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
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.