Managing Risk After Intracerebral Hemorrhage in Concomitant Atrial Fibrillation and Cerebral Amyloid Angiopathy
Author(s) -
Thomas B. Stoker,
Nicholas R. Evans
Publication year - 2016
Publication title -
stroke
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.397
H-Index - 319
eISSN - 1524-4628
pISSN - 0039-2499
DOI - 10.1161/strokeaha.116.013323
Subject(s) - medicine , intracerebral hemorrhage , cerebral amyloid angiopathy , concomitant , atrial fibrillation , stroke (engine) , cardiology , emergency department , psychiatry , disease , dementia , mechanical engineering , subarachnoid hemorrhage , engineering
A 77-year-old right-handed functionally independent man presented after waking with a right-sided frontal headache, associated with 3 episodes of vomiting. His headache progressed during the following 20 minutes, prompting presentation to the Emergency Department. He reported an unsteady gait but no focal weakness or sensory disturbance. He was known to be in atrial fibrillation (AF), for which he was anticoagulated with warfarin. His other comorbidities included a previous pulmonary embolus, hypertension, and benign prostatic hypertrophy.On examination, there was no focal neurological deficit, and his Glasgow Coma Scale score was 15. In view of his severe headache while therapeutically anticoagulated, he was investigated with an urgent computed tomography scan of his head. This demonstrated a 58 by 37 mm right temporal lobe hemorrhage (Figure 1). His international normalized ratio on admission was 2.13, which was corrected with vitamin K and prothrombin complex. The hemorrhage was managed conservatively with blood pressure control, initially requiring a labetalol infusion followed by oral lisinopril and doxazosin.Figure 1. Noncontrast axial computed tomography of head showing a right temporal lobe intracerebral hemorrhage (maximum diameter 58×37 mm) and associated mass effect with sulcal effacement.He remained neurologically stable throughout his admission. He was discharged 14 days later with a minor deficit in short-term memory but no other focal neurological deficit. His modified Rankin score was 1. In view of the acute hemorrhage, anticoagulation was withheld because further hemorrhagic risk was deemed to outweigh antithrombotic benefit.Magnetic resonance imaging was performed 1 month after discharge and demonstrated evolution of the hematoma (Figure 2A and 2B). Gradient echo images also demonstrated a small right parietal lobe hemorrhage (Figure 2C). These findings were suggestive of cerebral amyloid angiopathy (CAA) as the cause of his presenting right temporal lobe hemorrhage.Figure 2. Magnetic resonance imaging (MRI) of head performed 1 month after intracerebral hemorrhage. …
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