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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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102
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RadCases.thieme.com RadCases Interventional Radiology
■
Imaging Findings
A B C
(A) Ultrasound image of the left axilla shows a large, multicystic, multiseptated structure (arrows). (B) T2-weighted coronal and axial MRI scans show
the same structure (arrows) with diusely intense cystic spaces and hypointense septations. (C) A drain was placed, 40 mL of proteinaceous uid was
aspirated from the cysts (arrow), and 30 mL of doxycycline (10 mg/mL) was infused into the cystic spaces. The catheter was left to suction overnight and
then removed. Axillary swelling resolved and no further treatment was required.
■ Dierential Diagnosis
• Lymphatic malformation (LM): The most likely diagnosis
given the clinical history and the multiseptated, cystic
appearance on ultrasound and MRI scans.
• Vascular malformations may have this appearance: To
rule out this entity, Doppler ultrasound images would
show no ow, and infused MRI scans would show no
enhancement within the cystic spaces.
■ Essential Facts
• LMs are categorized as simple, low-ow vascular
malformations. Other anomalies in this category include
capillary malformations and venous malformations (VMs).
• LMs are lined by a single layer of endothelium and further
classied by the size of their channels. Microcystic LMs
have a network of microscopic channels. Macrocystic LMs
have larger channels and spaces, typically multiseptated.
• LMs contain proteinaceous uid, lymphocytes, and
erythrocytes. Lesions are often mixed and have both
macrocystic and microcystic components.
• Imaging considerations:
◦ Doppler ultrasound is rst-line imaging for distinguishing
macrocystic LMs from VMs. Although both are low-ow
malformations, LMs usually have large, cystic spaces of
dierent sizes, multiple septations, intraluminal debris,
and no discernable intraluminal ow.
◦ MRI can distinguish macrocystic and microcystic LMs
from VMs. Macrocystic LMs have cystic spaces that are
nonenhancing within the lumen, and septations that
may enhance in rings and arcs. No ow voids are visible,
and spaces are hypointense on T1-weighted images and
hyperintense on T2-weighted images. Microcystic LMs
are distinguishable from VMs by their typical lack of
enhancement.
• Treatment considerations:
◦ LMs are candidates for interventional treatment if
they cause signicant deformity, repeated infections,
functional impairment, or pressure-associated tissue loss.
◦ Percutaneous sclerotherapy is rst-line therapy for
macrocystic components of LMs; limited reports
describe its use to treat microcystic LMs.
◦ Other options include laser or radiofrequency ablation
and surgical resection. Limited studies of surgical
resection show high recurrence and complication rates
and poor cosmetic results.
• Percutaneous sclerotherapy:
◦ Individual, dominant cystic spaces are punctured under
ultrasound guidance and injected with contrast to
determine size and intercyst communication. A needle
or a small-caliber catheter can be used; the latter is
useful to facilitate complete drainage prior to injection
of the sclerosing agent.
◦ Agents for LMs include OK-432 (most common),
which is lyophilized powder of Streptococcus pyogenes
incubated with benzylpenicillin, bleomycin, and
doxycycline. Agents used to treat VMs have also been
used successfully for LMs, including ethanol, sodium
tetradecyl sulfate, and polidocanol.
◦ Sclerosing agent is injected to match the volume
removed from the LM, and in some cases, a pigtail
catheter is left to suction larger spaces for a period of
hours to days to facilitate complete obliteration.
◦ Follow-up surveillance with ultrasound is performed
every month, and repeat sclerotherapy is performed
at the time of ultrasound if necessary. MRI may be
necessary to follow up for larger, more extensive LMs.
◦ Clinical success of sclerotherapy for macrocystic LMs
ranges from 75 to 100%.
◦ Almost all complications are minor and include
local pain, blistering, ulceration, and cellulitis.
