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Blunt chest trauma: a clinical chameleonKaveh Eghbalzadeh,1 Anton Sabashnikov,1 Mohamed Zeriouh,1 Yeong-Hoon Choi,1 Alexander C Bunck,2 Navid Mader,1 Thorsten Wahlers1

ABstrActThe incidence of blunt chest trauma (BCT) is greater than 15% of all trauma admissions to the emergency departments worldwide and is the second leading cause of death after head injury in motor vehicle accidents. The mortality due to BCT is inhomogeneously described ranging from 9% to 60%. BCT is commonly caused by a sudden high-speed deceleration trauma to the anterior chest, leading to a compression of the thorax. All thoracic structures might be injured as a result of the trauma. Complex cardiac arrhythmia, heart murmurs, hypotension, angina-like chest pain, respiratory insufficiency or distention of the jugular veins may indicate potential cardiac injury. However, on admission to emergency departments symptoms might be missing or may not be clearly associated with the injury. Accurate diagnostics and early management in order to prevent serious complications and death are essential for patients suffering a BCT. Optimal initial diagnostics includes echocardiography or CT, Holter-monitor recordings, serial 12-lead electrocardiography and measurements of cardiac enzymes. Immediate diagnostics leading to the appropriate therapy is essential for saving a patient’s life. The key aspect of the entire management, including diagnostics and treatment of patients with BCT, remains an interdisciplinary team involving cardiologists, cardiothoracic surgeons, imaging radiologists and trauma specialists working in tandem.

BAckgroundBlunt chest trauma (BCT) is the second leading cause of death after head injury in vehicular acci-dents.1 The incidence of this trauma has been inconsistently reported in the literature; however, a rough estimate of around 15% of all trauma admis-sions to emergency departments seems reason-able.2 3 Similarly, analogous inhomogeneity exists in terms of mortality rates described in previous studies, ranging between 9% and 60% and exceeds 50% within the first 24 hours.3–5 The main reasons for this disparity seem to be its versatile presenta-tion patterns with involvement of various organs and tissues within the chest and the presence of a wide range of differential diagnoses. Approximately 90% of BCT cases are managed by insertion of a chest tube before any other consideration, whereas the remaining 10% require direct surgical interven-tions.6 7

The aim of this article was to present a compre-hensive overview of BCT with a main focus on cardiac involvement, as this category is usually associated with the most life-threatening complica-tions.3 8 Even though BCT represents a relatively rare condition, its high clinical impact explains the need for accurate diagnostics and early manage-ment in order to manage serious complications and death in a number of cases (see table 1).

Mechanisms of BctBCT typically occurs after direct impact to the anterior chest caused by high-speed sudden decel-eration or compression of the thorax, usually in motor vehicle accidents. Generally, mobile intra-thoracic viscera are injured by less-mobile skeletal structures of the thorax. Massive compression of the anterior chest can lead to heart contusions of varying severities as well as injuries to the ascending aorta, the innominate artery and the thoracic verte-brae.2 In cases of osteal fractures of the sternum (figure 1), sharp bone margins may tear the right ventricular chamber or the ascending aorta due to their direct anatomical neighbourhood to the sternum.9 10 However, apart from the sternum, frac-tures of other skeletal structures, such as ribs and thoracic or lumbar vertebrae, are often involved in this form of trauma.11 Naturally torsion or traction forces are seen as the common pathomechanism for damage to the heart and the thoracic aorta during BCT. As the descending aorta is directly fixed to the chest wall, a tear between the mobile part of the ascending aorta and aortic arch and stabilised part of the descending aorta can be frequently observed. The proximal descending aorta is fixed to the pulmonary artery through ligamentum arte-riosum, the remnant of the ductus arteriosus, and therefore the least mobile part of the aorta. Typi-cally this tear junction is located directly adjacent to the isthmus.12 High intraventricular pressure caused by trauma may injure cardiac valves and the myocardium itself depending on the cardiac cycle.2 The most vulnerable cycle might be end-diastole when the impact of the BCT increases intraven-tricular pressure due to the mechanical compres-sion of the distended ventricles.13 A complete heart block during BCT can be caused by either elec-trical or structural injury to the heart.14 In contrast to contusio cordis with predominantly structural character of the damage, commotio cordis might cause sudden death after the blunt impact on the precordium with subsequent ventricular fibrillation even without any evidence of structural injury to the myocardium.14 15 However, cardiac chamber or great vessel ruptures may occur not only as a result of BCT, but a growing number of reports also describe isolated coronary artery injuries including ruptures, dissections and other types of injuries.16

