Материал: Advanced Imaging of the Abdomen - Jovitas Skucas

ABDOMINAL VASCULATURE

A retrospective study of renovascular hypertension patients who underwent percutaneous transluminal renal angioplasty, percutaneous transluminal renal artery stent placement, or renal arterial bypass grafting found similar procedure success rates (91% to 98%), but complication rates were 13% for angioplasty, 16% for stent placement, and 38% for bypass grafting (114); of interest is that the number of antihypertensive medications returned to baseline in all patients by 12 months. In the Dutch Renal Artery Stenosis Intervention Cooperative Study Group, patients with hypertension and atherosclerotic renal artery stenosis were randomly assigned to either undergo percutaneous transluminal renal angioplasty or receive drug therapy (115); 3 months later no significant differences were evident in either systolic or diastolic blood pressures in the two groups.

Surgical Bypass

The initial therapy for renal artery stenosis consisted of aortorenal bypass surgery, which then was replaced by hepatorenal, splenorenal and other bypass, patch angioplasty, and renal artery endarterectomy. Retrospective surgical studies from the late 1980s and 1990s established standards for postoperative 5-year survival of 52% to 65% or higher and improvements in hypertension and renal insufficiency, and most current authors compare

their angioplasty and stenting results against these standards. These comparisons are difficult to place in proper perspective because surgical studies tended to contain “sicker” patients with their correspondingly greater morbidity and mortality. Currently surgical therapy in many institutions is limited to a few specific indications, including failed angioplasty and stenting.

Angioplasty

Percutaneous transluminal revascularization consists of balloon angioplasty, at times supplemented by stenting. If necessary in high-risk patients, carbon dioxide is used as a primary intravascular contrast agent during angioplasty, supplemental when necessary by iodinated contrast.

Angiography is generally used initially to evaluate the success of angioplasty; Doppler US is used by some investigators to assess patency during subsequent follow-up. Roughly half of patients with underlying fibromuscular dysplasia who undergo successful angioplasty are cured and most of the rest are improved, results far superior to those achieved in patients with atherosclerotic disease (Fig. 17.27).

Percutaneous angioplasty appears less appropriate for the relatively uncommon ostial stenosis. A randomized, prospective study compared transluminal angioplasty alone and angioplasty

with stent placement in patients with ostial atherosclerotic renal artery stenosis (116); the primary success rate, defined as a <50% residual stenosis, of angioplasty alone was 57% compared with 88% for stenting. The 6-month postprocedure primary patency rate was 29% for angioplasty alone, and 71% for stenting. Among patients undergoing angioplasty alone, 29% required secondary stenting for angioplasty failure, with these patients then having a success rate similar to those with primary stenting. The authors concluded that primary stenting is a superior procedure for patients with ostial stenosis.

Stenoses can be dilated in patients with renovascular hypertension due to nonspecific aortoarteritis (Takayasu’s disease); the restenosis rate, evident by recurrence of hypertension and restenosis, found at angiography, was 16% at 22 months (117).

Complete renal artery occlusions have been successfully revascularized. Sufficient data are not available to draw firm conclusions about angioplasty for this indication.

Angioplasty complications include renal artery dissection and rupture, embolization of atheromatous fragments, and artery thrombosis. Even including complications due to femoral angiography, angioplasty is associated with fewer complications than surgical correction.

Doppler US detection of residual renal artery stenosis one day after percutaneous revascularization of atherosclerotic renal arteries appears to be a predictor for future restenosis (118).

Stenting

Currently, percutaneously implanted renal artery stents have a role in stenoses that are not amenable to angioplasty, those due to failed therapy, and in a setting of ostial stenosis. Percutaneous renal artery stent insertion has been performed for renal artery involvement in aortic dissection (119). Problems with dissection and residual stenosis are largely overcome with stenting. A review of published studies of stent placement up to 1998, comparing results of renal arterial stent placement and renal percutaneous transluminal angioplasty, concluded that stenting is technically superior and clinically comparable to angioplasty (120); stenting achieves a lower restenosis rate (17%) than

ADVANCED IMAGING OF THE ABDOMEN

angioplasty (26%). The complication rates are similar, but stenting results in fewer patients with a postprocedure residual stenosis. The importance of a postprocedure residual stenosis is its association with a significantly higher rate of eventual restenosis.

