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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3627_Библиотеки_им_академика_М_И_Перельмана
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RadCases.thieme.com RadCases Interventional Radiology
■
Imaging Findings
A B, C
(A) Coronal reformatted, arterial-phase, contrast-enhanced CT scan shows the left superior epigastric artery (arrow) immediately caudal to the stomal site.
No extravasation. Adjacent image shows the more proximal segment of superior epigastric artery (arrow). (B) Selected internal mammary arteriogram
shows a large branch (arrow) of the superior epigastric artery encircling the stomal site. (C) This branch was embolized with coils (arrows) placed distal and
proximal to the stomal site. No further bleeding was noted.
■ Dierential Diagnosis
• Iatrogenic superior epigastric artery hemorrhage.
■ Essential Facts
• Major complications of percutaneous gastrostomy tube
(pGT) placement (3–6%) include sepsis, peritonitis,
major wound infections, peritoneal leakage of bowel
contents, hemorrhage, dislodgment of the pGT prior to
tract formation, and traversal of nontarget structures that
leads to signicant morbidity.
• Minor complications (, 10%) include mild wound infections
responding to antibiotics, delayed dislodgment, clogging,
leakage after stomal tract maturation, and minor bleeding.
• Bleeding can occur by puncture of systemic arterial
branches (most commonly) or varices, and it is typically
self-limiting. Injury to medium-sized arterial branches
such as the gastroepiploic (most commonly), the
gastroduodenal, the left gastric, or the short gastric
arteries usually requires arterial embolization.
• Injury of the superior epigastric artery causes a rectus
sheath hematoma and bleeding at the stomal site.
Embolization is performed by catheterizing the feeding
internal mammary artery and performing selective coil
embolization of the superior epigastric proximal and distal
to the aected segment to avoid reperfusion by the inferior
epigastric artery. This “back door–front door” technique is
performed whenever possible for iatrogenic arterial injury.
• During pGT placement, the most common arterial injury
requiring embolization is the gastroepiploic artery, which
courses along the greater curvature of the stomach and
may cross the intended stomal site (mid-body of the
stomach) in cases of inadequate gastric insuation or
anomalous gastric positioning.
• Dislodgment of a pGT after mature tract formation
and the related condition of buried bumper syndrome
(progressive impaction of the internal pGT retainer
within hypertrophied gastric mucosa) lead to an
uninjectable pGT with erythema and swelling. Treatment
is replacement through the existing tract. Continued
use of the pGT for enteral feeding can lead to major
complications such as abscess or necrotizing fasciitis,
requiring percutaneous drainage or surgical debridement.
• Dislodgment of a pGT prior to mature tract formation
(, 2 weeks) causes leakage of feeds into the peritoneum if
no gastropexy anchors have been left in place. Peritonitis
may result. Treatment is laparotomy, peritoneal lavage,
and if the pGT can be salvaged, surgical gastropexy.
• Traversal of the colon often presents with sepsis and
peritonitis requiring laparotomy, peritoneal lavage, and
intravenous antibiotics. Delayed presentation after tract
maturation is described and may not require surgery.
• Malignant seeding of the tract has been described in
patients with head and neck cancer who are undergoing
pull-type pGT placement (bumper-retained pGT pulled
down esophagus to stomach). Push-type (antegrade
dilation using the Seldinger technique) may be preferable
in these patients.
Pearls and Pitfalls
Routine imaging prior to uoroscopic pGT placement is
unnecessary, but existing studies should be reviewed to
exclude abnormal gastric positioning and intervening
normal or pathologic structures that may prevent safe
placement.
Radiographs and CT scans that show superimposition
of the colon and stomach do not contraindicate pGT
placement because in most cases, air insuation of the
stomach leads to inferior displacement of the colon.
For additional guidance of pGT placement, oral barium
contrast may be given the evening prior to pGT
placement to demonstrate the transverse colon.
Sonography can be used if hepatic, splenic, or vascular
interposition is suspected.
CT guidance of pGT placement may be required for
nonroutine cases, particularly after prior gastric surgery.
Case 67
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133
A B
C D
■ Clinical Presentation
A 45-year-old man presents with numbness, tingling, and swelling of the hands.
