .001), and initial FIO2 on NIV (odds ratio 1.04 [95% CI 1.01-1.08, P = .002) independently predicted NIV failure with an area under the curve of 0.88. Only NIV failure independently predicted death in multivariate analysis (area under the curve = 0.70).
546 _aEnglish
650 _a*Noninvasive Ventilation
650 _a*Respiratory Distress Syndrome
650 _a*Respiratory Insufficiency
650 _a*Sepsis
650 _aHumans
650 _aRespiratory Distress Syndrome/th [Therapy]
650 _aRespiratory Insufficiency/et [Etiology]
650 _aRespiratory Insufficiency/th [Therapy]
650 _aRetrospective Studies
650 _aSepsis/co [Complications]
650 _aSepsis/th [Therapy]
651 _aMedStar Washington Hospital Center
656 _aInternal Medicine Residency
656 _aRespiratory Therapy
657 _aJournal Article
700 _aAl-Ahmad, Ma'moon
700 _aDrescher, Gail S
790 _aAl-Ahmad MM, Drescher GS
856 _uhttps://dx.doi.org/10.4187/respcare.08599
_zhttps://dx.doi.org/10.4187/respcare.08599
942 _cART
_dArticle
999 _c6272
_d6272