Книги по МРТ КТ на английском языке / Advanced Imaging of the Abdomen - Jovitas Skucas

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complications (47); part of the reason may be that radiologists tended to perform cavography prior to filter placement and surgeons did not. A review of over 1700 implanted filters at one institution (up to 1998) found a 6% prevalence of observed postfilter pulmonary emboli, fatal in 4% of patients, with most fatal pulmonary emboli occurring a median of 4 days after filter insertion (48); the prevalence of observed postfilter caval thrombosis was 3%. Intrafilter clots are not uncommon. Benefit must be balanced against risk.

Other filter complications include malposition, filter tilting, and insufficient opening. Ideally, a filter is positioned between the ileal vein confluence and renal veins. A filter cephalad to the renal veins risks renal vein thrombosis. Mild filter tilting is common, but the ability to trap clots is reduced with excessive tilting. Likewise, insufficient filter opening reduces a filter’s clot trapping ability. A filter is designed to prevent pulmonary emboli, and the evidence of such an embolus after filter placement represents filter failure. In such a situation the filter should be investigated for migration, strut failure, or inferior vena cava thrombosis. Filter migration occurs either caudal or cranial.Vena caval thrombosis is a recognized filter complication, regardless of filter design. Some caval thrombi are asymptomatic. Even without a thrombus, extremity venous stasis tends to accentuate after filter placement. Rare complications include myocardial infarction due to filter migration and pericardial tamponade.

Filter perforation is rare. Anecdotal reports describe caval penetration resulting in pancreatitis and even biliary obstructive. Filter struts can fracture and migrate, including to the kidneys. Rare reports describe penetration of a vertebral body and caval perforation leading to small bowel volvulus.

Caval filters are recognized on contrastenhanced SGE MRI because of their symmetry and magnetic artifacts.

Incidentally, J-tipped guidewires should be used with care around filters; these guidewires are at risk for entrapment.

Aneurysms

Inferior vena cava aneurysms are very rare. Most are believed to be congenital. Acquired

ones are secondary to trauma or an arteriovenous fistula. Some are asymptomatic and are incidentally discovered when CT or MR are performed for other reasons. Sagittal reconstruction is helpful in their visualization.

Visceral Vessels

Vasculitides

Systemic vasculitis often involves small visceral vessels, with resultant ischemia leading to ulcerations, perforation, or evolving into a stricture. Vasculitis can involve any part of the gut, even the duodenum, which has a rich blood supply. It often affects multiple bowel segments, in distinction to thromboemboli, which tend to affect continuous segments. De novo duodenal ischemia is almost always secondary to a vasculitis. Concomitant splenic and renal involvement also suggest a vasculitis.

Behçet’s Syndrome

A chronic multisystemic disorder, Behçet’s syndrome is of unknown etiology. Whether Behçet’s syndrome has a primary ischemic basis is debatable; some authors classify it not under ischemia but in a separate category. Also, some authors separate Behçet’s syndrome into two forms: complete and incomplete. In Japan, Behçet’s colitis patients typically have no eye involvement, and these patients are classified under the incomplete form of Behçet’s syndrome.

Resected bowel in these patients reveals multiple punched-out inflammatory ulcers, mostly in the ileocecal region; most ulcers are on the antimesenteric border. Histopathology reveals a nonspecific vasculitis. Granulomas are not identified. Clinically, many patients develop erythema nodosum, arthralgias, oral and genital ulcers, and a relapsing iritis. Gastrointestinal symptoms are common, with abdominal pain and recurrent aphtha mimicking Crohn’s disease, ulcerative colitis, or another vasculitis. An acute presentation with bowel perforation and peritonitis is not uncommon. An occasional patient presents with prolonged fever. The diagnosis can be difficult; in 1990 the International Study Group for Behçet’s Disease proposed specific diagnostic criteria consisting of oral ulcers and at least two of the following: genital ulcers, specific eye lesions, skin lesions, and a

skin pustule test. A diagnosis of Behçet’s syndrome is established mostly on clinical grounds rather than on histopathologic findings.

