- Email: [email protected]
Blunt traumatic rupture of the thoracic aorta: A report of an unusual mechanism of injury
Blunt Traumatic Rupture of the Thoracic Aorta: A Report of an Unusual Mechanism of Injury i
GEOFFREY A. ANSWINI, MD, MARK k. STURDEVANT, MD, RONALD F. SING, DO, AND DAVID G. JACOBS, MD Classic teaching suggests that blunt thoracic aortic rupture (BTAR) results from high-speed deceleration injury mechanisms. Our recent experience with a patient who sustained fatal aortic rupture resulting from a low-speed crushing injury emphasizes the importance of maintaining a high index of suspicion for BTAR, even in patients with "lowrisk" injury mechanisms. Several potential pathophysiologic mechanisms of BTAR are discussed. (Am J Emerg Med 2001;19:579-582. Copyright ©2001 by W.B. Saunders Company) Blunt traumatic aortic rupture (BTAR) is an often lethal injury, believed to be caused by high-speed deceleration mechanism. Prompt diagnosis is critical and therefore, early angiography or chest computed tomography (CT) scanning is essential in patients with high-speed deceleration mechanisms and abnormal mediastinal contours on initial chest radiograph. 1-7 Some investigators advocate aortography for patients with "normal" chest radiographs if the traumatic mechanism is sufficiently suggestive, 8,9 while an abnormal mediastinal contour on chest radiograph is usually not considered an indication for aortography if the injury mechanism is inconsistent with BTAR. Thus, a clear understanding of the injury mechanisms causing BTAR is needed to appropriately select patients who will benefit from contrast studies of the thoracic aorta. Here, we report a patient with BTAR caused by a low-speed, nondeceleration mechanism.
CASE REPORT A 46-year-old man, employed as a landscaper, was riding on a large, commercial-sized standing lawnmower when the vehicle overturned on a hill, landing on top of him. He arrived at the emergency department (ED) with a Glasgow Coma Scale score of 10, a pulse rate of 100 beats/min and a blood pressure of 130/80 mm/hg. Mild respiratory distress was noted, with an abdominal breathing pattern and minimal chest wall movement. The patient was noted to have no rectal tone and no evidence of motor or sensory function in his lower extremities. He was intubated and resuscitated in the ED and begun on high-dose methylprednisolone. Initial laboratory examination showed a hemoglobin of
From the Department of General Surgery, Carolinas Medical Center, Charlotte, NC. Manuscript received and accepted April 14, 2001. Address reprint requests to David G. Jacobs, MD, FACS, Department of Surgery/MEB 601, 1000 Blythe Boulevard, Charlotte, NC 28203. E-mail: [email protected] Key Words: Thoracic aorta, blunt rupture. Copyright © 2001 by W.B. Saunders Company 0735-6757/01/1907-0009535.00/0 doi: 10.1053/ajem.2001.28034
14.5gm/dL, PaO2 of 384 tort (FIO 2 = 100%), a base excess of -5mEq/L, and a lactate of 6.1 mEq/L. A portable anterior-posterior (AP) chest radiograph revealed fractures of the left seventh and fight fifth ribs and an abnormal mediastinal contour (Fig 1). AP and lateral thoracic/lumbar spine films revealed a T12 vertebral body compression fracture, bilateral-transverse process fractures at L1, and bilateral twelfth rib fractures. A C T scan of the abdomen and pelvis was significant for a left hemothorax and retropulsed bony fragments into the spinal canal at T12. Because the mechanism of injury was not believed to be compatible with the diagnosis of aortic disruption, no further diagnostic studies of the thoracic aorta were obtained. After completion of these studies, the patient was transferred to the trauma intensive care unit, where a left tube thoracostomy was placed along with a central venous line and an arterial line. The patient's initial central venous pressure (CVP) was 7 cm H20. The chest tube initially drained 1,000 mL of blood, and a hemoglobin drawn 6 hours after admission was noted to be 9.5 g/dL. The patient's vital signs remained stable and over the next several hours, he maintained a brisk urine output and his chest tube drainage diminished substantially. He was transfused with 2 units of packed red blood cells, and his hemoglobin level increased to 11.1 g/dL Thirty-six hours after admission, the patient had an abrupt increase in bloody drainage from his left chest tube. The patient rapidly deteriorated to pulseless electrical activity, and advanced cardiac life support (ACLS) was immediately instituted along with transfusion of packed red blood cells. A left thoracotomy was performed at the bedside, and a large amount of blood and clot were evacuated from the left chest. The descending thoracic aorta was cross-clamped, and direct cardiac massage was started. An actively bleeding intercostal artery adjacent to the fractured left seventh rib was ligated, but no other sites of active hemorrhage were identified. Ventricular fibrillation ensued, and cardioversion and standard ACLS medications were unsuccessful at restoring a sinus rhythm. The patient became asystolic and was pronounced dead. A postmortem examination revealed 2 transverse tears of the descending thoracic aorta, distal to the ligamentum arteriosum. These measured 3.0 cm and 2.5 cm (Fig 2A2B). Both were associated with hemorrhage into the adventitia and surrounding adipose tissue. The patient was also noted to have a contused left lung base and a bruised and lacerated lumbar spinal cord distal to the T12 vertebral fracture. 579
