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31 Right-Sided Thrombus
389
Fig. 31.5 A right ventricular outow tract thrombus seen
in a patient during cardiac arrest. (a) A parasternal longaxis view showing a mobile thrombus in the right ventricular outow tract. (b) A parasternal short-axis view at
the level of the aortic valve showing the same thrombus in
the right ventricular outow tract with associated thrombus in the proximal main and right pulmonary artery
a
b
Fig. 31.6 Apical 4-chamber views showing a side-byside comparison between the difference in contrast
enhancement in true thombus and a mass. (a
ventricular thrombus with contrast-ehanced images show-
) A right-
ing a lling defect within the right ventricle. (b) A
right-ventricular malignant mass showing contrast uptake
and enhancement of the mass
390
K. El-Kersh and B. A. Jalil
In contrast echocardiography, thrombi show no
enhancement as they are avascular, while malignant tumors show enhancement due to abnormal
neovascularization and high vascularity, and
myxomas show partial enhancement due to poor
blood supply [14]. The adjunctive use of
3- dimensional echocardiographic imaging may
permit better visualization of thrombi and allow
their volumetric measurements, similar to its use
in intracardiac masses [15].
Transesophageal echocardiography (TEE) has
distinct advantages of higher-resolution imaging
and confers superior sensitivity in the right-heart
chambers’ surveillance and thrombi detection
[16]. An added benet of using TEE in RST is the
ability to detect small thrombi that are beyond the
resolution of TTE and accurately determine their
morphology and size (Fig.31.7 and Video 31.11).
The use of cardiac magnetic resonance (CMR)
Fig. 31.7
Transesophageal
echocardiogram of the
right atrial appendage
showing a mobile
thrombus
imaging has also been reported to detect RST and
may be a valuable alternative in patients with a
high suspicion of RST who cannot undergo TEE
imaging [12]. Some clots are very small and may
be better delineated on CMR as seen in Fig.31.8
and Video 31.12.
A careful review of contrast chest computed
tomography (CT) images may also be helpful in
evaluating patients with RST. Contrasted chest
CTs may show lling defects within the right
heart chambers as shown in Fig.31.9. This may
help strengthen the suspicion of a thrombus seen
initially on TTE or vice versa. Additionally, computed tomography imaging of the abdomen in the
case of tumor thrombus associated with renal cell
carcinoma and magnetic resonance imaging of
the liver in patients with hepatocellular carcinoma may be useful in conrming a suspected
tumor thrombus seen on echocardiography.
31 Right-Sided Thrombus
Fig. 31.8 Cardiac
magnetic resonance
image showing a small
globular appearing right
atrial thrombus
Fig. 31.9 Computer
tomography image of
the chest with contrast
showing a lling defect
in the apex of the right
ventricle
391
Clinical Implications
In patients with RST on echocardiography without
documented PE, it is imperative to evaluate these
patients for the presence of concurrent PE.Mobile
RSTs are associated with an increased mortality in
the setting of acute PE, especially in the presence
of right ventricular dysfunction [17, 18]. Despite
the noted higher mortality, the current guidelines
don’t include the presence or absence of RST in
the formal PE risk assessment, which mainly utilizes hemodynamic instability, clinical parameters
of severity or comorbidities, right ventricular dysfunction, and elevated cardiac biomarkers such as
392
K. El-Kersh and B. A. Jalil
troponins in early risk assessment [4]. It is difcult
to differentiate tumors, tumor thrombi, and true
thrombi based on their sonographic appearance; it
is important to consider contrast-enhanced echocardiography and the use of multimodality imaging, including TEE and CMR, to better differentiate
the ndings on TTE.
There is a risk of RST causing hemodynamic
instability; initial triage should include an individualized approach to consider monitoring these
patients who may be at a higher risk of hemodynamic collapse in the intensive care unit.
Multidisciplinary Pulmonary Embolism Response
Teams (PERT) can be a valuable resource in triage
and treatment decision- making. Treatment decisions can be affected by several factors, including
the center’s experience, bleeding risk, size and
location of the thrombus, overall clot burden, right
ventricular dysfunction, and presence of patent
foramen ovale [20]. Besides anticoagulation, systemic thrombolysis, catheter- directed therapy
including catheter embolectomies such as
AngioVac systems, and surgical embolectomy can
be considered in the treatment of mobile RST [20].