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■
Imaging Findings
A, B
(A) Conventional venography with the right arm in neutral position shows minimal to no compression at the thoracic outlet (arrow). (B) Conventional
arteriography with the left arm in neutral position shows mild stenosis of the subclavian artery at the thoracic outlet (arrow). (C) Abduction of the right
arm results in subclavian vein compression (arrow). This eect was bilateral. (D) Abduction of the left arm results in subclavian artery compression (arrow).
This eect was bilateral.
■ Dierential Diagnosis
• Thoracic outlet syndrome (TOS): Indicated by arterial
and venous compression at the thoracic outlet that
worsens with abduction.
■ Essential Facts
• TOS is compression of the brachial plexus, subclavian
vein, and subclavian artery within the thoracic outlet by
normal or anomalous structures. Nerve (brachial plexus)
compression is the most common type of TOS (95%),
followed by venous compression (3–4%) and arterial
(1–2%) compression.
• Contributing structures include the rst rib, the anterior
scalene muscle, the tendon of the subclavius muscle,
exostoses, posttraumatic pseudarthroses, and anomalous
cervical ribs.
• Associations include a history of musculoskeletal injury,
motor vehicle accident, and subluxation.
• Presentation depends on which structures are
compressed and may include symptoms of nerve
compression such as numbness or weakness, symptoms
of venous compression such as arm swelling, and
symptoms of arterial compression such as exercise
fatigue, pallor, pain, muscle cramping, and blue digits.
Left untreated, arterial TOS can lead to stenosis, poststenotic dilatation, luminal irregularity, frank aneurysm
formation, and distal thromboembolism.
• Physical exam and imaging of TOS include stress
maneuvers:
◦ Adson’s maneuver consists of pulse and symptom
evaluation during inhalation with the head turned
toward the symptomatic side and the arm extended.
◦ Wright’s test consists of pulse and symptom evaluation
during hyperabduction and external rotation of the arm.
• Radiographs commonly show cervical ribs, osteophytes,
healed fractures, or exostoses.
• Doppler ultrasound may show no ow or doubling of
peak systolic velocity from neutral to hyperabduction.
• CT angiography is performed in hyperabduction and may
show arterial compression, subclavian artery defects, and
the structure causing compression.
• Conventional angiography may be the best test to detect
distal thromboembolism (digital arteries) and facilitate
performance of thrombolysis. Injections should be
performed in the neutral and hyperabducted positions.
• Treatment options:
◦ Endovascular thrombolysis and thrombectomy treat
arterial or venous thrombosis and distal arterial
thromboembolism. These options can be performed
prior to surgical management.
◦ Surgical management involves resection of the rst rib,
cervical rib or bony exostosis, release of the insertion of
the anterior scalene muscle, resection of the subclavius
muscle tendon, and in cases of xed, severe subclavian
artery stenosis or aneurysm, arterial bypass, or surgical
reconstruction. Acute upper extremity ischemia
associated with TOS portends a poor postsurgical
outcome.
◦ Some endovascular options used only after surgical
decompression include angioplasty to treat xed
stenoses, webs, and synechiae, as well as stent grafts to
treat aneurysms.
Pearls and Pitfalls
ü Postsurgical results are good to excellent in 86% and
poor to fair in 13% of cases.
ü Arterial and venous compression can be an incidental
nding in 50% of asymptomatic patients. Treatment is
reserved for the clinical syndrome described.
C, D
Case 68
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A
■ Clinical Presentation
A 42-year-old man with a history of hypertension presents with chest pain and a painful, cold right leg.
■ Further Work-up
B
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■
Imaging Findings
A, B C, D
(A) Three-dimensional, volume-rendered, contrast-enhanced CT scan of the posterior aspect of the aorta shows a linear aortic lling defect (arrows)
bisecting the aorta and extending into the right iliac arteries. The density of the left half (large arrowhead) is lower than that of the right half (small arrowhead).