580
AMERICAN JOURNAL OF EMERGENCY MEDICINE • Volume 19, Number 7 • November 2001
FIGURE 1. Portable AP chest radiograph shows an abnormal mediastinal contour.
DISCUSSION Most patients (80% to 90%) who sustain BTAR die immediately of exsanguination; thus, only 10% to 20% survive for medical treatment.l-9 Prompt diagnosis and expedient surgical repair of BTAR is of paramount importance in the initial management of the trauma patient. The evaluating physician must review the patient's vital signs, physical findings, mechanism of injury, and chest radiograph and determine if the patient is at risk for BTAR. Patients who sustain rapid deceleration forces to the chest and have an abnormal mediastinal contour (Table 1) on chest radiograph need further work-up for BTAR to include either spiral CT scanning of the chest or aortography. Case reviews based on autopsy studies report that motor vehicle collisions cause up to 95% of BTARs; most of the other 5% are caused by falls from great heights or crushing chest injuries.l°-~7 Most of the traumatic aortic injury mechanisms proposed in the literature combine features of rapid deceleration and chest compression. One large series evaluated the mechanisms of aortic rupture in 142 fatally injured persons and concluded that rapid chest deceleration/compression induces torsional and shearing forces that cause transverse laceration and rupture of the aorta, most commonly at the ligamentum arteriosum.12 Another large series evaluated 116 patients with BTAR between 1969 and 1989 and made similar observations. 5 BTAR is generally attributable to the action of violent forces applied directly or indirectly to the chest at the moment of impact. To better understand the mechanisms causing this injury, several studies correlated clinical and post mortem observations of injured individuals with the mechanisms of injury and presumed patient kinematics. These studies identified various mechanisms of injury that
alone or in combination can explain the development of aortic tears. These include: (1) Chest crushing-compression causing displacement of the heart downward and to the left after impact on the sternum (ruptures ascending aorta), [°'19-22 (2) Rapid deceleration of the moving body producing tension-stress on the wall of the aorta at points where it is tethered (most commonly the ligamentum arteriosum), 10-14"17"1s'22"23(3) The "shovelling effect" which is upward displacement of the heart and mediastinum from a cranially directed impact on the lower chest (ruptures proximal descending aorta), 19 (4) The osseous pinch (described later in text), 2~-25 (5) Increased intravascular pressure and/or hemodynamic forces (water-hammer effect) after a blow on the chest or rapid deceleration25,26 The common denominator among all of these theories is that the forces causing BTAR are associated with high velocity impacts. In this case report, the described mechanism of injury did not involve a high-velocity impact; therefore aortic disruption was not suspected. This caused a delay in diagnosis. The most likely mechanism causing aortic injury in our patient is the osseous pinch. This mechanism was first described in 1990 by Crass et al and suggests that aortic injuries may be caused by a pinching of the aorta between the spine and the anterior bony thorax during chest compression after abrupt deceleration, 24 Compressive forces from blunt thoracic trauma cause the anterior thoracic osseous structures (manubrium, first rib, medial clavicles) to rotate posteriorly and inferiorly about the axes of the posterior rib articulations. Sufficiently large forces cause the anterior osseous structures to impact the vertebral column and shear the interposed vascular structures, namely the thoracic aorta. Both Parmley et al and Zehnder expressed doubt that the usual deceleration forces encountered in
ANSWINI ET AL • MECHANISM OF BLUNT TRAUMATIC AORTIC RUPTURE
581
FIGURE 2. (A) Post mortem examination of the thoracic aorta reveals one 3.0 cm and one 2.5 cm tear just distal to the take off of the left subclavian artery. (2B) A close-up view of the 2 thoracic aorta tears. trauma were sufficient to rupture the aorta. 17,23 Many studies have shown experimentally that the tensile strength of the aorta exceeds the forces generated in deceleration injuries. 11,15,23-26 The pinch mechanism is even more plausible when the atypical lacerations of the aorta at the arch and the great vessels are taken into account. This mechanism potentially explains why vehicles hitting pedestrians, falls TABLE 1.
