Материал: Advanced Imaging of the Abdomen - Jovitas Skucas

or abscess, at times it is worthwhile obtaining Doppler US to exclude an aneurysm from the differential diagnosis. Some aneurysms contain a thrombus, making their identification even more difficult.

Currently DSA is considered the gold standard in evaluating splanchnic aneurysms. Evidence is accumulating that CTA is nearly as accurate, but MRA is still in the background although potentially it will evolve into a viable alternative.

In general, once a visceral aneurysm is detected, repair should be considered. Some smaller aneurysms are followed with serial US. These aneurysms tend to increase in size with time and are at increased risk of rupture. Many of these aneurysms undergo primary surgical repair. Angiographic embolization is a viable option but some surgeons still consider this therapy only in the presence of a surgical contraindication.

Temporarily occlusion of a splanchnic feeding vessel during transcatheter embolization appears to decrease the risk of rupture and bleeding during the procedure.

Celiac Artery

Aneurysms of the celiac artery are uncommon. Most are associated with medial degeneration and tend to be silent. These aneurysms can be treated by embolization. Celiac artery occlusion may be tolerated with such a technique as long as patent collateral vessels are present.

Splenic Artery

Underlying atherosclerosis is common in patients with splenic artery aneurysms. A mycotic cause is rare. Prevalence of these aneurysms is higher in women, and pregnancy and multiparity appear to predispose to their formation. Splenic artery aneurysms are uncommon in the pediatric age group, with most aneurysms in this age group being traumatic in origin. Portal hypertension in association with splenomegaly appears to predispose to splenic artery aneurysm formation. They also occur after liver transplantation.

Ultrasonography, MRI, and arteriography in a man with Ehlers-Danlos syndrome, type IV, identified kidney and liver cysts and splenic artery and hypogastric artery aneurysms (58),

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suggesting a common connective tissue defect for these conditions.

Most splenic artery aneurysms are asymptomatic until they rupture into the peritoneal cavity or an adjacent structure, including the bowel. They are prone to rupture during pregnancy, with rupture being most common during the third trimester, leading to high maternal and fetal mortality. Spontaneous rupture of splenic artery aneurysms occurs after liver transplantation. A rare splenic artery aneurysm erodes into the splenic vein and leads to portal hypertension. An occasional such patient develops a mesenteric steal syndrome.

Splenic artery aneurysms can present as a cystic tumor in the pancreatic tail; Doppler US identifies arterial blood. Rupture into the pancreatic duct results in succus pancreaticus.

Most of these aneurysms are saccular in outline. They are either intraor extrasplenic in location and occur most often in the distal portion of the splenic artery (close to the spleen). Their size varies considerably, with larger ones being more prone to rupture.

Splenic artery aneurysms can be diagnosed by Doppler US, CT, MRI, or angiography. Gray-scale US does not detect them readily; calcifications tend to produce artifacts. One limitation of Doppler US is that a completely thrombosed aneurysm is missed.

Hepatic Artery

Hepatic artery aneurysms occur in the common hepatic, right and left hepatic, or any branch artery. Most are secondary to atherosclerosis; less common etiologies include trauma, abscess, or inflammation, such as pancreatitis. Rarer causes are related to Marfan’s syndrome, EhlersDanlos syndrome, lupus erythematosus, and even von Willebrand’s disease (59). Some traumatic aneurysms are secondary to instrumentation, such as liver biopsy, or various attempts at drainage procedures.

The major complication of hepatic artery aneurysms is rupture, an event associated with a high morbidity and mortality. Most bleeding is intraperitoneal, or, with erosion into the duodenum, an upper gastrointestinal hemorrhage ensues. Occasionally an aneurysm evolves into an arteriobiliary fistula and results in hemobilia.

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Three-dimensional CTA is useful in detecting and defining these aneurysms.