The most common site of gastrointestinal involvement is the ileocecal region, followed by the colon, small bowel, and, least often, esophagus. Gastric disease is rare. Imaging in affected individuals reveals inflammatory polyps and either aphtha or deep ulcers. In general, deep or punched-out ulcers in either the distal ileum or right colon should suggest Behçet’s syndrome.A perforation is not an uncommon acute event. A retrospective CT study of patients with intestinal Behçet’s syndrome found intestinal polyps in 36% and thickened bowel wall in 32% (49); enhancement ranged from mild to marked. Both polyps and a thickened bowel wall were more common in patients with complications. Also, severe perienteric infiltration was seen only in patients with complications. Adjacent lymph nodes can be deformed by chronic ileocecal ulcerations.

Most therapy is unsatisfactory in patients with Behçet’s syndrome. Some patients’ clinical symptoms improve and imaging abnormalities clear after the start of a low residue diet. Even thalidomide treatment has been helpful.

Patients with Behçet’s syndrome are prone to develop aortic and arterial aneurysms (50). Stent-grafts are helpful, although artery occlusion is a complication. Thromboses of inferior vena cava, portal vein, and smaller veins also develop.

Postoperative recurrence after bowel resection is common and generally is close to an anastomosis.

Periarteritis Nodosa

Periarteritis nodosa (polyarteritis nodosa), a necrotizing inflammation (arteritis) of small and medium-sized artery walls, eventually results in organ ischemia, with renal arteries more often involved than liver vessels. Hypertension is common. These patients develop arterial aneurysms and stenoses, generally at sites of arterial bifurcation—characteristic but not pathognomonic findings; these findings also occur in other arteritides. Aneurysms tend to be small, saccular, at times having an irregular outline.

Contrast CT shows patchy renal uptake bilaterally due to scarring; wedge-shaped defects

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develop secondary to focal ischemia. The imaging appearance is nonspecific.

Henoch-Schönlein Purpura

Henoch-Schönlein purpura (nonthrombocytopenic purpura) is a vasculitis of unknown etiology affecting mostly children. Usually a characteristic lower extremity purple rash precedes abdominal symptomatology, with some exceptions. Abdominal pain and bleeding in these patients presumably is secondary to intramural bleeding or a serohemorrhagic effusion.

Imaging reveals a predilection for proximal small bowel involvement. With extensive involvement, a small bowel study reveals intramural fluid as fold thickening and thumbprinting (Fig. 17.8). An intramural hematoma occasionally acts as a lead point for an intussusception. Computed tomography identifies segmental small bowel mural thickening, a nonspecific finding.

In children with Henoch-Schönlein purpura, US detects dilated small bowel segments, decreased motility, and eccentric bowel wall thickening.

Figure 17.8. Henoch-Schönlein purpura resulting in bowel wall edema (arrows) and fold infiltration.

Allergic Granulomatous Vasculitis

(Churg-Strauss Syndrome)

Allergic granulomatous angitis (Churg-Strauss syndrome) is a necrotizing vasculitis leading to ischemia due to arterial occlusion. Some patients develop ulcerative colitis–like findings. Symptoms tend to improve with steroid therapy, but disease recurs when steroids are discontinued.

Degos’ Disease

Degos’ disease (malignant atrophic papulosis) is a rare, progressive disease leading to occlusion of small and medium-size arteries. Bowel involvement results in perforations, peritonitis, and fistulas.

Degos’ disease is in the differential diagnosis of small bowel ulcerations.

