Objectives: Acute respiratory distress syndrome develops commonly in critically ill patients in response to an injurious stimulus. The prevalence and risk factors for development of acute respiratory distress syndrome after spontaneous intracerebral hemorrhage have not been reported. We sought to determine the prevalence of acute respiratory distress syndrome after intracerebral hemorrhage, characterize risk factors for its development, and assess its impact on patient outcomes.
Design: Retrospective cohort study at two academic centers.
Patients: We included consecutive patients presenting from June 1, 2000, to November 1, 2010, with intracerebral hemorrhage requiring mechanical ventilation. We excluded patients with age less than 18 years, intracerebral hemorrhage secondary to trauma, tumor, ischemic stroke, or structural lesion; if they required intubation only during surgery; if they were admitted for comfort measures; or for a history of immunodeficiency.
Measurements and Main Results: Data were collected both prospectively as part of an ongoing cohort study and by retrospective chart review. Of 1,665 patients identified by database query, 697 met inclusion criteria. The prevalence of acute respiratory distress syndrome was 27%. In unadjusted analysis, high tidal volume ventilation was associated with an increased risk of acute respiratory distress syndrome (hazard ratio, 1.79 [95% CI, 1.13–2.83]), as were male sex, RBC and plasma transfusion, higher fluid balance, obesity, hypoxemia, acidosis, tobacco use, emergent hematoma evacuation, and vasopressor dependence. In multivariable modeling, high tidal volume ventilation was the strongest risk factor for acute respiratory distress syndrome development (hazard ratio, 1.74 [95% CI, 1.08–2.81]) and for inhospital mortality (hazard ratio, 2.52 [95% CI, 1.46–4.34]).
Conclusions: Development of acute respiratory distress syndrome is common after intubation for intracerebral hemorrhage. Modifiable risk factors, including high tidal volume ventilation, are associated with its development and in-patient mortality.
1Department of Critical Care Medicine, University of Pittsburgh Medical Center, Pittsburg, PA.
2Department of Emergency Medicine, Brigham and Women’s Hospital, Boston, MA.
3Division of Burn, Trauma and Surgical Critical Care, Department of Surgery, Brigham and Women’s Hospital, Boston, MA.
4Harvard Medical School, Boston, MA.
5Department of Emergency Medicine, Massachusetts General Hospital, Boston, MA.
6Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Boston, MA.
7Department of Medicine, Massachusetts General Hospital, Boston, MA.
8Department of Neurology, Massachusetts General Hospital, Boston, MA.
9Pulmonary and Critical Care Unit, Massachusetts General Hospital, Boston, MA.
10Department of Respiratory Care, Massachusetts General Hospital, Boston, MA.
11Department of Radiology, Massachusetts General Hospital, Boston, MA.
12Department of Radiology, Brigham and Women’s Hospital, Boston, MA.
13Division of Neurocritical Care and Emergency Neurology, Massachusetts General Hospital, Boston, MA.
*See also p. 2055.
Supported, in part, by a grant from the Emergency Medicine Foundation/Emergency Medicine Resident’s Association, the Wuerz Award from the Department of Emergency Medicine at Brigham and Women’s Hospital, and by the National Institutes of Health (R01NS073344, R01NS059727, and 5K23NS059774).
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Dr. Hess has consulted for Philips Respironics, ResMed, Breathe Technology, and Pari. Dr. Greenberg has consulted for Hoffman La-Roche, received grants 5R01AG026484-08 and 5R01NS070834-03, and received payment for lectures from U of Texas-Grand Rounds. Dr. Rosand has received grant support from the National Institutes of Health. Dr. Goldstein has received grant support from the Mass Medical Society, the National Institutes of Health and NINDS. He has consulted for CSL Behring. The remaining authors have disclosed that they do not have any potential conflicts of interest.
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