Koyama S, Kubo K, Takabayashi Y, Miyahara T, Kawashima A, Fujimoto K, Honda T, Matsuzawa Y, Kobayashi T, Sekiguchi M
First Department of Internal Medicine, Shinshu University School of Medicine, Matsumoto, Japan.
Nihon Kyobu Shikkan Gakkai Zasshi. 1993 Jun;31(6):775-9.
A 29-year-old male climber developed high altitude pulmonary edema (HAPE), progressing from headache and dyspnea to disturbance of consciousness in the Japan Alps. He was admitted to Shinshu University Hospital. Physical examination on admission revealed a cyanotic patient with coarse crackles and wheezes in bilateral lungs. Chest X-ray film showed bilateral patchy infiltrates. Arterial blood gases indicated severe hypoxemia, and respiratory alkalosis; pH 7.452, PO2 35.5 Torr, PCO2 31.6 Torr. Right heart catheterization showed noncardiogenic pulmonary edema, analysis of bronchoalveolar lavage (BAL) fluid was as follows; cells 2.05 x 10(5)/ml (alveolar macrophages 61.5%, neutrophils 25.5%, lymphocytes 13.0%), protein concentration 91 mg/dl. Cellular and protein analysis of BAL has been shown to be of value to clarify the pathogenesis of the permeability edema in patients with HAPE.
一名29岁的男性登山者在日本阿尔卑斯山患上了高原肺水肿(HAPE),症状从头痛和呼吸困难发展到意识障碍。他被送往信州大学医院。入院时体格检查发现患者面色青紫,双肺有粗湿啰音和哮鸣音。胸部X光片显示双侧斑片状浸润。动脉血气分析显示严重低氧血症和呼吸性碱中毒;pH值7.452,氧分压35.5托,二氧化碳分压31.6托。右心导管检查显示为非心源性肺水肿,支气管肺泡灌洗(BAL)液分析结果如下:细胞数2.05×10⁵/ml(肺泡巨噬细胞61.5%,中性粒细胞25.5%,淋巴细胞13.0%),蛋白浓度91mg/dl。BAL的细胞和蛋白分析已被证明有助于阐明HAPE患者通透性水肿的发病机制。