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CHAPTER 28 Acute Aortic Syndromes: Diagnosis and Management 299
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conditions. It should be noted that penetrating aortic ulcer is
Diagnosis
The findings on CT, MRI, TEE, and aortography in patients with
penetrating aortic ulcer are characteristic, allowing for differentiation of penetrating aortic ulcer from classic aortic dissection. In
contrast to aortic dissection, an intimal flap or false lumen is not
present; in addition, significant, often advanced atherosclerotic
disease of the aorta, most commonly the descending thoracic
aorta, is evident. An echolucent intramural hematoma with overlying advanced atherosclerotic disease is the most common TEE
finding in patients with acute penetrating aortic ulcer. Careful
evaluation may demonstrate a crater-like ulceration with surrounding atheroma. When the intramural hematoma undergoes
thrombosis, it becomes echogenic, creating the appearance of an
increase in aortic wall thickness. The intramural hematoma may
extend proximally or distally for a variable distance from the entry
site. Additional findings in patients with penetrating aortic ulcer
include aortic pseudoaneurysm or saccular aneurysm. Using CT,
penetrating atherosclerotic ulcer manifests as focal involvement
with adjacent subintimal hematoma and is often associated with
aortic wall thickening or enhancement. Magnetic resonance
imaging is superior to conventional CT in differentiating acute
intramural hematoma from atherosclerotic plaque and chronic
intraluminal thrombus and allows unenhanced multiplanar
imaging (Fig. 28.7). Spiral CT involves shorter examination
times and allows high-quality two- and three-dimensional image
reconstruction. CT angiography can demonstrate complex spatial
relationships, mural abnormalities, and extraluminal pathologic
strongly associated with abdominal aortic aneurysm, which
is seen concomitantly in 42% of patients. Therefore imaging
of the abdominal aorta should be included in the initial
evaluation.
122
Management
The optimal treatment for penetrating aortic ulcer is not well
defined. Treatment is individualized, as the natural history of
penetrating aortic ulcer and indications for surgery are evolving.
Although careful follow-up is necessary, many penetrating aortic
ulcers involving the descending thoracic aorta can be managed
nonoperatively in the acute setting. The natural history of an
intramural hematoma involving the descending thoracic aorta
has been shown by serial noninvasive imaging studies to follow
a course of resorption of the hematoma and compensatory aortic
dilation in the region of the involved aorta in 85% of patients
over 1 year.
be treated medically initially, with special emphasis placed on
impulse control therapy, preferably with a β-adrenergic blocking
agent.
persistent symptoms, or hypertension that is difficult to control
are indications for surgery. When saccular or pseudoaneurysm
is the result of a penetrating atherosclerotic ulcer of the aorta,
surgery is also recommended. Thoracic endograft technology is
being applied to patients with penetrating aortic ulcer involving
the descending thoracic aorta with high procedural success and
a low perioperative morbidity and mortality.
120,121
Patients with an intramural hematoma should
123
Ascending aortic involvement, progressive aortic dilation,
124–127
A
Fig. 28.7 Magnetic resonance (MR) imaging in a patient with multiple penetrating aortic ulcers.
(A) Transverse imaging plane shows a penetrating aortic ulcer in the proximal descending thoracic
aorta (arrow). (B) MR angiogram with gadolinium enhancement shows severe atherosclerotic
changes of the descending thoracic aorta and a penetrating aortic ulcer in the proximal descending
thoracic aorta (arrow).
B
300 PART IV Noncoronary Diseases: Diagnosis and Management
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AORTIC INTRAMURAL HEMATOMA
Aortic intramural hematoma (IMH) is an acute, potentially lethal
disorder that is similar to but pathologically distinct from acute
aortic dissection. Although hemorrhage into the aortic media
occurs in both disorders, an intimal tear with resultant false
lumen is not present in IMH. The prevalence of IMH among
patients with acute aortic syndromes has been reported to be
5% to 20%.
diagnosis of IMH are similar to aortic dissection, as are the
classification scheme and general principles of management.