diAgnosticsThere is currently no gold standard for the diagnos-tics of BCT, which includes a wide range of possible presentations with individual symptoms. Complex cardiac arrhythmia, heart murmurs, hypotension, angina-like chest pain, dyspnoea or distention of the jugular veins may, however, indicate potential

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to cite: Eghbalzadeh K, Sabashnikov A, Zeriouh M, et al. Heart 2018;104:719–724.

1Department of Cardiothoracic Surgery, University Hospital Cologne, Cologne, Germany2Department of Radiology, University Hospital Cologne, Cologne, Germany

correspondence toDr Anton Sabashnikov, Department of Cardiothoracic Surgery, University Hospital of Cologne, Cologne 50937, Germany; a. sabashnikov@ gmail. com

Received 8 August 2017Revised 23 October 2017Accepted 3 November 2017Published Online First 4 December 2017

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cardiac injury. Whereas on admission to the emergency depart-ment a large proportion of patients with BCT do not show respi-ratory insufficiency and cardiac symptoms indicative of BCT, clinicians should be prepared for rapid changes in clinical condi-tion of such patients as various complications can first occur within 72 hours.4 17 Therefore, the relevance of complete diag-nostics including CT scan should not be underestimated after typical trauma mechanisms, even when the first impression on patient’s clinical condition does not indicate severe injury.

Whenever possible patients should first undergo physical examination, Holter-monitor recordings, serial 12-lead ECG and measurements of cardiac enzymes. Cardiac enzymes, such as creatine kinase MB (CK-MB), might be elevated depending on the severity and localization of the trauma and are therefore not always specific.18 Furthermore, in some cases cardiac enzymes might even not be elevated despite significant cardiac injury, such as in case of a cardiac contusion.2 Arrhythmia in general is a very unspecific sign and may also not always be associated with the presence of a BCT.

In terms of radiologic imaging a plain chest radiograph is considered a sufficient indication for inserting a chest tube in presence of a pneumothorax. However, the radiographic exam-ination shows no pathological findings in up to 44% of patients suffering an aortic injury.19 On the basis of the Guidelines of the Eastern Association for the Surgery of Trauma (EAST) every patient presenting with specific chest radiograph pathologies,

such as widened mediastinum, tracheal deviation and loss of aortopulmonary window (figure 2) after a high-speed deceler-ation trauma or suspicious of an aortic injury should undergo a CT scan of the chest using intravenous contrast, which is superior to catheter-based angiography.8 20 On the other hand, catheter-based angiography shows highest sensitivity in cases of coronary artery involvement after BCT.21 Also, a great amount

table 1 Overview of the most important injuries after BCT

relative incidence clinical presentation imaging findings Acute management outcome

Blunt aortic injury ~1% of all vehicular high-speed accidents

Lethal, when ruptured; symptomless; mid-scapular back pain; malperfursion syndrome

X-ray: loss of aortopulmonary window; CT scan see figure 3

Systolic BP <120 mm Hg; surgery or EVR

30% die within 24 hours, mortality: surgery 18.9% vs 7.9% EVR

Myocardial contusion Up to 24% of all BCTs (from autopsy reports)

Symptomless up to therapy-refractory hypotension/low-cardiac ouput; arrhythmias

No specific imaging findings (1) 12-Lead ECG, CK+CK/MB, Holter monitor; (2) fluid and vasopressor; (3)  mechanical circulatory support

Cardiac failure improves with time, complete reconvalenscence possible

Valvular rupture <100 case reports Typical symptoms of valve insufficiency, depending on the affected valve

Valve rupture in electrocardiography 

Surgical valve repair or replacement

Excellent long-term outcome

Coronary dissection <100 case reports Symptoms of MI, pericardial effusion, low-cardiac output

True and false lumen in angiography or coronary CT angiography

(1) Coronary stenting; (2) surgical revascularisation

Early intervention associated with good outcome

BCT, blunt chest trauma; BP, blood pressure; CK-MB, creatine kinase MB; EVR, endovascular repair; MI, myocardial infarction.

