Ultrasound in cardiac trauma

    Ultrasound in cardiac trauma Theodosios Saranteas MD, Andreas F. Mavrogenis MD, Christina Mandila MD, John Poularas MD, Fotios Panou PII: DOI: Reference:

S0883-9441(16)30680-3 doi: 10.1016/j.jcrc.2016.10.032 YJCRC 52335

To appear in:

Journal of Critical Care

Please cite this article as: Saranteas Theodosios, Mavrogenis Andreas F., Mandila Christina, Poularas John, Panou Fotios, Ultrasound in cardiac trauma, Journal of Critical Care (2016), doi: 10.1016/j.jcrc.2016.10.032

This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

ACCEPTED MANUSCRIPT Ultrasound in cardiac trauma

T

Theodosios Saranteas, MD;* Andreas F. Mavrogenis, MD#;

RI P

Christina Mandila, MD;≠ John Poularas, MD;≠ Fotios Panou†

SC

From the *Department of Anaesthesiology, the #First Department of Orthopaedics and the †Second department of Cardiology, National and Kapodistrian University of

MA NU

Athens, School of Medicine, ATTIKON University Hospital, Athens, Greece, and the ≠Intensive care unit, General state hospital of Athens, Athens Greece

ED

Running head: US in cardiac trauma

AC

CE

PT

Conflicts of Interest: All authors declare no conflicts of interest.

Correspondence Andreas F. Mavrogenis, MD First Department of Orthopaedics

National and Kapodistrian University of Athens, School of Medicine 41 Ventouri Street, 15562, Holargos, Athens, Greece Tel/Fax: 0030-210-6542800 E-mail: [email protected]

ACCEPTED MANUSCRIPT Abstract In the perioperative period, the emergency room or the intensive care unit accurate

T

assessment of variable chest pain requires meticulous knowledge, diagnostic skills

RI P

and suitable usage of various diagnostic modalities. Additionally, in polytrauma patients, cardiac injury including aortic dissection, pulmonary embolism, acute

SC

myocardial infarction, and pericardial effusion should be immediately revealed and

MA NU

treated. In these patients, arrhythmias, mainly tachycardia, cardiac murmurs, or hypotension must alert physicians to suspect cardiovascular trauma, which would potentially be life threatening. Ultrasound

of

the

heart

using

transthoracic

and

transesophageal

ED

echocardiography are valuable diagnostic tools that can be used interchangeably in conjunction with other modalities such as the electrocardiogram (ECG) and computed

PT

tomography (CT) for the diagnosis of cardiovascular abnormalities in trauma patients.

CE

Although ultrasound of the heart is often underutilized in the setting of trauma, it does have the advantages of being easily accessible, noninvasive, and rapid bed-side

AC

assessment tool. In this review article aims to analyze the potential cardiac injuries in trauma patients, and to provide an elaborate description of the role of echocardiography for their accurate diagnosis.

Keywords: Ultrasound; Cardiac trauma; Emergency; Intensive care.

ACCEPTED MANUSCRIPT Introduction In the perioperative period, the emergency room or the intensive care unit (ICU)

T

accurate assessment of variable chest pain requires meticulous knowledge, diagnostic

RI P

skills and suitable usage of various diagnostic modalities. Aortic dissection, pulmonary embolism, acute myocardial infarction, and pericardial effusion are

SC

common traits of acute chest pain [1-4]. Additionally, in polytrauma patients, cardiac

MA NU

injury should be immediately revealed and treated; in these patients, arrhythmias, mainly tachycardia, cardiac murmurs, or hypotension must alert physicians to suspect cardiovascular trauma, which would potentially be life threatening [5-7]. Transthoracic (TTE) and transesophageal (TEE) echocardiography are

ED

valuable diagnostic tools that can be used interchangeably in conjunction with other modalities such as the electrocardiogram (ECG) and computed tomography (CT) for

PT

the diagnosis of cardiovascular abnormalities in trauma patients. Echocardiography

CE

can be employed successfully to assess and monitor cardiovascular hemodynamics by examining the left ventricular function and the cardiac preload through measurements

AC

of the heart chambers and inferior vena cava (IVC) diameters, in addition to excluding any fatal cardiac pathology such as cardiac tamponade, rupture of the coronary arteries and valvular dysfunction [4,8]. Although TTE is often underutilized in the setting of trauma, it does have the advantages of being easily accessible, noninvasive, and rapid bed-side assessment tool. Considering the fact that throughout the perioperative period heart function and its abnormalities cannot be easily evaluated by TEE in awake patients, and that TTE is an absolutely non-invasive and innocuous monitoring modality, its application to appraise patients’ hemodynamic status is very important [4]. Currently, pocket-sized ultrasound devices have been available for TTE [9,10]. These devices have a size almost similar to a smart phone

ACCEPTED MANUSCRIPT and are equipped with a single or dual transducer; they can provide B-mode imaging, color-flow Doppler, and two-dimensional (2D) measurements of cardiac structures, as

T

well as a recording of still images and video clips [9,10].

RI P

This review article aims to analyze the potential cardiac injuries in trauma patients, and to provide an elaborate description of the role of echocardiography for

Hemorrhage and hypotension

MA NU

SC

their accurate diagnosis.

In trauma patients with hypotension, the emergency physician should promptly recognize a non-cardiac injury as a cause, such as hemorrhage with subsequent

ED

hypovolaemia. In this setting, the echocardiogram can clearly reveal a small and underfilled left ventricle with preserved or hyperdynamic function (video 1) [4, 9,11].

PT

Additionally, in patients with a medical history of hypertension and left ventricular

CE

hypertrophy, the hypovolemia/bleeding can lead to dynamic left ventricular out-flow tract obstruction due to systolic anterior motion of the mitral valve. Additionally,

AC

secondary mitral regurgitation can be identified; surprisingly, in these patients, right heart catheterization will reveal high pulmonary occlusion pressures due to mitral valve regurgitation (video 2) [11]. In these cases, physicians can be misled and consider a status of intravascular volume overload. Failure to appraise properly this phenomenon may result in excessive administration of diuretics and vasopressors, which instead to improve they worsen hemodynamics [11]. Therefore, in patients with progressive hypotension, without restoration but even with deterioration of blood pressure after administration of intravenous vasopressors, physicians should suspect hypovolemia and ongoing bleeding as a cause of the hemodynamic instability.

ACCEPTED MANUSCRIPT The echocardiogram per se cannot lead to the diagnosis of hemorrhage; a hyperdynamic left ventricle can be an indirect sign of hypovolemia, but this is not

T

always the case. For instance, a hyperdynamic ventricle could result from low

RI P

peripheral resistance as occurs in sepsis or post-traumatic systemic inflammatory response syndrome [11].

