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Predictors of Mortality in Acute Lung Injury During the Era

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Predictors of Mortality in Acute Lung Injury During the Era Acutelunginjury Predictors of mortality in acute lung injury during the Thorax: first published as 10.1136/thx.2007.093658 on 19 June 2008. Downloaded from era of lung protective ventilation E Seeley,1 D F McAuley,2 M Eisner,1 M Miletin,1,3 M A Matthay,1 R H Kallet4 1 Departments of Medicine and ABSTRACT ratio,9 respiratory system compliance (Crs)3 and Anesthesia, Cardiovascular Background: Lung protective ventilation has been widely oxygenation index (OI).7 To our knowledge, no Research Institute, University of large study of mortality predictors has been California, San Francisco, adopted for the management of acute lung injury (ALI) and California, USA; 2 Respiratory acute respiratory distress syndrome (ARDS). Consequently, conducted in North America since the implemen- Medicine Research Group, ventilator associated lung injury and mortality have tation of the lung protective ventilation. Thus we Queen’s University of Belfast, decreased. It is not known if this ventilation strategy conducted a retrospective study of these variables Belfast, Northern Ireland, UK; changes the prognostic value of previously identified to identify early predictors of mortality in ALI/ 3 Department of Medicine, William Osler Health Centre, demographic and pulmonary predictors of mortality, such as ARDS after adoption of lung protective ventila- Toronto, Canada; 4 Department respiratory compliance and the arterial oxygen tension to tion. We hypothesised that this ventilation strat- of Anesthesia, University of inspired oxygen fraction ratio (PaO2/FiO2). egy may attenuate the predictive value of California, San Francisco at San Methods: Demographic, clinical, laboratory and pulmon- previously identified pulmonary specific measures. Francisco General Hospital, San Francisco, California, USA ary variables were recorded in 149 patients with ALI/ ARDS. Significant predictors of mortality were identified in METHODS Correspondence to: bivariate analysis and these were entered into multivariate Dr E J Seeley, University of analysis to identify independent predictors of mortality. Subjects California, San Francisco, 505 We studied patients in both medical and surgical Parnassus Ave, Box 0130, San Results: Hospital mortality was 41%. In the bivariate Francisco, CA 94143, USA; analysis, 17 variables were significantly correlated with intensive care units identified prospectively as part [email protected] mortality, including age, APACHE II score and the of ongoing clinical trials of ALI/ARDS between 1 presence of cirrhosis. Pulmonary parameters associated July 2002 and 30 June 2003. The study was done at Received 22 November 2007 the University of California Moffitt-Long Hospital, with death included PaO2/FiO2 and oxygenation index Accepted 2 June 2008 a tertiary university referral centre, and at San Published Online First ((mean airway pressure6FiO26100)4PaO2). In unad- Francisco General Hospital, a large, inner city 19 June 2008 justed analysis, the odds ratio (OR) of death for PaO2/FiO2 was 1.57 (CI 1.12 to 3.04) per standard deviation hospital and level 1 trauma centre. Retrospective data collection was approved by the institutional decrease. However, in adjusted analysis, PaO2/FiO2 was not a statistically significant predictor of death, with an review board of the University of California, San Francisco and given the retrospective nature of this OR of 1.29 (CI 0.82 to 2.02). In contrast, oxygenation http://thorax.bmj.com/ index (OI) was a statistically significant predictor of death study, the requirement for written informed con- in both unadjusted analysis (OR 1.89 (CI 1.28 to 2.78)) sent was waived. Patients were 18 years of age or and in adjusted analysis (OR 1.84 (CI 1.13 to 2.99)). older, had received mechanical ventilation and met Conclusions: In this cohort of patients with ALI/ARDS, OI the North American–European consensus confer- ence definition for ALI/ARDS.10 No exclusion was an independent predictor of mortality, whereas PaO / 2 criteria were used. Ventilator management was at FiO was not. OI may be a superior predictor because it 2 the discretion of the critical care team. However, integrates both airway pressure and oxygenation into a both hospitals had implemented the lung protective single variable. on October 1, 2021 by guest. Protected copyright. ventilation protocol of the ARDS Net trial. Despite advances in our understanding of the Data collection pathophysiology and treatment of acute lung The plan for data collection and the data analysis injury (ALI) and acute respiratory distress syn- strategy were defined prospectively, before review drome (ARDS), mortality remains high; approxi- of the medical records began. Data were recorded at mately 30–60% of patients die before hospital a daily reference time between 06:00 and 10:00. 