OBJECTIVES: Presentation, management and outcome following seizure after carotid endarterectomy (CEA). MATERIALS AND DESIGN: Prospective audit. RESULTS: Eight patients (0.8%) suffered a seizure (three bilateral) <30 days following 949 CEAs. Seizure was not associated with age, gender or presentation. Seven were treated hypertensives but four had labile BP pre-operatively. Five had severe bilateral carotid disease and four had vertebral/subclavian stenoses. Six had a >50% drop in middle cerebral artery blood flow velocity (MCAV) with clamping. Only three had >100% increase in MCAV with flow restoration. Five required treatment for post-operative hypertension. Two suffered seizures <36 hrs of CEA, the remainder were at 3-8 days. All eight had significantly elevated blood pressure at onset of seizures. Four underwent immediate MCAV monitoring and each was elevated. Emergency CT scanning/autopsy showed normal scans (n = 3), white matter oedema (n = 3), oedema and diffuse haemorrhage (n = 1), intracranial haemorrhage (n = 1). Seven developed a post-ictal neurological deficit (stroke = 5, TIA = 2). Overall, two patients either died or suffered a disabling stroke. CONCLUSIONS: Post-CEA seizure was associated with adverse outcome. Most were labile hypertensives with severe bilateral carotid/vertebral disease. MCAV changes suggested poor collateral recruitment, but no consistent pattern of early hyperperfusion emerged. It remains uncertain whether high MCAVs and severe hypertension after seizure onset are cause or effect. Clinicians treating these patients in acute medical units were generally unaware of the "post-CEA hyperperfusion syndrome" and tended to treat the hypertension less aggressively.
OBJECTIVES: Presentation, management and outcome following seizure after carotid endarterectomy (CEA). MATERIALS AND DESIGN: Prospective audit. RESULTS: Eight patients (0.8%) suffered a seizure (three bilateral) <30 days following 949 CEAs. Seizure was not associated with age, gender or presentation. Seven were treated hypertensives but four had labile BP pre-operatively. Five had severe bilateral carotid disease and four had vertebral/subclavian stenoses. Six had a >50% drop in middle cerebral artery blood flow velocity (MCAV) with clamping. Only three had >100% increase in MCAV with flow restoration. Five required treatment for post-operative hypertension. Two suffered seizures <36 hrs of CEA, the remainder were at 3-8 days. All eight had significantly elevated blood pressure at onset of seizures. Four underwent immediate MCAV monitoring and each was elevated. Emergency CT scanning/autopsy showed normal scans (n = 3), white matter oedema (n = 3), oedema and diffuse haemorrhage (n = 1), intracranial haemorrhage (n = 1). Seven developed a post-ictal neurological deficit (stroke = 5, TIA = 2). Overall, two patients either died or suffered a disabling stroke. CONCLUSIONS: Post-CEA seizure was associated with adverse outcome. Most were labile hypertensives with severe bilateral carotid/vertebral disease. MCAV changes suggested poor collateral recruitment, but no consistent pattern of early hyperperfusion emerged. It remains uncertain whether high MCAVs and severe hypertension after seizure onset are cause or effect. Clinicians treating these patients in acute medical units were generally unaware of the "post-CEA hyperperfusion syndrome" and tended to treat the hypertension less aggressively.
Authors: Narayan D Deshmukh; Rakeshsingh K Singh; Rakesh S Lalla; Anil P Karapurkar; Satish V Khadilkar Journal: Ann Indian Acad Neurol Date: 2019 Apr-Jun Impact factor: 1.383