(B) Aortogram with a pigtail catheter in the left half of the aorta (small arrowhead) shows strong opacication of the left lumbar and iliac arteries but only
faint opacication of right iliac arteries (large arrowhead) and no visible mesenteric, right lumbar, or renal arteries. (C) Sharp puncture from the left to the
right aortic lumens and balloon fenestration of the intimal ap. (D) Repeat aortogram from the left aortic lumen shows new right iliac (arrow) and femoral
opacication as well as new visualization of the right renal, right lumbar, and inferior mesenteric arteries.
■ Dierential Diagnosis
• Aortic dissection treated by endovascular intimal
fenestration.
■ Essential Facts
• Aortic dissection is a tear in the intima of the aorta with
dissection of blood into the media. Approximately 50% of
cases involve the descending aorta only, and 50% involve
either the ascending aorta only or the ascending and
descending aorta.
• The clinical presentation is usually ripping chest pain but
varies with location and involvement of great vessels,
aortic valve, pericardial sac, and coronary arteries. The
mortality rate is 1% per hour for the rst 48 hours.
• Risk factors include atherosclerotic disease, trauma, bicuspid
aortic valve, coarctation, pregnancy, cocaine use, cystic
medial necrosis, some connective tissue diseases (Marfan’s
syndrome, Ehlers–Danlos syndrome), and homocystinuria.
• Stanford classication:
◦ Type A: ascending aorta
◦ Type B: distal to subclavian artery origin
• DeBakey classication:
◦ Type I: ascending aorta, arch, descending aorta
◦ Type II: limited to ascending aorta
◦ Type III: limited to descending aorta distal to the origin
of the left subclavian artery
• Imaging options:
◦ CT/CT angiography (CTA), MR/MR angiography (MRA),
and transesophageal echocardiogram (TEE) have similar
diagnostic yields with high sensitivity and specicity
for dissection. TEE allows fast bedside examination of
unstable patients and may show type B entry/reentry
sites not visible on CTA and type A coronary involvement,
pericardial eusion, and aortic regurgitation.
◦ CT/CTA oers the best anatomic delineation of aortic
dissection from the arch to the pelvis and accurately
shows dissection aps, true and false lumens, and organ
perfusion and rupture.
◦ Conventional angiography provides excellent
demonstration of branch vessel perfusion by the
true and false lumen and is reserved for guidance
of endovascular treatment, surgical planning, or
evaluation and treatment of complications.
• Treatment options:
◦ Type A is treated surgically and emergently to prevent
propagation to the aortic root with rupture, pericardial
tamponade, or coronary artery obstruction. Options
include fenestration, open aortic grafts, and stent grafts.
◦ Type B is usually treated medically with
antihypertensives and analgesics unless there is
rupture, refractory hypertension, or organ ischemia
(present in this case). Organ ischemia may necessitate
endovascular options such as stents, stent grafts,
intimal fenestration, or some combination of these.
◦ Fenestration is puncturing across the intimal ap and
creating a rent between the false and true lumens to
restore perfusion to excluded organs. Balloon dilatation
of the rent is a common strategy.
◦ Stents and stent grafts can be used to tack down the
intimal ap, revascularize compromised branch vessels,
or seal the proximal entry point of the ap.
Pearls and Pitfalls
ü Stanford classication dictates treatment and has
largely replaced the DeBakey classication.
ü Cystic medial necrosis occurs with aging and connective
tissue diseases such as Marfan’s syndrome. Breakdown
of smooth muscle and connective tissue in the media
predisposes patients to dissection.
Case 69
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A B
■ Clinical Presentation
A 66-year-old man presents to his primary care physician with back pain for 3 months.
■ Further Work-up
C D
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■
Imaging Findings
C, D E
(A) Arterial-phase, contrast-enhanced CT scan shows a large, partially thrombosed aneurysm supplied by the splenic artery. (B) Additional slice shows that the
eerent splenic artery segment is of normal caliber. Therefore, the aneurysm involves the mid-portion of the splenic artery. Images A, B shown on previous
page. (C) Selective celiac arteriography shows the aneurysm to be saccular, with a narrow neck (arr ow). Left gastric branches (arrowhead) are not involved,
although in some cases, these branches can anastomose with splenic artery branches to feed splenic artery pseudoaneurysms. (D) Delayed image shows the
distal splenic artery to be of normal caliber (arrow). (E) The main splenic artery was embolized with coils (arrow) across the neck of the pseudoaneurysm.