Figure 1 Multiplanar reformations of a CT trauma scan in sagittal and axial view showing a fracture of the sternal manubrium with adjacent retrosternal haematoma and soft tissue emphysema after a motorcycle accident. The haematoma required no further intervention. No injury to the greater intrathoracic vessels was found.

Figure 2 CT image showing a retrosternal haematoma with signs of active bleeding after a blunt chest trauma. Corresponding chest X-ray with widened upper mediastinum and loss of the aortopulmonary window.

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of useful information can easily and quickly be obtained using transthoracic echocardiography, which can aid the physician in deciding on the appropriate therapy.22 As Liteplo et al suggested, all patients with hypotensive trauma should undergo FAST (Focused Assessment with Sonography in Trauma) and RELI-ABLE ultrasound. RELIABLE is an acronym and stands for right ventricular, effusion—pericardial, left ventricular, inferior vena cava, aorta, blood clot—venous, lungs—pneumothorax and ectopic pregnancy.22 23 In the current technological era, there is an optimal examination for almost every kind of injury avail-able. However, the most difficult part of the diagnostics is to identify potential latent problems in patients who were stable on admission, for example, pericardial effusion or late arrhythmic complications. Another important clinical challenge is the ability to promptly recognise emergent cases where surgical interven-tion, such as thoracotomy, needs to be performed immediately after the initial assessment—preferably in the operating theatre—as such patients are not likely to survive delayed therapy to be decided after further diagnostics.24

trAuMA to the heArt And greAt vesselsBlunt aortic injuryAmong all categories of BCT, blunt aortic injury (BAI) is the leading cause of death after vehicular accidents, as it is the second most leading cause of death for all trauma after head injuries.25 Survival is only possible if the rupture is covered by the surrounding tissue or haematoma. An immediate definite treatment of this life-threatening condition is of vital importance for survivors.26 Autopsy reports have shown that 30% of the survivors die within 24 hours after rupture and more than half of the patients die within the first week after injury.27 Overall BAI occurs in more than 1% of all high-speed vehicular accidents. However, this rare injury accounts for 16% of all trauma-related deaths.1

The typical mechanism of BAI is generally an abrupt decelera-tion generating maximum shearing forces on the transition zone between the fixed and the mobile aorta, usually in the region of the aortic isthmus (figures 3 and 4).12 Over 90% of aortic

ruptures are located in this region, whereas other locations including ascending, distal descending or abdominal aorta have been reported in individual cases.28 29 After the landmark study by Parmley et al angiography was considered the gold standard in diagnosis of the BAI for more than 40 years.27 Thereafter, some studies favoured transoesophageal echocardiography to be first-line imaging modality for the evaluation of trauma in patients suspicious of BAI due to its portability and diagnostic accuracy.30 Nowadays, the imaging method of choice is helical CT scan with an estimated sensitivity of 100% compared with 92% for angiography (figure 3).8 20 28 When BAI cannot be treated first in high-risk patients suffering from other major associated injuries or severe comorbidities, Fabian et al showed that antihypertensive therapy with a targeted systolic blood pres-sure of less than 120 mm Hg results in a significantly improved outcome for patients undergoing delayed repair of the aorta.31 In patients showing evidence of hypervolaemia and contained BAI, the major source of blood loss cannot be the aorta as that could prove to be fatal. For this reason, for patients with BAI and major associated injuries resulting in hypovolaemia, delayed repair with controlled systolic blood pressure is a valuable therapy option.