Although color Doppler US provides aneurysm flow characteristics, angiography not only defines its relationship with the hepatic artery but also provides access for therapy. These aneurysms are treated with Gianturco coils, gelatin sponge, polyvinyl alcohol fragments, occlusion with Ivalon particles, or other particles. Embolization controls bleeding in most patients. Percutaneous transluminal angioplasty is emerging as the preferred treatment modality for both intrahepatic and extrahepatic saccular aneurysms, and such an angioplastic technique has a high success rate. Biliary sepsis, liver insufficiency, and gan-

grenous cholecystitis are some of the complications. An occasional patient with an intrahepatic aneurysm, however, requires a partial hepatectomy.

Superior Mesenteric Artery

Aneurysms of the superior mesenteric artery and its branches are not common. These are often detected only after rupture. Some are infected or are associated with intramural dissection. An aneurysm close to the origin of the superior mesenteric artery was associated with a tight stenosis of the celiac artery (60). These aneurysms develop in patients with systemic lupus erythematosus (Fig. 17.11).

Superior mesenteric artery branch aneurysm embolization using small coils is occasionally performed.

Pancreaticoduodenal Arteries

The pancreaticoduodenal arteries have a greater predilection for aneurysms than expected. For unclear reasons a number of these aneurysms are associated with stenosis or occlusion of the celiac artery.

Some of these aneurysms are secondary to pancreatitis, with a septic etiology or prior trauma being postulated. Not all aneurysms progress if left untreated. Still, these aneurysms tend to rupture even when still small, bleed— extraperitoneally or even into the duodenum— and carry a high mortality rate.

These aneurysms are treated both by transcatheter embolization and surgically, and some are left untreated. Nevertheless, for those aneurysms associated with celiac axis stenosis, correction of the latter condition should also be considered. Surgical options include aneurysm resection or even arterial ligation, although with rupture a partial pancreatectomy may be required to control bleeding.

Other Aneurysms

Aneurysms are rare in the inferior mesenteric artery. An occasional one is associated with obstruction of the superior mesenteric or celiac artery.

Less common sites for an aneurysm include the gastroepiploic artery; rupture of these aneurysms carries a high mortality rate. A gastroduodenal artery aneurysm developed a few months after an episode of acute biliary pancreatitis (60). An occasional middle colic artery aneurysm is reported. These aneurysms are also embolized.

Small vessel aneurysms are rare, but a mycotic source or periarteritis nodosa should be suspected with some of them.

Dissection

A complication of transcatheter arterial embolization is dissection of the feeding trunk. With attempted transcatheter arterial embolization of hepatocellular carcinomas, the two most

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common sites of dissection are celiac artery and proper hepatic artery; long-term follow-up of these dissections reveals recanalization in approximately one third, a residual narrowed lumen in another third, and complete obstruction in the rest.

A hepatic artery dissection is rare. Superior mesenteric artery dissection is also rare. Threedimensional CT can identify the false lumen, intimal flap, and both entry and exit points.

Portal Vein

Portal Hypertension

It should be kept in mind that some authors use the term portal hypertension rather broadly and include under this topic splenic vein obstruction and resultant gastric varices, a condition without portal vein hypertension. Others use left-sided portal hypertension and localized portal hypertension to describe splenic vein obstruction. Isolated splenic vein obstruction is discussed in a later section. Some conditions, such as splenic vein thrombosis extending into the portal vein, involve both veins and are covered in this section.

Pressure and Blood Flow Measurements

Normal portal venous pressure ranges from 5 to 10mmHg, which is 4 to 6mmHg higher than inferior vena cava pressure. Portal hypertension is said to be present if portal venous pressure exceeds 10mmHg, is more than 5mmHg above inferior vena caval pressure, or if splenic vein pressure is more than 15mmHg. Clinically, a useful assumption is that portal hypertension is present if portal pressure is more than twice the normal range, but keep in mind that the portal vein–inferior vena cava pressure gradient is more significant in evaluating portal hypertension than an actual pressure.

