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
NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript 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 immunodefciency.
Interventions-None.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.
Keywordsacute lung injury; hemorrhagic stroke; mechanical ventilation; tidal volume; ventilator-induced lung injuryThe development of neurogenic pulmonary edema after a neurologic insult has been recognized for over a century (1). Neurologic injury leads to systemic inflam-mation, increases pulmonary vascular hydrostatic pressure and endothelial permeability, and potentiates pulmonary inflammation (2-5). The histopathologic features observed in patients who die with neurogenic pulmonary edema are virtually identical to those observed with acute respiratory distress syndrome (ARDS) (6, 7), and many have suggested that these two entities are pathophysiologically identical (8, 9).ARDS occurs in up to 20-25% of cases of spontaneous sub-arachnoid hemorrhage and traumatic brain injury (TBI) and is a major driver of morbidity and cost in these patients (4,(10)(11)(12)(13)(14). Spontaneous intracerebral hemorrhage (ICH) is arguably the most devastating form of neurologic injury, with 1-month mortality rates in excess of 40% and death or severe d...