neurogenic pulmonary edema神经源性肺水肿.pdfVIP

Davison et al. Critical Care 2012, 16:212 /content/16/2/212 R E V I E W Neurogenic pulmonary edema Danielle L Davison, Megan Terek and Lakhmir S Chawla* This article is one of eleven reviews selected from the Annual Update in Intensive Care and Emergency Medicine 2012 (Springer Verlag, DOI: 10.1007/978-3-642-25716-2) and co-published as a series in Critical Care. Other articles in the series can be found online at /series/annualupdate2012. Further information about the Annual Update in Intensive Care and Emergency Medicine is available from /series/8901. Introduction Epidemiology Neurogenic pulmonary edema (NPE) is a clinical Because much of the clinical information on NPE has syndrome characterized by the acute onset of pulmonary been derived from case reports and autopsy series, the edema following a signifi cant central nervous system true incidence of NPE is unknown and is likely under- (CNS) insult. h e etiology is thought to be a surge of reported. Any acute CNS insult, including spinal cord catecholamines that results in cardiopulmonary dysfunc- trauma, can result in pulmonary edema. In patients with tion. A myriad of CNS events, including spinal cord SAH, reports of NPE incidence range from 2% to 42.9% injury, subarachnoid hemorrhage (SAH), traumatic brain [3,9,10]. Clinically, the likelihood of developing NPE injury (TBI), intracranial hemorrhage, status epilepticus, following SAH correlates with increasing age, delay to meningitis, and subdural hemorrhage, have been asso- surgery, vertebral artery origin, and the