Abstract
Neurogenic pulmonary edema (NPE) is a clinical syndrome characterized by the acute onset of pulmonary edema following a significant central nervous system (CNS) insult. The etiology is thought to be a surge of catecholamines that results in cardiopulmonary dysfunction. A myriad of CNS events, including spinal cord injury, subarachnoid hemorrhage (SAH), traumatic brain injury (TBI), intracranial hemorrhage, status epilepticus, meningitis, and subdural hemorrhage, have been associated with this syndrome [1–5]. Although NPE was identified over 100 years ago, it is still underappreciated in the clinical arena. Its sporadic and relatively unpredictable nature and a lack of etiologic-specific diagnostic markers and treatment modalities may in part be responsible for its poor recognition at the bedside. In this manuscript, we will review the anatomical origin of NPE, outline the various possible pathophysiologic mechanisms responsible for its development, and propose a clinical framework for the classification of NPE.
Highlights
Neurogenic pulmonary edema (NPE) is a clinical syndrome characterized by the acute onset of pulmonary edema following a significant central nervous system (CNS) insult
Among the traumatic brain injury (TBI) patients who died within 96 hours, the incidence of NPE rose to 50% [2]
Prevented increases in pulmonary perfusion pressure and pulmonary vascular resistance (PVR) and associated increases in lung water, Qs/pulmonary shunt (Qt), dead space (VD), and hypoxemia induced by intracranial pressure (ICP) elevation [50]
Summary
Other articles in the series can be found online at http://ccforum.com/series/annualupdate2012. Further information about the Annual Update in Intensive Care and Emergency Medicine is available from http://www.springer.com/series/8901
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