Case #001

Sudden focal deficits in an older patient are a stroke until proven otherwise, and the first job is to remove the mimics that are treatable in their own right. The normal capillary glucose does most of that work, since hypoglycaemia reproduces focal deficits convincingly and would have been reversed at the bedside. Expressive aphasia with right-sided weakness places the lesion in the left hemisphere, and the rhythm strip supplies the mechanism. The QRS complexes are narrow but spaced irregularly, no two intervals alike, and not one is preceded by a P wave, only a fibrillating baseline: atrial fibrillation, which without anticoagulation throws emboli, and this one lodged in the left middle cerebral artery. Everything after that is a timing question. Onset was witnessed 45 minutes ago, so the 4.5-hour window for a plasminogen activator such as alteplase or tenecteplase is open, the CT excludes the haemorrhage that would forbid it, and a pressure of 168/92 sits under the 185/110 ceiling that has to be met before the drug runs. Thrombolysis alone is not enough here: a proximal MCA occlusion is a large clot that intravenous drug clears unreliably, and perfusion shows a small infarcted core inside a much larger territory that is still salvageable. That mismatch is what justifies retrieving the clot mechanically as well, and it is why the thrombectomy window stretches to 24 hours where imaging can still show tissue worth saving. Antiplatelets wait 24 hours after lysis.