Clinical investigations were performed in 27 patients with high altitude pulmonay edema (HAPE) . The altitude of the onset was relatively low altitude (from 2, 680 m to 3, 190 m above sea level) . Symptoms included marked shortness of breath, undue dyspnea, cough, and stridor. Physical examinations revealed cyanosis, tachycardia, and rales. Neurological disturbances such as headache, vomiting, memory disturbance, clouding of consciousness or coma were accompanied.
Laboratory data showed hemoconcentration and leucocytosis, but relative thrombocytepenia was observed at the beginning of treatment, compared with the data at the leaving hospital. CPK increased remarkably and CRP was positive. Arterial blood gasometric analysis showed hypoxemia and respiratory alkalosis.
Chest roentgenograms at the beginning of treatment revealed prominent, dilated main pulmonary artery, and a coarse patchy mottling with confluencies. The distribution of shadow was often asymmetric and involved any parts of the lung fields. The right ventricle enlargement was also observed. During recovery, the prominence of the pulmonary vasculature receded, and there was a spectacular clearing of infiltrates.
Hemodynamic studies demonstrated that HAPE was a noncardiogenic type of pulmonary edema. The characteristics were followed by 1. pulmonary hypertension, which was not normalized by 100% oxygen inhalation, 2. normal pulmonary arterial wedge pressure, 3. normal cardiac output, and 4. increased pulmonary arteriolar resistance.
The edema fluid aspirated through endotracheal tube was protein-rich fluid.
These findings may suggest that HAPE is due to the increase in microvascular permeability.
