Risk Factors And Management Of Hemorrhage After Endovascular Therapy Of Cerebral Arteriovenous Malformations

Research backgroundA cerebral arteriovenous malformation (cAVM) is the most common cerebral vascular dysplasia, which is reported to be present in50%of the deformity.It is thought to be caused by short-circuit between the cerebral arteriovenous, which produces a series of brain hemodynamic disorder arises from lack of capillary network between arteries and veins of the brain lesion resulting in arterial vein connected directly and may eventually lead to clinical signs and symptoms.In the past two decades, with advances in technology and the continuous development of methods and means of research, surgical techniques and experience continuously improve intravascular embolic material and medical imaging theory and equipment continued to emerge, the research and treatment of brain AVM has also been rapid development. Endovascular treatment is becoming one of the main treatment of cerebral AVM due to its little damage, quick recovery and repeatable advantage. Meanwhile, effectiveness and complications of embolization has become a hotspot of cerebral arteriovenous malformations.Intracranial hemorrhage is the most serious complications with extremely high mortality after the cerebral arteriovenous malformation embolization. However, its risk factors, prevention measures and long-term prognosis are is involved little. Beside, the risk factors of intracranial hemorrhage after cerebral arteriovenous malformation embolization have been in controversy.Domestic and international studies of intracranial hemorrhage after cerebral arteriovenous malformation embolization are mainly concentrated on the causes of bleeding. Poor drainage of residual malformation arise from the draining veins damaging due to embolic agents and increased pressure within the residual malformation are considered to the most important reason for cerebral AVM nidus rupture after partial embolization. In addition, the local hemodynamic changes causing the nidus rupture of the weak parts after embolization, the embolic agents sticky tube, the microcatheter guide wire punctured deformity group and postoperative normal perfusion pressure breakthrough may be related to the intracranial hemorrhage after cerebral arteriovenous malformation embolization. The conclusion of each reported differences in the analysis of risk factors. The main consideration may be associated with the patient’s age, AVM size and volume reduction. Preventive measures are unfeasible due to the uncertainties of risk factors. Controlling blood pressure strictly is recognized to be one of prevention of intracerebral hemorrhage after embolization of cerebral arteriovenous malformation. However, the control range of blood pressure and the time are still controversial. Additionally, domestic and foreign reports different management of intracranial hemorrhage after cerebral arteriovenous malformation embolization, for example, trepanation and drainage, evacuation of hematoma, spinal puncture and conservative treatment methods which need further specification.In this study, we retrospective collected the large number of cAVM cases and view the general characteristics of the patients, the imaging features of cerebral AVM and treatment process, and the results of relevant factors analysis system to identify the risk factors of intracranial hemorrhage after embolization of cerebral arteriovenous malformation for the purpose of guiding the clinical prevention and treatment decision making in the future..ObjectiveTo identify the risk factors of hemorrhage after endovascular therapy of cerebral arteriovenous malformations (cAVMs), and illustrate the prevention and management on this event as well as its postembolization outcomes evaluation for the purpose of guiding the clinical prevention and treatment decision made hemorrhage after endovascular therapy of cAVMs in the future.MethodWe retrospectively reviewed the records in263patients with cerebral AVMs from January2002to June2012. The study comprised patients with previously untreated AVMs presenting to Southern Medical University Zhujiang Hospital. Patients with dural arteriovenous fistulas, Galen malformations, cAVMs associated aneurysms, and other types of brain vascular malformations were excluded. Baseline clinical characteristics includ mRS score of the admission in patients, AVM sizes, location, Spetzler-Martin grading scale, venous drainage, volume reduction, embolization sessions, postoperative complications, and follow-up mRS score, etc. All embolization techniques were carried out by the same proficient endovascular therapists in Department of Neurosurgery, Interventional Therapy Centre. All endovascular embolization were carried out using the transfemoral approach with patients under monitored anesthetic care general at a biplane angiography unit. Each embolization was preceded by superselective angiograms, usually in two planes. Following careful analysis of the superselective angiogram, Italy glue with lipiodol mixture was used to occlude the vascular nidus once the microcatheters were advanced into position. After completion of the embolization, a control angiography was generally performed in2planes. Postprocedure, heparin therapy was routinely