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High-Altitude Cerebral Edema Evaluated With Magnetic Resonance Imaging
Clinical Correlation and Pathophysiology
Peter H. Hackett, MD;
Philip R. Yarnell, MD;
Richard Hill, MD;
Kenneth Reynard, MD;
Joseph Heit, MD;
John McCormick, MD
JAMA. 1998;280:1920-1925.
Context.— Because of its onset in generally remote environments, high-altitude cerebral edema (HACE) has received little scientific attention. Understanding the pathophysiology might have implications for prevention and treatment of both this disorder and the much more common acute mountain sickness.
Objectives.— To identify a clinical imaging correlate for HACE and determine whether the edema is primarily vasogenic or cytotoxic.
Design.— Case-comparison study.
Setting.— Community hospitals accessed by helicopter from mountains in Colorado and Alaska.
Patients.— A consecutive sample of 9 men with HACE, between 18 and 35 years old, 8 of whom also had pulmonary edema, were studied after evacuation from high-altitude locations; 5 were mountain climbers and 4 were skiers. The control group, matched for age, sex, and altitude exposure, consisted of 3 subjects with high-altitude pulmonary edema only and 3 who had been entirely well at altitude. Four patients with HACE were available for follow-up imaging after complete recovery.
Main Outcome Measures.— Magnetic resonance imaging (MRI) of the brain during acute, convalescent, and recovered phases of HACE, and once in controls, immediately after altitude exposure.
Results.— Seven of the 9 patients with HACE showed intense T2 signal in white matter areas, especially the splenium of the corpus callosum, and no gray matter abnormalities. Control subjects demonstrated no such abnormalities. All patients completely recovered; in the 4 available for follow-up MRI, the changes had resolved entirely.
Conclusions.— We conclude that HACE is characterized on MRI by reversible white matter edema, with a predilection for the splenium of the corpus callosum. This finding provides a clinical imaging correlate useful for diagnosis. It also suggests that the predominant mechanism is vasogenic (movement of fluid and protein out of the vascular compartment) and, thus, that the blood-brain barrier may be important in HACE.
From the School of Health Professions, University of Alaska (Dr Hackett), and the Departments of Emergency Medicine (Dr Hackett) and Radiology (Drs Hill and McCormick), Alaska Regional Hospital, Anchorage; Department of Medicine, University of Washington School of Medicine, Seattle (Dr Hackett); and St Anthony Hospital (Drs Yarnell, Reynard, and Heit) and Department of Neurology, University of Colorado School of Medicine (Dr Yarnell), Denver. Dr Hackett is now with St Mary's Hospital and Medical Center, Grand Junction, Colo.
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December 9, 1998
JAMA. 1998;280(22):1965.
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