Pathogenesis
Although hemorrhage into the aortic media occurs in both acute
aortic dissection and IMH, an intimal tear with resultant false
lumen is not present in IMH. Although the mechanism is not
certain, two mechanisms have been described: hemorrhage within
the aortic wall owing to rupture of the vasa vasorum or rupture
owing to an atherosclerotic penetrating aortic ulcer.
evolves very dynamically in the short term to regression, dissection, or aortic rupture.
of IMH is the development of aortic aneurysm or pseudoaneurysm. Lesions of the ascending aorta appear to represent the
early stage of a classic dissection in some patients.
regression without changes in aortic diameter is observed in
one-third of cases, and progression to classical dissection is less
common (between 8% and 16%).
in the acute phase is the best predictor of IMH regression without
complications, and absence of echolucent areas and atherosclerotic
ulcerated plaque are associated with evolution to aortic aneurysm.
hypertension (50% to 84% of patients) but has also been reported
in association with trauma (e.g., auto accident or iatrogenic) in
6% of cases in a meta-analysis.
Classification
The classification scheme for IMH is the same as is used for
classic aortic dissection (see earlier section on aortic dissection).
Patients with IMH are more likely to have type B lesions than
those with classic aortic dissection (e.g., 60% vs. 35%).
Clinical Features
Clinically, patients with acute IMH have a similar presentation
to those with acute aortic dissection. Sudden, severe chest and/
or back pain, as occur in classic aortic dissection, are common
in IMH.
common with ascending (type A) lesions, whereas interscapular
back pain is more common with descending (type B) lesions.
In contrast to aortic dissection, manifestations associated with
aortic branch vessel disease (e.g., myocardial infarction, stroke,
aortic regurgitation, visceral vessel compromise, and paraplegia)
are relatively uncommon with type A IMH.
Diagnosis
The noninvasive imaging methods used to diagnose IMH are
the same as those used in the diagnosis of acute aortic dissection
(TEE, CT, MRI). Exclusion of a dissecting intimal flap is a
62,128,129
The clinical presentation and noninvasive
130
IMH
131
The most frequent long-term outcome
132
Complete
128,133
A normal aortic diameter
131
IMH is most often associated with long-standing
128,129,134
128
129
Although not specific, anterior chest pain is more
Fig. 28.8 Computed tomographic scan with contrast enhance-
ment in a patient with sudden and severe chest pain shows a
circumferential intramural hematoma involving the mid-descending
thoracic aorta (arrow).
prerequisite for the diagnosis of IMH. Specific findings on TEE
for IMH include crescentic or circumferential regional thickening
of the aortic wall exceeding 7 mm, echolucent areas within the
involved aortic wall, displaced intimal Ca2+, and absence of an
intimal flap (Video 28.4). CT and MRI will typically demonstrate
a crescentic or circular high attenuation area along the aortic
wall that does not enhance with contrast
Management
In general, the acute management of IMH and acute aortic
dissection are similar. Initial treatment places emphasis on impulse
control therapy (see section on management of acute aortic
dissection). β-Blockade is indicated in all patients without absolute
contraindications to their use. Patients with ascending aortic
involvement have a reduction in early mortality with surgical
intervention as compared with medical management (14% vs.
129
36%).
with medical or surgical management (14% vs. 20%). Therefore,
surgical intervention is usually recommended in patients with
type A IMH, whereas aggressive medical therapy is the most
common course for patients with type B IMH.
and survive the acute phase of the illness often occurs, although
the rate of progression can be reduced in patients treated with
β-blocker therapy acutely.
presentation may also predict which patients are most likely to
135
have disease progression (aortic diameter >5 cm predicting
progression), potentially identifying a high-risk group that would
benefit from early surgical intervention. Interestingly, in patients
with ascending aortic IMH managed medically (due to advanced
age and comorbid medical conditions), the mortality rate is
much lower as compared with patients with type A aortic dissection who do not undergo surgery.
The full reference list for this chapter is available at
ExpertConsult.com.
Patients with type B lesions have a similar mortality
Progression of disease in patients who are managed medically
135
136
(Fig. 28.8).
Aortic diameter at the time of initial
132
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OUTLINE
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Anatomy and Physiology of the Normal Pericardium, 301
Clinical Presentation of Pericardial Disease, 301
Acute Pericarditis, 302
Clinical Diagnosis, 302
Treatment of Acute Pericarditis, 303
Pericardial Effusion, 303
Cardiac (Pericardial) Tamponade, 304
29
Acute Pericardial Disease
Jacob Luthman, Brian D. Hoit
Low Pressure Tamponade, 306
Causes of Tamponade in the CICU, 306
Treatment of Cardiac Tamponade, 306
Constrictive Pericarditis, 307
Conclusion, 307
Pericardial disease is encountered less frequently than myocardial
disease in the cardiac intensive care unit (CICU). However, its
ability to mimic ischemic heart disease and congestive heart
failure can make the diagnosis of pericardial disease challenging
at times. While many patients with pericardial disease have a
subacute or chronic presentation, the astute clinician must always
consider pericardial disease in patients who present with hemodynamic embarrassment and shock in the CICU, for the failure
to recognize cardiac tamponade can have dire consequences.
