The hyperperfusion syndrome represents a highly debated clinical entity, without having yet any clinically identifiable limits. The correlation of clinical with pre- and postoperative magnetic resonance imaging (MRI) findings following carotid endarterectomy in patients with a possible hyperperfusion syndrome was investigated.Prospective clinical and laboratory study.At the Aretaieio University Hospital.Comparison to the postoperative clinical symptomatic and MRI findings. Patients. We studied 30 patients (mean age 66.6) of whom 14 (46.6%) were asymptomatic, 16 (53.4%) were symptomatic, 17 (56.6%) were hypertensive, 18 (60%) hyperlipidaemic, 5 (16.6%) diabetic and 17 (56.6%) had coronary artery disease.Twenty-one patients (70%) exhibited disturbances such as ipsilateral headache, seizures, vomiting or facial pain; immediate postoperative MRI scans revealed new ischaemic foci in 4 (19%) without any objective neurological findings. Lesions displayed in postoperative MRI scans did not always cause symptoms and normal findings on MRI did not exclude the presence of symptoms. Hypertension favoured the presence of subjective disturbances, without necessarily any change in the MRI appearances. Preoperative MRI and clinical findings did not contribute to the identification of patients who might have exhibited postoperative symptoms. Thus, the symptomatology remains unclear and open to debate, as a variety of other conditions may produce the same clinical picture postoperatively.Subjective disturbances, objective neurological findings and MRI abnormalities with or without hypertension may appear independently after carotid endarterectomy, a fact which makes the pathogenesis of the hyperperfusion syndrome more difficult to elucidate.
Abstract: Endovascular repair of abdominal aortic aneurysms (AAA) is an alternative to conventional surgical aortic reconstruction. However the presence of renal artery stenosis (RAS) and/or accessory renal arteries may alter the endovascular approach in these cases. We present two cases with infrarenal aneurysms and a coexisting unilateral renal artery stenosis (first case) and accessory renal artery (second case). In both patients endovascular treatment was undertaken. In the first patient a stent was placed for the RAS and an aortic endograft with suprarenal fixation for the aneurysm. In the second patient the placement of an aortic endograft with suprarenal fixation occluded the accessory renal artery. In the first patient renal function was normal pre- and post-intervention. In the second patient, renal function was normal pre-intervention but showed a slight deterioration postoperatively, returning to normal after 10 days. Both patients were normotensive pre- and post-intervention. In conclusion, RAS and AAA may be treated by the placement of a stent and a stent-graft simultaneously. During endovascular repair of AAA, a significant accessory renal artery (around 3 mm in diameter) may safely be excluded in patients with otherwise normal renal function.
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