Major complications are exceedingly rare when
OK-432, bleomycin, and doxycycline are used for LM
sclerotherapy, but they may include airway impairment
(for neck lesions), skin necrosis, and nerve damage.
Pearls and Pitfalls
LMs that occur with Klippel–Trénaunay syndrome often
have components common to that condition, such as
capillary malformations and VMs.
Microcystic LMs may be indistinguishable from
some VMs because both may have a network of
very small channels that appears echogenic with no
detectable ow.
Case 52
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A
■ Clinical Presentation
A 40-year-old woman presents to interventional radiology after a recent hysterectomy complicated by ureteral injury.
B
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■
Imaging Findings
A B C
(A) Percutaneous nephrostomy was performed using a two-stick technique because of the lack of hydronephrosis. First, intravenous contrast (50 mL)
was injected. Then, a lower pole calyx was rapidly accessed under uoroscopic guidance (arrowhead). Continued injection of dilute contrast through that
needle enabled partial distention of the collecting system and subsequent puncture of a second calyx suitable for catheter access (arrow). (B) Antegrade
nephrostogram shows transection of the distal ureter (large arrow) with leakage of contrast and lling of a large collection (small arrows) separate from
the urinary bladder (arrowhead). (C) After placement of a nephroureterostomy catheter for 4 weeks, antegrade nephrostogram shows an intact ureter
without leakage or obstruction.
■ Dierential Diagnosis
• Iatrogenic ureteral injury.
■ Essential Facts
• For most indications, retrograde endourologic access has
replaced percutaneous access as the rst-line therapeutic
or diagnostic option.
• Indications for percutaneous nephrostomy access:
◦ Relief of urinary obstruction
◦ Diagnostic evaluation of the urinary tract
◦ Therapeutic intervention
◦ Urinary diversion
• Urinary diversion:
◦ This is performed to drain urine and facilitate healing of
urinary tract leakage, stulas, and hemorrhagic cystitis.
◦ Retrograde diversion involves cystoscopic placement of
a plastic, double-J retrograde ureteral stent (RUS).
◦ Percutaneous options include nephrostomy (PCN),
nephroureterostomy (PCNU), and cystostomy catheters.
• Ureteral leakage and stulas are treated using RUS as a
rst-line option in most institutions. If RUS fails, is not
feasible, or results in persistent leakage, percutaneous
options are used.
• Ureteral injury:
◦ May be iatrogenic (80%) or traumatic. The majority
of iatrogenic injuries result from hysterectomy, other
surgical procedures, and endourologic procedures.
◦ Early injury diagnosed within a few days of occurrence
is primarily surgically repaired.
◦ Delayed injury is often treated with a RUS. Complete
ureteral transection and large leaks require PCN
placement to divert urine; smaller partial transections
may heal with either RUS, PCN, or PCNU placement.
◦ Percutaneous urinoma drainage serves a dual purpose
to provide both drainage and a means for monitoring
persistent leakage over time.
• Urinary tract stulas are most commonly iatrogenic,
with the majority caused by surgical procedures such
as hysterectomy. Other causes include malignancy,
retroperitoneal and pelvic infection and inammation,
and radiation therapy.
• Ureteral stulas:
◦ Common types include ureterovaginal, ureteroenteric,
and ureterocutaneous stulas.
◦ Treatment is usually RUS placement, but continued
leakage requires PCN placement.
• Vesicular stulas:
◦ Common types include vesicovaginal and
vesicocutaneous stulas.
◦ Benign stulas may heal with bilateral PCN placement.
Antegrade, percutaneous, bilateral balloon occlusion
of both ureters with PCN diversion has been described,
with variable success.
◦ Malignant stulas without a surgical option may
require permanent occlusion of the ureters. The
most common method is coil and Gelfoam packing,
which results in both mechanical and inammatory
obstruction. Lifelong PCNs are required after
ureteral occlusion.
