脑动静脉畸形导致出血的多层螺旋CT血管造影的相关因素分析

目的 探讨多层螺旋CT血管成像(MSCTA)显示脑动静脉畸形(AVM)合并出血的影像学相关因素.方法 通过比较脑AVM出血组和未出血组之间MSCTA所显示的供血动脉、畸形血管团、引流静脉特点.结果 脑出血组与未出血组两组间MSCTA所显示得畸形血管团部位、大小、引流静脉条数、引流静脉是否受损以及有无合并动脉瘤比率差异有统计学意义.结论 MSCTA提示导致AVM的血管压力增高的深部位、小病灶、单支引流静脉或引流静脉狭窄、闭塞以及合并动脉瘤是脑AVM合并出血的密切相关因素.MSCTA为临床治疗提供依据和借鉴.     

脑动静脉畸形导致出血的影像学相关因素分析

目的探讨多层螺旋CT血管成像（MSCTA）显示脑动静脉畸形（AVM）合并出血的影像学相关因素。方法通过比较脑AVM出血组和未出血组之间MSCTA所显示的供血动脉、畸形血管团、引流静脉特点。结果脑出血组与未出血组两组间MSCTA所显示得畸形血管团部位、大小、引流静脉条数、引流静脉是否受损以及有无合并动脉瘤比率差异有统计学意义。结论 MSCTA提示导致AVM的血管压力增高的深部位、小病灶、单支引流静脉或引流静脉狭窄、闭塞以及合并动脉瘤是脑AVM合并出血的密切相关因素。MSCTA为临床治疗提供依据和借鉴。     

脑动静脉畸形出血的危险因素

目的探讨脑动静脉畸形(BAVM)出血的危险因素。方法收集DSA确诊的BAVM患者105例,分析BAVM出血的危险因素。结果单因素分析表明,BAVM破裂出血的危险因素有病灶位置、大小,供血动脉类型、数目,引流静脉类型、数目、形态及是否合并动静脉瘘;多因素Logistic分析发现,病灶位置、大小,供血动脉类型、数目,引流静脉数目及是否合并动静脉瘘是出血的危险因素,而引流静脉扩张可能是保护因素。结论病灶位于幕下或大脑深部、畸形团3cm、单支静脉引流、单纯穿支动脉供血及多支供血动脉、合并动静脉瘘是BAVM出血的危险因素。     

静脉动脉化皮瓣修复拇指软组织缺损30例

目的:探讨应用筋膜蒂皮瓣修复拇指软组织缺损出现血供障碍时改用静脉动脉化皮瓣修复的方法及临床效果。方法:2015年3月-2019年5月,在切取第1掌骨背筋膜蒂岛状皮瓣修复拇指软组织缺损时,出现皮瓣血供障碍30例,将皮瓣内主干静脉与受区指掌侧固有动脉吻合,改成静脉动脉化皮瓣进行修复。其中男20例,女10例,年龄18~50岁...     

影响断指再植成活率的多因素分析

目的 研究患的年龄、血红蛋白含量、吻合动静脉比例对断指再植成活率的影响。方法 回顾性分析1999年1月一2002年11月844例1231指的断指再植资料，对断指再植成活率与患的年龄、血红蛋白含量、吻合动静脉比例的关系进行统计学分析。结果 年龄因素不影响断指再植的成活率；急血红蛋白含量与断指再植的成活率呈明显正相关；甲根以远平面的断指再植用放血疗法的成活率明显低于吻合1条静脉的成活率；甲根至远侧指间关节平面的断指再植，吻合动脉数多于静脉数时，成活率明显下降；在中节和近节平面吻合动、静脉的比例数不影响成活率，但在近节平面吻合2条动脉的指端血运良好。结论 年龄不应作为筛选断指再植的条件；术后要注意及时纠正贫血；动静脉比例影响断指再植的成活率。     

锁骨下动脉窃血综合征(文献综述)

