The decedent was an 87-year-old female (nonsmoker) with a history of hypertension, peripheral vascular disease, chronic renal insufficiency, coronary artery disease, and congestive heart failure, and a 20-year known history of a surgically untreatable intracranial aneurysm. She presented to an outside hospital 14 days prior to death, reporting acute onset of severe headache and neck stiffness. Imaging studies showed Fisher grade 4 subarachnoid hemorrhage, with a ruptured left supraclinoid carotid artery giant aneurysm (Hunt-Hess grade 2) (). The patient (who was unresponsive following the CT study) was intubated, treated with dexamethasone, mannitol, and phenytoin, and was transferred to our institution.
Figure 1 Pre-procedure Imaging: A) Post contrast CTA of the brain source image shows laterally projecting enhanced saccular aneurysm in the left supraclinoid ICA (arrow), and B) conventional cerebral angiogram (lateral projection of selective left internal carotid (more ...)
She was treated with routine subarachnoid hemorrhage management strategies, and being a poor surgical candidate, underwent embolization of the aneurysm 12 days prior to her death. During the procedure, a 6 French 80 cm shuttle sheath (Cook Inc., Bloomington, IN) was inserted into the right common femoral artery over a 0.035 Cook Bentson guidewire (Cook Inc., Bloomington, IN). A Simmons 2 catheter (Terumo Medical, Somerset, NJ) was inserted and advanced into the aorta. However, due to an excessively tortuous aortic arch, it was not possible to select the left common carotid artery. A 5F VTK catheter (Cook Inc., Bloomington, IN) and 0.038 Terumo Glidewire (Terumo Medical, Somerset, NJ) were instead used to advance the shuttle sheath into the left common carotid artery. An Echelon 10 microcatheter (ev3 Neurovascular, Irvine, California) and fasDasher 14 microguidewire (Boston Scientific Neurovascular, Fremont, California) were used to catheterize the aneurysm. A total of 7 Guglielmi Detachable coils (Boston Scientific Neurovascular, Fremont, CA) and 12 Matrix2 coils (Boston Scientific Neurovascular, Fremont, CA) were used to fill the aneurysm. Following the procedure, the aneurysm showed no residual contrast filling.
Post-procedure, the patient was slow to regain consciousness but was symmetric in spontaneous movements. The day following the procedure, she developed right hemiparesis. She never fully regained consciousness and was clinically diagnosed with a left middle cerebral artery (MCA) territory infarct. MRI (postoperative day 2) revealed areas of hyperintense signal on T2-weighted and FLAIR sequences with associated diffusion restriction within the left frontal, temporal, parietal, and occipital lobes, with involvement of the left insular cortex, caudate nucleus and putamen, representing acute infarcts in the left MCA and posterior cerebral artery (PCA) territories (). Multiple small, scattered areas of acute infarct were visualized in the cerebellum (bilateral hemispheres, ), pons, right parieto-occipital lobes, right centrum semiovale, and right caudate head. Given the presence of multiple infarcts involving several bilateral vascular territories, findings were suggestive of embolic stroke. Concurrent MR angiogram showed stable occlusion of the aneurysm with diminished flow signal intensity in Sylvian branches of the left MCA, signifying possible emboli in the distal MCA territory.
A right frontal ventriculostomy catheter was placed 11 days before death, and medical workup ensued to determine the origin of the emboli. Bilateral upper extremity, carotid, axillary, subclavian, brachial, and radial arteries were unremarkable by Doppler ultrasound studies. Echocardiography with contrast (bubble study) showed thickening of the aortic and mitral valves with a right-to-left shunt, indicating patent foramen ovale. Based on these findings, a cardiac source for the patient’s emboli could not be clinically excluded.
Over the next week, the patient developed cyanosis of the digits, necrosis of the tongue, polymicrobial pneumonia, urinary tract infection, and progressively worsening renal function. Despite percutaneous tracheostomy with ventilatory support and institution of intravenous inotropic agents, the patient developed cardiorespiratory collapse and died.