Thrombus-in-transit across a PFO represents a
unique challenge. Despite limited evidence, in this
situation, surgical embolectomy can be considered
due to the risk of stroke and intracranial hemorrhage with other therapeutic modalities [19].
Evolving Evidence
Due to the lack of prospective randomized trials
that evaluate different treatment modalities of
mobile RST, there is no consensus on optimal
management strategy and an individualized treatment approach should be considered in each case.
Summary Points
• RST can be associated with pulmonary embo-
lism (thrombus-in-transit) or catheters/
devices.
• The echocardiographic appearance of RST
can be grouped into three patterns (type A,
type B, and type C).
• Mobile RSTs are associated with increased
mortality in the setting of acute pulmonary
embolism.
• Individualized treatment approaches should
be considered in patients with mobile RST.
• Multidisciplinary PERT can be a valuable
resource in management.
Questions
1. A 45-year-old female without known prior
medical problems, presented to the emergency room after a syncopal episode. She was
hypoxic, requiring oxygen at 6 L/min via
nasal cannula, had sinus tachycardia with a
heart rate of 145/min, a respiratory rate of 28/
min, and her blood pressure was 87/36mmHg.
She was given a bolus of 500 ml lactated
Ringer’s solution without improvement in her
blood pressure, and she was subsequently
started on a norepinephrine infusion. A contrast chest computed tomography showed a
saddle pulmonary embolism, and she was
started on a heparin infusion. An emergent
echocardiogram showed severe right ventricular dilation with severely depressed right
ventricular function. An incidental note was
made of a highly mobile serpiginous density
in the right atrium concerning a clot-in- transit.
What is the next best step in the management
of this patient?
A. Continue anticoagulation with heparin
and repeat serial echocardiograms to evaluate the right atrial density.
B. Switch intravenous heparin to subcutane-
ous low-molecular-weight heparin.
C. Review the thrombolytics contraindica-
tion checklist and treat the patient with
systemic thrombolytics in the absence of
contraindications.
D. Review the thrombolytics contraindica-
tion checklist and prepare the patient for
catheter-directed thrombolysis in the
absence of contraindications.
Answer: C
Explanation: The patient has a high-risk
acute pulmonary embolism evidenced by
31 Right-Sided Thrombus
393
hemodynamic instability and signicant right
ventricular dysfunction. Furthermore, she has
a right atrial thrombus-in-transit. In the
absence of contraindication, systemic thrombolysis is the treatment of choice in this case
(answer C). Anticoagulation alone (answers A
and B) or catheter-directed thrombolysis
(answer D) is not the treatment of choice in
high-risk pulmonary embolism complicated
with thrombus-in-transit in the absence of
contraindication for systemic thrombolysis.
2. A 65-year-old male with COVID-19 infection
was admitted to the ICU and was intubated for
progressive acute hypoxic respiratory failure.
Over the course of this ICU stay, his oxygen
requirement gradually improved. His Fio2
and positive end-expiratory pressure were
weaned gradually in anticipation of extubation. You were alerted about a sudden worsening in the patient’s oxygen requirement and
the development of circulatory failure, necessitating the initiation of vasopressors. A pointof- care ultrasound showed bilateral lung
sliding, preserved left ventricular ejection
fraction without regional wall motion abnormalities, dilated inferior vena cava at 2.3cm
without respiratory variations, and a mobile
density in the right ventricular outow tract.
Soon after, the patient became pulseless with
asystole on the cardiac monitor, and cardiopulmonary resuscitation was initiated. What
is the most likely cause of the patient’s cardiac
arrest?
A. Acute pulmonary embolism
B. Anterior wall myocardial infarction
C. Tension pneumothorax
D. Hypovolemic shock
Answer: A
Explanation: The sudden deterioration in
oxygenation and hemodynamics in the presence of a mobile density in the right ventricular
outow tract on point-of-care ultrasound is
highly suggestive of acute pulmonary embolism (answer A) as the cause of cardiac arrest.