Pearls and Pitfalls
Hemorrhagic cystitis is caused by diuse vascular and
epithelial injury to the bladder due to radiation or
cyclophosphamide therapy. Bilateral PCN placement is
required for diversion when cystoscopic fulguration and
irrigation techniques fail.
Both RUS and percutaneous diversion have been applied
to urinary tract leakage and stulas, but depending on
location, etiology, and local expertise, one option may
be preferred.
Case 53
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A B
■ Clinical Presentation
A 53-year-old man presents with a history of hepaticojejunostomy for biliary obstruction, and he now has increasing
serum bilirubin.
■ Further Work-up
C D
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■
Imaging Findings
A
(A) MR cholangiopancreatography shows diuse beading (arrow) and pruning (arrowhead) of the intrahepatic segmental bile ducts and nonvisualization
of the extrahepatic bile duct. (B) Even with diuse intrahepatic involvement (arrows), percutaneous biliary drainage (PTBD) was attempted to relieve
complete obstruction of the extrahepatic bile duct (arrowhead). This application of PTBD is controversial because it may introduce infection and worsen
obstruction in patients with diuse intrahepatic disease. (C) A biliary brush (arrow) was used to obtain a biopsy sample to exclude malignancy. (D) An
internal–external biliary drain was placed with the distal end (arrow) coiled in the small bowel.
B
■ Dierential Diagnosis
• Primary sclerosing cholangitis (PSC): The most likely
diagnosis, given the diuse intra- and extrahepatic duct
occlusions and irregularity.
• Cholangiocarcinoma may present with common duct
occlusion and diuse intrahepatic duct involvement:
Biopsy was performed in this case to rule out malignancy.
• Ascending cholangitis may mimic or be caused by primary
sclerosing cholangitis: This entity typically occurs due to
more distal duct obstruction.
• AIDS-related cholangitis and/or cytomegalovirus infection:
Can cause cholangiopathy identical to PSC.
■ Essential Facts
• PSC is a progressive biliary disease of unknown etiology
(possibly autoimmune) causing cholestasis. More
common in males (2:1), PSC may occur in children, but
onset is more typically at 30 to 40 years of age.
• Pathophysiology is unclear, but autoimmune, genetic,
and infectious etiologies have been postulated.
• Associations include inammatory bowel disease
(ulcerative colitis [UC] Crohn’s); 70% of patients with
PSC have UC, and 4% of patients with UC have PSC.
• Clinical presentation ranges from nonspecic fever, pruritus,
pain, and weight loss; to signs and symptoms of biliary
obstruction; to cirrhosis with portal hypertension; to liver
failure. Gray stools and dark urine may result from renal,
rather than gastrointestinal, excretion of conjugated bilirubin.
• Cholangiography via endoscopic retrograde
cholangiopancreatography (ERCP), MR
cholangiopancreatography (MRCP), or percutaneous
cholangiography shows bile duct irregularity with
diuse foci of annular narrowing and dilation, producing
a beaded and pruned appearance. Both intra- and
extrahepatic ducts may be aected. May progress to
involve segmental and hilar bile ducts. ERCP and MRCP
are the rst-line and least invasive tests.
C
• CT scan or ultrasound image may show hepatomegaly and
biliary obstruction in acute and subacute cases, or cirrhosis,
splenomegaly, ascites, and varices in chronic cases.
• Biopsy (percutaneous or transjugular) of the liver often
results in nonspecic ndings but may exclude other
causes of biliary obstruction such as cholangiocarcinoma.
• Treatment options:
◦ Medical therapy has not been shown to prevent
disease progression. Choleretic agents (bile acids) may
reduce cholestasis.
◦ Percutaneous or endoscopic balloon dilatation may buy
time to liver transplantation for focal intrahepatic or
extrahepatic PSC.
◦ Endoscopic plastic stent placement or percutaneous
biliary drainage (PTBD) is an option for extrahepatic as
well as single dominant intrahepatic strictures.
