Lumbar artery

Endoleaks are a major concern for those engaged in EVAR (Table 3, Fig. 4). This phenomenon describes the continuation of blood flow into the extragraft portion of the aneurysm (20). Endoleaks are related to the graft itself or other factors such as the presence of large patent lumbar arteries (21). The presence of an endoleak increases the chance of rupture. Diagnostic imaging plays an important role in the detection of endoleaks intraprocedural angiograms, surveillance CT scans, or duplex ultrasounds. 

Segmental arteries supply the spine with blood, including the vertebral bodies, paraspinal muscles, dura, nerve roots, and spinal cord. All these tissues, with the exception of the spinal cord, receive their blood supply from segmental arteries (one on each side) or their equivalents. In particular, the segmental supply of the thoracolumbar region is derived from intercostal and lumbar arteries arising from... 

Compared with brain ischemia spinal cord strokes are caused by more diverse etiologies. Up-to-now there is no satisfactory and accepted classification of spinal infarcts. Etiologies include circulatory arterial and venous disorders. From a clinical and pathoanatomical point of view it seems reasonable to differentiate between acute ischemic myelomalacia and subacute to chronic vascular myelopathy (Table 17.1). In most cases MRI enables the differentiation of these two main etiologies. A deficient spinal arterial blood flow generally has various causes, ranging from the occlusion of intercostal or lumbar arteries to affection of the intrinsic arteries of the spinal cord. ... 

Many causes of acute spinal cord infarction (of arterial and venous origin) have been reported (Table 17.2). They include diseases of the aorta and aortic surgery, thromboembolic events and cartilaginous disc embolism, vasculitis, coagulopathy, radiation-induced vasculopathy, toxic effects of contrast medium, epidural anesthesia, periradicu-lar nerve root therapy with crystalline corticoids, decompression illness, shock or cardiac arrest, lumbar artery compression and other etiologies... 

In most patients the dural fistula is supplied by a thoracic or lumbar artery. Deep located fistulas of the lumbosacral region are rare and beset with particular diagnostic problems mainly due to the unusual anatomic and hemodynamic conditions. In these cases MRI should be focused on the lumbosacral region. The arterialized dilated vein of the filum can be detected in 3-mm slices after paramagnetic contrast administration even if the flow is very slow. 

If the diagnosis of a compression of a lumbar artery has been established by dynamic spinal DSA showing complete occlusion of the lumbar artery, surgical section of the diaphragmatic crus may prevent irreversible infarction in this rare condition. 

Type I endoleak is caused by failure to achieve a circumferential seal at either the proximal (type lA) or distal end (type IB) of the stentgraft. Type IC endoleak is due to non-occluded iliac artery in patients with aorto-mono-iliac stent and femoral-femoral bypass. With type I endoleak, the aneurysm is perfused directly from the aorta or the iliac arteries (inflows). The leak usually communicates through a channel (sometimes multiple channels) with the aneurysmal sac. There are several outflow vessels, mainly lumbar arteries and inferior mesenteric artery (IMA) that communicate with the channel and or the sac (Figs. 14.1,14.2). The pressure within a type I leak is systemic. The tension on the aortic wall remains high. 

A type II endoleak corresponds to the retrograde filling of the aneurysm mainly from lumbar arteries and/or IMA but also in rare situations from sacral, gonadal or accessory renal artery (Figs. 14.3,14.4). 

Fig. 14.5a,b. Type III endoleak due to a hole in the fabric, a Aortogram demonstrates the endoleak (large black arrow) with IMA (small black arrow) and a lumbar artery (white arrow) acting as an outflow vessel, b The wire is passed through the hole in the aortic aneurysm (arrow)... 

Fig. 14.6a-c. Type III endoleak due to incomplete seal at the junction between components, a Angiogram from left groin demonstrates a type III endoleak (white arrow) and a lumbar artery (black arrow), b Palmaz stent placement inflated to 12 mm.c Control angiogram shows no more endoleak... 

The occlusion of the iliac artery is usually sufficient to treat the leak. However, in cases of long-term type IC endoleak, many outflow vessels may have developed and the leak may communicate with multiple lumbar arteries and the IMA. These enlarged vessels might be source of late type II endoleak. Thus, we usually embolize both the outflow vessels and the sac before occluding the iliac artery. Another attractive technique to achieve the occlusion of the common iliac artery is to perform an endovascular internal to external iliac artery bypass using stentgraft. This technique can allow the exclusion of the common iliac preserving the internal iliac artery. 

In some situations, the sac can be accessed from internal iliac artery through iliolumbar and lumbar arteries. 