SC

Small diameter cardiac chambers may provide a reliable evidence of low

MA NU

cardiac preload. However, in practice, when the cardiac function is evaluated by TTE or TEE, physicians generally do not have preoperative baseline values of left/right ventricular (LV/RV) diameter, therefore, they cannot reliably assess the relative changes in these diameters [12, 13]. The collapsibility index of the IVC (IVCCI) has

ED

been frequently employed serially for the assessment of patients’ hemodynamic status. The stroke volume (SV) and/or cardiac output (CO) through pulse wave (PW)

PT

Doppler techniques, the mitral annular velocities (TDI Doppler) and mitral inflow

CE

velocities (PW Doppler) seem to be time consuming and cumbersome, and are not routinely used in acute settings for haemodynamic monitoring purposes [13-15]. In

AC

fact, hypovolemic patients can be identified using ultrasound measurements including the size of the IVC and the IVCCI. Right atrial pressures (RAP) are calculated by measuring the IVCCI during inspiration (sniffing test or quite breathing tests) using the following formula [13-15]:

IVCCI = 100 x (IVC maximal diameter – IVC minimal diameter) / IVC maximal diameter.

Inspiration in spontaneously breathing patients causes negative intrathoracic pressure and a decrease in IVC diameter. The transthoracic echocardiographic subcostal window can be used to view the IVC. M-mode imaging allows high–frame

ACCEPTED MANUSCRIPT rate measurements of size changes throughout the respiratory cycle. Assessment of baseline values is not obligatory when evaluating dynamic measurements such as the

T

IVCCI. In fact, fluctuations of IVC diameter throughout respiration test are closely

RI P

associated with central venous pressure (CVP) (videos 3 and 4). An IVC diameter of <2.1 cm with IVCCI >50% (sniffing test) suggest a normal RAP of 3mmHg (range,

SC

0-5mmHg), whereas an IVC diameter of >2.1 cm with IVCCI <50% suggest a high

MA NU

RAP of 15mmHg (range, 10-20mmHg). In cases that IVC diameter and collapse does not fit the above categories, an intermediate value of 8 mmHg (range, 5-10 mmHg) should be applied. During quite inspiration, a cut-off value of 20% has been suggested for the estimation of the IVCCI [13,16]. In addition, IVCCI assessment for

ED

hemodynamic purposes is not ideal because measurements in mechanically ventilated patients and in patients suffering from constrictive pericarditis, pericardiac fluid

PT

accumulation and pulmonary disorders do not yield accurate results [16,17]. More

CE

important, in mechanically ventilated patients caution is necessary as collapsibility of the IVC will not occur during respiration due to positive intrathoracic pressures;

AC

therefore, the IVCCI should not be used to monitor RAP in this setting [16,17].

Cardiac ventricles trauma Injury of the myocardial walls can be seen either in blunt or penetrating trauma; myocardial injuries range from simple myocardial contusions, usually the most innocuous, to myocardial rupture that invariably causes fatal consequences [18-21]. The distribution of injury amongst the different cardiac chambers mainly pertains to the anterior location of the right heart in the chest cavity. Therefore, right ventricle and atria injuries are the most common cardiac injuries accounting for 17-32% and 865%, respectively [18,19]. More specifically, in blunt trauma the heart can be

ACCEPTED MANUSCRIPT compressed in the bony thorax as it is well encompassed between the ribs, the sternum and the thoracic vertebra. Additionally, severe abdominal compression can

T

lead to rapid increase in blood flow to the heart via the IVC, thus leading to

RI P

chambers’ rupture from abrupt increase of intracardiac pressures [20,21]. Because of its anterior location, the right ventricle is the most vulnerable to

SC

cardiac trauma. The anteroapical region of the left ventricle is also vulnerable,

MA NU

particularly to left lateral collisions. At echocardiography, right or left ventricular dysfunction may be seen, often in a regional (non-coronary) distribution (video 5). The contused area may show increased echogenicity and thickness because of tissue edema (Fig. 1). Dilation of cardiac chambers (particularly in right ventricular trauma)

ED

can be visualized and may indirectly lead to the diagnosis of myocardial injury [2025]. Dysfunction of the left or right ventricle can lead to sluggish blood flow into the

PT

heart chambers predisposing to thrombus formation (Fig. 2). Traumatic rupture of the

CE

heart can also occur in fatal blunt chest injury; atria rupture in this case is considered far more common than ventricular rupture [20-25].

AC

In penetrating cardiac trauma, if the injuries are not fatal, myocardial laceration and perforations can occur, eventually weakening the wall of the ventricle and in due course contributing to the formation of ventricular aneurysms [26,27]; thrombi can be seen within the sac of the aneurysms [27-29]. Generally, in chest trauma TTE is easily available, but image quality may be very poor because of pneumothorax and chest-wall injuries [23,25]. Cardiac dysfunction can be also faced in polytrauma patients with non cardiac trauma (video 6). Traumatic brain injury can cause a systemic massive catecholamine release stemming from activation of the central neuroendocrine axis, which, in turn, may lead to an abrupt surge in the sympathetic nervous system outflow [30]. This is a

ACCEPTED MANUSCRIPT potential mechanism that aims to maintain the cerebral perfusion in the presence of raised intracranial pressure (ICP). In this setting, hyper activation of the sympathetic

T

nervous system may have deleterious adverse effects on the heart. Neurogenic

RI P

cardiovascular dysfunction may induce minimal clinical manifestation, but in severe cases detrimental outcome such as cardiogenic shock may occur [31]. Myocardial

SC

stunning is the main trait of this clinical entity. Impaired left ventricular function with

MA NU

multiple wall motion abnormalities is often associated with this condition. Myocardial wall abnormalities predominately reflect the distribution of sympathetic nerves rather than a certain vascular distribution of a diseased coronary artery. More specifically, any regional wall motion abnormalities extending beyond a single

pheochromocytoma

or

myocarditis

can

be

considered

as

stress-induced

PT

cardiomyopathy [32,33].

ED

epicardial artery distribution in the absence of obstructive coronary disease,

CE

Takotsubo is a particular form of stress-related cardiomyopathy syndrome mimicking an acute coronary event [34]. Takotsubo cardiomyopathy can present as

AC

an isolated apical dysfunction of the left ventricle with apical/mid-ventricular akinesis compensated by basal hyper-kinesis. Four types of takotsubo cardiomyopathy have been recognized. Apical takotsubo cardiomyopathy accounts for the majority of cases (81.7%), followed by the midventricular (14.6%), basal (2.2%) and focal (1.5%) forms. Ventricular thrombi (1.3%) may develop within the hypo-kinetic left ventricle (video 7) [35]. Beyond the striking echocardiogram, markedly prolonged S-T segment, arrhythmias, S-T segment elevation, T-wave inversion may contribute to the correct diagnosis [34,35].

ACCEPTED MANUSCRIPT Coronary arteries trauma Blunt coronary arterial injury is extremely rare but may occur after direct trauma with

T

intimal disruption and thrombosis with fatal consequences. Injury almost invariably

RI P

occurs with severe myocardial contusion, and usually involves the left anterior descending coronary artery that lies anterior in the chest beneath the sternum [36-40].

SC

Additionally, in blunt injuries major compression of the heart in the chest cavity

MA NU

produces a sudden increase in intraventricular pressures. Coronary vessels injury occurs by transfer of this pressure wave from the heart chambers down to coronary sinus and then to the coronary vascular system. Additionally, rapid elevation of intraaortic pressure caused by sudden external impact to the upper abdomen may lead to

ED

coronary vessels disruption, particularly during cardiac systole where the aortic valve is closed during the traumatic impact [36-43]. Sequelae of such injuries may be life

ventricular

failure,

and

delayed

ventricular

rupture

[36-43].