In a follow-up study of consecutive patients, renal arterial stent placement did not significantly improve primary patency of proximal and truncal renal arterial stenoses over that achieved by balloon percutaneous transluminal angioplasty (121); stents did, however, improve patency of ostial stenoses.

In general, stenting for angioplasty failure does relieve stenosis, but hypertension is cured only in half or fewer patients; likewise, arrest of clinical renal failure occurs only in about half or so of patients after stenting.

Renal artery stent obstruction can be evaluated with contrast enhanced MRI.

Acute complications of renal artery stent placement include renal artery thrombosis, renal artery emboli, cholesterol embolization to lower limbs, and femoral hematoma.

Renal Ablation/Embolization

Occasionally percutaneous transcatheter renal ablation is considered in patients with uncontrolled hypertension or nephrotic syndrome. A long-term improvement in hypertension and nephrotic syndrome can be achieved with this procedure, often with a lower morbidity and mortality than for comparable surgical nephrectomy.

Transcatheter embolization should be considered in the hypertensive patient with an accessory renal artery or a branch artery stenosis not amenable to usual therapy and if the involved artery supplies only a small renal segment. Eventual scarring and some loss of renal function will occur.

Renal Artery Aneurysm

Renal artery aneurysms can be subdivided into true aneurysms,dissecting aneurysms,arteritisrelated aneurysms, and simply aneurysmal dilatation. True aneurysms are saccular, extraparenchymal, and located at bifurcations.

ABDOMINAL VASCULATURE

Several etiologies account for these aneurysms: elastic tissue degeneration, possibly on a congenital basis, and atherosclerosis predominate, with an occasional one being secondary to trauma. The prevalence of renal artery aneurysms increases with age, with only a rare one found in children. They are a rare cause of hypertension; in some patients an aneurysm manifests with pain or hematuria, although most patients are asymptomatic.

Small intrarenal aneurysms develop in patients with polyarteritis nodosa, Wegener’s granulomatosis, and lupus erythematosus. Dilated renal arteries and aneurysms occur in Behçet’s disease.

An occasional true aneurysm ruptures, at times resulting in a loss of that kidney. Similar to rupture of a splenic artery aneurysm, rupture of a renal artery aneurysm during pregnancy carries a high maternal and fetal mortality. Repair of a known aneurysm should be considered prior to conception. Rupture is not necessarily related to hypertension. Calcifications in an aneurysm do not protect against rupture. Some ruptures evolve into an arteriovenous fistula.

Ring-like calcifications are detected with conventional radiography in less than a third of renal artery aneurysms.

Renal artery aneurysms are readily detected with arteriography. Most are also identified during arterial phase helical CT; precontrast and delayed postcontrast CT images show an isodense mass similar to a neoplasm. A majority are saccular in shape, with a minority fusiform or dissecting. Imaging also detects an occasional thrombosed aneurysm.

Some renal artery aneurysms dissect spontaneously or dissect secondary to trauma, including catheter manipulation. A minority of dissections occur bilaterally. Patients with a dissecting aneurysm can develop hypertension.

Arteriography should be diagnostic of a dissecting aneurysm. At times urography reveals delayed contrast excretion, although often this study is normal.

Renal artery aneurysms have been treated with an ex vivo surgical technique and autotransplantation. Of note is that follow-up of aneurysmectomy reveals a better cure rate of hypertension than in patients with renal artery stenosis. Before ascribing hypertension to an

aneurysm, however, a stenosis in another artery should be excluded.

Renal Vein Occlusion

Adults

Renal vein thrombosis is often associated with an underlying renal cell carcinoma or inferior vena caval thrombosis. Less common factors are dehydration, coagulopathy, nephrotic syndrome, pancreatitis and other retroperitoneal inflammation, systemic lupus erythematosus, intrinsic renal disorders such as glomerulonephritis, and as an occasional complication of acute pyelonephritis. The prevalence of thrombosis is sufficiently high in nephrotic syndrome to warrant screening these patients for renal vein thrombosis.

