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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3676_Библиотеки_им_академика_М_И_Перельмана
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C. Brown and C.S. White
a
bc
de
Fig. 11.18 (a) cMPR. Type A aortic dissection (long
arrow) extending proximally to the aortic root and adja-
cent to the ostium of the left main coronary artery (LM).
Metal artifact from bioprosthetic aortic valve (arrow-
head). TL true lumen, FL false lumen. (b) Volume render-
ing. The false lumen (FL) has lower intensity on volume
rendered 3D reconstruction. A felt strip (short arrow) has
been placed in the proximal aorta to reinforce the suture
lines related to the previous aortic valve replacement. (c–
e) Axials and coronal: Type A aortic dissection—
Contributed by J. Lee and C. Smuclovisky
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11.18 Case 11.17 Contributed by
Lee and C. Smuclovisky
J.
11.18.1 History
An 82-year-old male presented with a history of
chronic myocardial infarct (MI), CABG, and aortic aneurysm repair.
11.18.2 Findings
There is a large chronic transmural MI involving
the anteroseptal and apical segments of the left
ventricle. The status was post CABG and ascending aortic aneurysm repair (Fig. 11.19a–c).
11.18.3 Diagnosis
The diagnosis is chronic transmural left ventricular MI.
11.18.4 Discussion
and subendocardial scarrings are visualized. The
typical appearance of a transmural MI is thinning
of the wall with low density from the scar. The
scar may also contain calcification. Functional
CTA demonstrates hypokinesis or akinesis in
area of the MI. Subendocardial scars are identified as areas of low density in the subendocardial
wall.
Transmural MI may develop aneurysmal dilatation, which may lead to a thrombus formation
in the left ventricle (Fig. 11.19d, e). Rupture of
the LV wall is most commonly fatal, and if the
patient survives, can occasionally lead to formation of a pseudoaneurysm.
11.18.5 Pearls and Pitfalls
Normal left ventricular apical thinning may
mimic an infarct. Normal LV systolic function with thickening in the apical segment
and lack of significant disease in the LAD is
helpful in substantiating the conclusion of a
normal variant.
Chronic myocardial infarcts of the left ventricle
are well identified with CTA. Both transmural
ab
Fig. 11.19 (a) Volume rendering. Large anteroseptal and
apical MI (arrows). Status post CABG and ascending aortic aneurysm repair. (b and c) Axial, sagittal. Transmural
MI. Thinning and low density throughout the scar
(arrows). Focal calcification in the infarcted wall (arrow-
head). (d and e) Oblique sagittal and axial. LV aneurysm
containing thrombus in another patient (arrow)
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C. Brown and C.S. White
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Fig. 11.19 (continued)
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11.19 Case 11.18 Contributed by
Lee and C. Smuclovisky
J.
11.19.1 History
A 51-year-old female presented with a history of
a dilated cardiomyopathy and previous surgery
for mitral and tricuspid insufficiency.
11.19.2 Findings
There are hyperdense C-shaped rings in the
mitral and tricuspid annuli (Fig. 11.20a–c).
11.19.3 Diagnosis
The diagnosis is surgical mitral and tricuspid
repair with Cosgrove-Edwards (CE) annuloplasty
rings.
11.19.4 Discussion
The patient had viral myocarditis in the previous
2 years with subsequent development of a dilated
cardiomyopathy that was complicated by severe
mitral and tricuspid regurgitation. Since she was
not a candidate for heart transplant, surgical
repair of the valves was performed. Diseased cardiac valves may be replaced or repaired. The CE
annuloplasty rings are commonly used to repair
the mitral and also tricuspid valves.
11.19.5 Pearls and Pitfalls
On CTA, the CE appears as a thin hyperdense
C-shaped band in the annulus.
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C. Brown and C.S. White
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de
bc
f
Cosgrove-Edwards
annuloplasty ring
Carpentier-McCarthy-Adams
IMR ETlogix
mitral annuloplasty ring
g
GeoForm
mitral annuloplasty ring
j
Myxo ETlogix
mitral annuloplasty ring
Fig. 11.20 (a) Coronal. Cosgrove-Edwards (CE) annulo-
plasty ring in the mitral annulus (arrow). (b) Sagittal. CE
annuloplasty ring in the tricuspid annulus (arrow). (c)
Axial. Partial visualization of the CE rings in the mitral
Carpentier-Edwards Classic
mitral annuloplasty ring
Carpentier-Edwards Physio
mitral annuloplasty ring
and tricuspid annuli (arrows). (d–j) Surgical diagram and
six different surgical devices used for valve repair (d–j,
courtesy of Edwards Life sciences, Irvine, CA)
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11.20 Case 11.19
11.20.1 History
A 62-year-old female presented to the emergency
department with substernal chest pain and shortness of breath.