CE

arrhythmias,

PT

threatening, and include myocardial infarction, formation of thrombi and emboli,

Echocardiography and colour Doppler techniques may provide important evidence

AC

since an injury of the coronary vessels can be translated in regional wall motion abnormalities of the left ventricle with or without synchronous right ventricular dysfunction. Obviously, additional work up including coronary angiography may confirm the diagnosis of the injured coronary circulation [23,44,45].

Cardiac valves trauma Blunt cardiac injury can cause valvular trauma including the pulmonary, mitral, aortic, tricuspid and even bioprosthetic valves, which may lead to valvular regurgitation. Pre-existing cardiac valvular disease is associated with increased risk of developing significant valvular disorder after both blunt and penetrating trauma [46-

ACCEPTED MANUSCRIPT 50]. Such acute injuries usually manifest as a combination of tachycardia, left ventricular dysfunction and eventually cardiogenic shock. Penetrating injuries of the

T

cardiac valves are not as common as blunt injuries. The former is frequently

RI P

complicated by valve leaflet perforation and laceration. Penetrating cardiac trauma and valve lacerations often cause minimal valvular regurgitation in the initial phase

SC

that may gradually progress into significant regurgitation lesion requiring

MA NU

cardiovascular surgery [51-52].

Tricuspid valve trauma is the most frequent valvular blunt trauma. Severe elevation of right intraventricular pressure has been shown to result in injury of the tricuspid valvular apparatus including both the chordae and papillary muscles [52].

ED

Furthermore, the right ventricle is immediately behind the sternum, which makes it more vulnerable to blunt trauma [53]. Rupture of the valve is more likely to occur

PT

during cardiac diastole when the right ventricular pressures are low, and more

CE

particularly when the right ventricle is compressed between the sternum and the vertebrae column; in that way, right ventricular pressures soar and lead to rapid

AC

tricuspid valve closure, thus very swiftly and forcefully opposing tricuspid blood flow during the cardiac diastole. The most frequently reported injury is chordae rupture, followed by rupture of the anterior papillary muscle and leaflet tear, primarily of the anterior leaflet [54]. The right ventricle has also been shown to be susceptible to indirect injury by a sudden increase in intracardiac pressure stemming from compression forces to the upper abdomen [54-56]. Post-traumatic aortic valve regurgitation may occur in polytrauma patients of any age and is often observed with sternum or multiple rib fractures [57,58]. Aortic valve trauma occurs during systole or early diastole because of compressive forces that may arise following a deceleration injury. At this point, the pressure in the aorta

ACCEPTED MANUSCRIPT increases and the aortic valve closes while the left ventricle contracts with maximum force [57,58].

T

Mitral valve dysfunction is very rare in traumatic chest injuries; once it occurs,

RI P

important clinical and echocardiographic signs are visualized. In deceleration injuries, sudden heart displacement as the result of anterior movement of the chest causes

SC

accelerated blood flow toward the myocardium and the mitral valve. This wave

MA NU

causes a sudden increase in intracardiac pressure and pushes on the closed valve causing extension of mitral valve supporting apparatus (chordae and papillary muscles). This pressure wave predisposes to mitral valve injuries extending from leaflet tear to chordae and papillary muscles rupture (Fig. 3A) [47,59,60].

ED

In terms of echocardiography, valvular regurgitation can be easily detected with colour flow imaging (Fig. 3B). Hyperdynamic ventricles can be visualized as an

PT

attempt to compensate the abrupt rise in cardiac preload produced by the acute mitral

CE

regurgitation. TEE has an important role in depicting not only the valves but all the perivalvular anatomy, thus enabling physicians to perceive well the exact mechanism

AC

of valvular regurgitation [46-50].

Pericardial bleeding/Cardiac tamponade Cardiac tamponade is accumulation of blood in the pericardium that occurs when a sufficient volume of blood develops enough pressure to hamper cardiac filling. At admission, the patients experience hypotension and distended neck veins. Echocardiography is an extremely helpful diagnostic tool for the diagnosis of pericardial bleeding/cardiac tamponade [61,62]. Gunshot or stab wounds, blunt trauma to the chest, accidental perforation or broken ribs, are frequent causes of traumatic cardiac tamponade. Although cardiac

ACCEPTED MANUSCRIPT tamponade in trauma is most commonly associated with penetrating injuries, blunt trauma of the chest may also cause pericardial bleeding originating from the heart

T

itself, the major or the pericardial vessels. Although blunt rupture of pericardial

RI P

vessels is rare, it may be the most severe form of all blunt cardiac injuries [63-67]. As well as the heart can be traumatized due to direct impact onto the chest wall, an

SC

increase of intrathoracic pressure from compressive forces to the abdomen can induce

MA NU

multiple injuries in the pericardium on both the diaphragmatic and pleural surfaces [63-68]. Slow bleeding (often from pericardial laceration) may lead to tamponade developing late. Therefore, it may be necessary to repeat the imaging work up and clinical evaluation, over the next hours, days, or even weeks after the injury [69].

ED

The optimal echocardiographic modality for detection and evaluation of cardiac tamponade is the 2-dimentional echocardiography for visualization of

PT

pericardial blood effusion. The size of echo-free space depends on the amount of fluid

CE

in the pericardial sac [69]. Normally, there may be very small amount of pericardial fluid (5-10ml) between the two layers in the posterior atrioventricular junction on

AC

parasternal long axis view. As effusion increases, the echo free space extends circumferentially around the heart. Gelatinous echodense materials can rarely be seen floating within the pericardial fluid (video 8). Loculated effusions are more common when merely a scarring of the pericardium has occurred [62,70]. The diastolic collapse of the right atrium (greater than a third of systole) and the diastolic collapse of the right ventricle (absent in right ventricle hypertrophy or myocardial

wall

infiltrations)

are

probably

the

most

known

signs

on

echocardiography, and are the signs that occur most frequently in cardiac tamponade. These signs are better visualized on 2-dimensional echocardiogram with 4-chamber apical and subcostal views [70-73]. Abnormal reciprocal changes in ventricular size

ACCEPTED MANUSCRIPT during respiration (septum movement toward the LV with inspiration, and toward the RV during expiration), exaggerated respiratory changes in aortic, mitral and tricuspid

T

flows, dilatation of the inferior vena cava with no respiratory changes in its diameter

RI P

(sensitive, but less specific for cardiac tamponade) (Fig. 4), and blunted systolic and diastolic flows in hepatic veins are also supportive findings for the diagnosis of

SC

cardiac tamponade [70-73]. Additionally, in patients with acute cardiac tamponade,

MA NU

such as those with cardiac trauma, the amount of effusion may be quite small, and either the clinical and echocardiographic signs may be difficult to recognize due to the critical patients’ condition. In such cases, clinical suspicion of the disorder is life saving [70-73].

ED

Pericardial wounds that open into the pleura may be associated with free bleeding into the pleural space. Such patients will experience signs and symptoms of

PT

hemothorax, hypovolemia, shock and hypoxia. In these cases, combined lung and

CE

heart ultrasonography may provide for immediate diagnosis (Fig. 5) [74]. Additionally, TTE-guided pericardiocentesis may minimize the risk of pneumothorax

AC

and cardiac wall puncture by providing direct visualization of the fluid-filled space through sub costal views (Fig. 6) [75]. Nevertheless, all the aforementioned data must be considered in combination with those from the clinical evaluation in order to achieve a comprehensive interpretation of the cardiovascular status and to guide decision-making.

