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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
11.5 Case 11.4
11.5.1 History
A 59-year-old female presented to the emergency
department with chest pain and shortness of
breath.
11.5.2 Findings
There are pulmonary emboli and bilateral main
pulmonary arteries and segmental arteries.
There is right ventricular strain (Figs. 11.4 and
11.5).
11.5.3 Diagnosis
The diagnosis is extensive pulmonary emboli
with right ventricular strain.
11.5.4 Discussion
Pulmonary embolism (PE) is a common yet
deadly disease that is responsible for 100,000
deaths in the USA annually. Risk factors for PE
are similar to those for DVT and include malignancy, surgery, joint replacements, prolonged
immobilization, pregnancy, and hypercoagulable
disorders.
Common symptoms of PE are dyspnea, chest
pain, and cough. The most common sign on physical exam is tachycardia. Because many patients
may be asymptomatic, a high level of suspicion
must be maintained among those who are at high
risk. PE is often a lethal disease because it may
cause right heart failure and subsequent death due
to arrhythmias or cardiac shock in up to 30% of
patients if not treated. Typical treatment is immediate anticoagulation and supportive therapy
although more invasive therapy may be necessary
in patients with hemodynamic compromise.
Fig. 11.4 (a) Axial. Thrombus in the right main pulmo-
nary artery (long arrow) and left lung segmental pulmonary arteries (short arrows). (b) Axial. Flattening of the
interventricular septum (arrow) indicates right ventricular
strain. Normally, the interventricular septum bows outward from the left ventricle
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a
c
d
b
Fig. 11.5 (a) Axial. Massive pulmonary embolism with a
large saddle embolus in the main pulmonary artery (arrows).
(b) Axial. Extensive bilateral thrombus in the proximal pulmonary arteries (arrows). (c and d) Axial and sagittal.
The presence of right ventricular strain, which
can be assessed by right ventricular dilation and
flattening of the intraventricular septum, is a negative prognostic indicator in patients with PE.
Historically, the gold standard for diagnosis
was pulmonary angiography. However, today
similar diagnostic results are achieved with CT
angiography.
Arrows pointing to a partial filling defect in an arterial branch
to the right lower lobe (c) and proximal right pulmonary
artery (d), which sometimes can have the appearance of an
eyeball defect—Contributed by J. Lee & C. Smuclovisky
11.5.5 Pearls and Pitfalls
Timing of the contrast injection is crucial.
Opacification extending from the main pulmonary arteries to the subsegmental arteries must be
achieved to confidently rule out PE.
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C. Brown and C.S. White
11.6 Case 11.5
11.6.1 History
A 65-year-old male underwent a preoperative
study for aortic valve replacement. He has history
of coronary artery disease and prior coronary
artery bypass graft.
11.6.2 Findings
There is right-sided pleural effusion with septal
thickening and ground glass opacities in both
lung bases (Fig. 11.6).
11.6.3 Diagnosis
Pleural effusion due to volume overload.
11.6.4 Discussion
Pleural effusions can be classified as either transudative or exudative. Transudative effusions are caused
by increased plasma hydrostatic pressure, decreased
plasma oncotic pressure, or a combination of
the two. The most common cause of transudative
effusions is left heart failure, which causes increased
plasma hydrostatic pressure from vascular congestion. Other causes include volume overload and diseases characterized by hypoalbunemia, such as
hepatic disease or nephrotic syndrome. Exudative
effusions are caused by infection, inflammation, and
malignancy.
Pulmonary edema can develop in setting of
volume overload or congestive heart failure.
Radiographically, this is demonstrated by the
presence of septal lines due to increased interstitial fluid as well as ground glass opacities due to
increased fluid in the alveoli.
Thoracentesis can be performed to sample the
pleural fluid, which can then be analyzed to help
distinguish transudative effusions from exudative
effusions. Typically, a transudative effusion has a
pleural/serum protein ratio less than 0.5, pleural/
serum LDH ratio less than 0.6, and pleural LDH
less than 200 IU/L.
11.6.5 Pearls and Pitfalls
Transudative effusions usually have density on
CT of 0–20 HU. Exudative effusions tend to have
density greater than 20 HU.
Fig. 11.6 (a) Axial. Soft tissue window shows right-sided pleural effusion with density of simple fluid. (b) Axial. Lung
windows show septal thickening and ground glass opacities in both lung bases
bc
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11.7 Case 11.6 Contributed by
Lee and C. Smuclovisky
J.
11.7.1 History
An 89-year-old male presented with a history of
increasing shortness of breath and atypical chest
pain.
11.7.2 Findings
There is a pericardial effusion (Fig. 11.7a, b).