锁骨下动脉窃血综合征(简称窃血综合征)是由于远离脑部的血管即锁骨下动脉或无名动脉近心端的阻塞,导致脑血流经脑 Willis 氏动脉环、经同侧椎动脉“虹吸”引流,使部分脑血流逆行灌入患侧上肢,从而引起脑局部缺血,主要是椎-基底动脉供血不全而致的一组症状与体征。1960年意大利医师在血管造影时,证实了此综合征的椎-基底-椎动脉的侧支引流,1961年 Rob,C.详细讨论了此一侧支引流,同年 Reivich 等报告了两例。在同期的新英格兰医学     

股骨头缺血性坏死的血管造影表现及分型

目的通过对股骨头供血动脉行超选择性数字减影血管造影(DSA)探导股骨头缺血性坏死(ANFH)的血流动力学改变及其意义。方法对171例(228髋)ANFH及正常对照10例(10髋)作了股骨头供血动脉超选择性血管造影。ARCO分期:Ⅰ期,12髋;Ⅱ期,101髋;Ⅲ期,108髋;Ⅳ期,7髋。经患髋对侧股动脉穿刺插入4~5 F Cobra导管,越过髂总动脉分叉,插至患侧股骨头供血动脉。造影条件为碘必乐(300 mgI/ml)每秒1.5 ml,3幅/s,总量8~10 ml。结果228髋中有223髋有异常血管造影表现,占98%。ANFH的血管造影表现:Ⅰ型,动脉端闭塞,118髋(52%),其中Ⅰa型,动脉主干闭塞,68髋(30%),Ⅰb型,动脉分支闭塞,50髋(22%);Ⅱ型,毛细血管闭塞,21髋(9%);Ⅲ型,静脉端闭塞,19髋(8%);Ⅳ型,混合型,65髋(29%)。结论ANFH股骨头血流动力学改变是复杂的,其发病机制不可能用单一原因,如股骨头供血障碍,微循环的淤滞或静脉流出道阻塞加以解释,可能是多种因素,多阶段发生的疾病。     

椎动脉-小脑后下动脉梭形动脉瘤的手术治疗

目的 探讨手术治疗椎动脉-小脑后下动脉梭形动脉瘤的方法.方法 回顾性分析2007年12月至2010年2月收治的5例椎动脉-小脑后下动脉梭形动脉瘤患者的临床特点、手术方法及疗效.5例患者均为男性,年龄40～55岁,平均47岁.其中动脉瘤破裂出血4例,1例表现为后枕部阵发性头痛.所有患者均采用远外侧入路,翻开皮肌瓣后,先于枕部肌群内分离枕动脉,开颅后显露同侧小脑后下动脉尾襻,并于此处行枕动脉-小脑后下动脉吻合重建小脑后下动脉血流,再行动脉瘤孤立术或切除术.术后进行随访,观察疗效.结果 5例患者术后1例无神经功能缺失;3例有后组脑神经功能障碍;1例出现颅内血肿,二次手术后并发对侧肢体偏瘫.行数字减影血管造影或CT血管造影检查,吻合口通畅,动脉瘤不显影.随访2～29个月,平均18个月,4例预后良好,1例对侧肢体轻偏瘫.结论 枕动脉-小脑后下动脉搭桥+动脉瘤孤立或切除术是治疗椎动脉-小脑后下动脉梭形动脉瘤的有效方法,但需结合实际情况,选择个体化的治疗方案.     