Thoracic aorta trauma Traumatic disruption of the thoracic aorta or its branches is a common cause of sudden death in patients with blunt thoracic trauma. Blunt trauma to the thorax usually causes dissection of the ascending aorta at the area of ligamentum Botalli

ACCEPTED MANUSCRIPT (aortic isthmus). More than 80% of cases are due to severe deceleration injury, especially in motor vehicle collisions at a speed of >70km/h. Despite the severe

T

nature of the injury, the clinical signs of aortic trauma are often occult and the

RI P

diagnosis is easily missed [76-83]. There are 2 known classifications of aortic aneurysms, Stanford’s and De Bakey’s. A new classification has also been proposed class

1

(classic

aortic

dissection),

SC

including

class

2

(intramural

MA NU

hematoma/haemorrhage), class 3 (subtle-discrete aortic dissection), class 4 (plaque rupture and ulceration), and class 5 (traumatic and iatrogenic aortic dissection) [80]. Transesophageal echocardiography (TEE) is a non-invasive procedure that has been suggested by many authors as the diagnostic modality of choice to supplant

ED

aortography in the evaluation of aortic trauma [76,77]. The multicenter European Cooperative Study reported that TEE was at least equal to computed tomography

PT

(CT) and aortography for the diagnosis of aortic dissection with a sensitivity of 90%

CE

[78]. In the past, aortography was the gold standard for the diagnosis of aortic trauma [78]. Currently, TEE is reported to have a sensitivity of 94-100% and a specificity of

AC

77-100% for identifying an intimal flap [76-78]. Recent studies have reported a sensitivity and specificity of 100% for TEE, helical CT scans, and magnetic resonance imaging, whereas conventional CT scans (probably the most widely used technique) is less accurate (sensitivity 83-94% and specificity 87-100%) [83]. Enhanced CT is a very reliable technique for the diagnosis of aortic dissection, with a specificity approaching that of aortography [78-83]. TTE may be used for the diagnosis of aortic aneurysms solely located in the proximal portion of the aorta (video 9). The limitations of TTE include poor visualization of intramural hematoma, and inability for thorough identification of the upper segment of ascending aorta or entry tear location. A multiplane approach

ACCEPTED MANUSCRIPT permits visualization of the entire ascending aorta in the majority of patients. Contrast enhancement substantially improves TTE for the diagnosis of aortic dissection [84].

T

However, negative initial aortic imaging with TTE always entails a second imaging

RI P

study with higher specificity.

Endoluminal stent grafting has recently been introduced as a new therapeutic

SC

modality in patients with acute type B aortic dissection in which the primary tear is

MA NU

located distal to the left subclavian artery and for whom surgery is an absolute indication. Although this procedure is usually performed in the operating room under fluoroscopy and angiographic guidance, there are several restrictions for patients with aortic dissection in whom the anatomy and subsequently the ideal angulation of the

ED

thoracic aorta in the chest is difficult to obtain by a mobile C-arm [84,85]. By virtue of the ability to visualize these anatomic portions of the thoracic aorta, intravascular

PT

ultrasound imaging (IVUS) and TEE (video 10) has occasionally been put forward to

CE

fluoroscopy during endovascular thoracic aortic repair [84-87].

AC

Fat embolism

Fat embolism consists of circulation of fat globules in the lung parenchyma and peripheral circulation following major trauma. Fat embolism syndrome (FES) is a serious sequel of fat embolism that lead to an extensive scale of clinical symptoms and signs [88,89]. It is most commonly seen after fractures of long bones and the pelvis, and it is more common in closed rather than open fractures. FES typically presents 24-72 hours after trauma. Rarely, manifestations emerge as early as 12 hours or as late as 2 weeks. The classic triad of respiratory changes, neurological abnormalities and petechial rash is the common clinical trait of this syndrome [88,89].

ACCEPTED MANUSCRIPT During hip replacement, acetabular and femoral canal preparation and especially intramedullary instrumentation cause bone marrow extravasation and

T

release of fat emboli in the systemic circulation [90]. In total hip arthroplasty patients,

RI P

fat embolism is believed to be related to the high intramedullary pressures caused by instrumentation during the procedure [91].

SC

Echocardiography can reveal large quantities of echogenic material [92,93].

MA NU

Although both TTE and TEE can be used to reveal the fatty material in the right atrium or the IVC after lower extremity trauma (Fig. 8 and video 11) [92,93]. Multiple small masses of 1-10 mm diameter can be visualized, as well as large discrete echogenic masses up to 8 cm. Studies using intraoperative TEE have detected

ED

fat embolism in 41% of patients during fixation of long bone fractures [92]. The dimension of the hemodynamic and blood gas analytical changes correlate well with

PT

the intensity of the echocardiographically proved emboli [93,94]. Pulmonary fat

CE

embolism will also lead to increased pressures in the pulmonary circulation and subsequently in the right atrium; dilatation of the right ventricle, interventricular

AC

septum shift to the left ventricle or open of the flap valve of the fossa ovalis that enables embolic material to cross to the left side of the heart may be also depicted with echocardiography [95].

Deep Vein and cardiac thromboembolism Venous thromboembolism (VTE) is a common complication in the perioperative period in injured patients. Risk factors for DVT in these patients include surgical trauma, catheters, immobility and use of muscular blockade agents. In trauma patients, trauma itself can trigger a systemic hyper-coagulant reaction due to excessive activation of the coagulation cascade and increased fibrinolytic inhibition

ACCEPTED MANUSCRIPT [96-99]. These factors alone or together with the presence of foreign materials such as central venous catheters can contribute synergistically to formation of thrombi [100-

T

102]. TTE and TEE have been used in the perioperative setting for the exclusion of

RI P

thrombi and other procoagulant states such as spontaneous echo contrast in the great veins and/or cardiac chambers, (Fig. 9; videos 12 and 13), as well as to aid the

SC

diagnosis of pulmonary embolism [100-102]. IVC identification with TTE can also

MA NU

confer visualization of IVC filters inserted for prevention from pulmonary embolism, thus ruling out complications such as filter migration in the right atrium or thrombosis [103].

ED

Future perspectives

Three-dimensional echocardiography (3DE) has gain popularity the last years and

PT

thus far it supplements 2-dimentional echocardiography. Recent advances in 3D-TEE

CE

allow for better assessment of valvular heart disease or guidance of interventional procedures [104,105]. In this setting, 3DE may provide beneficial information on the

AC

anatomy of the valves due to its better anatomic and spatial resolutions [104]. Unlike mitral and aortic valves, simultaneous visualization of the 3 tricuspid leaflets cannot be achieved with 2-dimensional echocardiography due to valve orientation with respect to the imaging planes; therefore, multiple imagine planes should be received to clearly delineate the anatomy of the tricuspid valve. Although tricuspid regurgitation is a rare sequel of cardiac trauma, 3D-TEE provides a surgeon view of the three leaflets of the valve and allows for precise localization of the lesion aiding the surgical planning [106,107].

