title: Neurogenic pulmonary edema and other mechanisms of impaired oxygenation after aneurysmal subarachnoid hemorrhage.
abstract: BACKGROUND
  Aneurysmal subarachnoid hemorrhage (SAH) affects 30,000 patients per year, causing neurologic morbidity and mortality. The etiology of hypoxemia and its role in comorbidity are controversial and unknown.
  
  
  OBJECTIVE
  To identify the incidence and etiologies of oxygenation abnormalities following SAH and to determine its impact on length of hospital stay (LOS).
  
  
  METHODS
  We retrospectively reviewed 70 consecutive SAH patients' records, including review of computed tomography scans, chest X-rays, arterial blood gases, electrocardiograms, echocardiograms, blood pressure, carbon monoxide, central venous pressure, and pulmonary capillary wedge pressure. Fluid balance and chest X-ray interpretation on admission and at time of worst alveolar-arterial oxygen difference was assessed, as was length of hospital stay.
  
  
  RESULTS
  Fifty six (80%) patients had impaired oxygenation (alveolar-arterial oxygen difference>00 mmHg). Of these 56, 50% had normal chest X-rays. Patients were euvolemic and normodynamic with mean central venous pressure 8.8+/-4.1 mmHg and had normal cardiac output 6.8+/-2.4 L/min. The most frequent etiologies of hypoxemia based on composite data assessment were pneumonia 8/56 (14%), fulminant neurogenic pulmonary edema 9/56 (16%), atelectasis 5/56 (27%), and cryptogenic (57%). The mean length of stay was doubled in the impaired oxygenation group 19.3 days+/-14.6 compared with 7.1+/-4.3 days in the normal oxygenation group (p<0.001; df=36). Likewise, the patients with fulminant neurogenic pulmonary edema had a prolonged length of stay of 13.4+/-6.2 (p<0.002; df=27) compared with the normal oxygenation group. Neither the occurrence of vasospasm nor delayed neurologic deficit influenced the incidence of poor oxygenation (p<0.93).
  
  
  CONCLUSIONS
  Oxygenation abnormalities after SAH occur more frequently than previously suspected. They are frequently the result of noncardiogenic and hydrostatic causes and contribute to an increased length of hospital stay.
authors.affiliation: Division of Neurosurgery, Department of Neurology, University of California, Los Angeles 90028, USA. PVespa@mednet.ucla.edu
authors.forename: Paul M
authors.initials: PM
authors.lastname: Vespa
authors.forename: Thomas P
authors.initials: TP
authors.lastname: Bleck
mesh_terms: D000328:Adult; D000368:Aged; D001784:Blood Gas Analysis; D002302:Cardiac Output / Q000502:physiology; D006801:Humans; D000860:Hypoxia / Q000453:epidemiology / Q000209:etiology* / Q000503:physiopathology*; D015994:Incidence; D007902:Length of Stay; D008171:Lung Diseases / Q000150:complications* / Q000503:physiopathology*; D008875:Middle Aged; D011669:Pulmonary Wedge Pressure / Q000502:physiology; D012189:Retrospective Studies; D013345:Subarachnoid Hemorrhage / Q000097:blood / Q000150:complications* / Q000503:physiopathology*