Radiographic Clues to Aortic Injury on Chest Radiograph Widened (>8 cm) mediastinum Depressed (>140 degrees) left mainstem bronchus Loss of aortic knob contour Lateral deviation of trachea Deviation of nasogastric tube in esophagus Anterior displacement of trachea Left apical pleura hematoma "cap" Calcium "layering" in aortic arch Massive left-side hemothorax Fracture of thoracic spine, clavicle, sternum, or scapula Loss of paraspinal stripe Loss of aorticopulmonary "window"
from heights, and crushing chest injuries cause aortic rupture. We believe that the osseous pinch mechanism caused the aortic injury in this patient and that this must be seriously considered in the evaluation of all trauma patients when ruling out BTAR. What then, should be the approach to the patient with an abnormal mediastinal contour, without the classic rapid deceleration, high-risk mechanism? The decision to evaluate the mediastinum in all of these patients will produce many negative studies and subject many patients to IV contrast and unnecessary intrahospital transport. However, it will obviate the catastrophic outcomes associated with missed aortic injuries. It is imperative to remember all of the possible mechanisms of BTAR, including the osseous pinch, when determining which patients require contrast studies of the aortic arch. We suggest that any patient with an abnormal mediastinal contour on initial chest radiograph and a rapid deceleration or transthoracic, crush-type of injury undergo either aortography or spiral CT scanning of the chest. Blunt traumatic rupture of the thoracic aorta remains a diagnostic challenge, and further prospective studies may
582
AMERICAN JOURNAL OF EMERGENCY MEDICINE • Volume 19, Number 7 • November 2001
delineate a cost-effective, yet sensitive, way to expeditiously and efficiently identify this often fatal injury. REFERENCES 1. Gammie JS, Shah AS, Hattler BG, et al: Traumatic aortic rupture: diagnosis and management. Ann Thor Surg 1998;66:12951300 2. Galli R, Pacini D, Di Bartolomeo R, et al: Surgical indications and timing of repair of traumatic ruptures of the thoracic aorta. Ann Thorac Sur 1998;65:461-464 3. Tribble CG, Crosby IK: Traumatic rupture of the thoracic aorta. South Med J 1988;81:963-968 4. Von Oppell UO, Dunne 1-1, De Groot MK, et al: Traumatic aortic rupture: Twenty-year meta-analysis of mortality and risk of paraplegia. Ann Thorac Surg 1994;58:585-593 5. Kodali S, Jamieson WRE, Leia-Stephens M, et al: Traumatic rupture of the thoracic aorta; a 20-year review: 1969-1989. Circulation 1991 ;84 111:40-46 (suppl) 6. Ayella RJ, Hankins JR, Turney SZ, et al: Ruptured thoracic aorta due to blunt trauma. J Trauma 1977;17:199-205 7. Symbas PJ, Horsley WS, Symbas PN: Rupture of the ascending aorta caused by blunt trauma. Ann Thorac Surg 1998;66:113-117 8. Mattox KL: Approaches to trauma involving major vessels of the thorax. Surg Clin N A 1989;69:77-91 9. Mattox KL: Injury to the thoracic great vessels, in Moore EE, Mattox KL, Feliciano DV (eds): Trauma (ed 2). Norwalk, CT, Appleton I_ang, 1991, pp 393-408 10. Shkrum MJ, McClafferty KJ, Green RN, et al: Mechanisms of aortic injury in fatalities occurring in motor vehicle collisions. J Forensic Sci 1999;44:44o56 11. Greendyke RM: Traumatic rupture of aorta. Special reference to automobile accidents. JAMA 1996;195:119-122 12. Feczko JD, Lynch L, Pless JE, et al: An autopsy case review of 142 non-penetrating (blunt) injuries of the aorta. J Trauma 1992; 33:846-849
