[Hypoxemia in the acute stage of hypertensive intracerebral hemorrhage, with special reference to increased extravascular lung water].

Respiratory responses to acute brain damage have been well documented. Severe hypoxemia of unknown origin has often been seen in the acute stage of intracerebral and subarachnoid hemorrhage. Neurogenic pulmonary edema is a particular concern in the neurosurgical intensive care setting. In this study, the extravascular lung water volume (EVLW), alveolar-arterial oxygen difference (AaDO2), and intrapulmonary shunt (QS/QT) were measured in 17 patients with hypertensive intracerebral hemorrhage in the acute stage. The mean AaDO2, QS/QT, and EVLW values were 19.1 mmHg, 7.7%, and 5.49 ml/kg, respectively. The mean pulmonary arterial, central venous, and pulmonary capillary wedge pressures were all within the normal ranges. Eight patients with an AaDO2 of 20 mmHg or more manifested abnormal increases in QS/QT and EVLW, the mean values of which were 10.3% and 6.52 ml/kg, respectively. Nine patients with an AaDO2 of less than 20 mmHg exhibited normal QS/QT and EVLW, with mean values of 5.4% and 4.57 ml/kg, respectively. There was a significant, direct correlation between AaDO2 and EVLW. AaDO2 and EVLW in 11 measured cases either stayed normal or normalized within 4 weeks. These results suggest that acute congestive heart failure and/or pulmonary hypertension were not the main causes of the increase in AaDO2 and EVLW; the increase in EVLW might be explained by increased permeability of pulmonary vessels. The results of this study suggest that an increase in EVLW is causally related to hypoxemia. Further studies of lung water are necessary if we are to better understand respiratory abnormalities associated with acute-stage hypertensive intracerebral hemorrhage.