• Am. J. Crit. Care · Sep 2006

    Neurogenic pulmonary edema due to traumatic brain injury: evidence of cardiac dysfunction.

    • Mabrouk Bahloul, Anis N Chaari, Hatem Kallel, Abdelmajid Khabir, Adnène Ayadi, Hanène Charfeddine, Leila Hergafi, Adel D Chaari, Hedi E Chelly, Chokri Ben Hamida, Noureddine Rekik, and Mounir Bouaziz.
    • Service de Réanimation Médicale, Centre Hospitalier Universitaire Habib Bourguiba, Sfax, Tunisia. bahloulmab@yahoo.fr
    • Am. J. Crit. Care. 2006 Sep 1;15(5):462-70.

    BackgroundAcute neurogenic pulmonary edema, a common and underdiagnosed clinical entity, can occur after virtually any form of injury of the central nervous system and is a potential early contributor to pulmonary dysfunction in patients with head injuries.ObjectiveTo explore myocardial function in patients with evident neurogenic pulmonary edema after traumatic head injury.MethodsDuring a 1-year period in a university hospital in Sfax, Tunisia, information was collected prospectively on patients admitted to the 22-bed intensive care unit because of isolated traumatic head injury who had neurogenic pulmonary edema. Data included demographic information, vital signs, neurological status, physiological status, and laboratory findings. All of the patients had computed tomography and plain radiography of the neck and determination of cardiac function.ResultsAll 7 patients in the sample had cardiac dysfunction. Evidence of myocardial damage was confirmed by echocardiography in 3 patients, pulmonary artery catheterization in 3 patients, and/or postmortem myocardial biopsy in 4 patients. Echocardiography studies, repeated 7 days after the initial study in one patient and 90 days afterward in another, showed complete improvement in wall motion, with a left ventricular ejection fraction of 0.65.ConclusionAll patients who had neurogenic pulmonary edema due to traumatic head injury had myocardial dysfunction. The mechanisms of the dysfunction were multiple. The great improvement in wall motion seen in 2 patients indicated the presence of a stunned myocardium. Further studies are needed to understand the mechanisms of this cardiac dysfunction.

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