1–3 discharge. Lung protective ventilation, a strategy Arterial blood gases (ABG) used to calculate PaO2/ that targets lower tidal volumes (Vt) and limits FiO2 were drawn during this reference period. It is plateau pressure (Pplat) to less than 30 cm H2Ois the policy of the respiratory care departments that the only clinical intervention that has shown a ABG are not obtained within 20 min of suctioning mortality benefit in large randomised trials.45 and recruitment manoeuvres are not standard Observational studies performed before wide- treatment in our hospital system and were unlikely spread application of lung protective ventilation to confound the ABG measurements. A reference identified demographic, pulmonary specific and quasi-static respiratory compliance (Crs) was found clinical variables that predict mortality in ALI/ to reflect average daily Crs in a subset of subjects.11 ARDS.2 3 6–9 These included age, Severe Acute Clinical data were abstracted from the medical Physiology Score (SAPS II), Acute Physiology and record for up to 7 days or until death or extuba- Chronic Health Evaluation (APACHE II) score, tion, whichever occurred first. These data included cirrhosis, immunosuppression and pulmonary the aetiology of ALI/ARDS, coexisting medical specific variables, including the arterial oxygen illnesses, use of glucocorticoids or other causes tension to fraction of inspired oxygen (PaO2/FiO2) of immunosuppression, fluid intake/output and 994 Thorax 2008;63:994–998. doi:10.1136/thx.2007.093658 Acute lung injury Table 1 Clinical characteristics of 149 with patients with ALI/ARDS or non-survivors and the variables enumerated above were compared using bivariate analysis. Continuous normally dis- Thorax: first published as 10.1136/thx.2007.093658 on 19 June 2008. Downloaded from Characteristic tributed variables were compared using a Student’s t test and Age (years) 48.6 (17.4) categorical variables were compared using a x2 test. Select Gender variables that were statistically significant, or of a priori clinical Female (n (%)) 49 (33) significance, were then introduced into a forward, stepwise, Male (n (%)) 100 (67) logistic regression model. SAS computer software (SAS SAPS II 44.3 (14.6) Institute, Cary, North Carolina, USA) was used for statistical APACHE II 19.9 (7.8) analysis. All interval data are presented as mean (SD). The LIS 2.6 (0.5) goodness-of-fit of the logistic regression model was assessed Mechanical ventilation variables with the Hosmer–Lemeshow test. Standard regression diagnos- Vt (ml/kg PBW) 7.6 (2.1) tics and goodness-of-fit testing indicated that the logistic PEEP (cm H2O) 7.6 (3.0) f 22.5 (8.1) regression models were adequate. Results were considered to be statistically significant if p,0.05. FiO2 0.8 (0.2) PaO2/FiO2 (kPa) 19.2 (9.5) OI (cm H2O/kPa) 89.3 (59.3) RESULTS pH 7.34 (0.1) Between 1 July 2002 and 30 June 2003, 149 patients with ALI/ Base deficit 23.44 (6.4) ARDS were identified at the two hospitals and their data were Crs (ml/cm H2O) 28.2 (10.3) incorporated into this study (table 1). Patients with ALI/ARDS Aetiology of ALI/ARDS (n (%)) had moderately severe lung injury characterised by a low Crs Pneumonia 47 (32) and marked impairment in oxygenation (average PaO2/ Sepsis 33 (22) FiO219.2 kPa). On the day of ALI/ARDS diagnosis, patients Aspiration 16 (11) were ventilated with an average of 7.6 (SD 2.1) ml/kg PBW that Probable TRALI 11 (7) subsequently decreased to 7.0 (2.1) ml/kg PBW on day 2, 6.8 Trauma 10 (7) (1.8) ml/kg PBW on day 3 and 6.6 (1.4) ml/kg PBW on day 4. Pancreatitis 8 (5) ALI/ARDS was the result of direct pulmonary injury in 48% Other or unknown 24 (16) Underlying medical conditions (n (%)) of patients, while 52% had an indirect or extrapulmonary cause. Cirrhosis 22 (14) At enrolment, 19% of patients had a PaO2/FiO2 between 27 and HIV/AIDS 18 (12) 41 kPa (200–300 mm Hg) and 81% had a PaO2/FiO2 ,27 kPa Heart transplant 8 (5) (200 mm Hg). All but one patient initially diagnosed with ALI Metastatic cancer (solid tumour) 7 (4) developed ARDS (PaO2/FiO2 ,27 kPa) within 48 h. Haematological cancer 5 (3) The overall hospital mortality in our cohort of patients with Bone marrow transplantation 3 (2) ALI/ARDS was 41% (61/149; 95% confidence interval (CI) 33% to http://thorax.bmj.com/ Data are mean (SD) or n (%). 49%), which was higher, but not significantly different from the AIDS, acquired immunodeficiency syndrome; ALI, acute lung injury; ARDS, acute mortality predicted by APACHE II (36%) and SAPS II (33%). Most respiratory distress syndrome; APACHE, Acute Physiology and Chronic Health patients had a variety of chronic comorbid conditions: 26% were Evaluation; Crs, respiratory system compliance; f, respiratory frequency; FiO2, inspired immunosuppresed and 15% had cirrhosis. Patients originally oxygen fraction; HIV, human immunodeficiency virus; LIS, lung injury score; OI, oxygenation index; PaO2, arterial oxygen partial pressure; PBW, predicted body diagnosed with ALI had a lower mortality compared with patients weight; PEEP, positive end expiratory pressure; SAPS II, Severe Acute Physiology with ARDS (31% vs 44%), but this difference was not statistically Score II; TRALI, transfusion related lung injury; Vt, tidal volume.
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