ACCEPTED MANUSCRIPT Conclusion We performed this study to emphasize on the valuable role of echocardiography for

T

evaluation of cardiac injury in polytrauma patients in the emergency room or the ICU.

RI P

We provided illustrations and videos of echocardiography of trauma patients with cardiac injuries such as aortic dissection, pulmonary embolism, acute myocardial

SC

infarction and pericardial effusion that are common traits of acute chest pain in the

MA NU

trauma setting. We believe that this study would be useful for the emergency

AC

CE

PT

ED

physicians to diagnose cardiovascular trauma.

ACCEPTED MANUSCRIPT References 1.

Papanikolaou J, Makris D, Karakitsos D, Saranteas T, Karabinis A,

T

Kostopanagiotou G, Zakynthinos E. Cardiac and central vascular functional

RI P

alterations in the acute phase of aneurysmal subarachnoid hemorrhage. Crit Care Med 2012;40(1):223-32.

Saranteas T, Alevizou A, Tzoufi M, Panou F, Kostopanagiotou G. Transthoracic

SC

2.

MA NU

echocardiography for the diagnosis of left ventricular thrombosis in the postoperative care unit. Crit Care 2011;9:15(1):R54. 3.

Saranteas T, Kostopanagiotou G, Tzoufi M, Drachtidi K, Knox GM, Panou F. Incidence of inferior vena cava thrombosis detected by transthoracic

ED

echocardiography in the immediate postoperative period after adult cardiac and general surgery. Anaesth Intensive Care 2013;41(6):782-7. Saranteas T, Mavrogenis AF. Holistic ultrasound in trauma: An update. Injury.

PT

4.

5.

CE

2016;47(10):2110-6.

Wolbrom DH, Rahman A, Tschabrunn CM. Mechanisms and Clinical

AC

Management of Ventricular Arrhythmias following Blunt Chest Trauma. Cardiol Res Pract 2016;2016: Epub 2016 Feb 11 6.

de Biasi AR, Seastedt KP, Eachempati SR, Salemi A. Common Cause of Mortality in Trauma but Manageable Nonetheless. Circulation 2015;132(6):53745

7.

Roy-Shapira A, Levi I, Khoda J. Sternal Fractures: a red flag or a red herring? J Trauma 1994;37:59-61.

8.

Kimura BJ, Bocchicchio M, Willis CL, Demaria AN. Screening cardiac ultrasonographic examination in patients with suspected cardiac disease in the emergency department. Am Heart J 2001;142:324.

ACCEPTED MANUSCRIPT 9.

Platz E, Solomon S. Point-of-Care Echocardiography in the Accountable Care Organization. Circulation: Cardiovascular Imaging 2012;5:676-82.

T

10. Saranteas T, Panou F, Manikis D, Mavrogenis A, Kostopanagiotou G,

RI P

Papadimos T. Pocket-sized transthoracic echocardiography for intraoperative monitoring of heart function in spontaneously breathing patients and the optimal

SC

acoustic window. Br J Anaesth 2016;116(4):556-7.

MA NU

11. Feigenbaum H. ICU and operative/perioperative applications: In Feigenbaum, H, Armrstrong WF, Ryan T (eds) Feigenbaums’s Echocardiography, 6th edn. Philadelphia: Lippincott Williams and Wilkins, 2005;pp 637-41. 12. Jozwiak M, Monnet X, Teboul JL. Monitoring: from cardiac output monitoring

ED

to echocardiography. Curr Opin Crit Care 2015;21(5):395-401. 13. Saranteas T, Manikis D, Papadimos T, Mavrogenis AF, Kostopanagiotou G,

PT

Panou F Intraoperative TTE inferior vena cava monitoring in elderly orthopaedic

CE

patients with cardiac disease and spinal-induced hypotension. J Clin Monit Comput 2016. [Epub ahead of print]

AC

14. Machare-Delgado E, Decaro M, Marik PE. Inferior vena cava variation compared to pulse contour analysis as predictors of fluid responsiveness: a prospective cohort study. J Int Care Med 2011;26:116-24. 15. Porter TR, Shillcutt SK, Adams MS, Desjardins G, Glas KE, Olson JJ, Troughton RW. Guidelines for the use of echocardiography as a monitor for therapeutic intervention in adults: a report from the American Society of Echocardiography. J Am Soc Echocardiogr 2015;28(1):40-56. 16. Rudski LG, Lai WW, Afilalo J, et al. Guide lines for the echocardiographic assessment of the right heart in adults: a report from the American Society of Echocardiography endorsed by the European Association of Echocardiography, a

ACCEPTED MANUSCRIPT registered branch of the European Society of Cardiology and the Canadian Society of Echocardiography. J Am Soc Echocardiogr 2010;23(7):691-2.

T

17. Via G, Tavazzi G, Price S. Ten situations where inferior vena cava ultrasound

of view. Intensive Care Med 2016;42(7):1164-7.

RI P

may fail to accurately predict fluid responsiveness: a physiologically based point

SC

18. Schultz JM, Trunkey DD. Blunt cardiac injury. Crit Care Clin 2004;20(1):57-70.

MA NU

19. Mattox KL, Flint LM, Carrico CJ, Grover F, Meredith J, Morris J, Rice C, Richardson D, Rodriquez A, Trunkey DD. Blunt cardiac injury. J Trauma 1992;33(5):649-50.

20. Chirillo F, Totis O, Cavarzerani A, Bruni A, Farnia A, Sarpellon M, Ius P, Valfrè

ED

C, Stritoni P. Usefulness of transthoracic and transoesophageal echocardiography in recognition and management of cardiovascular injuries after blunt chest

PT

trauma. Heart 1996;75(3):301-6.

CE

21. Sybrandy KC, Cramer MJ, Burgersdijk C. Diagnosing cardiac contusion: old wisdom and new insights. Heart 2003;89:485-9.

AC

22. Crown LA, Hawkins W. Commotio cordis: clinical implications of blunt cardiac trauma. Am Fam Physician 1997;55:2467-0. 23. Karalis DG, Victor MF, Davis GA, McAllister MP, Covalesky VA, Ross JJ Jr, Foley RV, Kerstein MD, Chandrasekaran K. The role of echocardiography in blunt chest trauma: a transthoracic and transesophageal echocardiographic study. J Trauma 1994;36(1):53-8. 24. Brathwaite CE, Rodriguez A, Turney SZ, Dunham CM, Cowley R. Blunt traumatic cardiac rupture. A 5-year experience. Ann Surg 1990;212:701-4.

ACCEPTED MANUSCRIPT 25. Weiss RL, Brier JA, O’Connor W, Ross S, Brathwaite CM. The usefulness of transesophageal echocardiography in diagnosing cardiac contusions. Chest

T

1996;109:73-7.

RI P

26. Tesinsky L, Pirk J, al-Hiti H, Malek I. An isolated ventricular septal defect as a consequence of penetrating injury to the heart. Eur J Cardiothorac Surg

SC

1999;15:221-3.

MA NU

27. Jenson B, Kessler RM, Follis F, Wernly JA. Repair of atrial septal defect due to penetrating trauma. Tex Heart Inst J 1993;20:241-3. 28. Bland EF, Beebe GW. Missiles in the heart: a 20 year follow-up report of world war cases. N Engl J Med 1966;274:1039-46.

