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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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162
https://t.me/med1917
RadCases.thieme.com RadCases Interventional Radiology
■
Imaging Findings
A
(A) Selective left renal angiogram shows a large pseudoaneurysm (arrowhead) and rapid shunting from the renal artery (large arrow) to the renal vein
(small arrow). (B) Successful coil (arrows) embolization of arterial branches supplying the pseudoaneurysm and the arteriovenous stula.
■ Dierential Diagnosis
• Acquired renal arteriovenous stula: Suspected because
of the involvement of only a few arterial branches, the
presence of a pseudoaneurysm, and a history of diabetic
nephropathy that most likely required percutaneous
biopsy.
• Congenital renal arteriovenous malformation: Often
involves multiple small arteriovenous communications.
■ Essential Facts
• Renal arteriovenous shunts may be congenital (rare) or
acquired and are caused by abnormal communication of
intrarenal (lobar or interlobar) arteries and veins.
• Congenital renal arteriovenous shunts are usually
arteriovenous malformations (AVMs), distinguishable by
the presence of multiple arteriovenous communications.
Types include:
◦ Cirsoid: multiple coiled, tortuous channels that form a
“mass”
◦ Cavernous: single artery to single vein, interposed by a
dilated cavernous vessel
• Acquired renal arteriovenous shunts are usually
arteriovenous stulas (AVFs) distinguishable by only a
few arteriovenous communications.
• AVFs usually result from trauma, from iatrogenic causes
such as percutaneous renal biopsy or nephrostomy, or
from malignancy. Arteriovenous shunting is common
within malignant tumors such as renal cell carcinoma, but
it is uncommon in the setting of benign renal tumors. AVFs
may be idiopathic and/or associated with renal aneurysms.
• Clinical presentation may include gross hematuria
(most common), pain (ischemic), hypertension (reninangiotensin mediated), and high-output cardiac failure. A
bruit may be detected. Congenital AVMs are more likely
than acquired AVFs to be symptomatic.
• Imaging options:
◦ Imaging studies may show the arteriovenous
communications, early draining veins, and
complications such as vascular thrombosis, infarction,
hemorrhage, and blood clot within the renal collecting
system.
◦ Ultrasound may show turbulent ow within enlarged
vessels upon Doppler interrogation, and large high-ow
vessels are seen on color Doppler.
◦ Multidetector CT and MR angiographic studies can be
performed using dynamic renal protocols in which
noncontrast imaging is followed by multiple, sequential
contrast-enhanced scans through the level of the
kidney.
• Treatment options:
◦ Embolization (rst line) using coils or microcoils.
Typically, only one or two arterial feeders are identied
and treated in the case of AVFs.
◦ Catheter-directed alcohol sclerosis with concurrent
balloon occlusion of the feeding artery. These options
may become necessary for congenital AVMs when
multiple arteriovenous communications are present.
◦ Nephrectomy (partial or complete) for large AVMs or
after technical failure of embolization for AVFs.
Pearls and Pitfalls
AVFs may be associated with pseudoaneurysms. Coil
embolization treats both entities.
A total of 15% of renal biopsies result in arteriovenous
communication, most of which resolve spontaneously.
Angiography immediately after biopsy may reveal
one of these transient AVFs and lead to unnecessary
treatment.
Complications of endovascular treatment methods
include nontarget embolization or sclerosis, infarction,
renal failure, contrast reaction, and arterial injury.
Renal function should be assessed prior to diagnostic
and therapeutic options to avoid:
Renal failure due to excessive use of iodinated
contrast material.
Renal failure due to coil embolization or surgical
excision of excessive parenchymal distributions.
B
Case 82
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A B
■ Clinical Presentation
A 38-year-old woman presents with hypertension that is increasingly refractory to medical management.