Repair of the aortic disruption can be performed either surgi-cally via left thoracotomy with an incision in the fourth inter-costal space using unilateral ventilation of the right lung or interventionally through endovascular repair.8 32 Perioperative and postoperative complications of the surgical approach can be reduced by using a left atrium to left femoral artery bypass with a centrifugal pump, through a venoarterial cardiopulmonary bypass or a Gott shunt inserted between the ascending and the thoracic descending aorta.33 Endovascular repair is performed by positioning a stent graft using a guide wire under angiog-raphy.34 Figure 5 shows an aortic tear treated by a thoracic endovascular stent graft. According to the guidelines for the evaluation and management of blunt traumatic aortic injury by endovascular repair as a less invasive approach (EAST) is consid-ered to carry a significantly lower risk of blood loss, mortality, paraplegia and a comparable risk of procedure-related stroke.8 The overall mortality was lower at 7.9% as reported in 37 studies involving 2588 patients for the endovascular repair cohort compared with 18.9% for the surgical approach (risk ratio (RR)

Figure 3 Three-dimensional rendering, curved reformation and an axial CT image of a severe laceration of the aortic arch with formation of a pseudoaneurysm after a velocity accident of a motorcyclist. This injury was successfully treated by thoracic endovascular aortic repair procedure. A concomitant compression fracture of the sixth thoracic vertebra resulted in spinal cord injury and incomplete paraplegia.

Figure 4 Stented aneurysm of the aortic arch. The male patient suffered a blunt aortic injury during a motorcycle accident. A tear is directly adjacent to the isthmus. Unfortunately, the patient died before arrival to the hospital.

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0.54; 0.41–0.7).8 The Incidence of paraplegia was also lower for endovascular versus open repair (0.5% vs 3%), taking the guidelines of the EAST as the basis. Furthermore, the guidelines published in 2015 recommend a delayed repair due to decreased mortality and paraplegia.8 However, the incidence of stroke was slightly higher in the endovascular group accounting for 2.5% compared with 1% for the open repair. Nonetheless, it has to be emphasised that the quality of evidence regarding different approaches for aortic repair after BAI is low to moderate and therefore requires further investigations.8

Myocardial contusionThe second most frequent injury leading to death after BCT is myocardial contusion. The right ventricular wall is anatomically in close proximity to the dorsal sternum and represents the most vulnerable structure in cases of myocardial contusion. Compared to myocardial concussion, where only an abnormal myocardial wall motion with no anatomic or cellular injury is present, a myocardial contusion is associated with a manifest myocardial tissue damage.35 However, myocardial concussion should not be considered a benign entity, as it may cause severe rhythm distur-bances. Autopsies of patients who died of BCT revealed myocar-dial contusion in up to 24% of the cases.27 36 Postmortem autopsy is the only way to retrospectively ensure the definite diagnosis of this category of BCT, whereas clinical diagnosis is often difficult and therefore the incidence is reported with wide discrepancy.35 Although myocardial damage can also result in ECG changes or myocardial enzyme release, such as troponin and CK-MB, these findings remain unspecific in most cases of BCT including myocardial contusion. Echocardiography is considered to be of higher specificity as echocardiography findings were shown to correlate with complications in a large meta-analysis by Maenza et al. Unfortunately, the sensitivity of echocardiography was reported to be considerably lower compared with ECG and enzyme kinetics.36 37 Furthermore, Hammer et al analysed CT findings after myocardial contusions and reported on poor sensitivity of specific CT findings, such as myocardial hypoen-hancement. Therefore, CT scan is not recommended as a reli-able screening tool for detecting myocardial contusion.35 The pathomechanism of cardiac contusion is based on the myocar-dial damage at the cellular level. Histologically, red blood cell extravasation into and between myocardial muscle fibres and a selective necrosis of the fibres is observed.38 This phenomenon might cause enzyme release, which can be identified via a blood

test. Necrosis of myocardial muscle fibres is characterised by infiltrates of polymorphonuclear leucocytes. Haemorrhage is generally absorbed and the contusion heals by patchy and irreg-ular scar formation.27 In contrast, repair of ischaemic myocardial injury shows generalised fibrosis. Consequently, the diagnosis of the non-penetrating pathology termed myocardial contusion can only be ensured by histological examination postmortem. In case of an existing penetration the diagnosis of myocardial contusion cannot be made.