Systemic Lupus Erythematosus

Some patients with systemic lupus erythematosus develop a gastrointestinal vasculitis with resultant symptoms of diarrhea and pain. The final end point is ischemic bowel disease. In affected patients with acute abdominal pain, CT reveals bowel wall thickening, a target-like appearance and mesenteric vascular engorgement and haziness, findings suggesting ischemic bowel disease (51). In distinction from more common bowel ischemia, bowel wall thickening tends to be multifocal, varies in length, and is not confined to a single vascular field. Unless irreparable damage ensues, the changes should revert to normal after therapy (Fig. 17.9).

A three-phase Tc-99m–pyrophosphate scintigram appears useful in these patients; a positive scan suggests a vasculitis.

Antiphospholipid Antibody

Syndrome

Study of antiphospholipid antibody syndrome belongs mostly in the hematologist’s domain. Abdominal imaging enters the picture when venous and arterial thromboses develop in patients with serum antiphospholipid antibodies and thrombocytopenia. Abdominal pain and abdominal distention are the most common clinical presentations. Spontaneous abortions also occur.

Both antiphospholipid antibodies and lupus anticoagulant alter hemostasis and induce a hypercoagulable state. This syndrome exists as a primary form and also in association with systemic lupus erythematosus. Both forms manifest similar clinical findings, although lupus usually leads to venous thrombosis only.

Patients with antiphospholipid syndrome develop major vascular thromboses, including the aorta, inferior vena cava, portal vein, superior mesenteric vein, and splenic vein (52). Resultant ischemia is either localized or diffuse and can progress to infarction and necrosis and involve kidneys, liver, spleen, stomach, and bowel. Adrenal infarction can develop without evident hemorrhage (53). Pancreatitis and hepatic dysfunction associated with portal hypertension develop in some. Inferior vena cava or hepatic vein thrombosis can lead to Budd-Chiari syndrome. In some patients thromboemboli recur at the same site; in others they tend to be limited to either the arterial or venous side. Imaging detection of unusual or recurrent thrombi, especially in a younger patient, should suggest this entity. Histology simply reveals extensive small artery, arteriolar, and venous occlusive disease.

Other Vasculitides

Pseudoxanthoma elasticum is a connective tissue disorder consisting of characteristic skin lesions, angioid streaks in the eyes, and occlusive vascular disease. Presumably the latter findings are responsible for the occasional gastric hemorrhage developing in this condition. Some patients develop ischemic bowel perforations before manifesting peripheral findings.

Dermatomyositis is a vasculitis also affecting the gastrointestinal tract. Underlying ischemia

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leads to edema, ulcers, gangrene, and, if severe enough, eventual bowel perforation.

A distinct form of vasculitis consisting of a giant cell phlebitis in a 16-year-old girl led to an ischemic colonic stricture (54); arterioles and arteries were not involved.

Ischemia

Clinical

Adults

Acute intestinal ischemia is a result of arterial thrombosis, arterial embolism, venous thrombosis, a vasculitis, or a nonocclusive low blood flow state. (Ischemic enterocolitis is discussed in Chapters 4 and 5, and gastrointestinal tract bleeding is discussed Chapter 4). From a clinical viewpoint, intestinal ischemia is best subdivided into acute and chronic types; some authors also include a subacute category.

Acute intestinal ischemia often presents as an abdominal catastrophe, evolving rather swiftly into a major infarction. Mortality remains high even with rapid diagnosis and ready availability of surgical consultation.

Nonocclusive mesenteric ischemia is difficult to detect and is probably underdiagnosed. Presenting symptoms tend to be vague and wide-ranging. The jejunum is involved in most patients. At its extreme, nonocclusive ischemia leads to necrosis, gangrene, and perforation. Computed tomography, US, and MRI are not reliable in the early detection of this condition, and mesenteric angiography should be considered in a clinical setting of suspected acute mesenteric ischemia.

Mesenteric ischemia can ensue with an aortic dissection involving the origin of the superior mesenteric artery or even compressing it; at times stenting relieves the ischemia.

