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神经源性肺水肿及动脉瘤性蛛网膜下腔出血后氧合受损的其他机制。

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

作者信息

Vespa Paul M, Bleck Thomas P

机构信息

Division of Neurosurgery, Department of Neurology, University of California, Los Angeles 90028, USA.

出版信息

Neurocrit Care. 2004;1(2):157-70. doi: 10.1385/NCC:1:2:157.

Abstract

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.

摘要

引言

动脉瘤性蛛网膜下腔出血(SAH)每年影响30000名患者,导致神经功能障碍和死亡。低氧血症的病因及其在合并症中的作用存在争议且尚不明确。

目的

确定SAH后氧合异常的发生率和病因,并确定其对住院时间(LOS)的影响。

方法

我们回顾性分析了70例连续SAH患者的记录,包括计算机断层扫描、胸部X线、动脉血气、心电图、超声心动图、血压、一氧化碳、中心静脉压和肺毛细血管楔压的检查。评估入院时及肺泡-动脉氧分压差最差时的液体平衡和胸部X线解读情况,以及住院时间。

结果

56例(80%)患者存在氧合受损(肺泡-动脉氧分压差>00 mmHg)。在这56例患者中,50%的胸部X线检查结果正常。患者血容量正常、血流动力学正常,平均中心静脉压为8.8±4.1 mmHg,心输出量正常,为6.8±2.4 L/min。根据综合数据评估,低氧血症最常见的病因是肺炎8/56(14%)、暴发性神经源性肺水肿9/56(16%)、肺不张5/56(27%)和隐源性(57%)。氧合受损组的平均住院时间增加了一倍,为19.3天±14.6天,而正常氧合组为7.1±4.3天(p<0.001;自由度=36)。同样,与正常氧合组相比,暴发性神经源性肺水肿患者的住院时间延长至13.4±6.2天(p<0.002;自由度=27)。血管痉挛的发生和延迟性神经功能缺损均未影响氧合不良的发生率(p<0.93)。

结论

SAH后的氧合异常比之前怀疑的更为常见。它们通常是由非心源性和流体静力因素导致的,并且会导致住院时间延长。

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