13. Smith RS, Chang FC: Traumatic rupture of the aorta: still a lethal injury. Am J Surg 1986;152:660-663 14. Strassman G: Traumatic rupture of the aorta. Am Heart J 1947;33:508-515 15. Lundevall J: Traumatic rupture of the aorta with special reference to road accidents. Acta Path Microbiol Scand 1964;62:29-33 16. Hartford JM, Fayer RL, Shaver TE, et al: Transection of the thoracic aorta: Assessment of a trauma system. Am J Surg 1986; 151:224-229 17. Parmley LF, Mattingly TW, Manion WC, et al: Non-penetrating traumatic injury of the aorta. Circulation 1958;17:1086-1101 18. Applebaum A, Karp RB, Kirklin JW: Surgical treatment for closed thoracic aortic injuries. J Torac Cardiovasc Surg 1976;71: 458-460 19. Voigt GE, Wilfert K: Mechanisms of injuries to unrestrained drivers in head-on collisions. SAE Report No.: 690811. Warrendale, PA, Society of Automotive Engineers, Inc., 1969 20. Moffat RC, Roberts VL, Berkas EM: Blunt trauma to the thorax: Development of pseudoaneurysms in the dog. J Trauma 1966;6:666-680 21. Louhimo I: Heart injury after blunt thoracic trauma. An experimental study on rabbits. Acta Chit Scand 1968;380:1-60 (suppl) 22. Sevitt S: The mechanisms of traumatic rupture of the thoracic aorta. Br J Surg 1977;64:166-173 23. Zehnder MA: Delayed post-traumatic rupture of the aorta in a young healthy individual after closed injury. Angiology 1956;7:252267 24. Crass JR, Cohen AM, Motta AO, et al: A proposed new mechanism of traumatic aortic rupture: The osseous pinch. Radiology 1990;176:645-649 25. Cohen AM, Crass JR, Thomas HA, et al: CT evidence for the "osseous pinch" mechanism of traumatic aortic injury. A JR Am J Roentgenol 1992;159:271-274 26. Lundevall J: The mechanism of traumatic rupture of the aorta. Acta Pathol Microbiol Scand 1964;62:34-46
GEOFFREY A. ANSWINI, MD, MARK k. STURDEVANT, MD, RONALD F. SING, DO, AND DAVID G. JACOBS, MD Classic teaching suggests that blunt thoracic aortic rupture (BTAR) results from high-speed deceleration injury mechanisms. Our recent experience with a patient who sustained fatal aortic rupture resulting from a low-speed crushing injury emphasizes the importance of maintaining a high index of suspicion for BTAR, even in patients with "lowrisk" injury mechanisms. Several potential pathophysiologic mechanisms of BTAR are discussed. (Am J Emerg Med 2001;19:579-582. Copyright ©2001 by W.B. Saunders Company) Blunt traumatic aortic rupture (BTAR) is an often lethal injury, believed to be caused by high-speed deceleration mechanism. Prompt diagnosis is critical and therefore, early angiography or chest computed tomography (CT) scanning is essential in patients with high-speed deceleration mechanisms and abnormal mediastinal contours on initial chest radiograph. 1-7 Some investigators advocate aortography for patients with "normal" chest radiographs if the traumatic mechanism is sufficiently suggestive, 8,9 while an abnormal mediastinal contour on chest radiograph is usually not considered an indication for aortography if the injury mechanism is inconsistent with BTAR. Thus, a clear understanding of the injury mechanisms causing BTAR is needed to appropriately select patients who will benefit from contrast studies of the thoracic aorta. Here, we report a patient with BTAR caused by a low-speed, nondeceleration mechanism.