Cholesterol embolization is associated with atheromatous plaques, angiography, vascular surgery, and even thrombolytic therapy. Such embolization can lead to mesenteric ischemia, gastrointestinal hemorrhage and bowel infarction and perforation (55). Clinically, these patients often also develop extremity ischemia and renal insufficiency. Eosinophilia is detected in some.

Although fibromuscular dysplasia is common in the renal arteries, it is unusual in visceral

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arteries; it is an occasional cause of ischemia, especially in a younger patient. Angiography reveals a characteristic “string of beads” appearance seen with fibromuscular dysplasia.

Mesenteric ischemia is more common in patients undergoing chronic hemodialysis than in the general population, probably due to atherosclerosis.

Heroin-related mesenteric ischemia is well known. Ischemia also develops after intranasal cocaine use.

Most chronic ischemia, especially in the elderly, is caused by either arterial stenosis due to atherosclerosis or a vasculitis. It is more common in women. Patients with chronic ischemia present with intestinal angina, weight loss, anemia, and diarrhea. Stenoses and occlusions range from a single visceral artery being involved to a combination of vessels. Collateral flow from the internal iliac or other arteries is not unusual. On a chronic basis, at times the arc of Buehler enlarges to the point that it provides most of the arterial blood supply to the liver and spleen.

Infants and Children

Gastric ischemia in a neonate is usually a complication of acute anoxia or shock. Intestinal ischemia in children is often superimposed on underlying congenital vascular or metabolic abnormalities. Thus vascular thromboemboli are a known complication in a setting of homocystinuria, a rare inborn error of amino acid metabolism manifesting as a multisystemic disease associated with mental retardation and vascular disease, consisting of premature arteriosclerosis and thrombosis.

Does the use of umbilical artery catheters in newborns impair mesenteric blood flow? Doppler US performed before and after removal of umbilical artery catheters found that after catheter removal mean peak celiac artery systolic blood flow velocity increased from 50cm/sec to 62cm/sec and superior mesenteric artery flow from 52cm/sec to 72cm/sec (56); end diastolic blood flow velocity and vessel diameters did not change significantly.

Umbilical arteriovenous fistulas are uncommon. They can be either congenital or acquired. Even in a neonate an arteriovenous fistula between the umbilical artery and umbilical vein can result in bowel ischemia. Bowel perfu-

sion improves in some after umbilical vein ligation.

Imaging

Angiography is the historic gold standard in suspected acute mesenteric ischemia. It is more time-consuming and often less available than CT, which is the current examination of choice in many centers. Mesenteric CTA detects superior mesenteric artery embolism or thrombosis and superior mesenteric vein thrombosis with a sensitivity approaching that of angiography. In addition to acute ischemia, CT also evaluates other causes of an acute abdomen.

Conventional radiography findings in patients with intestinal ischemia reflect the underlying spectrum of pathologic changes. They are normal initially or reveal variable degrees of gaseous bowel distention and fluid levels. Dynamic CT findings range from early ischemic ileus, bowel wall edema, and hematoma manifesting as bowel wall thickening, major vessel stenosis, or occlusion (either arterial or venous) to eventual bowel wall necrosis identified as intramural gas and lack of bowel wall contrast enhancement. In patients requiring surgery for acute mesenteric ischemia, detection of at least one of these CT findings achieves a specificity of over 90% but a considerably lower sensitivity. At times a contrast-enhanced CT target sign is evident during the arterial phase, especially if ischemia is due primarily to venous obstruction.

Gas–fluid levels and dilated bowel loops, both nonspecific signs of acute mesenteric ischemia, are seen equally well with conventional radiography and CT. Major ischemia leads to gas within the bowel wall (pneumatosis intestinalis) and mesenteric and portal vein gas. With few exceptions, in adults detection of mesenteric and portal venous gas implies mesenteric infarction. Such gas occasionally migrates to the internal spinal venous plexus, presumably from the pelvic veins. Pneumoperitoneum and even pneumoretroperitoneum are uncommon manifestations of bowel ischemia and presumably reflect a perforation. Some authors preach the superiority of CT in detecting portal venous gas and probably rightly so, although a formal comparison with conventional radiography is lacking. Nevertheless,

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sition in the steady state (GRASS) MRA identifies any stenosis in celiac and superior mesenteric arteries.