Mean normal portal vein blood velocity is about 15 to 30cm/sec and varies both with respiration and cardiac phase but is hepatopetal. With portal hypertension venous blood flow exhibits a complex pattern. For instance, in some patients hepatopetal flow in the fasting state changes to a to-and-fro flow after a meal and then to hepatofugal flow.

Intraoperative flow measurements show that hepatic artery blood flow is approximately two

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thirds that of the portal vein; hepatic artery flow increases significantly with temporary occlusion of the portal vein. Theoretically, percutaneous Doppler US should be able to measure liver and portal venous blood flow; in practice, blood flow measurements vary considerably.

Hepatic venous pressure gradients are obtained by hepatic vein catheterization and portal blood flow velocity and portal vein congestion index measured by duplex Doppler US. No significant correlation exists between venous pressure gradients and Doppler measurements in patients with cirrhosis and portal hypertension, but a significant linear correlation is evident if patients with patent paraumbilical veins are excluded (61).

Duplex portal vein US in patients before TIPS diagnosed portal hypertension with a sensitivity and specificity of 80% if a portal vein diameter >1.25cm or portal vein velocity <21cm/sec were detected, but US could not grade hypertension (62). On the other hand, in cirrhotic patients portal blood velocity does not differentiate between those with or without endoscopic evidence of esophageal varices or congestive gastropathy and, in general. Doppler US cannot identify those cirrhotic patients at risk for upper gastrointestinal bleeding.

Phase-contrast MRA has been used to measure portal blood flow. In general, MRA results correlate with data obtained by Doppler US. Phase contrast MRA also provides azygos vein flow changes during the cardiac cycle; flow rates are considerably greater in patients with chronic liver disease and portal hypertension than in healthy individuals. Potentially, such information aids in evaluating progression of diffuse liver disease.

An endoscopic balloon technique measures esophageal variceal pressure. This pressure correlates only partly with portal venous pressure, probably due to the presence of other collateral channels.

Etiology and Pathogenesis

Occasionally portal hypertension is associated primarily with increased portal blood flow, such as an arterioportal fistula, but most often it develops due to increased resistance to portal venous blood flow. A rare malignant vascular intrahepatic tumor leads to portal hyperten-

sion; these tumors result in increased portal blood flow due to shunting, intrahepatic portal obstruction caused by massive tumor growth,or both. Occasionally portal hypertension is idiopathic (Banti’s syndrome).

Increased Flow

Portal hypertension due to increased blood flow is most often a result of a systemic artery-to- portal vein shunt, either intraor extrahepatic in location. These shunts, or fistulas, extend to the splenic vein, superior mesenteric vein, or portal vein, including its intrahepatic branches. They can be congenital or acquired. A congenital artery-to-portal vein fistula should be suspected with infantile portal hypertension. At times portal hypertension manifests clinically only years after a fistula is established.

Increased Resistance

Table 17.1 lists some of the causes of portal hypertension due primarily to increased resistance to portal blood flow. Of interest is that portal venous pressure tends to be slightly elevated in some disorders not usually associated with portal hypertension. Thus portal pressure is increased in patients with biliary obstruction, decreasing after biliary decompression. Rarer causes of prehepatic portal venous obstruction include adenopathy at the liver hilum.A number of patients with abdominal tuberculosis and periportal adenopathy have portal hypertension (63). Similarly, periportal lymphoid infiltration in lymphoma or leukemia can result in portal hypertension.

With presinusoidal intrahepatic obstruction the hepatic vein wedged pressure is normal. Thus patients with hepatic schistosomiasis have hyperkinetic systemic and splanchnic circulations but a normal hepatic venous pressure gradient and hepatic blood flow; in those with esophageal varices a normal hepatic venous pressure gradient is indicative of presinusoidal portal hypertension. Of note is that portal hypertension in schistosomiasis patients is not due to fibrosis only but is multifactorial; hemodynamic values are not significantly different between patients with and without liver fibrosis. A rare cause of portal hypertension is portal vein invasion by an intrahepatic peripheral cholangiocarcinoma.