◦ For diuse, predominantly intrahepatic PSC, PTBD is
often ineective and may actually worsen symptoms of
biliary obstruction.
◦ A transjugular intrahepatic portosystemic shunt
procedure may become necessary for cirrhosis-related
portal hypertension and/or refractory ascites.
◦ For extrahepatic strictures, surgical
choledochoenterostomy or liver transplantation may
become necessary for end-stage liver disease.
ü Pearls and û Pitfalls
8û Ascending cholangitis may occur as a repeated
complication of biliary obstruction due to PSC.
8û Cholangiocarcinoma occurs in 10 to 15% of patients
with PSC.
8û Diuse involvement of segmental and hilar ducts limits
the utility of focused treatment by balloon dilatation,
drain placement, or plastic stent placement. Attempts
at these interventions may result in systemic spread
of infection while exacerbating rather than alleviating
duct obstruction. Such cases typically require liver
transplantation.
D
Case 54
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A
■ Clinical Presentation
A 65-year-old man presents with a history of intermittent abdominal pain. He is afebrile without leukocytosis.
■ Further Work-up
B
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■
Imaging Findings
A B
(A) Sagittal, arterial-phase, contrast-enhanced CT scan shows a saccular outpouching of the celiac artery (arrow). (B) A selected superior mesenteric
arteriogram shows multiple aneurysms aecting primary branches (arrows) and diuse ectasia of the superior mesenteric artery.
■ Dierential Diagnosis
• Segmental arterial mediolysis (SAM): Indicated by
predominantly celiac branch involvement.
• Mycotic pseudoaneurysms: Typically saccular and
multifocal.
• Vasculitis such as giant cell or Takayasu’s arteritis: May
present with aneurysms, but more commonly presents
with involvement of the aorta and primary artery ostia.
• Ehlers–Danlos syndrome and other collagen vascular
diseases: Can present with vascular ectasia and
aneurysms.
■ Essential Facts
• SAM is a rare disorder, usually aecting the elderly, that
is fatal in . 50% of patients in the acute phase.
• SAM has a predilection for the celiac artery distribution
but also occurs in the superior and inferior mesenteric
arteries and in the renal arteries.
• Patients present with abdominal pain from dissection
or thrombosis with bowel ischemia; hypotension,
distension, or anemia may occur from gastrointestinal or
peritoneal hemorrhage.
• In the acute phase, SAM results in deposition of brin
and collagen in the media without inammatory
inltrate; in the late phase, there is reparative remodeling
of the vessel wall.
• Angiography (CT angiography, MR angiography, or
conventional) during the acute phase of SAM shows
segments of arterial dilation, narrowing, and beading.
Occlusion may result from thrombosis, dissection, or
stricture. Aneurysms may rupture or erode into adjacent
structures such as bile ducts, bowel, or peritoneum.
Imaging in the late phase of SAM (delayed 6 months)
shows resolution of beading and dilation, often leaving a
smooth arterial wall.
• Treatment considerations:
◦ Mild or asymptomatic (incidentally discovered)
cases may be followed clinically to the late phase,
occasionally with serial imaging studies.
◦ Coil embolization is recommended for large aneurysms
to prevent rupture and for aneurysms complicated by
pain, hemorrhage, or thromboembolism.
◦ Saccular aneurysms are usually amenable to
embolization, but fusiform aneurysms may require
ligation and bypass, although stent grafts may play an
increasing role in such cases.
◦ Surgical bypass or thrombectomy is considered second-
line treatment when endovascular options fail or are
not feasible.
Pearls and Pitfalls
Unlike bromuscular dysplasia, which also aects
the mesenteric arteries, SAM has a predilection for
the celiac distribution, occurs in an older population,
has a high mortality rate from aneurysmal rupture
and bowel ischemia, undergoes spontaneous
repair and remodeling, and is typically not treated
with angioplasty.
Unlike vasculitis, SAM is not associated with
inammatory inltration and does not respond to
steroids and immunosuppressants.
