Neurogenic pulmonary oedema. A review of the pathophysiology with clinical and therapeutic implications.

Five cases of neurogenic pulmonary oedema (NPE) are described. The causes were mechanical trauma to the skull, subarachnoid haemorrhage and epileptic seizure. In every case a frank pulmonary oedema was diagnosed that resolved within a few days. Treatment of the underlying disease resulted in a favourable outcome. The literature has been reviewed. The basic mechanism seems to be an increased intracranial pressure (ICP) precipitating an increased central sympathetic nerve activity mediated via peripheral alpha- or beta-adrenergic discharge. NPE results from a predominant alpha-receptor stimulation with massive increase in pre- and afterload. The major therapeutic efforts should be directed towards the underlying cause and, in addition, mechanical ventilation with passive hyperventilation is vital. High positive end-expiratory pressure should not be used without strict monitoring of ICP.