■ Dierential Diagnosis
• Splenic artery aneurysm.
■ Essential Facts
• The splenic artery is the most common location for
visceral artery aneurysms and pseudoaneurysms (SAAs:
splenic artery aneurysms) and the second most common
location overall after the aortoiliac artery. They account
for 60% of cases, are more common in women, peak in
the sixth decade of life, and range in size from , 1 cm to
. 8 cm in diameter.
• The most common etiology is pancreatitis. Segmental
arterial mediolysis (SAM) and bromuscular dysplasia
(FMD) may cause aneurysms of the main splenic artery
and segmental branches. Mycotic aneurysms from septic
emboli usually aect peripheral branches and branch
points. Unlike FMD, SAM has a predilection for the celiac
distribution. Other causes of SAAs include Ehlers–Danlos
syndrome type IV, Marfan’s syndrome, pregnancy,
portal hypertension, splenomegaly, and atherosclerosis.
Wegener’s granulomatosis and polyarteritis nodosa can
cause microaneurysms of the visceral arteries.
• Patients are usually asymptomatic (incidentally
discovered SAAs) but may present with pain and
compressive symptoms. Rupture occurs in 2 to 10% of
cases (more common in pregnant women in the third
trimester) with a high rate of mortality (35–90%).
Rupture presents with left upper quadrant pain radiating
to the scapula and hypotension.
• Imaging considerations:
◦ CT scan may show signs of pancreatitis: a round,
enhancing structure on arterial-phase images and a
hematoma lling the lesser sac, suggesting a ruptured
SAA. The combination of rupture into the lesser sac and
peritoneum is called the “double rupture phenomenon”
and is typically catastrophic.
• Treatment options:
◦ Treatment is recommended for large SAAs (. 2 cm),
symptomatic SAAs, or rapidly enlarging SAAs.
Surveillance CT scans every 6 to 12 months are
sometimes recommended with aneurysms , 2 cm,
particularly in older patients (. 60 years of age).
◦ Fusiform or wide-necked SAAs of the main splenic artery
are routinely managed by embolization with coils or
plugs proximal and distal to the aneurysm (back door–
front door) or by surgical ligation at these locations.
Collateral ow reconstitutes the more distal splenic
artery and branches via the short gastric, left gastric,
gastroepiploic, and pancreatic branches, preventing
splenic infarction and abscess in the majority of cases.
◦ Saccular, narrow-necked, or branch artery SAAs may
be treated by packing the aneurysm with coils or
embolizing the feeding branch.
◦ Large aneurysms of the splenic hilum are treated with
splenectomy; distal pancreatectomy may be required if
the body and tail of the pancreas are involved.
◦ Unruptured mycotic aneurysms are treated with
antibiotics prior to embolization.
◦ Intrasplenic aneurysms are treated by coil embolization
of the aected branch(es) or by splenectomy.
◦ Covered stents and ow-diverting stents have been
described, particularly for proximal aneurysms of the
main splenic artery. This segment is less tortuous and
more amenable to stent placement.
Pearls and Pitfalls
ü Mycotic aneurysms tend to occur at branch points and
may result from thromboembolism. The most common
source of peripheral artery thromboembolism is the heart.
ü Pseudoaneurysms are distinguished from aneurysms
by disruption of one or more layers of the arterial
wall. Causes include pancreatitis, peptic ulcer disease,
trauma, and iatrogenic injury.
Case 70
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A B
139
■ Clinical Presentation
A 49-year-old man presents from an outside hospital after placement of a percutaneous biliary drain to relieve obstructing
jaundice associated with back and abdominal pain.
■ Further Work-up
C D
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■
Imaging Findings
C, D
(A, B) Coronal reformatted contrast-enhanced CT images show a large aneurysm or pseudoaneurysm adjacent to the hepatic artery (HA), displacing
the pancreatic head. Low density adjacent to the sac may represent intraluminal thrombus or edema within the pancreatic head. Peripancreatic edema
surrounds the body and tail consistent with pancreatitis. An internal–external biliary drain is in place. Images A, B shown on previous page. (C, D) Conventional aortogram shows the sac (arrows) communicating directly with the HA (arrowhead) at the expected location of the gastroduodenal artery (GDA),
which is not opacied. No neck separates the sac from the HA. (E) The sac was traversed with a 5-Fr catheter to select the more distal GDA (arrow). The
sac is actually a markedly enlarged GDA. (F) The GDA (small arrow) and one of its branches as well as the entire sac (large arrow) were embolized with coils.