C
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RadCases.thieme.com RadCases Interventional Radiology
■
Imaging Findings
A B
(A, B) MR angiographic images show narrowing of the distal thoracic aorta (large arrow), ectasia of the proximal abdominal aorta, fusiform carotid artery
aneurysm (small arrow), and possible narrowing of the proximal celiac artery (arrowhead). (C) Posterior aortic CT angiographic image shows critical steno-
sis of the bifurcation of the right renal artery aecting both the anterior and posterior divisions (arrowhead). (D) Angioplasty was performed, but delayed
arterial occlusion resulted in renal atrophy and calcication (arrowhead).
■ Dierential Diagnosis
• Takayasu’s arteritis: Indicated by the appearance of the
aorta and the involvement of its major branches.
• Giant cell arteritis: Can aect the aorta and its major
branches but typically aects older individuals.
■ Essential Facts
• Takayasu’s arteritis (TA) is a chronic, slowly progressive,
cell-mediated inammatory vasculitis that most
commonly aects the aorta, its major branches, and the
pulmonary arteries. Incidence is 6 in 1,000 worldwide.
• TA presents in all ages and ethnicities but is most common
in women (80% of cases) under 30 years of age, more
common in Sephardic Jews, and uncommon in Caucasians.
• Early (acute, active phase) TA is the active inammatory
condition presenting with fever, pain, fatigue, bruit, and
hypertension.
• Late (chronic, “burned-out”) TA results from symptoms
of arterial obstruction such as pulseless brachial arteries,
stroke from carotid involvement, and hypertension from
renal artery stenosis.
• Vascular manifestations include stenosis, occlusion, ectasia,
and frank aneurysm formation. The subclavian arteries (left
greater than right) are the most commonly aected aortic
branches, but involvement of any primary branch from
the brachiocephalic artery to the iliac arteries has been
described, as well as involvement of the pulmonary arteries.
• Renal involvement is common—usually ostial bilateral
stenosis associated with adjacent aortic stenosis.
• CT angiography and MR angiography are standard for
diagnosis and follow-up and should be performed with and
without contrast. Active-phase TA may show thickening and
high density of the aortic wall on the precontrast images,
enhancement in the postcontrast arterial and venous
phases, and a low attenuation ring in the arterial wall in the
venous phase. “Burned-out” TA may show smooth fusiform
stenosis, occlusion, or dilation (moderate to aneurysmal).
• Treatment considerations:
◦ Medical management of the active phase includes
steroids and immunosuppressant therapy.
◦ Revascularization options are reserved for
posttreatment “burned out” TA when acute
inammation has largely subsided and the erythrocyte
sedimentation rate has normalized.
◦ Endovascular options include angioplasty and stent
placement.
◦ Surgical options include open vascular bypass and
patch angioplasty. Delayed complications are common
(20–40%) and include anastomotic occlusion and
aneurysm formation.
• General renal angioplasty considerations:
◦ Blood pressure is strictly controlled before and during
the procedure.
◦ Low-dose aspirin (, 150 mg/d) is often initiated before
angioplasty and maintained for life.
◦ Clopidogrel (75 mg orally) is given pre-procedure if stent
placement is anticipated and is continued for 3 months.
◦ Heparin (100 IU/kg) is administered during the procedure.
◦ Antihypertensive medications are withheld for 24 hours
after the procedure.
◦ Femoral, radial, or brachial artery puncture can be used
for access.
◦ Nitroglycerin (100–200 mg intra-arterial) or nifedipine
(5–10 mg sublingual) is administered for vasospasm.
◦ A balloon that approximates the normal diameter of the
renal artery is inated up to three times.
◦ Balloon-expandable stents are placed if indicated.
Pearls and Pitfalls
Success:
Angiographic: , 30% residual stenosis, increase
Clinical: Cure if normal blood pressure (BP) without
Cumulative 5-year patency is 67%, and the need for
dissection, rupture, and access site complications.
C
in lumen diameter of . 50%, residual pressure
gradient , 20 mm Hg with a reduction of at least
15 mm Hg from initial.
medications, improved if . 15% reduction of
diastolic BP or a diastolic BP , 90 mm Hg on
medication, or failed if no improvement in BP.
reintervention is common.
D
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C D
■ Clinical Presentation
A 40-year-old woman presents with a long history of sharp, right-upper-quadrant abdominal pain.
