Rehabilitation after Hypoxic and Metabolic Brain Injury in a Mountain Climber

A patient in her 50s presented with altered mental status and shortness of breath at 4600 m elevation. After descent to the base of the mountain, the patient became comatose. She was found to have bilateral pulmonary infiltrates and a serum sodium of 102 mEq/L. She was rapidly corrected to 131 mEq/L in 1 day. Initial MRI showed intensities in bilateral hippocampi, temporal cortex and insula. A repeat MRI 17 days post injury showed worsened intensities in the bilateral occipital lobes. On admission to acute rehabilitation, the patient presented with blindness, agitation, hallucinations and an inability to follow commands. Midway through her rehabilitation course, antioxidant supplementations were started with significant improvement in function. Rapid correction of hyponatraemia may cause central pontine myelinolysis or extrapontine myelinolysis (EPM). In some cases of hypoxic brain injury, delayed post-hypoxic leucoencephalopathy (DPHL) may occur. Treatment options for both disorders are generally supportive. This report represents the only documented interdisciplinary approach to treatment of a patient with DPHL and EPM. Antioxidant supplementation may be beneficial as a treatment option for both EPM and DPHL.