Few symptoms are evident in adults if thrombosis develops gradually. On a chronic basis collaterals (sometimes called renal varices) develop, the kidney is no longer enlarged, and venous flow returns to the renal hilum. A complication of renal vein thrombosis is pulmonary emboli.

Renal vein thrombosis with the thrombus extending into the inferior vena cava can be misdiagnosed as a renal cell carcinoma. Precontrast CT of a renal vein thrombus revealed a hyperdense tumor.

With acute thrombosis, contrast-enhanced CT detects renal enlargement and a thrombuscontaining enlarged renal vein. The venous wall tends to enhance with contrast. Corticomedullary differentiation is prolonged and a nephrogram delayed. Extraperitoneal hemorrhage is not an uncommon association.

Ultrasonography detects an enlarged, hypoechoic kidney. Initially a thrombus is anechoic. A thrombus is better detected in the shorter right renal vein than in the left. Doppler US findings have been disappointing. With some thrombi, Doppler US does not detect renal vein flow, although often the obstruction is incomplete and flow is present, albeit slow. Normal arterial Doppler US does not exclude venous thrombosis.

Scant literature exists on the use of MRI for renal vein thrombosis, although based on results from other vascular sites MR should be well suited in this setting.

Neonates

Predisposing factors for renal vein thrombosis in the neonate are dehydration, sepsis, maternal diabetes, polycythemia, and umbilical vein catheter manipulation and the rare hereditary thrombophilia. Thrombosis can be limited to small renal veins or extend into the main renal vein or even inferior vena cava. Clinically, these neonates develop hematuria or hypertension.

Gray-scale US is usually the first imaging modality employed. A transient early finding of an intrarenal vein thrombus is a linear echogenic structure. With sufficiently extensive involvement the affected kidney enlarges and assumes a heterogenous appearance. Ultrasonography should also detect any associated vena caval thrombus. Some neonates also have adrenal hemorrhage. Color Doppler US suggests a lack of flow in the intrarenal veins and reversal of arterial diastolic flow. Contrast enhanced MRI reveals persistent cortical enhancement and a lack of medullary enhancement.

Sequelae of renal vein thrombosis in a neonate range from an atrophic kidney, to focal scarring, to the kidney reverting to an essentially normal appearance.

Renal and Ureteric Varices

Not all venous engorgement is due to renal vein obstruction. Portal hypertension has led to intrarenal segmental venous engorgement (renal varices). Rarely, intrarenal varices are idiopathic. Renal varices can lead to recurrent hematuria.

Computed tomography detects tubular contrast-enhancing perineal structures. Color Doppler US should detect these varices. Selective renal phlebography is diagnostic. Of note is that renal arteriography can miss these venous structures.

Ureteric varices are uncommon. Occasionally engorged gonadal veins lead to extrinsic compression and result in a characteristic serpiginous appearance. Somewhat similar findings are seen with dilation of a ureteral artery, generally in association with renal artery stenosis where the ureteral artery provides a collateral blood supply to the kidney.

Vascular Fistulas

A fistula involving the aorta can be either aortovascular or aortoenteric. Fistulas associated with aortic aneurysms were discussed earlier (see Aorta),as were portosystemic shunts and fistulas (see Collateral Veins).

Aortocaval Fistula

Most aortocaval fistulas are related to aortic aneurysms and resultant surgical correction. These patients tend to be elderly and in poor health. A rare malignant fibrous histiocytoma at the aortic bifurcation led to a pseudoaneurysm which evolved into an iliocaval fistula (122).

In a patient with oliguric renal failure and a suspected aortocaval fistula, angiography using carbon dioxide is an alternate diagnostic test. Aortocaval fistulas have been embolized with coils, cyanoacrylate, and other materials.