CASE REPORT A 46-year-old man, employed as a landscaper, was riding on a large, commercial-sized standing lawnmower when the vehicle overturned on a hill, landing on top of him. He arrived at the emergency department (ED) with a Glasgow Coma Scale score of 10, a pulse rate of 100 beats/min and a blood pressure of 130/80 mm/hg. Mild respiratory distress was noted, with an abdominal breathing pattern and minimal chest wall movement. The patient was noted to have no rectal tone and no evidence of motor or sensory function in his lower extremities. He was intubated and resuscitated in the ED and begun on high-dose methylprednisolone. Initial laboratory examination showed a hemoglobin of
From the Department of General Surgery, Carolinas Medical Center, Charlotte, NC. Manuscript received and accepted April 14, 2001. Address reprint requests to David G. Jacobs, MD, FACS, Department of Surgery/MEB 601, 1000 Blythe Boulevard, Charlotte, NC 28203. E-mail: [email protected] Key Words: Thoracic aorta, blunt rupture. Copyright © 2001 by W.B. Saunders Company 0735-6757/01/1907-0009535.00/0 doi: 10.1053/ajem.2001.28034
14.5gm/dL, PaO2 of 384 tort (FIO 2 = 100%), a base excess of -5mEq/L, and a lactate of 6.1 mEq/L. A portable anterior-posterior (AP) chest radiograph revealed fractures of the left seventh and fight fifth ribs and an abnormal mediastinal contour (Fig 1). AP and lateral thoracic/lumbar spine films revealed a T12 vertebral body compression fracture, bilateral-transverse process fractures at L1, and bilateral twelfth rib fractures. A C T scan of the abdomen and pelvis was significant for a left hemothorax and retropulsed bony fragments into the spinal canal at T12. Because the mechanism of injury was not believed to be compatible with the diagnosis of aortic disruption, no further diagnostic studies of the thoracic aorta were obtained. After completion of these studies, the patient was transferred to the trauma intensive care unit, where a left tube thoracostomy was placed along with a central venous line and an arterial line. The patient's initial central venous pressure (CVP) was 7 cm H20. The chest tube initially drained 1,000 mL of blood, and a hemoglobin drawn 6 hours after admission was noted to be 9.5 g/dL. The patient's vital signs remained stable and over the next several hours, he maintained a brisk urine output and his chest tube drainage diminished substantially. He was transfused with 2 units of packed red blood cells, and his hemoglobin level increased to 11.1 g/dL Thirty-six hours after admission, the patient had an abrupt increase in bloody drainage from his left chest tube. The patient rapidly deteriorated to pulseless electrical activity, and advanced cardiac life support (ACLS) was immediately instituted along with transfusion of packed red blood cells. A left thoracotomy was performed at the bedside, and a large amount of blood and clot were evacuated from the left chest. The descending thoracic aorta was cross-clamped, and direct cardiac massage was started. An actively bleeding intercostal artery adjacent to the fractured left seventh rib was ligated, but no other sites of active hemorrhage were identified. Ventricular fibrillation ensued, and cardioversion and standard ACLS medications were unsuccessful at restoring a sinus rhythm. The patient became asystolic and was pronounced dead. A postmortem examination revealed 2 transverse tears of the descending thoracic aorta, distal to the ligamentum arteriosum. These measured 3.0 cm and 2.5 cm (Fig 2A2B). Both were associated with hemorrhage into the adventitia and surrounding adipose tissue. The patient was also noted to have a contused left lung base and a bruised and lacerated lumbar spinal cord distal to the T12 vertebral fracture. 579
580
AMERICAN JOURNAL OF EMERGENCY MEDICINE • Volume 19, Number 7 • November 2001
FIGURE 1. Portable AP chest radiograph shows an abnormal mediastinal contour.
