The catastrophic basilar artery occlusion.

To cite: Liao W-H, Lai C-C, Huang S-H, et al. BMJ Case Rep Published online: [please include Day Month Year] doi:10.1136/bcr-2013201004 DESCRIPTION A 71-year-old man with hypertension presented to the emergency department with slurred speech, dizziness and four limbs weakness with left side predominance for 3.5 h. A non-contrast CTof head at arrival showed a hyperdense basilar artery (figure 1A) and the diagnosis of basilar artery occlusion (BAO) was made. Given the unavailability of intra-arterial treatment, he received recanalisation therapy with intravenous alteplase 4 h after the symptom onset; however, a rapid deterioration of consciousness was observed. On the next day, brainstem reflexes were absent and the follow-up CT of head showed extensive infarcts of basilar artery territory and hydrocephalus (figure 1B). The patient received supportive therapy and he passed away 1 week later. BAO, accounting for about 1% of all strokes, had been mostly fatal before the introduction of antithrombotic treatment. Past investigations have demonstrated that early intravenous or intra-arterial thrombolysis has a beneficial effect. Patients with acute ischaemic stroke would benefit from intravenous tissue plasminogen activator within 4.5 h after onset, and a shorter time from the onset to treatment is associated with a better outcome. Likewise, intra-arterial thrombolysis within 6 h would bring a more favourable outcome for BAO and the prognosis is always dismal beyond 9 h. The hyperdense basilar artery sign is specific for BAO; nonetheless, it is observed in about two-thirds of patients. In addition, diffusion-weighted MRI could detect early ischaemic damage of BAO. Unfortunately, a substantial proportion of patients with BAO died or became dependent despite the endeavours in early diagnosis and modern antithrombotics.