■ Dierential Diagnosis
(see below). An additional option is to BD-FD embolize
E, F
the HA across the GDA origin. This can be done
• Gastroduodenal artery (GDA) pseudoaneurysm caused
by pancreatitis resulting in biliary obstruction:
Malignancy causing the pancreatitis cannot be excluded.
without liver failure or infarction if there is adequate
portal venous ow and normal liver function, or
if there is adequate collateral supply to the more
distal HA (e.g., via the left-to-right gastric arteries).
Similarly, aneurysms of the main splenic artery are
■ Essential Facts
commonly treated by BD-FD embolization of the
main splenic artery; adequate perfusion to the
• This case reviews the wide array of treatment options for
visceral artery aneurysms or pseudoaneurysms (PSAs).
• Common etiologies:
◦ Local infection and inammation resulting from
conditions such as pancreatitis or cholecystitis are the
most common etiologies. Pancreatitis can cause true
aneurysms or PSAs, most commonly involving the
splenic, gastroduodenal, and gastroepiploic arteries.
◦ Septic thromboembolic disease most commonly originates
from endocarditis and causes mycotic aneurysms that are
commonly multiple and tend to occur at branch points.
◦ Trauma is a common cause of PSAs. In the abdomen,
hepatic and splenic lacerations are the most common
etiology of traumatic PSAs.
◦ Connective tissue diseases (e.g., Ehlers–Danlos syndrome),
vasculitis (e.g., Takayasu’s arteritis), and noninammatory
vasculopathies (e.g., segmental arterial mediolysis and
bromuscular dysplasia) can cause visceral aneurysms.
◦ Iatrogenic PSAs may be caused by percutaneous or
endoscopic puncture and intervention, by inadvertent
injury during surgery, or as a complication of arterial
anastomosis (e.g., liver transplantation).
• Endovascular treatment techniques for visceral artery
aneurysms and PSAs:
◦ Coil or plug embolization of the inow and outow, also
called back door–front door (BD-FD) embolization:
This option is optimal when there is adequate length
of aerent and eerent artery for placement of the
embolic agent and when the aected artery can be
safely sacriced.
In the presented case, no aerent GDA was present,
necessitating coil embolization of the sac itself
spleen is maintained by the gastroepiploic artery.
◦ Packing coils within the aneurysm:
This option is optimal for saccular aneurysms to
preserve the parent artery. A small neck facilitates
coil packing without coil loss into the parent artery,
as does the newer technology of retractable coils.
Visceral artery PSAs are prone to rupture when over-
packed.
For fusiform or wide-necked aneurysms, this option
is performed when the aected artery can be safely
sacriced.
◦ Stents:
Bare stents can be used in the parent artery of a wide-
neck saccular aneurysm to facilitate packing of the
aneurysm with coils while preventing coil migration.
Stent graft placement can be used to exclude
aneurysms and PSAs, as long as they are adequately
seated proximally and distally (to avoid a type I
endoleak) and as long as no feeding and draining
arteries will continue to perfuse the aneurysm or
PSA after stent graft placement (type II endoleak).
In the latter case, stent grafts can be combined with
coil embolization of the aneurysm.
◦ Percutaneous thrombin injection:
This technique is an option for narrow-neck PSAs.
For large-neck PSAs, the risk of distal embolization
may be too great for thrombin injection. Increments
of 100 IU of thrombin in 0.1 mL of saline are
slowly injected under ultrasound monitoring until
thrombosis is observed, typically requiring a total
of 200 to 750 IU of thrombin. Complications include
distal embolization and allergic reaction to thrombin.
Case 71
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C D
■ Clinical Presentation
A 33-year-old woman presents with chronic pelvic pain and varices of the buttocks and lower extremities.
BA
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