This chapter will provide clinicians with the tools to recognize,
diagnose, and manage patients with pericardial disease in the
CICU setting.
ANATOMY AND PHYSIOLOGY OF THE
NORMAL PERICARDIUM
The normal pericardium consists of a double-layered membranous
sac that envelops the heart and proximal portions of the great
vessels. The outer layer, or parietal (fibrous) pericardium, serves
to anchor the heart within the thorax, and becomes contiguous
with the adventitia of the great vessels. The inner layer, or visceral
pericardium, is a serosal monolayer that adheres firmly to the
myocardium as the epicardium, reflects over the origin of the
great vessels creating the oblique and transverse sinuses and
pericardial recesses (major contributors to the pericardial reserve
volume), and fuses with the tough, fibrous parietal layer. Under
normal physiologic conditions, there is typically less than 50 mL
of pericardial fluid (largely an ultrafiltrate of plasma) between
the layers of the pericardium.
While not essential for survival, the pericardium and fluid
within serves many important yet subtle functions. Briefly, the
pericardium limits distention of the cardiac chambers, facilitates
ventricular interaction and coupling of the atria and ventricles,
equalizes physical forces across the entire myocardial surface,
minimizes friction with surrounding structures, and provides
an anatomic barrier from the spread of infection.
1
CLINICAL PRESENTATION OF
PERICARDIAL DISEASE
Although there are relatively few disease processes that primarily
affect the pericardium, the pericardium can be affected by many
disease states (e.g., trauma, rheumatologic, infectious, metabolic,
neoplastic, and congenital disease). As such, the clinical presentation of pericardial disease varies from acute to chronic, and from
benign to life threatening, depending on the underlying etiology.
This propensity for varying clinical presentation and an ability
to mimic life-threatening disease processes (e.g., chest pain and
ST segment elevation seen with acute pericarditis mimicking
acute myocardial infarction [MI]) make the diagnosis of acute
pericardial disease challenging, particularly when time is of
the essence. Therefore, the astute intensivist must understand
which patients require evaluation for pericardial disease, be
able to rapidly and accurately diagnose pericardial disease,
and facilitate timely management. The major ways in which
pericardial disease may simulate ischemic syndromes are listed in
Box 29.1.
Clinically, diseases of the pericardium present in several ways.
Acutely, pericarditis, pericardial effusion (without hemodynamic
compromise), and cardiac tamponade remain the primary concern
in the CICU setting. Chronic and subacute presentations—
including chronic pericardial effusion, constrictive pericarditis,
and effusive-constrictive pericarditis—are less commonly observed
in the CICU and will not be discussed in any detail.
301
CHAPTER 29 Acute Pericardial Disease 301.e1
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Key Words
pericarditis
cardiac tamponade
pericardial effusion
pericardiocentesis
myocardial infarction
echocardiography
302 PART IV Noncoronary Diseases: Diagnosis and Management
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BOX 29.1 Major Ways in Which Pericardial
Disease May Simulate Ischemic Syndromes
Pericardial pain simulating ischemic pain
ST segment deviation suggesting myocardial ischemia
Dressler syndrome mistaken for reinfarction
Cardiac tamponade misinterpreted as heart failure
Severe tamponade mistaken for cardiogenic shock
Friction rub mistaken for murmur of acute mitral regurgitation
Friction rub mistaken for murmur of rupture of the ventricular septum
ACUTE PERICARDITIS
Acute pericarditis is the most common disorder involving the
pericardium, occurring in up to 0.2% of hospitalized patients
and in 5% of patients admitted to the emergency department
for nonischemic chest pain.
remains the most common etiology in the immunocompetent
host in developed countries (80% to 90% of cases), radiation
therapy, cardiac surgery (postpericardiectomy syndrome), and
invasive procedures have become important causes.
Mycobacterium tuberculosis pericarditis is more common in
underdeveloped countries and immunocompromised hosts.