Aortoenteric Fistulas

The most common cause of an aortoesophageal fistula is a thoracic aortic aneurysm. Esophageal perforation by an ingested foreign body is less common.

Most aortoduodenal fistulas develop in a setting of prior aortic aneurysm repair. Some are related to prior radiotherapy to this region. Rarely, duodenal tuberculosis or even a brucellar aortic aneurysm evolves into an aortoduodenal fistula.

A fistulous tract between an aortic graft and duodenum can be detected by CTA. If performed while the patient is bleeding, a temporal increase occurs in duodenal contrast agent accumulation (123).

Cavoenteric Fistulas

Most cavoenteric fistulas are secondary to trauma, tumor invasion, or prior radiotherapy. Thus a cavo-duodenal fistula developed after a right nephrectomy and radiotherapy for a urothelial tumor 20 months earlier (124). Anecdotal reports describe migrating caval filters resulting in duodenal perforation and a caroduodenal fistula (124).

ABDOMINAL VASCULATURE

Arterioportal Fistula

Clinically, arterioportal fistulas manifest through gastrointestinal bleeding, ascites, heart failure, or even diarrhea, findings induced by resultant portal hypertension, ischemia, or vascular erosions.

Dynamic MRA reveals arterioportal shunts as early focal regions of contrast enhancement (Fig. 17.28). Splenic arteriography is diagnostic.

Treatment of these fistulas is not clear. Some believe that embolization is the therapy of choice for acquired intrahepatic arterioportal fistulas but that extrahepatic ones should be corrected surgically. Successful transarterial embolization using coils and detachable balloons has been performed for these often highflow fistulas (Fig. 17.29).

Arteriovenous Fistula

An arteriovenous fistula is an abnormal communication that bypasses the usual capillary circulation.A congenital fistula usually has multiple connections between an artery and vein. Most acquired fistulas are traumatic in origin. Tumors eroding into vessels also result in fistulas. The most common acquired origin is from the hepatic artery.

Splenic arteriovenous fistulas are either congenital or acquired. The less common congenital ones tend to be intrasplenic in location and their imaging appearance mimics a hemangioma. Acquired fistulas are often associated

with atherosclerosis and trauma; an occasional one is related to pregnancy. They are identified by duplex Doppler US and arteriography.

Renal arteriovenous fistulas range from congenital to acquired. Some of these congenital fistulas do not manifest until adulthood. Among acquired ones are those secondary to prior vascular instrumentation or surgical manipulation, although many are idiopathic. Gross hematuria is the usual presentation with a renal fistula. Hypertension develops in some patients. Larger fistulas are associated with an enlarged feeding artery and draining vein. Loss of adjacent renal parenchyma and a resultant scar are evident with some fistulas. Similar to other sites, renal arteriovenous fistulas are detected by Doppler US. Renal arteriography defines the extent of a fistula and allows selective embolization.

At times scintigraphy of a vascular fistula suggests a hypervascular neoplasm.

Many congenital arteriovenous fistulas are difficult to treat with surgery, and recurrence is common.

Arterioureteral fistula

Arterioureteric fistulas are rare. Most are complications of vascular surgery, with atherosclerotic disease, chronic ureteral stenting or prior pelvic radiotherapy occasionally having a role. Clinical presentation consists of hematuria, often intermittent, ranging from mild to massive bleeding. Most aortoureteric fistulas are related to aortic prosthetic graft infections.

In the appropriate clinical setting, arteriography will define these fistulas, but some are initially not detected due to their intermittent bleeding. Some are associated with a pseudoaneurysm. Excretory urography and retrograde ureterography may simply show blood clots. Surgery is difficult in these patients. An empiric nephrectomy is considered in some patients with life-threatening bleeding, but it will miss a more distal site of bleeding. Arterial emboliza-

tion and endovascular stenting are immediate therapeutic options.

Arteriovenous Malformations

Most mesenteric arteriovenous malformations are a variant of an arterioportal fistula.

Angiography detects the larger arteriovenous malformations. Many are in the pelvis and present difficult management problems. Surgi-