• Neurocritical care · Jan 2004

    Neurogenic pulmonary edema and other mechanisms of impaired oxygenation after aneurysmal subarachnoid hemorrhage.

    • Paul M Vespa and Thomas P Bleck.
    • Division of Neurosurgery, Department of Neurology, University of California, Los Angeles 90028, USA. PVespa@mednet.ucla.edu
    • Neurocrit Care. 2004 Jan 1; 1 (2): 157-70.

    IntroductionAneurysmal 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.PurposeTo identify the incidence and etiologies of oxygenation abnormalities following SAH and to determine its impact on length of hospital stay (LOS).MethodsWe 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.ResultsFifty 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).ConclusionOxygenation 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.

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