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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3645_Библиотеки_им_академика_М_И_Перельмана
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Case 85 Portal Vein Embolization
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Figure 85.4
Figure 85.6
Figure 85.5
Findings
▶ Transhepatic access to the right posterior portal vein has been achieved, and a pigtail catheter is positioned in
the main portal vein (Fig. 85.4, arrow).
▶ Portal venogram in the AP (Fig. 85.4) and RAO (Fig. 85.5) projections demonstrates aberrant portal vein
branching pattern. e right posterior portal vein (arrow) is the rst branch of the main portal vein in this
so-called “Z-type” anatomy.
▶ Following embolization of the right portal vein (Fig. 85.6), there is redirection of ow to the future liver
remanant (FLR), in this case the le hemiliver.
Teaching Points
▶ e indication for portal vein embolization is to induce contralateral hepatic hypertrophy to facilitate
extended hepatic resection.
▶ Assessment of liver function may be functional or anatomic. Clearance of indocyanine green is an example of
functional assessment and is commonly used preoperatively in Asia. Liver volumetric analysis, an anatomic
measure, is more commonly used in the United States to assess resectability.
▶ Approximately 40% of patients have variant portal vein anatomy. is is important to recognize to prevent
embolization of nontarget vessels and ensure embolization of all target branches.
258
Management
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▶ In this case, embolization was performed with Embospheres©, although many agents can be used, including
particles, glue, and thrombin. Coils are generally not used as a single agent because of the rich intrahepatic
collaterals that reconstitued distal portal vein branches, but they may be used in combination with another
agent.
▶ In patients with compensated cirrhosis, an FLR of 40% is considered adequate, whereas in patients with
normal liver parenchyma an FLR of 20%–25% may be acceptable.
▶ Hypertrophy is commonly assessed by computed tomography or magnetic resonance volumetry 4 weeks aer
embolization. Typical increase in the ratio of future liver remnent/total liver volume is 8%–10% and the mean
hypertrophy of the FLR is 25%–30%. In patients with cirrhosis the hypertrophy is less pronounced.
▶ Ipsilateral portal vein access is preferred to minimize the risk of damage to the FLR.
Further Reading
Avritscher R, de Baere T, Murthy R, etal. Percutaneous transhepatic portal vein embolization:rationale, technique, and
outcomes. Semin Intervent Radiol. 2008; 25(2):132–145.
Covey AM, Brody LA, Getrajdman GI, etal. e incidence, patterns and clinical relevance of variant portal vein anatomy. Am J
Roentgenol. 2004; 183(4):1055–1064.
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Case 86
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History
▶ A31-Year-Old Asian Female with History of Crohn’s Disease and Sickle Cell Trait with Multiple Past
Hospitalizations for Chest Pain and Myalgia
Multiple prior chest computed tomographs (CTs) performed were all negative. Recently, the patient was
admitted with acute chest pain with the following imaging; ndings are new since 6months prior. Of note, the
patient had previously been on chronic steroid therapy.
Figure 86.1
Figure 86.3
Figure 86.2
Figure 86.4
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Case 86 Takayasu’s Arteritis with Ascending Aortic Aneurysm
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Figure 86.5
Figure 86.7 Figure 86.8
Figure 86.6
Figure 86.9
Figure 86.10
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Findings
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▶ CT scan on admission shows asymmetric stenosis of the right carotid artery with thickening of the arterial wall
(white arrows, Fig. 86.4). Additionally, an ascending aortic aneurysm is identied (white arrows, Figs. 86.6 and
86.7), which was not seen on prior CT scans from 6months prior (not shown). ickening of the walls of the
descending aorta (black arrow, Fig. 86.6) and carotid artery (black arrow, Fig. 86.5) are also identied.
▶ Figure 86.8 represents an ascending aortic angiogram showing a tulip bulb appearance of the ascending aorta
(white arrow). Taken alone, this could also reect aortic dilation from Marfan’s syndrome; however, it is
compatible with sequela of large-vessel vasculitis, given the remainder of ndings on the corresponding CT.
