London, United Kingdom 2013 Poster Session Red Cerebrovasc Dis 2013; 35 (suppl 3)1-854 367 161 Interesting and challenging cases Case report: A rare case of reversible neurological injury presenting as Transient Ischaemic Attack (TIA) Mimic- High Altitude Cerebral Oedema (HACE) A. Asokanathan1, A.Y. Allan2, S. Sethuraman3, D. Phiri4, L. Sekaran5 Luton and Dunstable NHS Foundation Trust, Luton, UNITED KINGDOM1, Luton and Dun-stable NHS Foundation Trust, Luton, UNITED KINGDOM2, Luton and Dunstable NHS Foundation Trust, Luton, UNITED KINGDOM3, Luton and Dunstable NHS Foundation Trust, Luton, UNITED KINGDOM4, Luton and Dunstable NHS Foundation Trust, Luton, UNITED KINGDOM5 Introduction We describe a case with clinical and neuroimaging features of high altitude cerebral oedema (HACE) presenting as TIA. HACE is a fatal metabolic encephalopathy associated with exposure to the hypobaric hypoxia of high altitude. It is a reversible white matter oedema usually occurring in unacclimatised individuals at altitudes above 3000m. Case History 26 year old man climbed to 3000m altitude in Himachal Pradesh, India. On return to base, he de-veloped headache and nausea, subsequently noting right arm and face weakness with slurred speech and unsteady gait. This resolved within 24 hours. He was assessed and treated as TIA at a local teaching hospital. On his return from India he was further investigated in our TIA Clinic. He had no vascular risk factors and no family history of vascular disease or migraine. He was a non-smoker, no alcohol intake or illicit drug use. There was no focal neurological deficit. MRA and MRV were normal. MRI head demonstrated bilateral white matter hyperintensity with re-striction on DWI (Fig 1) 1 month later repeat MRI head was completely normal (Fig 2) U/S Doppler, ECHO, bubble ECHO, 24h tape and thrombophilia screen were normal. Discussion Whilst pathogenesis is unknown, HACE is considered a form of vasogenic and cytogenic oedema as a result of high altitude-induced hypoxia. Symptoms are non-specific and may mimic TIA, stroke or intracranial tumours. Once HACE is diagnosed, descent is critical. Dexamethasone and a portable hyperbaric chamber may be used. It can be prevented by slow ascent and using acetazolamide. Conclusion HACE is a form of high altitude sickness. It may mimic TIA/stroke at altitudes greater than 3000m in unacclimatised individuals. As symptoms of HACE are non-specific, any neurological symptoms at high altitude should be considered as HACE unless another definitive diagnosis is made. Swift diagnosis and treatment are essential since it can quickly progress to coma and death within a few hours if not properly managed.
Karger_ESC London_2013
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