Tension pneumothorax (answer C) is less
likely in the presence of bilateral lung sliding
on ultrasound lung examination. Anterior wall
myocardial infarction (answer B) is less likely
in the absence of regional wall motion abnormalities. The dilation of the inferior vena cava
without respiratory variations argues against
hypovolemia (answer D).
References
1. Rose PS, Punjabi NM, Pearse DB.Treatment of right
heart thromboemboli. Chest. 2002;121(3):806–14.
2. Torbicki A, Galie N, Covezzoli A, Rossi E, De Rosa
M, Goldhaber SZ, etal. Right heart thrombi in pulmonary embolism: results from the international
cooperative pulmonary embolism registry. J Am Coll
Cardiol. 2003;41(12):2245–51.
3. Casazza F, Bongarzoni A, Centonze F, Morpurgo
M. Prevalence and prognostic signicance of rightsided cardiac mobile thrombi in acute massive pulmonary embolism. Am J Cardiol. 1997;79(10):1433–5.
4. Konstantinides SV, Meyer G, Becattini C, Bueno H,
Geersing GJ, Harjola VP, etal. 2019 ESC guidelines
for the diagnosis and management of acute pulmonary embolism developed in collaboration with the
European Respiratory Society (ERS). Eur Heart J.
2020;41(4):543–603.
5. Ferrari E, Benhamou M, Berthier F, Baudouy
M. Mobile thrombi of the right heart in pulmonary
embolism: delayed disappearance after thrombolytic
treatment. Chest. 2005;127(3):1051–3.
6. Shah A, Murray M, Nzerue C.Right atrial thrombi
complicating use of central venous catheters in hemodialysis. Int J Artif Organs. 2004;27(9):772–8.
7. Ducatman BS, McMichan JC, Edwards WD.Catheterinduced lesions of the right side of the heart. A oneyear prospective study of 141 autopsies. JAMA.
1985;253(6):791–5.
8. Supple GE, Ren JF, Zado ES, Marchlinski FE.Mobile
thrombus on device leads in patients undergoing ablation: identication, incidence, location, and association with increased pulmonary artery systolic
pressure. Circulation. 2011;124(7):772–8.
9. van Laecke S, Dhondt A, de Sutter J, Vanholder
R.Right atrial thrombus in an asymptomatic hemodialysis patient with malfunctioning catheter and patent
foramen ovale. Hemodial Int. 2005;9(3):236–40.
10. Wang Y, Yuan L, Ge RL, Sun Y, Wei G.Survival benet of surgical treatment for hepatocellular carcinoma
with inferior vena cava/right atrium tumor thrombus: results of a retrospective cohort study. Ann Surg
Oncol. 2013;20(3):914–22.
11. Chiappini B, Savini C, Marinelli G, Suarez SM, Di
Eusanio M, Fiorani V, etal. Cavoatrial tumor thrombus: single-stage surgical approach with profound
hypothermia and circulatory arrest, including a
review of the literature. J Thorac Cardiovasc Surg.
2002;124(4):684–8.
12. Tsang BK, Platts DG, Javorsky G, Brown MR.Right
ventricular thrombus detection and multimodality
394
K. El-Kersh and B. A. Jalil
imaging using contrast echocardiography and cardiac magnetic resonance imaging. Heart Lung Circ.
2012;21(3):185–8.
13. Horner SM, Bell JA, Swanton RH.Infected right atrial
thrombus—an important but rare complication of central venous lines. Eur Heart J. 1993;14(1):138–40.
14. Mansencal N, Revault-d’Allonnes L, Pelage JP,
Farcot JC, Lacombe P, Dubourg O.Usefulness of contrast echocardiography for assessment of intracardiac
masses. Arch Cardiovasc Dis. 2009;102(3):177–83.
15. Zaragoza-Macias E, Chen MA, Gill EA. Real
time three-dimensional echocardiography evaluation of intracardiac masses. Echocardiography.
2012;29(2):207–19.
16. Cohen GI, Klein AL, Chan KL, Stewart WJ, Salcedo
EE. Transesophageal echocardiographic diagnosis
of right-sided cardiac masses in patients with central
lines. Am J Cardiol. 1992;70(9):925–9.
