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

Neurogenic pulmonary edema (NPE) is an increase in interstitial and alveolar lung fluid that occurs as a direct consequence of acute or subacute central nervous system (CNS) injury. In this review we describe a patient who developed hypoxemic respiratory failure as a result of NPE following catastrophic subarachnoid hemorrhage (SAH). The patient displayed many of the characteristic 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 be 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 combination of pulmonary capillary leakage and elevated intravascular pressures, many questions about its pathophysiology remain unanswered. Data from animal models using therapeutic trials of antiadrenergic agents suggest a significant role for sympathetic nervous system activation and massive catecholamine release in the pathogenesis of this disorder. The most common causes of NPE include head trauma, seizures, cerebral hemorrhages, subarachnoid bleeds, and increased intracranial pressure of any etiology. As is generally observed with this disorder, conservative and supportive management of our patient's respiratory failure led to complete resolution of the NPE within 96 hours. Although NPE is an infrequent phenomenon, it should be considered in the differential diagnosis of all patients who develop respiratory complications soon after CNS injury.