▶ Active vasculitis is demonstrated as uorodeoxyglucose (FDG) avidity on positron emission tomography
(PET) imaging (white arrows, Fig. 86.9).
▶ Figure 86.10 shows 1-year follow-up aer ascending aortic aneurysm repair (white arrow).
Teaching Points
▶ Takayasu’s arteritis is an uncommon large-vessel vasculitis that can produce both stenosis and aneuryms. It is
more common in females.
▶ It is considered an autoimmune disease, but it is thought to have a multifactorial etiology.
▶ Classical presentation includes two phases:an acute (prepulseless) phase and a late (pulseless) phase.
■ Acute symptoms:oen constitutional—weight loss, fatigue, night sweats, and fevers. May also include joint
pain and arthritis.
■ Late symptoms:usually secondary to organ involvement such as upper-extremity claudication,
cerebrovascular insuciency, or carotid artery pain.
▶ While nonspecic, inammatory markers such as ESR and C-reactive protein may be elevated.
▶ Magnetic resonance imaging (MRI) or CT will show vessel wall thickening, stenosis, and/or aneurysm
formation.
▶ PET/CT has been suggested to monitor signs of inammation within the vessel wall.
▶ Current classication of Takayasu’s arteritis is as follows, based on artery involvement:
■ Type I—Arch vessels
■ Type IIA—Ascending aorta, arch, and branches
■ Type IIB—Type IIA + descending aorta
■ Type III—Descending and abdominal aorta and/or renal artery
■ Type IV—Abdominal aorta and renal artery
■ Type V—Combination of types IIB and IV
Management
▶ Main therapy is medical with a combination of steroids and/or immunosuppressive drugs. Long-term
prednisolone therapy can result in imaging improvement. Patients in the active phase are treated with a steroid
taper.
▶ Surgery for symptomatic stenosis or enlarging aneurysms should only be performed aer multidisciplinary
discussion and avoided during the active phase.
▶ Intervention during the active phase is associated with poor outcome. In the latent phase, angioplasty to treat
chronic stenosis can be considered. ere are scattered reports of endogra placement to treat aneurysmal
components.
Further Reading
Gotway MB, Araz PA, Macedo TA, etal. Imaging ndings in Takayasu’s arteritis. Am J Roentgenol. 2005; 184:1945–1950.
Tombetti E, Manfredi A, Sabbadini MG, etal. Management options for Takayasu arteritis. Expert Opin on Orphan Drug. 2013;
1:685–693.
262
History
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▶ A69-Year-Old Diabetic Male with Atherosclerosis and Upper igh/Buttock Claudication
Case 87
Figure 87.1
Figure 87.2
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Case 87 Leriche Syndrome
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Figure 87.3
Figure 87.4
Findings
▶ MIP from a contrast-enhanced magnetic resonance image (MRI) (Fig. 87.3) demonstrates abrupt cuto of
the abdominal aorta just below the origin of the superior mesenteric artery (arrow). e external iliac arteries
(stars) are reconstituted by collaterals, including prominent inferior epigastric arteries (hollow arrows) and
iliolumbar arteries (arrowhead).
▶ Arterial-phase axial contrast-enhanced computed tomography (CT) (Fig. 87.4) conrms complete occlusion
of the distal aorta and shows large inferior epigastric arteries (arrows) that serve as a collateral pathway to
reconstitute the external iliac arteries.
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Teaching Points
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▶ e constellation of bilateral buttock claudication, impotence (in men), and diminished femoral pulses is
termed “Leriche syndrome.” Symptoms may be unilateral or bilateral, depending on the level of obstruction
and ecacy of collateral pathways.
▶ Leriche syndrome occurs in the setting of atherosclerotic aortoiliac occlusive disease usually distal to origin
of the renal arteries. is is a dierentiating factor from mid-aortic syndrome, which is seen in children and
young adults and involves the origins of the renal arteries.