In the CICU setting, pericarditis is most often related to MI
and less commonly to cardiac or coronary interventions. Early
post-MI pericarditis occurs during the first few days after MI
and is caused by transmural necrosis with inflammation affecting
the adjacent pericardium. Pericardial involvement is related to
infarct transmurality and size and is associated with a poor
prognosis. It is often asymptomatic and is identified only by the
presence of a friction rub on physical examination. When patients
are symptomatic, it is essential to distinguish between recurrent
ischemic pain and pericardial pain. Late post-MI pericarditis
(Dressler syndrome) is one of the postcardiac injury (autoimmune)
syndromes, occurring from a week to a few months after MI; it
is less commonly seen in the modern era of early revascularization.
Patients may present with pleuritic chest pain, friction rub, fever,
leukocytosis, and sometimes pleural effusion or pulmonary
infiltrates. The diagnosis is clinical, although objective findings—
such as elevated inflammatory markers, electrocardiographic
changes, and pericardial effusion on echocardiogram (ECG)—can
be helpful.
Clinical Diagnosis
The diagnosis of acute pericarditis can be made in the presence
of at least two of the following criteria: (1) typical chest pain,
(2) a pericardial friction rub on auscultation, (3) changes on
the ECG, and (4) new or worsening pericardial effusion. Elevation
of inflammatory markers or evidence of pericardial inflammation
on other imaging modalities can help support the diagnosis in
atypical cases but are not part of the diagnostic criteria. Modest
elevations of troponin reflect concurrent myocardial inflammation. All patients suspected of having acute pericarditis should
have the following studies: an ECG, chest radiograph, complete
blood count, troponin level, serum C-reactive protein level, renal
function panel, blood cultures (if fever >38°C or signs of sepsis),
and a transthoracic echocardiogram.
2,3
While idiopathic/viral pericarditis
4,5
In contrast,
5
4
Chest pain is the most common presenting symptom and
typically has a sudden onset, variable severity and intensity, and
may radiate to the trapezius ridge. The pain is generally pleuritic,
becoming worse with inspiration, and is alleviated by sitting up
and leaning forward. The pericardial friction rub, auscultated
best at the left sternal border with the patient seated and leaning
forward, is considered pathognomonic for pericarditis.6 While
highly specific, its absence does not exclude pericarditis, as it may
be evanescent, and is heard in only one-third of patients with
acute pericarditis.4 Notably, the pericardial friction rub can be
monophasic, biphasic, or triphasic in nature and does not vary
with the respiratory cycle, which helps differentiate pericardial
from pleural friction rubs. While the friction rub remains an
accurate means of diagnosis, all patients presenting to the CICU
with chest pain deserve a thorough clinical examination, including
assessment of vital signs, jugular venous pressure (JVP) and
pulsation, blood pressure determination in each upper extremity,
auscultation for cardiac murmurs, and the evaluation for pulsus
paradoxus in order to alert the clinician to complications of
pericarditis (e.g., tamponade), or suggest alternate pathology
(e.g., MI or aortic dissection).
ECG changes are common in pericarditis and typically progress
through four stages: stage I, diffuse ST segment elevation and
PR segment depression; stage II, normalization of the ST and
PR segments; stage III, T-wave inversion that occurs after normalization of the ST segment; and stage IV (which is variably
present), normalization of the T waves. These “classic” ECG
changes of diffuse ST segment elevation and PR segment depression are seen in the first hours to days of the disease process and
have been shown to be present in only approximately 60% of
cases of pericarditis5 (Fig. 29.1). Distinguishing the ECG changes
of acute pericarditis from those of acute myocardial ischemia
can be challenging. In differentiating the two conditions, it should
be remembered that the ST segment elevation seen in pericarditis
starts at the J-point, is concave upwards and distributed throughout nearly all leads on the ECG (i.e., in multiple vascular territories), and is associated with PR depression and an absence
of Q-waves. In contrast, the ST segment change seen in ST elevation MI (STEMI) originates at the J-point, is convex (domeshaped), generally occurs in a single coronary vascular territory,
does not have associated PR segment changes, and may have
reciprocal ST segment changes in other vascular territories of
the myocardium. Sustained dysrhythmia is also more common
with myocardial ischemia as compared to acute pericarditis
(provided that the pericarditis is not the result of a transmural
infarction), although atrial arrhythmias complicate 5% to 10%
of cases of acute pericarditis. When pericarditis is associated
with an acute MI, the degree of ST elevation may be exaggerated,
the reciprocal ST segment changes of infarction masked, and
atypical T wave evolution or early normalization of inverted T
waves may be seen.