动脉化静脉皮瓣两种灌流方式比较的实验研究及临床应用

目的 探讨两种不同灌流方式对游离动脉化静脉皮瓣存活效果的影响。方法 将20只日本大耳白兔40侧后肢建立成吻合股动、静脉浅支的动脉化静脉皮瓣模型。采用自身对照，实验组为逆静脉瓣供血顺静脉瓣回流，对照组为顺静脉瓣供血逆静脉瓣回流。临床上采用逆静脉瓣供血顺静脉瓣回流方式的皮瓣5例。结果 实验组皮瓣存活16侧，部分存活2侧，坏死2侧。对照组皮瓣存活6侧，部分存活11侧，坏死3侧。两组差异有统计学意义（P〈0．05）。临床应用5例，4例完全存活，1例表皮坏死，脱痂后愈合。结论 建立适当的供血与回流比例是动脉化静脉皮瓣存活的关键，保证供血前提下增加静脉回流能提高动脉化静脉皮瓣的存活率。如果不能增加回流，减少超量的供血可提高皮瓣的存活。     

双功能超声和阴部内动脉造影检查在外伤动脉性勃起功能障碍诊断中的应用(附7例报告)

目的探讨双功能超声(DU)、阴部内动脉造影(IPA)在外伤动脉性勃起功能障碍诊断中的应用。方法7例骨盆骨折外伤引起阴茎动脉供血受损致勃起功能障碍患者进行DU和IPA检查。结果DU检查提示7例患者阴茎勃起动脉血液灌注血流动力学受到损害。IPA检查显示7例患者有阴茎动脉血供受损解剖形态学上的变化,包括阴部内动脉断裂、阴茎动脉主干断裂、阴茎动脉主干狭窄和髂总动脉假性动脉瘤病变。结论DU和IPA为阴茎动脉功能和解剖形态学“金标准”试验,DU提供了阴茎勃起动脉血供受损血流动力学改变的客观数据,而IPA显示了阴茎动脉受损解剖形态学上的变化,对损伤病变部位进行定位。对于外伤所致动脉性勃起功能障碍的患者首选DU检查。     

Do the morphological characteristics of arteriovenous malformations affect the results of radiosurgery?

OBJECT: The authors sought to determine which morphological features of arteriovenous malformations (AVMs) are statistically predictive of preradiosurgical hemorrhage, postradiosurgical hemorrhage, and neuroimaging-defined failure of radiosurgical treatment. In addition, correlation between computerized tomography (CT) scanning and angiography for the identification of AVM structures was investigated. METHODS: Archived CT dosimetry and available angiographic and clinical data for 268 patients in whom AVMs were treated with linear accelerator radiosurgery were retrospectively reviewed. Many of the morphological features of AVMs, including location, volume, compact or diffuse nidus, neovascularity, ease of nidus identification, number of feeding arteries, location (deep or superficial) of feeding arteries, number of draining veins, deep or superficial venous drainage, venous stenoses, venous ectasias, and the presence of intranidal aneurysms, were analyzed. In addition, a number of patient and treatment factors, including patient age, presenting symptoms, radiation dose, repeated treatment, and radiological outcome, were subjected to multivariate analyses. Two hundred twenty-seven patients were treated with radiosurgery for the first time and 41 patients underwent repeated radiosurgery. Eighty-one patients presented with a history of AVM hemorrhage and 91 patients had AVMs in a periventricular location. Twenty-six patients (10%) experienced a hemorrhage following radiosurgery. Of the 268 patients, 81 (30%) experienced angiographically defined cures, and 37 (14%) experienced MR imaging-defined cures. Eighty-six patients (32%) experienced neuroimaging-defined treatment failure, and 64 underwent insufficiently long follow up. A larger AVM volume (odds ratio [OR] 0.349; p = 0.004) was associated with a decreased rate of pretreatment hemorrhage, whereas periventricular location (OR 6.358; p = 0.000) was associated with an increased rate of pretreatment hemorrhage. None of the analyzed factors was predictive of hemorrhage following radiosurgery. A higher radiosurgical dose was strongly correlated with neuroimaging-defined success (OR 3.743; p = 0.006), whereas a diffuse nidus structure (OR 0.246; p = 0.008) and associated neovascularity (OR 0.428; p = 0.048) were each associated with a lower neuroimaging-defined cure rate. A strong correlation between CT scanning and angiography was noted for both nidus structure (p = 0.000; Fisher exact test) and neovascularity (p = 0.002; Fisher exact test). CONCLUSIONS: Patients presenting with AVMs that are small or periventricular were at higher risk for experiencing hemorrhage. A higher radiosurgical dose correlated strongly with neuroimaging-defined success. Patients in whom the AVM had a diffuse structure or associated neovascularity were at higher risk for neuroimaging-defined failure of radiosurgery. A strong correlation between CT scanning and angiography in the assessment of AVM structure was demonstrated.     