DISCUSSION Most patients (80% to 90%) who sustain BTAR die immediately of exsanguination; thus, only 10% to 20% survive for medical treatment.l-9 Prompt diagnosis and expedient surgical repair of BTAR is of paramount importance in the initial management of the trauma patient. The evaluating physician must review the patient's vital signs, physical findings, mechanism of injury, and chest radiograph and determine if the patient is at risk for BTAR. Patients who sustain rapid deceleration forces to the chest and have an abnormal mediastinal contour (Table 1) on chest radiograph need further work-up for BTAR to include either spiral CT scanning of the chest or aortography. Case reviews based on autopsy studies report that motor vehicle collisions cause up to 95% of BTARs; most of the other 5% are caused by falls from great heights or crushing chest injuries.l°-~7 Most of the traumatic aortic injury mechanisms proposed in the literature combine features of rapid deceleration and chest compression. One large series evaluated the mechanisms of aortic rupture in 142 fatally injured persons and concluded that rapid chest deceleration/compression induces torsional and shearing forces that cause transverse laceration and rupture of the aorta, most commonly at the ligamentum arteriosum.12 Another large series evaluated 116 patients with BTAR between 1969 and 1989 and made similar observations. 5 BTAR is generally attributable to the action of violent forces applied directly or indirectly to the chest at the moment of impact. To better understand the mechanisms causing this injury, several studies correlated clinical and post mortem observations of injured individuals with the mechanisms of injury and presumed patient kinematics. These studies identified various mechanisms of injury that
alone or in combination can explain the development of aortic tears. These include: (1) Chest crushing-compression causing displacement of the heart downward and to the left after impact on the sternum (ruptures ascending aorta), [°'19-22 (2) Rapid deceleration of the moving body producing tension-stress on the wall of the aorta at points where it is tethered (most commonly the ligamentum arteriosum), 10-14"17"1s'22"23(3) The "shovelling effect" which is upward displacement of the heart and mediastinum from a cranially directed impact on the lower chest (ruptures proximal descending aorta), 19 (4) The osseous pinch (described later in text), 2~-25 (5) Increased intravascular pressure and/or hemodynamic forces (water-hammer effect) after a blow on the chest or rapid deceleration25,26 The common denominator among all of these theories is that the forces causing BTAR are associated with high velocity impacts. In this case report, the described mechanism of injury did not involve a high-velocity impact; therefore aortic disruption was not suspected. This caused a delay in diagnosis. The most likely mechanism causing aortic injury in our patient is the osseous pinch. This mechanism was first described in 1990 by Crass et al and suggests that aortic injuries may be caused by a pinching of the aorta between the spine and the anterior bony thorax during chest compression after abrupt deceleration, 24 Compressive forces from blunt thoracic trauma cause the anterior thoracic osseous structures (manubrium, first rib, medial clavicles) to rotate posteriorly and inferiorly about the axes of the posterior rib articulations. Sufficiently large forces cause the anterior osseous structures to impact the vertebral column and shear the interposed vascular structures, namely the thoracic aorta. Both Parmley et al and Zehnder expressed doubt that the usual deceleration forces encountered in
ANSWINI ET AL • MECHANISM OF BLUNT TRAUMATIC AORTIC RUPTURE
581
FIGURE 2. (A) Post mortem examination of the thoracic aorta reveals one 3.0 cm and one 2.5 cm tear just distal to the take off of the left subclavian artery. (2B) A close-up view of the 2 thoracic aorta tears. trauma were sufficient to rupture the aorta. 17,23 Many studies have shown experimentally that the tensile strength of the aorta exceeds the forces generated in deceleration injuries. 11,15,23-26 The pinch mechanism is even more plausible when the atypical lacerations of the aorta at the arch and the great vessels are taken into account. This mechanism potentially explains why vehicles hitting pedestrians, falls TABLE 1.