Deoxyhemoglobin in blood cells is paramagnetic, but oxyhemoglobin is not. This difference can be used to measure superior mesenteric vein blood oxygen saturation in hemoglobin, obtained using flow-independent MR T2 data; it appears useful in confirming suspected chronic mesenteric ischemia. In patients without ischemia, superior mesenteric vein blood oxygen saturation increases after a meal, but in symptomatic patients with chronic mesenteric ischemia blood saturation tends to decrease. In spite of research on this topic for over a decade, the clinical relevance of such measurements is yet to be established.

In an occasional patient positive uptake of Tc-99m–HMPAO–labeled leukocytes appears to reflect underlying chronic ischemia rather than primary inflammation.

Therapy

Acute Ischemia

Different therapy is employed for acute and chronic ischemia. Without therapy, acute nonocclusive ischemia often progresses to infarction. The treatment of choice in some patients with nonocclusive ischemia is papaverine infusion via a vascular catheter. Resection and anticoagulation are therapies for infarcted bowel. Recurrent bowel ischemia is a complication of surgical bypass grafting for acute ischemia. Fibrinolytic therapy using urokinase, rather than surgical embolectomy, appears effective in a majority of patients with a mesenteric embolus and without evidence of intestinal infarction; others require laparotomy. The best sign of successful therapy is pain abatement; persistent pain suggested intestinal infarction.

Rather than surgical embolectomy, in selected individuals mechanical thrombolysis of mesenteric and portal vein thrombosis, using a jugular vein approach, is an alternate approach.

Chronic Ischemia

Either percutaneous transluminal angioplasty or a surgical bypass graft is employed in a setting of chronic mesenteric ischemia. At times transaortic endarterectomy is performed. All of

these techniques have their associated complications. The published success rates of percutaneous transluminal angioplasty are difficult to put in perspective because different criteria are used (e.g., size of postprocedure luminal diameter, restenosis rate, improved clinical status) and are operator dependent.

Similar to surgical mesenteric vascular graft placement, percutaneous transluminal angioplasty has a technical procedure success rate of about 90% and short-term clinical success of about 80%. Procedure-related mortality and the major complication rate appear similar for operative bypass grafting and percutaneous transluminal angioplasty; long-term pain relief is similar or better with grafting.

Splanchnic Aneurysms

Many splanchnic aneurysms contain only a portion of the vessel wall; therefore, strictly speaking these outpouchings should be called pseudoaneurysms, yet the term aneurysm has been adopted in most of the medical literature and is used here.

The most common site for abdominal aneurysms is in the splenic artery, although they occur widely. Detection of a splanchnic aneurysm in a young patient should suggest Ehlers-Danlos syndrome (57). Some patients with multiple visceral artery aneurysms have connective tissue fragility suggesting cystic medial necrosis, even without clinical features of Marfan syndrome; they are prone to excessive hemorrhage during angiography and appear to be at increased risk for developing complications during vascular catheterization procedures.

Pancreatitis and resultant pseudocysts lead to aneurysms in adjacent vessel. Other causes include trauma, such as biopsy, and infection resulting in mycotic aneurysms. Intestinal tuberculosis is an occasional cause of a mesenteric artery aneurysm, generally manifesting as massive gastrointestinal hemorrhage.

Many aneurysms calcify and are identified with conventional radiography. In general, the presence of rim calcifications suggests an atheromatous origin rather than mycotic or traumatic. Some of these aneurysms become quite large. Noncontrast imaging reveals a fluidfilled cavity similar to a cyst or abscess. Thus prior to attempted drainage of a suspected cyst

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