ED

29. Symbas PN, DiOrio DA, Tyras, DH, Ware RE, Hatcher CR Jr. Penetrating cardiac wounds: significant residual and delayed sequelae. J Thorac Cardiovasc

PT

Surg 1973;66:526-32.

CE

30. Wittstein IS, Thiemann DR, Lima JA, Baughman KL, Schulman SP, Gerstenblith G, Wu KC, Rade JJ, Bivalacqua TJ, Champion HC. Neurohumoral

AC

features of myocardial stunning due to sudden emotional stress. N Engl J Med 2005;352(6):539-48. 31. Nguyen H, Zaroff JG. Neurogenic stunned myocardium. Curr Neurol Neurosci Rep 2009;9:486-491. 32. Prasad A. Apical ballooning syndrome: an important differential diagnosis of acute myocardial infarction. Circulation 2007;115:e56-e59. 33. Medeiros K, O’Connor MJ, Baicu CF, et al. Systolic and diastolic mechanics in stress cardiomyopathy. Circulation 2014;129:1659-1667.

ACCEPTED MANUSCRIPT 34. Hurst RT, Prasad A, Askew JW III, Sengupta PP, Tajik AJ. Takotsubo cardiomyopathy:

a

unique

cardiomyopathy

with

variable

ventricular

T

morphology. JACC Cardiovasc Imaging 2010;3:641-649.

RI P

35. Templin C, Ghadri JR, Diekmann J, et al Clinical Features and Outcomes of Takotsubo (Stress) Cardiomyopathy. N Engl J Med 2015;373(10):929-38.

SC

36. Kulshrestha P, Das B, Iyer KS, Sampath KA, Sharma ML, Rao IM, Venugopal

MA NU

P. Cardiac injuries--a clinical and autopsy profile. J Trauma 1990;30(2):203-7. 37. Olsovsky MR, Wechsler AS, Topaz O. Cardiac trauma. Diagnosis, management, and current therapy. Angiology 1997;48(5):423-32. 38. Pretre R, Chilcott M. Blunt trauma to the heart and great vessels. N Engl J Med

ED

1997;336(9):626-32.

39. Sabbah HN, Stein PD, Hawkins ET, Viano DC, Vostal JJ. Extrinsic compression

PT

of the coronary arteries following cardiac trauma in dogs. J Trauma

CE

1982;22:937-43.

40. Gaspard P, Clermont A, Villard J, Amiel M. Non-iatrogenic trauma of the

AC

coronary arteries and myocardium: contribution of angiography—report of six cases and literature review. Cardiovasc Intervent Radiol 1983;6:20-9. 41. Fu M, Wu CJ, Hsieh MJ. Coronary dissection and myocardial infarction following blunt chesttrauma. J Formos Med Assoc 1999;98:136-40. 42. Tun A, Khan IA. Myocardial infarction with normal coronary arteries: the pathologic and clinical perspectives. Angiology 2000;52:299-304. 43. Shapiro MJ, Wittgen C, Flynn MS, Zuckerman DA, Durham RM, Mazuski JE. Right coronary artery occlusion secondary to blunt trauma. Clin Cardiol 1994;17:157-9.

ACCEPTED MANUSCRIPT 44. Meluzín J, Groch L, Toman J, Hornácek I, Fischerová B. Rupture of the coronary artery after blunt nonpenetrating chest wall trauma detected by color echocardiography:

a

case

report.

J

Am

Soc

Echocardiogr

T

Doppler

RI P

2000;13(11):1043-6

45. García-Fernández MA, López-Pérez JM, Pérez-Castellano N, Quero LF, Virgós-

SC

Lamela A, Otero-Ferreiro A, Lasara AM, Vega M, Moreno M, Pastor-Benavent

MA NU

JA, Bermejo J, García-Pardo J, Gil de la Peña M, Navia J, Delcán JL. Role of transesophageal echocardiography in the assessment of patients with blunt chest trauma: correlation of echocardiographic findings with the electrocardiogram and creatine

kinase

monoclonal

measurements.

Am

Heart

J

ED

1998;135(3):476-81.

antibody

46. Yousaf H, Ammar KA, Tajik AJ. Traumatic pulmonary valve injury following

PT

blunt chest trauma. Eur Heart J Cardiovasc Imaging. 2015;16(11):1206.

CE

47. Pasquier M, Sierro C, Yersin B, Delay D, Carron PN. Traumatic mitral valve injury after blunt chest trauma: a case report and review of the literature. J

AC

Trauma 2010;68(1):243-6. 48. Reddy VK, Nanda S, Bandarupalli N, Pothineni KR, Nanda NC. Traumatic tricuspid papillary muscle and chordae rupture: emerging role of threedimensional echocardiography. Echocardiography 2008;25(6):653-7. 49. Kim S, Park JS, Yoo SM, Kim KH, Yang WI, Sung JH, Kim IJ, Lim SW, Cha DH, Moon JY. Traumatic aortic regurgitation combined with descending aortic pseudoaneurysm secondary to blunt chest trauma. Cardiovasc J Afr 2014;23;25(5):e5-8.

ACCEPTED MANUSCRIPT 50. Repossini A, Giroletti L, Rosati F, Chiari E, Corsetti G, Muneretto C. Chest Blunt Trauma: An Uncommon Cause of Aortic Stentless Bioprosthesis

T

Dysfunction. Ann Thorac Surg 2015;100(3):1094-6.

RI P

51. Parmley LF, Manion WC, Mattingly TW. Nonpenetrating traumatic injury of the heart. Circulation 1958;18:371-6.

SC

52. Rywik T, Sitkowski W, Cichocki J, Rajecka A, Suwalski K. Acute mitral

MA NU

regurgitation caused by penetrating chest injury. J Heart Valve Dis 1995;4:293-5. 53. Rashid MA, Wikström T, Ortenwall P. Cardiac injuries: a ten-year experience. Eur J Surg 2000;166(1):18-21.

54. Banning AP, Durrani A, Pillai R. Rupture of the atrial septum and tricuspid valve

ED

after blunt chest trauma. Ann Thorac Surg 1997;64(1):240-2. 55. Bortolotti U, Scioti G, Milano A, Guglielmi C, Benedetti M, Tartarini G,

PT

Balbarini A. Post-traumatic tricuspid valve insufficiency. 2 cases of delayed

CE

clinical manifestation. Tex Heart Inst J 1997;24(3):223-5. 56. Perlroth MG, Hazan E, Lecompte Y, Gougne G. Chronic tricuspid regurgitation

AC

and bifascicular block due to blunt chest trauma. Am J Med Sci 1986;291(2):119-25. 57. Pretre R, Faidutti B. Surgical management of aortic valve injury after nonpenetrating trauma. Ann Thorac Surg 1993;56(6):1426-31. 58. Parry GW, Wilkinson GA. Traumatic aortic regurgitation. Injury 1997;28(910):679-80. 59. Hammer MM, Raptis DA, Cummings KW, Mellnick VM, Bhalla S, Schuerer DJ, Raptis CA.Imaging in blunt cardiac injury: Computed tomographic findings in cardiac contusion and associated injuries. Injury 2016;47(5):1025-30.