Schmid R, Gurke L, Aschwanden M, et al (2002) CT-guided percutaneous embolization of a lumbar artery maintaining a Type II endoleak. J Endovasc Ther 9 198-202... 

Occasionally, communications between branches of an uninvolved IIA and distal lumbar arteries can create type-II endoleaks (Fig. 15.1). This can be a more technically challenging situation and embolization of the distal branches should be attempted only if growth of the aneurysm sac has been documented (see Sect. 15.2.1). 

Fig. 15.1. a Contrast. enhanced CT of abdomen shows an abdominal aortic aneurysm with patent lumbar and inferior mesenteric arteries. Patient developed a type 11 endoleak after endograft placement, b Non-contrast CT shows glue embolization of the lumbar arteries and the sac through a branch of the internal iliac artery... 

Occasionally, communications between various branches of the IIA and the lumbar arteries may cause retrograde flow into the sac of an aortic aneurysm creating a type-II endoleak. Microcatheter traversal of the entire length of these conununications may not always be possible. Under such circumstances, liquid embolic agents have been employed to occlude the feeder arteries. As mentioned above, this practice may cause ischemic radiculopathy if the targeted vessels are either lateral sacral or iliolumbar arteries. It may be more prudent to coil embo-lize these arteries and use alternative approaches to deal with the possible residual type-II endoleak (see Chap. 14). 

Type II retrograde blood flow into the aortic lesion from collateral branches (e.g. lumbar arteries)... 

Fig. 23.9. a Type II endoleak after EVAR of an abdominal aortic aneurysm, with a bifurcation graft. The endoleak is filled from a retrograde flow out of a lumbar artery (arrow), b Type III endoleak after EVAR of an abdominal aneurysm. The graft is ruptured (arrowhead), leading to this type of endoleak... 

The ASA is transversely reinforced by branches of deep cervical arteries at the neck and by posterior intercostal (PIA) and upper lumbar arteries at the trunk. Both of the latter derive segmentally from the descending thoracic and abdominal aorta and range between 0.5 and 5mm in diameter (Boll et al. 2006). The PIA and lumbar arteries send rami dorsales, from which again the radicular arteries (synonymous with radicomed-ullary artery or spinal branch) as feeders of the spinal cord originate. The radicular arteries divide soon into anterior and posterior branches that support either the anterior or the posterior spinal arteries. 

Standard transverse images reconstructed from a 3D data set with overlapping thin slices may be sufficient for visualization of the posterior intercostal and lumbar arteries as well as of their proximal rami dorsales. The AKA or other anterior radicular arteries of significant dimension may be localized on transverse sections as well, if a second vessel with arterial contrast begins to accompany the usually sohtary ASA in the thoracolumbar region (Fig. 24.2). 

Perforating arteries, an important collateral pathway to the kidney, arise from the intraparenchymal branches of the renal artery and exit from the kidney to anastomose with various retroperitoneal arteries [18]. In addition to the main renal artery and perforating arteries, the superior, middle, and inferior capsular arteries should be considered as well. The superior capsular artery may arise from the inferior adrenal artery, main renal artery, or aorta. The middle capsular artery, which may consist of one or more branches, arises from the main renal artery. The inferior capsular artery may originate from the gonadal artery, an accessory or aberrant lower pole, or even the main renal artery. These vessels form a rich capsular network that anastomoses freely with perforating arteries and other retroperitoneal (especially lumbar) arteries and also with internal iliac, intercostal, and mesenteric arteries [18]. 

Palliation of symptoms in nonoperable patients was also included in some outcome analyses. The details of symptoms and therapeutic effects of renal artery embolization are generally lacking, but studies generally reported thathematuria, pain, and paraneoplastic symptoms were alleviated. In one study, severe hematuria resolved in 11 of 14 patients, and incomplete embolization of the tumor blood supply from parasitized lumbar arteries resulted in persistent hematuria in 3 of 14 patients [11]. In another study, malignant hypercalcemia resolved after embolization [10]. Kalman and Varenhorst concluded that a small group of patients with specific, tumor-related symptoms may benefit from embolization. However, the palliative effect of embolization cannot be evaluated from the available data, and the effectiveness of the procedure awaits validation. 

Trauma and vascular processes are the most common causes of neurological symptoms. Needle punctures and catheters may injure the spinal cord, nerve roots, bone, ligaments, or the blood vessels in the area. Vascular pathology includes thrombosis and embolization of the spinal arteries, arterial spasm without intraluminar clotting, and severance of the intercostal and lumbar arteries, and the risk of vascular complications if there is compression of the vessels due to tumours or vertebral processes, or by the presence of arteriosclerotic and thrombotic changes in the aorta. Other causes of neurologicjd sequelae are infections, chemicals, and previous neurological disease. 

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