There was multivessel non-obstructive calcified
plaques in the coronary arteries (not shown).
11.7.3 Diagnosis
The diagnosis is pericardial effusion.
11.7.4 Discussion
The pericardial space normally contains up to
50 mL of fluid, which serves as lubrication for the
visceral and parietal layers of the pericardium.
Pericardial effusion is defined as an abnormal
amount fluid or density in the pericardium.
Etiologies include infectious, noninfectious, and
autoimmune. The cause in this case was idiopathic.
The cause of increased fluid production
depends on the underlying etiology. Transudate
fluid accumulation results from obstruction of
fluid drainage, which occurs through lymphatic
channels. Exudate fluids occur secondary to
inflammatory, infectious, malignant, or autoimmune processes affecting the pericardium.
Clinical manifestations of pericardial effusion
are mostly dependent on the rate of accumulation
of fluid in the pericardial sac. Rapid accumulation
may cause elevated intrapericardial pressures
a
de
Fig. 11.7 (a and b) Axial and sagittal. Pericardial effu-
sion (arrows). (c and d) Axial and sagittal. Thickened
pericardium with scattered calcifications (arrows). (e)
Axial: Constrictive pericarditis (arrows). Thickened and
partially calcified pericardium causing compression of the
ventricles with secondary dilatation of the atria (LA left
atrium; RA right atrium)
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C. Brown and C.S. White
with as little as 80 mL, while slowly progressing
effusions can contain up to 2 L with minimal or
no symptoms. CT can detect small amounts of
fluid in the pericardium and reported as little as
50 mL. Pericarditis can lead to fibrosis and calcifications (Fig. 11.7c, d) in the pericardium that
can lead to constrictive pericarditis (Fig. 11.7e),
which impedes normal diastolic filling.
11.7.5 Pearls and Pitfalls
It is not uncommon to normally visualize a small
amount of fluid in the inferior pericardial recess
in asymptomatic patients. With a pericardial effusion, fluid extends superiorly surrounding the
heart anterior and posteriorly.
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11.8 Case 11.7 Contributed by
Lee and C. Smuclovisky
J.
11.8.1 History
An 81-year-old asymptomatic male presented
with an abnormal nuclear stress test and silent
MI.
11.8.2 Findings
There is a 3.9-cm water density mass inseparable
from the free wall of the right atrium located in
the cardiophrenic angle (Fig. 11.8a, b).
a
b
11.8.3 Diagnosis
The diagnosis is pericardial cyst.
11.8.4 Discussion
Most pericardial cysts are congenital and are discovered, as in this case, as an incidental finding.
Less common are inflammatory pericardial cysts.
These include pseudocysts as well as encapsulated and loculated pericardial effusions.
Pericardial scarring may trap portions of an intrapericardial exudate or hemorrhage producing a
pocket or cyst-like structure (Fig. 11.8c).
Fig. 11.8 (a and b) Axial and coronal. Pericardial cyst in
the right cardiophrenic angle (arrows). (c) Axial. Different
patient with a large chronic myocardial infarct in the territory of the LAD (triple arrows), with a trapped fluid col-
lection (single arrow) in the left cardiophrenic angle.
There is a small amount of fluid (arrow head) in the pericardium. (d) Axial. Bronchogenic cyst, on a different
patient (arrows)
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Cysts occur anywhere in the pericardium and
are mostly commonly located in the right cardiophrenic angle. Pericardial cysts are usually less
than 3 cm in diameter and most are unilocular,
have smooth borders, and contain clear fluid. The
cyst arises from the parietal pericardium and consists of a single layer of mesothelial cells. Rarely,
cysts can be associated with chest pain, dyspnea,
cough, and significant arrhythmias, likely secondary to compression and erosion of the adjacent tissues.
The diagnosis on CT is established by the
location, ovoid/triangular shape, thin walls, and
homogeneous water density. These cysts have
similar appearance and histology as broncho-
genic cysts (Fig. 11.8d). Pericardial cysts may be
hyperdense on CT, likely from containing mucoid
or proteinaceous material or both that may mimic
a solid mass.
11.8.5 Pearls and Pitfalls
Differential diagnosis of a pericardial cyst would
include a bronchogenic cyst that is trapped in or
on the pericardium, lymphangiomas, and necrotic
tumors. Pericardial diverticula are less common
and resemble cysts except that a comparable
developmental abnormality has left a communication with the pericardial cavity.
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11.9 Case 11.8 Contributed by
Lee and C. Smuclovisky
J.
