Neurocritical care · 2004
Neurogenic pulmonary edema and other mechanisms of impaired oxygenation after aneurysmal subarachnoid hemorrhage.
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Vespa Paul M, Bleck Thomas P
Аннотация
INTRODUCTION: 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.
PURPOSE: 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).
CONCLUSION: 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.
PURPOSE: 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).
CONCLUSION: 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.