ACCEPTED MANUSCRIPT 60. Wilke A, Kruse T, Hesse H et al. Papillary muscle injury after blunt chest trauma. J Trauma 1997;43(2):360-1.

RI P

modern medicine. Curr Cardiol Rep 2002;4(1):13-21

T

61. Maisch B, Ristic AD. The classification of pericardial disease in the age of

62. Reid CL, Kawanishi DT, Rahimtoola SH, Chandraratna PA. Chest trauma:

SC

evaluation by two-dimensional echocardiography. Am Heart J 1987;113(4):971-

MA NU

976.

63. Reddy PS, Curtiss EI, Uretsky BF. Spectrum of hemodynamic changes in cardiac tamponade. Am J Cardiol 1990;66:1487-91.

64. Sugg WL, Rea WJ, Ecker RR, Webb WR, Rose EF, Shaw RR. Penetrating

1968;56(4):531-45.

ED

wounds of the heart. An analysis of 459 cases. J Thorac Cardiovasc Surg

PT

65. Jorden RC. Penetrating chest trauma. Emerg Med Clin North Am 1993;11(1):97-

CE

106.

66. Kang N, Hsee L, Rizoli S, Alison P. Penetrating cardiac injury: overcoming the

AC

limits set by Nature. Injury 2009;40:919-27. 67. Marshall DT. The spectrum of findings in cases of sudden death due to blunt cardiac trauma--commotio cordis. Am J Forensic Med Pathol 2008;29:1-4. 68. Farhataziz N, Landay M. Pericardial rupture after blunt chest trauma. J Thorac Imaging 2005; 20:50-2. 69. Fowler NO. Cardiac tamponade. A clinical or an echocardiographic diagnosis? Circulation 1993;87:1738-41. 70. Tsang TS, Oh JK, Seward JB. Diagnosis and management of cardiac tamponade in the era of echocardiography. Clin Cardiol 1999;22(7):446-52.

ACCEPTED MANUSCRIPT 71. Fowler NO, Gobel N. The hemodynamic effects of cardiac tamponade: mainly the result of atrial, not ventricular, compression. Circulation 1985;1:154-7.

T

72. Levitov A, Frankel HL, Blaivas M, Kirkpatrick AW, Su E, Evans D,

RI P

Summerfield DT, Slonim A, Breitkreutz R, Price S, McLaughlin M, Marik PE, Elbarbary Guidelines for the Appropriate Use of Bedside General and Cardiac

SC

Ultrasonography in the Evaluation of Critically Ill Patients-Part II: Cardiac

MA NU

Ultrasonography. Crit Care Med 2016;44(6):1206-27.

73. Kapoor PM. Echocardiography for cardiac tamponade. Ann Card Anaesth 2016;19(2):338.

74. Saranteas T, Santaitidis E, Valtzoglou V, Kostopanagiotou G. Emergency lung

ED

ultrasound examination for the diagnosis of massive-clotted haemothorax in two cardiac surgery patients. Anaesth Intensive Care 2012;40(3):564-5.

PT

75. Callahan JA. Two-dimensional echcoardiographically guided pericardiocentesis:

CE

experience in 117 consecutive patients. Am J Cardiol 1985;55:476-9. 76. Isselbacher EM. Thoracic and abdominal aortic aneurysms. Circulation

AC

2005;11:816-28.

77. Ahrar K, Smith DC, Bansal RC, Razzouk A, Catalano RD. Angiography in blunt thoracic aortic injury. J Trauma 1997;42(4):665-9. 78. Erbel R, Engberding R, Daniel W, Roelandt J, Visser C, Rennolet H, and the European Cooperative Study Group for Echocardiography. Echocardiography in diagnosis of aortic dissection. Lancet 1989;1:457-61. 79. O’Conor CE. Diagnosing traumatic rupture of the thoracic aorta in the emergency department. Emerg Med J 2004;21(4):4149.

ACCEPTED MANUSCRIPT 80. Svenson LG, Labil SB, Eisenhauer AC. Intimal tear without hematoma: an important variant of aortic dissection that can elude current imaging techniques.

T

Circulation 1999;99:1331-6.

RI P

81. Shiga T, Wajima Z, Apfel CC, Inoue T, Ohe Y. Diagnostic accuracy of transesophageal echocardiography, helical computed tomography, and magnetic

SC

resonance imaging for suspected thoracic aortic dissection: systematic review

MA NU

and meta-analysis. Arch Intern Med 2006;166(13):1350-6. 82. Nienaber CA, von Kodolitsch Y, Nicolas V, Siglow V, Piepho A, Brockhoff C, Koschyk DH, Spielmann RP. The diagnosis of thoracic aortic dissection by noninvasive imaging procedures. N Engl J Med 1993;328(1):1-9.

ED

83. Pepi M, Campodonico J, Galli C, Tamborini G, Barbier P, Doria E, Maltagliati A, Alimento M, Spirito R. Rapid diagnosis and management of thoracic aortic

PT

dissection and intramural haematoma: a prospective study of advantages of

CE

multiplane vs. biplane transoesophageal echocardiography. Eur J Echocardiogr 2000;1(1):72-9.

AC

84. Evangelista A, Avegliano G, Aguilar R, Cuellar H, Igual A, González-Alujas T, Rodríguez-Palomares J, Mahia P, García-Dorado D. Impact of contrast-enhanced echocardiography on the diagnostic algorithm of acute aortic dissection. Eur Heart J 2010;31(4):472-9. 85. Lee DY, Williams DM, Abrams GD. The dissected aorta. Part II. Differentiation of the true from the false lumen with intravascular US. Radiology 1997;203:3236. 86. Moskowitz DM, Kahn RA, Konstadt SNS Mitly H, Hollier LH, Marin ML. Intraopcrative transesophageal echocardiography as an adjuvant to fluoroscopy

ACCEPTED MANUSCRIPT during endovascular thoracic aortic repair. Eur J Vasc Endovasc Surg 1999;17:22-27.

T

87. Dounis G, Saranteas T, Mandila C, Papanikolaou I, Poularas J, Kostopanagiotou

RI P

G, Karabinis A. Intimal tear of the descending aorta and stent-graft repair in a trauma patient: the role of transesophageal ultrasound examination in the ICU.

SC

Acta Anaesthesiol Scand 2008;52(8):1172-4.

MA NU

88. Johnson MJ, Lucas G. Fat embolism syndrome. Orthopaedics. 1996;19:41-4. 89. Mellor A, Soni N. Fat embolism. Anaesthesia 2001;56:145-54. 90. Arroyo JS, Garvin KL, McGuire MH. Fatal marrow embolization following a porous-coated bipolar hip endoprosthesis. J Arthroplasty 1994;9(4):449-52.

ED

91. Watson JT, Stulberg BN. Fat embolism associated with cementing of femoral stems designed for press-fit application. J Arthroplasty 1989;4:133-137.

PT

92. Pell AC, Christie J, Keating JF, Sutherland GR. The detection of fat embolism

CE

by transoesophageal echocardiography during reamed intramedullary nailing. A study of 24 patients with femoral and tibial fractures. J Bone Joint Surg Br

AC

1993;75(6):921-5.