11.20.2 Findings
There is a well-circumscribed hypodense hepatic
lesion that measures 7 cm. The lesion demonstrates
peripheral nodular enhancement (Fig. 11.21).
11.20.3 Diagnosis
Hepatic hemangioma.
11.20.4 Discussion
Hepatic masses in adults have a broad differential
diagnosis of both benign and malignant diseases.
Common benign etiologies include hepatic hemangioma (also called cavernous hemangiomas),
focal nodular hyperplasia (FNH), hepatic adenoma, and idiopathic noncirrhotic portal hypertension. Malignant etiologies include hepatocellular
carcinoma, cholangiocarcinoma, and metastatic
disease. Parasitic infections and abscesses are less
common etiologies. These lesions can often be
diagnosed noninvasively by the presence of characteristic imaging features in conjunction with the
patient’s history and risk factors.
Hepatic hemangiomas are the most common
benign hepatic tumor and have been estimated to
occur in up to 20% of the population. They are
more common in females by a 3:1 ratio. These
lesions can be solitary or present in multiple
lobes of the liver. Most patients are asymptomatic, but lesions larger than 4 cm may cause
abdominal pain, nausea, or early satiety due to
mass effect. Rarely, hemorrhage or thrombosis
within the tumor can cause acute right upper
quadrant pain.
On contrast-enhanced CT imaging, hepatic
hemangiomas have early peripheral nodular
enhancement and delayed filling in a centripetal
pattern. Imaging is usually sufficient for diagnosis. Biopsy of this lesion carries risk of hemorrhage and is not usually necessary for confirmation
of the diagnosis.
Fig. 11.21 Axial. Soft tissue windows show a large
hypodense mass (large arrow) with peripheral nodular
enhancement (short arrow)
11.20.5 Pearls and Pitfalls
MRI and ultrasound can be used to assist in distinguishing hepatic hemangiomas from more
serious conditions such as metastatic disease.
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11.21 Case 11.20
11.21.1 History
An 84-year-old male underwent imaging to
assess his coronary arteries. His history is significant prior coronary artery bypass graft for left
anterior artery (LAD) disease.
11.21.2 Findings
There is a well-circumscribed 2 cm lesion in the
right adrenal gland. The density is somewhat
lower than that of soft tissue (Fig. 11.22).
11.21.3 Diagnosis
Adrenal adenoma.
11.21.4 Discussion
Adrenal adenomas are common findings with use
of advanced imaging such as multi-detector
CT. Multiple studies have estimated that they are
present in 5% or more of the general population.
Adrenal adenomas are most often unilateral and
nonfunctional. In one study, only 1% of adrenal
lesions found incidentally proved to be adrenal
carcinoma. Other important differential diagnoses include metastasis, pheochromocytoma, cyst,
and hemorrhage.
Certain imaging characteristics can be used to
distinguish benign from malignant adrenal lesions.
Lesions that are smaller than 3 cm are most likely
benign, while lesions greater than 5 cm are more
likely malignant. Lesions with density less than 10
HU on a non-contrast CT are lipid-rich and most
likely benign. On contrasted CT imaging, benign
lesions typically have rapid contrast washout,
while malignant lesions have delayed contrast
washout. Moreover, lesions that show no growth
on follow-up imaging are usually benign.
Fig. 11.22 Axial. Soft tissue window shows a hypodense
mass within the right adrenal gland (arrow)
11.21.5 Pearls and Pitfalls
A density slightly lower than that of soft tissue is
often typical of adrenal adenomas. However,
dedicated abdominal CT or MRI is often necessary to further characterize incidentally found
adrenal lesions.
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11.22 Case 11.21
11.22.1 History
An 81-year-old female underwent coronary
artery imaging after a positive stress test.
11.22.2 Findings
The abdominal aorta is abnormally enlarged
(4.3 cm) and contains mural thrombus (Fig. 11.23).
11.22.3 Diagnosis
Abdominal aortic aneurysm (AAA).
11.22.4 Discussion
Early recognition and treatment of this disease is
important because a ruptured AAA is a lifethreatening emergency. It is estimated that about
15,000 deaths are attributed to AAA in the USA
each year.