While transthoracic echocardiography has little utility in
evaluating the pericardium itself, it is invaluable for diagnosing
acute pericarditis and its complications (pericardial effusion and
tamponade) and for recognizing alternative diagnoses. Because
of its noninvasive nature and widespread availability, both the
European Society of Cardiology (ESC) and the American Society
CHAPTER 29 Acute Pericardial Disease 303
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III III
V
1
Fig. 29.1 Echocardiogram of a patient with acute viral pericarditis. Characteristic features include
ST segments elevated concave upward and not localized. T waves are upright in leads with ST
segment elevation. Reciprocal repolarization changes are seen in aVR and V
depressed.
V
2
V
3
of Echocardiography recommend that a transthoracic ECG be
performed in all patients with suspected acute pericarditis.
6
Leukocytosis and elevations in the erythrocyte sedimentation
rate and C-reactive protein are nonspecific indicators of inflammation and therefore are not useful for the diagnosis of pericarditis; however, they do have prognostic value. For example,
in an Italian study of 156 consecutive patients with idiopathic
or viral pericarditis, hs-CRP elevation at 1 week was a significant
independent risk factor for recurrence of disease (hazard ratio
[HR], 2.36).7 Cardiac troponin has also been evaluated in acute
idiopathic or viral pericarditis as a marker for myocardial involvement. In one study, 38 of 118 consecutive patients with pericarditis
were found to have troponin elevations. However, after a mean
follow-up of 24 months, a similar rate of recurrent pericarditis
and constrictive pericarditis was noted among those with positive
and negative troponin values and no cases of tamponade were
detected in the cohort with positive troponin values.
8
An exhaustive diagnostic evaluation is not recommended in
the immunocompetent patient owing to the diminished value
of testing compared to the cost incurred and the low probability
of any result having a significant impact on management.
However, following a basic evaluation, patients with fever greater
than 38°C, subacute onset of symptoms, immunosuppression,
trauma, oral anticoagulation therapy, evidence of myopericarditis,
moderate or large pericardial effusion, or cardiac tamponade
are considered high risk and should be admitted to the hospital
(and, if appropriate, to the CICU) for further evaluation of a
specific etiology of the pericarditis.
9
Treatment of Acute Pericarditis
Aspirin and nonsteroidal antiinflammatory drugs (NSAIDs)
are a mainstay of therapy for idiopathic acute pericarditis.
The open-label Colchicine for Acute Pericarditis (COPE) trial
prospectively studied aspirin monotherapy compared to aspirin
plus colchicine for acute idiopathic pericarditis. The addition of
aV
R
V
4
aV
L
V
5
. PR segments are
1
aV
F
V
6
colchicine to aspirin led to a statistically significant reduction
in symptom persistence at 72 hours (11.7% vs. 36.7%) and a
significant reduction in the recurrence rate at 18 months (10.7%
vs. 32.2%), with the number needed to treat to prevent one recurrence being five.10 Multiple subsequent randomized controlled
trials and systematic reviews have documented similar efficacy
of colchicine in acute idiopathic pericarditis.
11–13
Treatment for early post-MI pericarditis is generally supportive, as most cases are self-limiting. Symptomatic patients
may be treated with high-dose acetylsalicylic acid (ASA) for 1 to
2 weeks. The addition of colchicine may be helpful in reducing
inflammation and reducing the risk for recurrent pericarditis.
NSAIDs and glucocorticoids should be avoided because of the
possibility of harmful effects in the early post-MI setting and the
increased risk of recurrent pericarditis. Patients with an associated
pericardial effusion generally do not need to have antiplatelet
therapy or anticoagulation withheld. However, those with large or
enlarging pericardial effusions or signs of tamponade may need
cessation of anticoagulation to avoid hemorrhagic conversion of
the pericardial effusion. An exhaustive review of specific regimens
is beyond the scope of this chapter. The interested reader is
referred to the excellent review by Schwier and Tran.
14
Pericardial Effusion
While the presence of a pericardial effusion can be suggested by
the history and physical examination, ECG, and chest radiograph,
many are discovered incidentally during the evaluation for other
cardiopulmonary processes, as there are no symptoms directly
attributed to the effusion until it produces hemodynamic effects. In
contrast, patients with a hemodynamically significant pericardial
effusion usually present with chest pain and fullness along with
signs and symptoms related to impaired cardiac function—such
as fatigue, dyspnea, hypotension, pulsus paradoxus, elevated JVP,
and edema—all of which can also be present in cardiomyopathy
or disease processes affecting the right heart.
2
Less commonly,
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