Location of intracranial aneurysms associated with cerebral arteriovenous malformation: statistical analysis

Distributions of cerebral aneurysms by site were compared statistically in 78 reported cases associated with arteriovenous malformation, including our five cases, and cases with solitary intracranial aneurysms without arteriovenous malformation. When the feeder of an arteriovenous malformation was one of the branches of anterior, middle, or posterior cerebral arteries, the aneurysms were located on these respective arteries much more frequently than expected in the general aneurysmal population. This was statistically significant. Our results strongly suggest that abnormal hemodynamic stresses on the arteries from which the feeders branch out to arteriovenous malformations play a significant role in the development of intracranial aneurysms on these arteries.     

Unruptured intracranial aneurysms and arteriovenous malformations: frequency of intracranial hemorrhage and relationship of lesions

Among 91 patients with unruptured intracranial arteriovenous malformations (AVM's), 16 patients had 26 unruptured intracranial saccular aneurysms. An actuarial analysis showed the risk of intracranial hemorrhage among patients with coexisting aneurysm and AVM to be 7% per year at 5 years following diagnosis compared to 1.7% for patients with AVM alone. The difference in length of survival free of hemorrhage was significant (log-rank, p less than 0.0007). Several angiographic and clinical parameters were investigated to better understand the relationship of these lesions. The aneurysms occurred in similar percentages in patients with small, medium, and large AVM's. Twenty-five aneurysms were on arteries feeding the malformation system, almost equally distributed proximally and distally. Eleven aneurysms were atypical in location, and all arose from primary or secondary branch feeders to the malformation; 24 were on enlarged feeding arteries. Eleven (16%) of the 67 patients with high-flow AVM's had associated aneurysms, compared with five (21%) of the 24 patients with low-flow AVM's. Four (16%) of 25 low-shunt malformations and 12 (18%) of 65 high-shunt malformations had associated aneurysms. All five aneurysms associated with low-shunt malformations were on a direct arterial feeder of the malformation. These data suggest that the intracranial AVM's predispose to aneurysm formation within AVM feeding systems and that the mechanism is not simply based upon the high blood flow or high arteriovenous shunt in these systems.     

Retrograde thrombosis of feeding arteries after removal of arteriovenous malformations

Five cases of retrograde thrombosis of former feeding arteries after removal of an arteriovenous malformation (AVM) are reported. The clinical features of these patients were studied and compared to those of 71 patients without this complication. The following characteristics were found to correlate with retrograde thrombosis: 1) advancing age of the patient; 2) large AVM size; and 3) markedly dilated and elongated feeders. It is suggested that the slow flow in the former feeding arteries that was observed immediately after AVM removal and pathological changes in these vessels due to long-standing hemodynamic stresses contributed to the development of retrograde thrombosis. Neurological manifestations related to retrograde thrombosis were noted in three of the five cases. Although infrequent, this complication should be considered as a serious possibility following removal of an AVM.     