Abdominal aortic aneurysms are defined as
a focal dilation of the aorta to more than 50%
of its normal size. Most men and women have
an aortic diameter less than 2 cm; therefore,
the upper limit of normal is considered to be
3 cm.
Risk factors for AAA include smoking,
increasing age, male gender, atherosclerosis, and
family history of AAA. Up to 8% of men over 65
are found to have AAA. One study found that
prevalence in men peaked at age 80, while prevalence in women kept increasing with age. Patients
under age 50 are extremely unlikely to have a
clinically significant AAA.
Management of asymptomatic, unruptured
AAA is based on size. Elective treatment is recommended for aneurysms greater than 5.5 cm or
those with growth rate greater than 1 cm per year.
In patients who do not meet these criteria, the risk
of surgery is greater than the risk of rupture, and
it is recommended that they undergo serial
surveillance.
Fig. 11.23 Axial. The abdominal aorta is enlarged with
mural thrombus (arrows)
11.22.5 Pearls and Pitfalls
The U.S. Preventative Services Task force recommends a one-time screening with ultrasound
to detect AAA in men between ages 65 and 75
with history of smoking.
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11.23 Case 11.22
11.23.1 History
A 35-year-old male presented to the emergency
department with shortness of breath and chest
pain.
11.23.2 Findings
The liver is enlarged and demonstrated low density due to fatty infiltration (Fig. 11.24).
11.23.3 Diagnosis
Hepatic steatosis (fatty infiltration).
11.23.4 Discussion
Fatty infiltration of the liver is a nonspecific finding that can occur in response to insult from
injury, toxins, or other diseases. When hepatic
steatosis is present without any known cause, the
condition is termed nonalcoholic fatty liver disease (NAFLD). The risk of NAFLD is that it may
progress to cirrhosis and ultimately liver failure.
NAFLD is subdivided into two entities: nonalcoholic fatty liver (NAFL) and nonalcoholic steatohepatitis (NASH). Histologically, NASH shows
evidence of hepatocellular injury and fibrosis, which
is absent in NAFL.
NAFLD is estimated to have a 20% worldwide
prevalence. Risk factors include obesity, diabetes
mellitus, dyslipidemia, and metabolic syndrome.
Most patients are asymptomatic from NAFLD,
and a variable number present with hepatomegaly.
Biopsy is not always necessary for diagnosis, but
is the only way to distinguish NAFL from NASH.
Fig. 11.24 Axial. Soft tissue windows show fatty infiltration of the liver
11.23.5 Pearls and Pitfalls
Fatty infiltration of the liver reduces its attenuation to lower than that of the spleen. A normal
liver has attenuation higher than that of the spleen.
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11.24 Case 11.23
11.24.1 History
A 51-year-old male presented to the emergency
department with chest pain.
11.24.2 Findings
There are compression fractures of T6, T7, and
T10. There is no retropulsion of bony fragments
into the spinal canal (Figs. 11.25 and 11.26).
11.24.3 Diagnosis
Multi-level thoracic compression fractures.
11.24.4 Discussion
Vertebral body compression fractures most commonly occur in the setting of osteoporosis,
malignancy, infection, and trauma. Compression
fractures are frequently located in the midthoracic spine or at the thoracolumbar junction.
Acute compression fractures can be caused by
minor trauma such as bending, lifting, or coughing, and most of patients present with severe back
pain. Chronic compression fractures may progress slowly over time, and patients may present
with asymptomatic loss of height and kyphosis.
Neurologic impairment can occur if there is associated compression of the spinal cord or nerve
roots. In cases of severe kyphosis of the thoracic
spine, patients can develop impaired respiratory
function.
Pain caused by compression fractures can be
managed conservatively with a back brace to provide support for the spine. Vertebroplasty and
kyphoplasty are also effective techniques to
reduce pain. To perform a vertebroplasty, cement
is injected percutaneously through the pedicles
into the vertebral body to stabilize and prevent
further collapse of the vertebral body. The technique for kyphoplasty is similar, except that it
also uses balloon inflation within the vertebral
body to help restore vertebral body height.
Surgery may be appropriate if there is spinal cord
compression with neurologic deficit or frank
instability of the spine.
Fig. 11.25 Sagittal. Bone show multiple compression
fractures (arrows) with loss of anterior vertebral body
height
11.24.5 Pearls and Pitfalls
Pathologic fractures should be followed up with
MRI to assess for malignancy or infection. MRI
will also evaluate for spinal cord compression.
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