Evidence from recent randomized controlled studies comparing intra-arterial (IA) therapy with intravenous tissue plasminogen activator highlighted the mismatch between recanalization success and clinical outcomes in patients presenting with acute ischemic stroke. There is emerging interest in the impact of arterial collateralization, as determined by leptomeningeal anastomoses (LMAs), on the treatment outcomes of IA therapy. The system of LMA constitutes the secondary network of cerebral collateral circulation apart from the Circle of Willis. Both anatomic and angiographic studies confirmed significant interindividual variability in LMA. This review aims to outline the current understanding of arterial collateralization and its impact on outcomes after IA therapy for acute ischemic stroke, underpinning the possible role of arterial collateralization assessment as a selection tool for patients most likely to benefit from IA therapy.
A seven years retrospective study was performed in 45 consecutive vascular injuries in the extremities to investigate the pattern of injuries, managements and outcomes. Motor-vehicle accidents were the leading cause of injuries (80%), followed by industrial injuries (11.1%) and iatrogenic injuries (4.4%). Popliteal and brachial artery injuries were commonly involved (20%). Fifteen (33.3%) patients had fractures, dislocation or fracture dislocation around the knee joint and 6 (13.3%) patients had soft tissue injuries without fracture. Traumatic arterial transection accounted for 34 (75.6%) cases, followed by laceration in 7 (15.6%) and 9 (6.7%) contusions. Associated nerve injuries were seen in 8 (17.8 %) patients using intra-operative findings as the gold standard, both conventional angiogram (CA) and computerized tomography angiogram (CTA) had 100% specificity and 100% sensitivity in determining the site of arterial injuries. The mean ischemic time was 25.31 hours (4 - 278 hours). Thirty-three (73.3 %) patients were treated more than 6 hours after injury and 6 patients underwent revascularization after 24 hours; all had good collateral circulation without distal pulses or evidence of ischemic neurological deficit. The mean ischemic time in 39 patients who underwent revascularization within 24 hours was 13.2 hours. Delayed amputation was performed in 5 patients (11.1%). Of the 6 patients who underwent delayed revascularization, one patient had early amputation, one -had delayed amputation following infection and multiple flap procedures while the rest of the patients' limbs survived. Joint stiffness was noted in 10 patients (22.2%) involving the knee joint, elbow and shoulder in two patients each. Infection was also noted in 5 patients (11.1%) with two of them were due to infected implants. Other complications encountered included nonunion (2 patients, 4.4%), delayed union (1 patient, 2.2%),limb length discrepancy (1 patient, 2.2%), hematoma (1 patient, 2.2%) and leaking anastomosis in one patient (2.2%). Volkmann's ischemic contracture occurred in 3 (6.7%) patients. There was no complication noted in 8 (17.8%) patients Three patients (6.7%) died of whom two were not due to vascular causes. We conclude that early detection and revascularization of traumatic vascular injuries is important but delayed revascularization also produced acceptable results.
A case of an intracerebral bleed in a young man with a rare combination of arteriovenous malformation (AVM) and unilateral moyamoya disease is presented. The location of the bleed in the left basal ganglia corresponded to the area supplied by the basal moyamoya vessels. The AVM which received supply from collateral moyamoya vessels as well as normal cerebral arteries was located in the ipsilateral parieto-occipital region posterior to the basal ganglia bleed. This is the first reported cerebral AVM co-existing with a unilateral moyamoya disease in the English literature. Unusual features of the case such as the unilaterality of the angiographic abnormalities, their coexistence and hypotheses as to their development are discussed.