Depending on the amount of myocardium involved, the damage at the cellular level might cause reduction in cardiac output potentially leading to cardiogenic shock in the worst-case scenario.38 In such circumstances symptom-oriented conservative treatment or implementation of mechanical circu-latory support as appropriate should be considered. Moreover, constant monitoring of vital parameters, including Holter-mon-itoring should be performed on intensive care unit for the first 24 hours after admission to identify possible arrhythmic compli-cations. Myocardial enzyme release markers, such as troponin and CK-MB, should be frequently performed as in patients with myocardial infarction (MI). As coronary involvement might equally lead to enzyme release and chest pain can be interpreted as being secondary to the trauma, Holter-monitor recordings and repetitive serial 12-lead electrocardiograms are the appro-priate examinations to differentiate between both pathologies. Whereas the injury itself is extremely difficult to identify compli-cating the establishment of the correct diagnosis and therapeutic strategy, most associated symptoms caused by myocardial contu-sion, such as cardiogenic shock or arrhythmias, can be treated independent from the cause. In cases of low-output syndrome or cardiogenic shock, continuously performed echocardiography represents an essential tool to evaluate the response to fluids and to facilitate the management of vasopressors versus afterload reduction therapy.

valve ruptureValve rupture after BCT is rare and unusual. However, its inci-dence cannot be accurately quantified. After its first description in 1830 by Plenderleath this phenomenon has inconsistently been described in the literature, mainly in form of case reports and case studies accounting for less than 100 cases reported by 2002.39 Studies with larger patient cohorts have also been limited to a low number of individual cases of BCT with involve-ment of valve injuries.27 40 In spite of its infrequent presentation, this category of injury is of high clinical relevance and interest for clinicians as appropriate and promising therapy options can be offered.

Aortic valve is the most frequently injured valve followed by mitral and tricuspid valves.39 Due to higher-pressure condi-tions in the left heart, the valves from the left cardiac chambers are more likely to be affected, whereas the cardiac cycle has its impact on the mechanism of injury.2 At the beginning of diastole, aortic valve is at a particular risk of developing an injury. At that time sufficient valve is closed and is subjected to maximal tension, whereas the pressure in the empty left ventricle is low. A sudden increase in intra-aortic pressure due to deformations caused by an external impact transmitted through the chest wall may lead to excessive forces directed towards the closed aortic valve. In combination with low left ventricular end-diastolic pres-sure, such an enormous pressure aortoventricular gradient may potentially destruct all leaflets.41 As valve rupture usually causes an insufficiency of the involved valve, characteristic clinical signs of valve pathology may be present, such as wide pulse pressure

Figure 5 CT angiography (CTA) in axial and coronal orientation showing a small aortic tear in the distal aortic arch after a car accident with unknown velocity. The lorry driver was stuck in his vehicle and required technical rescue. Concomitant injuries involved open head trauma, bilateral dissection of the internal carotid artery and serial rib fractures of the 1 st to fifth rib on the left side. On the CTA of the initial trauma scan, a large haematoma abutting the aortic arch was noticed causing broadening of the upper mediastinum. The aortic tear was successfully treated by a thoracic endovascular stent graft (thoracic endovascular aortic repair) and the haematoma resolved.

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amplitude in case of aortic regurgitation. In the same way, atrio-ventricular valves may be injured due to a massive increase in intraventricular pressure during systole. Therefore, depending on the valve affected, the clinical picture of a new regurgitation caused by a tear in a leaflet or papillary muscle is usually seen on admission.42 As with regurgitations of any other aetiology, diagnosis can be made via clinical examination, auscultation of a cardiac murmur and using echocardiography with Doppler and colour flow imaging.42 Moreover, haemodynamic condition on admission may strongly correlate with the severity of the valve pathology and also with the accompanying injuries of the patient with trauma. Interestingly, aortic and mitral insufficiency after trauma can also lead to an insidious progress of cardiac failure over several weeks, whereas in case of tricuspid insufficiency this process may even take several years.2 43Patients with acute heart failure due to the valve destruction should immediately undergo surgical repair, if full heparinisation is justifiable depending on the severity of other injuries, as valve replacement is associated with excellent long-term outcomes.41