▶ Collateral pathways that provide lower-extremity runo in the setting of aortoiliac occlusive disease include
(1)the “Winslow pathway” from the internal mammary or intercostal arteries to the external iliac arteries via
the inferior epigastric arteries (as in this case); (2)lumbar to iliolumbar arteries; (3)superior hemorrhoidal
(a branch of the inferior mesenteric artery) to inferior hemorrhoidal arteries; and (4)various additional
communications between branches of the internal iliac artery and femoral arteries (e.g., superior gluteal to
femoral circumex).
Management
▶ Diagnostic catheter angiography is rarely indicated because CT angiogram and magnetic resonance
angiogram can provide the morphologic and physiologic information required to plan intervention.
▶ Indications for intervention include disabling claudication and threatened limb.
▶ Surgical options include aortofemoral bypass, axillofemoral bypass, femoral-femoral bypass, and aortic
endarterectomy.
▶ In some cases, stent placement can be performed, with the best results in single lesions <3cm; however, this is
an uncommon cause of Leriche syndrome.
Further Reading
Hardman RL, Lopera JE, Cardan RA, etal. Common and rare collateral pathways in aortoiliac occlusive disease:a pictorial
essay. Am J Roentgenol. 2011; 197(3):W519–W524.
Kaufman J, Lee MJ. Abdominal aorta and iliac arteries. In:Vascular and Interventional Radiology:e Requisites. Elsevier-
Mosby; 2004:261–270.
265
History
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▶ A40-Year-Old Female Who Presents with Sudden Onset of Blue Fingers
Figure 88.1
Case 88
Figure 88.2
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Case 88 Thoracic Outlet Syndrome and Subclavian Artery Aneurysm
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Figure 88.3
Figure 88.4
Findings
▶ Aselective arteriogram of the right subclavian artery in neutral position (Fig. 88.3) shows a large aneurysm
(black arrow) involving the proximal right subclavian artery. is aneurysm is the source of emboli causing
blue ngers.
▶ Repeated arteriogram of the right subclavian artery with the arm abducted (Fig. 88.4) shows compression
of the subclavian artery (black arrow) at the thoracic outlet. Aneurysms secondary to thoracic outlet
compression usually occur just proximal to the area of compression, making this case atypical.
Teaching Points
▶ oracic outlet syndrome refers to compression of the neurovascular bundle by either normal or variant
anatomical structures. Commonly, these include the rst rib, the anterior scalene muscle, an anomalous
cervical rib, or the tendon of the subclavius muscle.
▶ Physical exam may reveal arm pain, skin color changes, or muscle cramping during abduction of the aected
limb.
▶ Sonography may reveal increased peak systolic velocities or cessation of ow when the arm is placed in the
hyperabducted position.
▶ To clinch the diagnosis of thoracic outlet syndrome at angiography, injections should be performed in both
a neutral and abducted position to assess anatomy, severity of compression, and associated ndings such as
aneurysm formation or distal emboli.
Management
▶ Surgical release of the thoracic outlet should be performed prior to any endovascular therapy, except in the
setting of limb ischemia or thrombus/emboli, where catheter-directed thrombolysis may be performed prior
to surgical resection.
▶ Endovascular stent gra placement has been used to exclude aneurysms following surgical release; however,
vascular bypass with aneurysm exclusion and resection may be required.
▶ Postsurgical angiography is performed to assess for residual stenosis, which may require further therapy.
▶ e patient in this case underwent rst-rib resection with excision of the aneurysm with interposition gra.
Further Reading
Criado E, Berguer R, Greeneld L. e spectrum of arterial compression at the thoracic outlet. J Vasc Surg. 2010; 52:406–411.
Demondion X, Herbinet P, Van Sint Jan S, etal. Imaging assessment of thoracic outlet syndrome. Radiographics. 2006;
26:1735–1750.
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