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■
Imaging Findings
A B D E
(A) Intermediate-phase contrast-enhanced CT image shows a well-circumscribed, homogeneous, hypodense liver lesion (arrow) with early peripheral
enhancement aecting segments 6 and 7. (B) Conventional proper hepatic arteriogram shows patchy peripheral enhancement of the lesion (arrows).
Hypertrophy of the segmental artery is noted (arrowhead). (C) Early-phase (shown on prior page) and late-phase (D) images show progressive, diuse
central pools and lakes of contrast pathognomonic for hemangioma (arrow). (E) Proper hepatic arteriogram after embolization shows no early enhance-
ment of the hemangioma and cessation of ow in the hypertrophied segmental artery (arrowhead).
■ Dierential Diagnosis
• Hemangioma: The only diagnosis required, given the
early peripheral enhancement on the contrast-enhanced
CT image, and gradual peripheral to central enhancement
from arterial- to venous-phase imaging on conventional
angiography.
■ Essential Facts
• Hemangiomas are benign networks of multiple
endothelial-lined vascular channels with increased cellular
turnover. They are the most common primary liver tumor
and the most common focal liver lesion after simple cysts.
They occur in up to 20% of people, are more common in
females, and represent 70% of benign liver tumors.
• Hemangiomas are classied as vascular tumors as
opposed to vascular malformations (International
Society for the Study of Vascular Anomalies). Other
vascular tumors include tufted angioma, kaposiform
hemangioendothelioma, hemangiopericytoma, pyogenic
granuloma, and spindle-cell hemangioendothelioma.
• Congenital hemangiomas are classied as either
rapidly involuting congenital hemangiomas (RICH) or
noninvoluting congenital hemangioma (NICH), presented
in this case.
• NICHs are usually asymptomatic and uncomplicated,
incidentally discovered on imaging studies, and remain
stable in size on subsequent imaging studies.
• Imaging ndings:
◦ Findings on contrast-enhanced cross-sectional
imaging studies and conventional angiograms are
pathognomonic and include progressive enhancement
from the periphery to the center of the lesion.
◦ Contrast pools in focal regions of the hemangioma in
the intermediate phases of enhancement.
◦ Washout of contrast is slow.
• Complications of hemangiomas include persistent pain,
rupture, compression of adjacent structures such as
bowel and blood vessels, high-output cardiac failure, and
Kasabach–Merritt syndrome (KMS).
• KMS occurs when large hemangiomas (anywhere in
the body) cause thrombocytopenia and a consumptive
coagulopathy. Mortality rate is 10 to 15%.
• Treatment options for symptomatic or complicated
hemangiomas:
◦ Medical therapy with monoclonal antibody and
chemotherapy
◦ Surgical resection (usually the rst-line intervention)
◦ Radiofrequency ablation
◦ Transarterial embolization (TAE):
Literature on nonsurgical management of
hemangiomas is limited, but TAE has been used
both as a method to devascularize prior to surgical
resection and as a primary treatment.
Embolization of the arterial supply is the most common
approach, although more aggressive combined arterial
and venous embolization has been described. Liquid
embolic agents, particles, and coils have been used.
Symptom relief and tumor shrinkage persisting at
6 and 12 months has been reported in some studies,
whereas others report minimal or no shrinkage.
Complications of TAE include postembolization
syndrome (pain, nausea, fever, hypertension,
leukocytosis, elevated liver function tests), liver abscess,
sepsis, renal failure, and nontarget organ injury.
Pearls and Pitfalls
Symptoms and complications, rather than size and
imaging appearance, determine the indication for
treatment, although some literature suggests that giant
(. 10 cm) hemangiomas may become complicated
more frequently.
Smaller hemangiomas may be dicult to characterize
by contrast-enhanced cross-sectional imaging. In
such cases, consider lesions such as focal nodular
hyperplasia, adenoma, and even hepatoma.
Case 84
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A
B C
■ Clinical Presentation
A 52-year-old man presents with painless jaundice, weight loss, and lethargy.