Association of intracranial aneurysm and arteriovenous malformation in childhood

The simultaneous occurrence in the same patient of an intracranial saccular aneurysm and an arteriovenous malformation (AVM) is a well-known phenomenon. Usually the aneurysms are related anatomically to the arteries supplying the AVM, and it is generally accepted that the aneurysms are caused by hemodynamic stresses resulting from the presence of an AVM. Because patients with both an AVM and an aneurysm are older than those presenting with an AVM alone, a time factor seems essential in the development of the aneurysm accompanying an AVM. In this article, the case reports of two children are presented. They both had a symptom-producing AVM and an attendant saccular aneurysm. The malformations were anatomically closely related and the significance of hemodynamic stresses in the development of the aneurysms cannot be neglected. However, in these two cases, the time factor obviously cannot be of vital importance. Therefore, another factor, possibly in the form of a vascular collagen defect, may be suspected as essential in the formation of aneurysms during childhood. The character of this defect is briefly discussed.     

Evaluation of cerebral AVM's using transcranial Doppler ultrasound

Blood flow velocities in basal cerebral arteries were recorded noninvasively in 28 patients with cerebral arteriovenous malformations (AVM's) and were correlated with the angiographic findings. In normal arteries remote from the AVM, flow velocities ranged from 44 to 94 cm/sec (median 65 cm/sec) with pulsatility indexes from 0.65 to 1.10 (median 0.87). This is consistent with findings in normal individuals. Arteries feeding the AVM's were identified by the high flow velocities (ranging from 75 to 237 cm/sec, median 124 cm/sec). The pulsatility index ranged from 0.22 to 0.74 (median 0.48). The difference of these results from findings in normal remote arteries was highly significant (p less than 0.001). Hyperventilation tests illustrated the hemodynamic difference between an AVM and normal cerebrovascular beds. Flow velocity measurements permitted noninvasive diagnosis of AVM's in 26 of the 28 patients. Furthermore, the identification of individual feeding arteries permitted good definition of the anatomical localization of individual AVM's. Flow velocity measurements combined with computerized tomography scans are useful in the diagnosis of AVM's. With the feeding artery's configuration identified on angiography, flow velocity measurements permit a new insight into the "hemodynamic dimension" of an AVM and its possible effects on adjacent normal brain-tissue perfusion in the individual patient.     

Distal aneurysms of the superior cerebellar artery and posterior inferior cerebellar artery feeding an associated arteriovenous malformation: case report.

The authors report a case of two distal aneurysms of the cerebellar arteries, one arising from the vermian branch of the posterior inferior cerebellar artery, the other arising from the hemispheric branch of the superior cerebellar artery, and both feeding an associated arteriovenous malformation (AVM). The aneurysm of the distal posterior inferior cerebellar artery was considered the source of a cerebellar hemorrhage because of the location of a hematoma in the cerebellar vermis. The life-threatening hematoma was evacuated in an emergency operation 6 hours after the acute onset of symptoms. The cerebellar aneurysms and the AVM were clipped or extirpated successfully after the patient's condition improved. The association of two rare types of aneurysms with an AVM strongly supports the theory that increased hemodynamic stress derived from the AVM plays an important role in aneurysm formation. The authors think that one should operate on the symptomatic lesion first or both the aneurysm and the AVM in the same operative procedure.     

Occlusive hyperemia versus normal perfusion pressure breakthrough after treatment of cranial arteriovenous malformations

Arteriovenous malformations (AVMs) are vascular lesions characterized by direct connections between feeding arteries and draining veins without an intervening capillary network. Two hypotheses, normal perfusion pressure breakthrough (NPPB) and occlusive hyperemia, prevail in the literature regarding the occasional development of hemorrhage and edema following AVM resection. The NPPB hypothesis was introduced in 1978. Since the occlusive hyperemia hypothesis was first postulated in 1993, however, a debate has persisted within the cerebrovascular community concerning which hypothesis better explains the complications of edema and?hemorrhage seen after AVM resection. Recent advances in cerebrovascular imaging and hemodynamic analysis have allowed a better evaluation of intracerebral changes following AVM resection. It is likely that these 2 hypotheses are not mutually exclusive and perhaps exist in a spectrum of hemodynamic alteration following AVM resection.