11.9.1 History
A 79-year-old male presented with chronic shortness of breath and atrial fibrillation.
a
11.9.2 Findings
There is a filling defect in the left atrial appendage (Fig. 11.9a).
b
Fig. 11.9 (a) Axial. Discrete low density in the left atrial
appendage (LAA) confirmed by transesophageal echocardiography (TEE) to represent a thrombus (arrow). (b) Axial.
Normal typical triangular appearance of the LAA (arrow) in
a different patient. (c) Axial: Anatomic variant of the LAA
with the apex toward the left sinus of Valsalva (arrow) in a
different patient. (d) Axial. False-positive CTA result.
Filling defect (arrow) in the LAA in a different patient with
a chronic dilated cardiomyopathy and no thrombus and
sluggish LAA on a TEE performed the following day
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11.9.3 Diagnosis
The diagnosis is chronic nonvalvular atrial fibrillation with a thrombus in the left atrial appendage
(LAA).
11.9.4 Discussion
The LAA is well identified on cardiac CT and is
contiguous anterior and superiorly with the left
atrium and located to the left of the main
pulmonary artery. The LAA typically has a triangular shape and enhances homogeneously
with IV contrast (Fig. 11.9b). Internal striations
in the apex of the appendage are also commonly
visualized. Anatomic variants of the LAA are
not infrequent and may appear redundant or
with the apex adjacent to the left sinus of
Valsalva (Fig. 11.9c).
The most common cause of thrombus in the
LAA is atrial fibrillation. Other causes include
mitral valvular disease, cardiomyopathy, and
platelet dysfunction. Atrial fibrillation is a common arrhythmia that is found in 1% of persons
older than 60 years to more than 5% of patients
older than 69 years. Nonvalvular atrial fibrillation
is the most common cardiac disease associated
with cerebral embolism. Close to half of the cardiogenic emboli in the USA occur in patients
with nonvalvular atrial fibrillation. Overall,
20–25% of ischemic strokes are due to cardiogenic emboli.
LAA thrombus is commonly difficult to identify on transthoracic echocardiography. The most
widely used diagnostic test to establish the presence of thrombus is transesophageal echocardiography (TEE). However, TEE is semi-invasive, and
cardiac CTA has shown the potential to diagnose
noninvasively thrombus in the LAA. Currently,
there are no definitive studies establishing that
CTA replaces TEE.
11.9.5 Pearls and Pitfalls
The LAA opacifies with contrast maximally in
end-systole. This is usually the 30–40% phase on
the cardiac CTA. LAA thrombus may be subtle
and should be suspected in patients with left
atrial (LA) enlargement (LA size 4.0 cm and
greater). A sluggish LAA may under fill initially
with contrast on CTA, giving the false appearance of a thrombus (Fig. 11.9d). Preliminary
studies suggest that delayed imaging of the heart
may avoid this pitfall.
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11.10 Case 11.9 Contributed by
Lee and C. Smuclovisky
J.
11.10.1 History
A 51-year-old male presented for workup of coronary artery disease.
11.10.2 Findings
There is an incidental 3.5-cm lobulated noncalcified mass in the left atrium attached to the posterior wall (Fig. 11.10a, b).
11.10.3 Diagnosis
The diagnosis is left atrial myxoma.
11.10.4 Discussion
The tumor was surgically resected and the pathology confirmed. Myxomas are benign and represent the most common type of primary cardiac
tumor. Approximately 90% are solitary and
pedunculated. About 75–85% occur in the left
atrial cavity. The mean age of patients with sporadic myxoma is 56 years. In the left atrium, the
usual site of attachment is in the area of the fossa
ovalis. Less often, myxomas also may arise from
the right atrium and either ventricle. Occasionally
myxomas, as in this case, arise from the posterior
left atrial wall or the appendage. The mobility of
the tumor depends on the extent of the attachment and length of the stalk. Clinical signs
include embolization and mechanical interference with the cardiac function. Myxomas may
also prolapse through the valve and cause destruction of the annulus or valve leaflets.
Familial cardiac myxomas represent approximately 10% of all myxomas. These may be associated with a syndrome called syndrome myxoma
or Carney’s syndrome that consists of myxomas
in other locations (breast or skin), spotty pigmentation, and endocrine dysfunction.
11.10.5 Pearls and Pitfalls
Not infrequently, mixing of IV contrast from the
superior vena cava with nonopacified blood from
the inferior vena cava causes a swirling artifact in
the right atrium that may mimic a thrombus or
tumor.
Fig. 11.10 (a and b) Axial and oblique sagittal. Lobulated 3.5-cm mass in the left atrium attached to the posterior wall
corresponding to a left atrial myxoma (arrow). (Courtesy of Dr. Constantino Pena, Miami, FL.)
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