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■
Imaging Findings
A D, EB, C
(A) Venous-phase contrast-enhanced CT image shows a hilar mass (arrow) with mild enhancement relative to liver parenchyma. Right and left intrahepatic
biliary dilatation is noted. (B) MR cholangiopancreatography shows bilateral biliary dilatation caused by obstruction of the right and left intrahepatic
ducts and proximal common bile duct (arrow). (C) Percutaneous cholangiogram veries bilateral partial hilar obstruction (arrow). (D) Temporary left-
sided internal–external biliary drain (arrow) was placed after bile duct biopsy. Biopsy revealed cholangiocarcinoma. (E) Permanent metal stent placement
(arrow) drains both right and left intrahepatic bile ducts. The internal–external drainage catheter was not replaced.
■ Dierential Diagnosis
• Malignant biliary obstruction: Caused by hilar
cholangiocarcinoma. Other neoplasms can mimic a
Klatskin tumor such as lymphoma, hepatocellular
carcinoma, and metastasis.
• Benign biliary obstruction: Unlikely, given the history, but
may be caused by inammatory or infectious etiologies
such as primary sclerosing cholangitis, ascending
cholangitis, stones, or sludge.
■ Essential Facts
• Malignant biliary obstruction results from pancreatic
adenocarcinoma (most commonly), cholangiocarcinoma,
gallbladder carcinoma, hepatocellular carcinoma,
lymphoma, and metastasis.
• Clinical presentation is painless jaundice, pruritus,
dark urine (bilirubin content), weight loss, nausea,
and vomiting. Fever and leukocytosis from infectious
cholangitis are uncommon.
• Imaging considerations:
◦ Imaging characterizes strictures, guides tissue
sampling, and stages malignancy.
◦ MR cholangiopancreatography (MRCP) and endoscopic
retrograde cholangiopancreatography (ERCP) are rstline for diagnosis and have similar sensitivity rates.
◦ ERCP is more invasive but provides access for tissue
acquisition and treatment.
◦ Percutaneous transhepatic cholangiography (PTC)
is second-line in most cases to avoid complications
of transhepatic access and external catheters. Brush
cytology, forceps biopsy, and core biopsy improve the
sensitivity of ERCP and PTC.
◦ CT and MRI are used to stage disease by detecting
distant metastases and invasion of regional vessels.
• Treatment considerations:
◦ Medical therapy is considered rst, depending on primary
malignancy. For example, obstruction by lymphoma may
resolve with treatment, so temporary endoscopic biliary
drainage (EBD), percutaneous biliary drainage (PTBD), or
retrievable covered stents may be better than permanent
self-expanding metal stents (SEMS).
◦ Curative resection is considered next but is rarely an
option because of advanced stage at presentation.
◦ EBD or PTBD via plastic catheters and stents is indicated
for biliary obstruction complicated by infection.
◦ PTBD is used only if EBD fails or is infeasible (e.g.,
Roux-en-Y), but additional exceptions exist. PTBD is
used for permanent biliary drainage when SEMS or
internal plastic stents fail or are infeasible and for
patients with hilar or segmental obstruction.
◦ EBD or PTBD via SEMS improves outcomes over plastic
stents for permanent relief of malignant obstruction.
◦ SEMS result in patency (150–250 days) that closely
matches survival for biliary and pancreatic cancer.
◦ To prevent tumor overgrowth, covered SEMS have
improved long-term patency in some studies, but there
is added cost and complications (stent migration).
Pearls and Pitfalls
Success rates of EBD and PTBD are comparable, but
recently, success and applicability of EBD have increased
because of endoscopic ultrasound–guided sharp
puncture techniques that bypass the obstructed papilla.
Contraindications to PTBD are relative and include
coagulopathy and ascites.
Preoperative EBD or PTBD for resection candidates is
controversial because increased postoperative infection
rates occurred in some studies.
Complication rates of EBD and PTBD are comparable.