reversed with the administration of protamine (10mg/1000U sodium heparin). Most patients were close monitored in an ICU for24hours after embolization. Basic management was performed, such as systolic blood pressure controlling, Sedative administration, keeping bowels open, etc.. All statistical data were analyzed with the SPSS statistical package (SPSS13.0). Multivariate was analyzed by unconditional logistic regression. Variables were chosen for the model based on previously established importance in regards to outcome for intracranial hemorrhage (e.g. Spetzler-Martin grading scale), the risk factors for intracranial hemorrhage of cAVMs by reported in the literature (such as hemorrhage history, venous drainage, cAVM locations, etc.), and known factors to influence intracranial hemorrhage after endovascular therapy of cAVMs(e.g. cAVM sizes, volume reduction). A value<0.05was considered statistical significant. The risk factors of hemorrhage after endovascular therapy of cAVMs were studied for guiding the treatment strategy. All patients who suffered from hemorrhage after endovascular therapy of cAVMs received clinical and angiographic follow-up for outcome evaluating.ResultsOf the total patient population,159(60.5%) were male and104(39.5%) were female. The mean patient age was29.18±12.04years (range,3-68years).73patients presented with an intracerebral hemorrhage caused by cAVMs.76patients developed epilepsy,56patients had headache without bleeding,24patients had neurological deficit,13patients had syncope, and21patients had asymptomatic. According to the Spetzler-Martin grading scale,40of the AVMs were ranked as Grades1,109were GradesⅡ,81were GradesⅢ, and29were GradesⅣ,4were GradesⅤ. A total of414embolization procedures were performed with a mean of1.6(range,1-8) per patient. Intracerebral hemorrhages occurred in17patients. A partial AVM reduction of >36.5%(OR=19.269;95%C.I.1.283-289.299, P=0.032) and hypertension (OR=7.962;95%C.I.1.121-56.567,P=0.038) were considered as risk factors for hemorrhage after endovascular therapy of cAVMs. A total of17patients with post-interventional alCH were monitored during the observation period, including10patients with parenchymal hemorrhage;5patients with subarachnoid hemorrhage;2patients with intraventricular hemorrhage. Among them,6patients with parenchymal hemorrhage are treated by hematoma dissection+nidus excision+decompressive craniectomy, the other4patients with conservative treatment;3patients with subarachnoid hemorrhage are treated spinal puncture, the other2cases with lumber cistern catheterization;2patients with intraventricular hemorrhage are treated by lumber cistern catheterization. All of the17patients were followed up for6-40months, an average of19.53±8.63months. Postoperative follow-up,1patient with vegetative state;1patient with right severe hemiplegia and left hemiparesis;3patients with right severe hemiplegia;2cases of left moderate hemiplegia;1case of left facioplegia;1cases of right facioplegia;1case of language dysfunction;3patients with intermittent headache;4cases had asymptomatic. mRS score:0points-in4cases,3cases of1points,2points in3cases,2cases of3points,4cases of4points,1case of5points.10patients underwent DSA follow-up,8patients had endovascular therapy again, when they were discharged from hospital two months later. Postoperative recovery of all patients is good and not happens to other complications again during follow-up.ConclusionsIntracranial hemorrhage is one of the most serious complications after the cerebral arteriovenous malformation embolization. In this study, patients who received a partial AVM reduction of≥36.5%in one session and who have hypertension history have a tendency of increasing hemorrhage after endovascular therapy of cAVMs. In order to prevent embolic material in the venous drainage stranded lead to the residual malformation poor drainage induced bleeding, endovascular embolization treatment should be careful and the thinner concentration adhesive liquid embolic material should be prepared when patients have venous drainage stenosis or venous drainage less than two. In addition, Large cerebral arteriovenous malformations should not be occluded nidus at one time, volume reduction should not exceed36.5%of AVM sizes, and twice embolization should interval of2weeks to2months. Patients should be absolute bed, defecation and sedative treatment after embolization for the purpose of prevent intracranial hemorrhage due to defecation difficulties and agitation with high blood pressure. Arterial blood pressure maintained at least72hours after embolization so that cerebral blood flow redistribution, prevent the normal perfusion pressure breakthrough is to reduce intracranial hemorrhage the after embolization. Patients with parenchymal hemorrhage should have conservative treatment if small amount of bleeding and not brain herniation signs. If not, hematoma dissection should be done immediate to avoid rebleeding, preferably together with the nidus resection. Decompressive craniectomy is recommended according to the situation; Intraventricular hemorrhage and subarachnoid hemorrhage generally recommended early lumbar puncture or lumbar catheter drainage, drainage BCSF prevent vasospasm caused by cerebral ischemia, cerebral infarction and other complications.