93. Saranteas T, Kostopanagiotou G, Panou F. Focused assessed transthoracic echocardiography for the diagnosis of fat embolism in an orthopedic patient with hip hemiarthroplasty. J Cardiothorac Vasc Anesth 2014;28(4):e40-1. 94. Pitto RP, Blunk J, Kössler M. Transesophageal echocardiography and clinical features of fat embolism during cemented total hip arthroplasty Arch Orthop Trauma Surg 2000;120(1-2):53-8. 95. Yeon HB, Ramappa A, Landzberg MJ, Thornhill TS. Paradoxic cerebral embolism after cemented knee arthroplasty: a report of 2 cases and prophylactic option for subsequent arthroplasty. J Arthroplasty 2003;18(1):113-20.

ACCEPTED MANUSCRIPT 96. Coleridge-Smith P, Labropoulos N, Partsch H, Myers K, Nicolaides A, Cavezzi A. Duplex ultrasound investigation of the veins in chronic venous disease of the

T

lower limbs--UIP consensus document. Part I. Basic principles. Eur J Vasc

RI P

Endovasc Surg 2006;31(1):83-92.

97. Knudson MM, Ikosi DG. Venous thromboembolism after trauma. Curr Opin Crit

SC

Care 2004;10:539-48.

MA NU

98. Burke DT. Venous thrombosis in traumatic brain injury. J Head Trauma Rehabil 1996;77:1182-85.

99. Zabalgoitia M, Halperin JL, Pearce LA, Blackshear JL, Asinger RW, Hart RG. Transesophageal

echocardiographic

correlates

of

clinical

risk

of

1998;31:1622-6.

ED

thromboembolism in nonvalvular atrial fibrillation. J Am Coll Cardiol

PT

100. Saranteas T, Poularas J, Mandila C, Kostopanagiotou GG, Karabinis A.

CE

Cardiovascular ultrasound in detecting central venous catheter thrombosis in the intensive care unit: splenectomy and antiphospholipid syndrome. Anaesth

AC

Intensive Care 2010;38(3):574-6. 101. Saranteas T, Mandila C, Poularas J, Papanikolaou J, Patriankos A, Karakitsos D, Karabinis A. Transesophageal echocardiography and vascular ultrasound in the diagnosis of catheter-related persistent left superior vena cava thrombosis. Eur J Echocardiogr 2009;10(3):452-5. 102. Karakitsos D, Saranteas T, Patrianakos AP, Labropoulos N, Karabinis A. Ultrasound-guided "low approach" femoral vein catheterization in critical care patients results in high incidence of deep vein thrombosis. Anesthesiology 2007;107(1):181-2.

ACCEPTED MANUSCRIPT 103. Karakitsos D, Saranteas T, Poularas J, Spyropoulos A, Karabinis A. Catheterrelated thrombosis and inferior vena cava filter implantation in a patient in the

T

intensive care unit: the role of ultrasound monitoring. Acta Anaesthesiol Scand

RI P

2007;51(7):961-2.

104. Houck RC, Cooke JE, Gill EA. Live 3D echocardiography: a replacement for

SC

traditional 2D echocardiography? AJR Am J Roentgenol 2006;187:1092-106.

MA NU

105. Hung J, Lang R, Flachskampf F, Shernan SK, McCulloch ML, Adams DB, Thomas J, Vannan M, Ryan T; ASE. 3D echocardiography: a review of the current status and future directions. J Am Soc Echocardiogr 2007;20(3):213-33. 106. Sugeng L, Shernan SK, Salgo IS, Weinert L, Shook D, Raman J, Jeevanandam

ED

V, Dupont F, Settlemier S, Savord B, Fox J, Mor-Avi V, Lang RM. Live 3dimensional transesophageal echocardiography initial experience using the fully-

PT

sampled matrix array probe. J Am Coll Cardiol 2008;52:446-9.

CE

107. Looi JL, Lee AP, Wong RH, Yu CM. 3D echocardiography for traumatic

AC

tricuspid regurgitation. JACC Cardiovasc Imaging 2012;5:1285-7.

ACCEPTED MANUSCRIPT Legends Figures

T

Figure 1. TEE modified four chambers view. Rupture of the lateral wall

RI P

of the RV (white arrow). The tricuspid annulus is hyperechoic and

LV: left ventricle, #: pericardial effusion.

SC

substantially thickened due to edema (black arrow). RV: right ventricle,

MA NU

Figure 2. TTE four chambers view. Trauma of the right atrium. Serial views of thrombus growing (arrow) within the right atrium. A: first day, B: third day after blunt thoracic trauma. The patient could not receive anticoagulants due to multiple injuries. RA: right atrium.

ED

Figure 3. TTE four chambers view. (A) Mitral valve posterior flail leaflet owing to chordae rupture (arrow). (B) Severe mitral regurgitation with

PT

significant flow convergence zone (arrow). LV: left ventricle, RV: right

CE

ventricle.

Figure 4. Patient with cardiac tamponade due to hemopericardium. (A)

AC

Significant respiratory fluctuation of the E component of mitral valve inflow Pulse Wave signal. (B) Dilatation of the inferior vena cava (IVC) with no respiratory changes in its diameter. Figure 5. Lung ultrasound. Pericardial wound that opens into the pleura. Massive haemothorax develops with the normal lung significantly compressed. Figure 6. TTE subcostal view. Pericardial haemorrhage (PH). (A) Before and (B) after pericardiocentesis. RA: right atrium, RV: right ventricle, LV: left ventricle.

ACCEPTED MANUSCRIPT Figure 7. TEE view of the thoracic aorta. Traumatic dissection of the thoracic aorta. TL: true lumen, FL: false lumen.

T

Figure 8. Multiple fatty emboli (arrows) from patients with lower limb

RI P

trauma, within the right atrium (RA) and the inferior vena cava (IVC). LA: left atrium.

SC

Figure 9. TEE mid oesophagus view of the proximal aorta (Ao) of a

MA NU

multi-trauma patient. The superior cava is depicted in long axis view with

AC

CE

PT

ED

a thrombus (T) within it.

ED

MA NU

SC

RI P

T

ACCEPTED MANUSCRIPT

AC

CE

PT

Figure 1

AC

CE

PT

ED

MA NU

SC

RI P

T

ACCEPTED MANUSCRIPT

Figure 2

AC

CE

PT

ED

MA NU

SC

RI P

T

ACCEPTED MANUSCRIPT

Figure 3

MA NU

SC

RI P

T

ACCEPTED MANUSCRIPT

AC

CE

PT

ED

Figure 4

ED

MA NU

SC

RI P

T

ACCEPTED MANUSCRIPT

AC

CE

PT

Figure 5

AC

CE

PT

ED

MA NU

SC

RI P

T

ACCEPTED MANUSCRIPT

Figure 6

PT

ED

MA NU

SC

RI P

T

ACCEPTED MANUSCRIPT

AC

CE

Figure 7

AC

CE

PT

ED

MA NU

SC

RI P

T

ACCEPTED MANUSCRIPT

Figure 8

AC

Figure 9

CE

PT

ED

MA NU

SC

RI P

T

ACCEPTED MANUSCRIPT