17. Barrios D, Rosa-Salazar V, Morillo R, Nieto R,
Fernandez S, Zamorano JL, etal. Prognostic signif-
icance of right heart thrombi in patients with acute
symptomatic pulmonary embolism: systematic review
and meta-analysis. Chest. 2017;151(2):409–16.
18. Koc M, Kostrubiec M, Elikowski W, Meneveau N,
Lankeit M, Grifoni S, etal. Outcome of patients with
right heart thrombi: the right heart thrombi European
registry. Eur Respir J. 2016;47(3):869–75.
19. Rivera-Lebron B, McDaniel M, Ahrar K, Alrifai A,
Dudzinski DM, Fanola C, etal. Diagnosis, treatment
and follow up of acute pulmonary embolism: consensus practice from the PERT consortium. Clin Appl
Thromb Hemost. 2019;25:1076029619853037.
20. Carroll BJ, Larnard EA, Pinto DS, Giri J, Secemsky
EA. Percutaneous Management of High-Risk
Pulmonary Embolism. Circ Cardiovasc Interv.
2023;16(2):e012166. https://doi.org/10.1161/
CIRCINTERVENTIONS.122.012166. Epub 2023
Feb 6. PMID: 36744463.
Diagnosing Acute Aortic
Syndromes withUltrasound
MeghanSnuckel andAndrewT.Levinson
32
Learning Objectives
1. Review aortic pathology relevant to critically
ill patients.
2. Describe image acquisition of the aorta via
transthoracic and transabdominal views.
3. Examine the diagnostic accuracy of TTE and
TEE for detecting acute aortic pathology.
4. Evaluate the evidence for the use of POCUS
in the rapid diagnosis of aortic syndromes.
Introduction
Imaging of the aorta with ultrasound can be critical in the rapid triage of the patient who presents
with back, abdominal, or chest pain and hypotension or shock. Acute aortic syndromes and emergencies in critically ill or injured patients include
ruptured abdominal aortic aneurysm, traumatic
aortic injury, aortic dissection, and aortic intraluminal thrombus. Acute aortic syndromes can
either be spontaneous or traumatic and are often
difcult to diagnose. Delayed diagnosis and mis-
Supplementary Information The online version contains supplementary material available at https://doi.
org/10.1007/978- 3- 031- 80038- 2_32.
diagnosis of acute aortic syndromes contribute to
signicant morbidity and mortality [1–3].
Risk factors for acute aortic pathology include
a history of connective tissue disease, family history, aortic valve disease, hypertension, known
prior aortic aneurysm, hyperlipidemia, COPD,
smoking history, and prior aortic endovascular
procedures or previous aortic surgeries [4].
Presenting symptoms of acute aortic pathology
can be non-specic and include chest pain, back
pain, abdominal pain, syncope, and focal neurological decits. Confounding the diagnosis is the
fact that a signicant percentage of patients with
acute aortic pathology may not have signicant
symptoms. Exam ndings may include diastolic
murmurs, pulse decit, and hypotension [2].
Aortic pathology can be detected and characterized by various radiographic modalities,
including chest radiography, contrast-enhanced
computed tomography (CT), trans-thoracic echocardiogram (TTE), trans-abdominal ultrasound,
trans-esophageal echocardiography (TEE), magnetic resonance imaging (MRI), and angiography. In trauma, a positive Focused Assessment
with Sonography for Trauma (FAST) exam
showing free uid in the abdomen may be an
indication for surgery in an unstable patient.
M. Snuckel · A. T. Levinson (*)
Division of Pulmonary, Critical Care, and Sleep
Medicine, The Warren Alpert Medical School,
Brown University, Providence, RI, USA
e-mail: andrew_levinson@brown.edu
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2025
M. J. Lanspa, A. T. Levinson (eds.), Echocardiography and Ultrasonography in the ICU,
Respiratory Medicine, https://doi.org/10.1007/978-3-031-80038-2_32
395
396
M. Snuckel and A. T. Levinson
Aortic Dissection
An aortic dissection results from a disruption in
the medial layer of the aorta, often in the setting
of an aortic intimal tear. Ultrasound ndings consistent with possible aortic dissection include
pericardial effusions, intimal aps, or an aortic
outow track diameter measuring more than
35mm [5] (Videos 32.8, 32.9, 32.10, and 32.11).
