Neurogenic pulmonary edema following catastrophic subarachnoid hemorrhage:A case report and pathophysiologic review

Citation
Am. Venkatesan et al., Neurogenic pulmonary edema following catastrophic subarachnoid hemorrhage:A case report and pathophysiologic review, J INTENS C, 16(5), 2001, pp. 236-242
Citations number
46
Categorie Soggetti
Aneshtesia & Intensive Care
Journal title
JOURNAL OF INTENSIVE CARE MEDICINE
ISSN journal
08850666 → ACNP
Volume
16
Issue
5
Year of publication
2001
Pages
236 - 242
Database
ISI
SICI code
0885-0666(200109/10)16:5<236:NPEFCS>2.0.ZU;2-L
Abstract
Neurogenic pulmonary edema (NPE) is an increase in interstitial and alveola r lung fluid that occurs as a direct consequence of acute or subacute centr al nervous system (CNS) injury. In this review we describe a patient who de veloped hypoxemic respiratory failure as a result of NPE following catastro phic subarachnoid hemorrhage (SAH), The patient displayed many of the chara cteristic symptoms, signs, and physiologic aberrations associated with NPE, including an altered level of consciousness, dyspnea, cyanosis, crackles, hypoxemia, and diffuse pulmonary infiltrates. These clinical features can b e mistaken for other causes of pulmonary edema and may lead to confusion in the diagnosis and therapeutic approach of hypoxemic respiratory failure in the setting of CNS injury. Although NPE is thought to be due to a combinat ion of pulmonary capillary leakage and elevated intravascular pressures, ma ny questions about its pathophysiology remain unanswered. Data from animal models using therapeutic trials of antiadrenergic agents suggest a signific ant role for sympathetic nervous system activation and massive catecholamin e release in the pathogenesis of this disorder. The most common causes of N PE include head trauma, seizures, cerebral hemorrhages, subarachnoid bleeds , and increased intracranial pressure of any etiology. As is generally obse rved with this disorder, conservative and supportive management of our pati ent's respiratory failure led to complete resolution of the NPE within 96 h ours. Although NPE is an infrequent phenomenon, it should be considered in the differential diagnosis of all patients who develop respiratory complica tions soon after CNS injury.