Major complications of ERCP/EBD include
pancreatitis (5–15%), gastrointestinal perforation,
sepsis, and hemorrhage from sphincterotomy and
endoscopic ultrasound–guided sharp puncture.
Major complications of PTC/PTBD (4–7%) include
sepsis, cholangitis, cholecystitis, pancreatitis, pleural
transgression, tumor seeding, and hemorrhage.
Complications of SEMS include cholangitis,
cholecystitis, pancreatitis, migration, and obstruction.
Case 85
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A
■ Clinical Presentation
A 2-year-old girl presents to the emergency department after a motor vehicle accident with hypotension and tachycardia
refractory to aggressive medical management. She is referred to interventional radiology.
■ Further Work-up
B
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■
Imaging Findings
A B C
(A) Contrast-enhanced CT scan shows a grade V liver laceration transecting the right lobe accompanied by a large hematoma (arrow). The laceration
involves the segmental vessels. (B) Selected right hepatic arteriogram shows extravasation (arrow) from multiple segmental branches. The right hepatic
artery originates from the superior mesenteric artery. (C) Aortogram shows successful coil embolization of the right hepatic artery (arrow). The left hepatic
artery (arrowhead) originates from the left gastric artery and remains patent without extravasation.
■ Dierential Diagnosis
• Traumatic hepatic laceration.
■ Essential Facts
• Traumatic hepatic laceration occurs during blunt injury
to the abdomen and is graded I to VI (see abbreviated
descriptions below):
I. , 1 cm parenchymal depth
II. 1 to 3 cm parenchymal depth
III. . 3 cm parenchymal depth
IV. 25 to 75% of hepatic lobe or 1 to 3 Couinaud
segments within a single lobe
V. . 75% of hepatic lobe or . 3 Couinaud segments
within a single lobe and/or juxtavenous hepatic
injuries (retrohepatic caval or hepatic venous
avulsion)
VI. Hepatic avulsion
• Imaging work-up:
◦ Stable patients undergo contrast-enhanced CT. CT/CT
angiography images show the grade and location of
laceration, associated injuries, injured vessels, active
extravasation, and the type of vessel injury.
◦ Conventional angiography is performed with the
intent to embolize and may show active extravasation,
pseudoaneurysm, arterial transection or dissection,
arterioportal stula, arterial spasm, or thrombosis.
• Treatment depends on the presentation and hospital
course.
◦ Medical management is rst-line for stable patients:
intravenous uids, blood products, and vasopressors.
◦ Transarterial embolization (TAE) is considered before
surgery for stable patients with evidence of continued
blood loss despite medical management, patients with
active extravasation, or patients with an arterial defect
such as a pseudoaneurysm or arterioportal stula.
Oxygen supply from the portal system minimizes the
risk of necrosis from TAE. After successful TAE, surgery
is usually unnecessary.
◦ Exploratory laparotomy involves sudden release of
the protective eects of abdominal tamponade and
is reserved for cases refractory to TAE and for cases
presenting with profound hypotension refractory to
uid resuscitation. Profound hypotension may indicate
bleeding from a source not amenable to TAE, such as
a ruptured or avulsed inferior vena cava, hepatic vein,
or portal vein. Repair with a covered stent has been
described, but emergent exploratory laparotomy is
usually indicated.
• Embolic agent used for TAE in these cases varies with the
underlying injury.
◦ Diuse bleeding resulting from a high-grade liver
laceration is often treated by injection of large-sized
particles (Gelfoam, polyvinyl alcohol, or trisacryl gel
spheres) into multiple arterial distributions.
◦ Focal bleeding sources such as arteriovenous stulas
and pseudoaneurysms are usually treated with coil
embolization.
◦ Injury to a large arterial branch may be treated with
coils, a combination of coils and Gelfoam, or covered
stent placement.
Pearls and Pitfalls
High-grade (IV or V) liver lacerations refractory
to medical management are best treated with
endovascular options rather than surgery in stable
patients.
Case 86
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A, B C
171
D E
■ Clinical Presentation
A 37-year-old woman presents with persistent pelvic pain 3 months after surgery at an outside hospital.
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