coronary involvementInvolvement of coronary arteries with subsequent MI after BCT is a rare phenomenon, which has only been reported on in single case reports or case studies. Analysing available evidence on this topic Christensen et al found a total of 77 cases of acute MI due to coronary injuries after BCT.44 Due to its anatomical position on less protected anterior ventricular wall left anterior descending (LAD) artery has been shown to be the most commonly injured coronary artery accounting for 76% of all coronary injuries45 The second most commonly injured coronary artery is the right coronary artery (RCA) with an incidence of 12%.45 A possible explanation for a relatively frequent RCA involvement is the fact that with every heart beat it moves anteriorly towards the sternum during systole. Another hypothesis postulates that rapid deceleration may also lead to a disruption of the RCA from its junction with the aortic root.46 Coronary artery injuries after BCT mainly include intimal tears, coronary dissections or ruptures, ruptures of pre-existing plaques and occlusions due to external epicardial haematomas.44 Coronary artery ruptures can be also fatal due to acute pericardial tamponade (figure 6). In

some cases normal appearance of coronary arteries in coronary angiogram may obscure the evidence of MI, whereas coronary spasm or spontaneous clot lysis may be responsible symptoms of ischaemia. In patients suspected of MI after BCT usual diagnos-tics with a serial 12-lead ECG and cardiac enzyme control should be performed. However, angina-like chest pain is generally not reported as a classical symptom after BCT as the symptoms might be partially concealed by other injuries of the thorax.44 Percuta-neous coronary intervention with stent placement is the optimal therapy for uncomplicated LAD and RCA lesions.47 Surgical myocardial revascularisation should be performed in cases of an unprotected left main coronary artery disease, contraindica-tions for antiplatelet therapy and history of bleeding diathesis.47 As patients with BCT regularly present with other concomitant injuries, the indication for stenting is limited due to the need for antiplatelet therapy, which may cause bleeding complica-tions. However, patients undergoing myocardial revascularisa-tion need a systemic anticoagulation with heparin representing another limitation. Patients with MI after BCT are usually young and are suffering a single vessel disease and therefore recover well and have good prognosis.44

other cardiac injuriesApart from more frequently described cardiac injuries after BCT mentioned above, there are still several other impressive clinical manifestations, which are exciting cases because of their rarity. Ruptures of cardiac chambers, or intrapericardial veins generally cause an acute tamponade leading to death before admission to the emergency department in most cases.2 The absolute minority of patients who survive rupture of a cardiac cavity usually have a tear in a low-pressure chamber.48 49 Moreover, some cases of asymptomatic haemopericardium leading to a constrictive pericarditis have been described in literature.9 38 A classical clinical presentation of a protracted constrictive myocarditis is severe diastolic dysfunction with indication for surgical pericardiectomy.50

conclusionBCT can cause a wide range of clinical presentations and inju-ries, making the diagnostics extremely challenging. Patients may initially appear haemodynamically stable and asymptomatic on admission, however suffering a life-threatening disease, which can lead to death, unless the problem is correctly recognised and appropriate timely therapy commenced. Due to the variety of presentations and severity of injuries, there are no fixed algo-rithms to identify the disease. However, simple clinical exam-ination, ECG, measurement of the cardiac enzymes and most importantly an immediate transthoracic echocardiography as easily available and rapid imaging option can save lives. Other specific techniques, such as angiography or CT scan of the chest, are often mandatory to confirm the diagnosis and initiate appropriate therapy. Finally, the most important aspect of the entire management of patients with BCT is an interdisciplinary team involving cardiologists, cardiothoracic surgeons, imaging radiologists and trauma specialists in order to emerge victorious against this clinical chameleon.

Acknowledgements We thank Dr Karl-Heinz Schiwy-Bochat for providing images from the Department of Forensic Medicine, University Hospital Cologne, Germany.

contributors KE wrote the manuscript. All authors contributed to the final manuscript, provided suggestions, prepared and revised the manuscript. KE, AS, MZ, Y-HC, ACB, NM, TW performed literature search and discussed the data. ACB was responsible for the imaging data collection and interpretation.

competing interests None declared.

Figure 6 A lethal pericardial effusion, which can potentially be caused by any blunt chest trauma independent from the underlying pathology. The heart is also presented in sections to demonstrate the extent of the tamponade.

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ethics approval The ethics committee of the University Department of Cologne approved the manuscript design.

Provenance and peer review Commissioned; externally peer reviewed.

© Article author(s) (or their employer(s) unless otherwise stated in the text of the article) 2018. All rights reserved. No commercial use is permitted unless otherwise expressly granted.

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