DeBakey and Stanford are two different classication systems to describe the location of aortic dissections that are used. DeBakey type I
includes the ascending aorta, arch, and descending thoracic aorta. Debakey type II, in contrast, is
limited to the ascending aorta, while Debakey
type III includes the descending aorta distal to the
left subclavian artery origin. Stanford classication type A includes the ascending aorta, while
type B does not involve the ascending aorta. Most
Stanford type B dissections are distal to the left
subclavian artery but may include the arch
involvement without involving the ascending
aorta [2]. Stanford type A dissections are mostly
managed surgically, while Stanford type B dissections involving the descending aorta are usually managed medically [3, 6].
Abdominal Aortic Aneurysm
An abdominal aortic aneurysm is dened as any
focal dilation along the abdominal aorta. The
aneurysm can be anywhere from an incidental
nding requiring incremental radiographic monitoring to emergent surgery. When evaluating aortic size with ultrasound, the accepted standard is
to measure the inner-to-inner maximum anteriorposterior aortic diameter [4].
At the level of the infrarenal aorta, an abdominal aortic aneurysm is considered to be present
when the inner-to-inner diameter exceeds 3.0cm
[3]. Surgery and/or endovascular repair should be
considered for symptomatic or quickly expanding. Aneurysms >4cm and poorly controlled diastolic blood pressure are risk factors for rupture
[3] (Video 32.5, 32.6, and 32.7).
Aortic Thrombus
Multiple etiologies of acute aortic clot (Video
32.6) have been described, including secondary
to aortic dissection, AAA, atrial brillation, and
other factors predisposing to hypercoagulability
[7]. Treatment may include systemic anticoagulation, anti-thrombotic therapy, maximal medical
therapy, and/or surgery.
Image Acquisition
Images of the aorta can be obtained by transthoracic and transabdominal views and by TEE.To
visualize the aorta, standard TTE views and
abdominal ultrasound are recommended.
For the thoracic aorta, transthoracic image
acquisition refers to the subcoastal views sections in Chap. 5: transthoracic echocardiography
views and windows. For TEE, see Chap. 9: TEE
views. Transthoracic views often allow imaging
of the ascending aorta and aortic arch, descending thoracic aorta, and the origins of the right brachiocephalic, left common carotid, and left
subclavian arteries. It is recommended that particular attention be placed on the parasternal and
apical and subcostal views with the patient supine
and/or in the left lateral decubital position [2].
It has also been described in the literature that
in patients with pneumonia and/or consolidation
patterns, the thoracic descending aorta and even
occasionally the aortic arch can be well visualized with TTE, positioning the probe on the left
lateral and posterior chest wall [8].
Abdominal aorta image acquisition and views
are well described in the literature [9]. For
abdominal views (Videos 32.1, 32.2, and 32.3),
the proximal (Image 32.1), mid (Images 32.2 and
32.3), and distal abdominal aorta (Images 32.4
and 32.5) should be visualized and measured
both in transverse and longitudinal views. The
aorta is visualized deep into the IVC.If there is
any confusion about whether the IVC or aorta is
being visualized, compression and the use of
Doppler signaling may be helpful.
32 Diagnosing Acute Aortic Syndromes withUltrasound
Image 32.1 Transverse
axis, proximal aorta,
“seagull sign”. AA
abdominal aorta, SA
splenic artery, HA
hepatic artery, CT celiac
trunk, IVC inferior vena
cava, VB vertebral body
Image 32.2 Transverse
axis, mid abdominal
aorta. AA abdominal
aorta, LRV left renal
vein, IVC Inferior vena
cava, SV splenic vein,
SMA superior
mesenteric artery
397
398
Image 32.3
Longitudinal view,
proximal and mid
abdominal aorta with
branching of the celiac
and superior mesenteric
artery. CT celiac trunk,
SMA superior
mesenteric artery
Image 32.4 Transverse
view, distal abdominal
aorta. AA Abdominal
aorta
M. Snuckel and A. T. Levinson