Unlike mycotic aneurysms, aneurysms of SAM are not
typically associated with arterial branch points.
Case 55
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A
■ Clinical Presentation
A 40-year-old woman with a history of a Whipple procedure complicated by abdominal abscess presents with elevated liver
function tests.
■ Further Work-up
B C
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■
Imaging Findings
A DB, C
(A) Coronal reformatted, venous-phase, contrast-enhanced CT scan shows portal vein thrombosis (arrow) and early venous collateralization. (B) From a
transhepatic approach, portal venography shows stasis of ow and a large thrombus (arrow). (C) After suction thrombectomy (right), venography shows
restoration of ow in the main portal vein (arrow) and its branches. (D) The transhepatic sheath was removed and the tract was embolized with coils (arrow).
■ Dierential Diagnosis
• Portal vein thrombosis.
■ Essential Facts
• Portal vein thrombosis (PVT) may be neoplastic (tumor
thrombus) or non-neoplastic. Non-neoplastic causes
include cirrhosis; prior abdominal surgery such as
liver transplantation; abdominal infections such as
diverticulitis, peritonitis, or appendicitis; abdominal
inammatory conditions such as Crohn’s disease; and
hypercoagulable states.
• Clinical presentation ranges from asymptomatic to fevers,
nausea, vomiting, and gastrointestinal bleeding to lactic
acidosis, peritonitis, and sepsis. Presentation varies with
variations in multiple pathophysiologic factors:
◦ The extent and rate of progression. Extension into the
superior mesenteric vein may result in mesenteric
ischemia indicated by serum lactic acidosis and
abdominal pain. Extension into the splenic vein
may result in bleeding, isolated gastric varices, and
splenomegaly.
◦ The presence of spontaneous recanalization and
the rate of compensatory venous collateralization.
Collaterals develop over a period of weeks to months.
◦ The presence of a mechanical obstruction (e.g.,
compression by tumor or anastomotic obstruction).
• Treatment options depend on etiology and
clinical presentation:
◦ Anticoagulation reduces symptoms and induces
recanalization in many patients with mild-to-moderate
symptoms and no mechanical obstruction.
◦ Catheter-directed venous thrombolysis (CDT)
and thrombectomy from either a transhepatic or
transjugular approach are options for persistent or
progressive PVT or when endovascular recanalization of
a mechanical obstruction is required.
◦ Mesenteric arterial thrombolysis is adjunctive to CDT
for cases involving the most proximal mesenteric veins.
◦ Surgical laparotomy with revascularization and possible
bowel resection is indicated when progression toward
intestinal ischemia is rapid or intestinal necrosis is
suspected.
Pearls and Pitfalls
PVT related to liver transplantation (LT):
PVT does not preclude LT but may complicate LT and
reduce graft survival.
Early PVT (, 30 days after LT) results in graft loss;
delayed PVT results in a high rate of graft loss.
Attempts at endovascular or surgical
revascularization are usually warranted because
potential pathways for collateralization have
been largely sacriced. In addition, portal venous
angioplasty, stent placement, or surgical revision is
typically indicated.
PVT related to cirrhosis:
Recanalization is often performed to maintain
or improve candidacy for LT and to prevent or
ameliorate the exacerbation of symptoms related to
portal hypertension.
Complete PVT is a contraindication to balloon-
occluded retrograde transvenous obliteration
(BRTO) in patients with isolated gastric varices,
because BRTO may result in mesenteric venous
ischemia in this setting.
Partial acute PVT may improve after BRTO because of
improved ow.
Transjugular intrahepatic portosystemic shunt
may prevent recurrence in acute cases and may
preserve candidacy for LT in both acute and chronic
cases.
Case 56
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A B
111
C D
■ Clinical Presentation
A 58-year-old woman presents to the interventional radiology clinic with an enlarging mass in the left groin.
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