Radiographic Clues to Aortic Injury on Chest Radiograph Widened (>8 cm) mediastinum Depressed (>140 degrees) left mainstem bronchus Loss of aortic knob contour Lateral deviation of trachea Deviation of nasogastric tube in esophagus Anterior displacement of trachea Left apical pleura hematoma "cap" Calcium "layering" in aortic arch Massive left-side hemothorax Fracture of thoracic spine, clavicle, sternum, or scapula Loss of paraspinal stripe Loss of aorticopulmonary "window"
from heights, and crushing chest injuries cause aortic rupture. We believe that the osseous pinch mechanism caused the aortic injury in this patient and that this must be seriously considered in the evaluation of all trauma patients when ruling out BTAR. What then, should be the approach to the patient with an abnormal mediastinal contour, without the classic rapid deceleration, high-risk mechanism? The decision to evaluate the mediastinum in all of these patients will produce many negative studies and subject many patients to IV contrast and unnecessary intrahospital transport. However, it will obviate the catastrophic outcomes associated with missed aortic injuries. It is imperative to remember all of the possible mechanisms of BTAR, including the osseous pinch, when determining which patients require contrast studies of the aortic arch. We suggest that any patient with an abnormal mediastinal contour on initial chest radiograph and a rapid deceleration or transthoracic, crush-type of injury undergo either aortography or spiral CT scanning of the chest. Blunt traumatic rupture of the thoracic aorta remains a diagnostic challenge, and further prospective studies may
582
AMERICAN JOURNAL OF EMERGENCY MEDICINE • Volume 19, Number 7 • November 2001
delineate a cost-effective, yet sensitive, way to expeditiously and efficiently identify this often fatal injury. REFERENCES 1. Gammie JS, Shah AS, Hattler BG, et al: Traumatic aortic rupture: diagnosis and management. Ann Thor Surg 1998;66:12951300 2. Galli R, Pacini D, Di Bartolomeo R, et al: Surgical indications and timing of repair of traumatic ruptures of the thoracic aorta. Ann Thorac Sur 1998;65:461-464 3. Tribble CG, Crosby IK: Traumatic rupture of the thoracic aorta. South Med J 1988;81:963-968 4. Von Oppell UO, Dunne 1-1, De Groot MK, et al: Traumatic aortic rupture: Twenty-year meta-analysis of mortality and risk of paraplegia. Ann Thorac Surg 1994;58:585-593 5. Kodali S, Jamieson WRE, Leia-Stephens M, et al: Traumatic rupture of the thoracic aorta; a 20-year review: 1969-1989. Circulation 1991 ;84 111:40-46 (suppl) 6. Ayella RJ, Hankins JR, Turney SZ, et al: Ruptured thoracic aorta due to blunt trauma. J Trauma 1977;17:199-205 7. Symbas PJ, Horsley WS, Symbas PN: Rupture of the ascending aorta caused by blunt trauma. Ann Thorac Surg 1998;66:113-117 8. Mattox KL: Approaches to trauma involving major vessels of the thorax. Surg Clin N A 1989;69:77-91 9. Mattox KL: Injury to the thoracic great vessels, in Moore EE, Mattox KL, Feliciano DV (eds): Trauma (ed 2). Norwalk, CT, Appleton I_ang, 1991, pp 393-408 10. Shkrum MJ, McClafferty KJ, Green RN, et al: Mechanisms of aortic injury in fatalities occurring in motor vehicle collisions. J Forensic Sci 1999;44:44o56 11. Greendyke RM: Traumatic rupture of aorta. Special reference to automobile accidents. JAMA 1996;195:119-122 12. Feczko JD, Lynch L, Pless JE, et al: An autopsy case review of 142 non-penetrating (blunt) injuries of the aorta. J Trauma 1992; 33:846-849
13. Smith RS, Chang FC: Traumatic rupture of the aorta: still a lethal injury. Am J Surg 1986;152:660-663 14. Strassman G: Traumatic rupture of the aorta. Am Heart J 1947;33:508-515 15. Lundevall J: Traumatic rupture of the aorta with special reference to road accidents. Acta Path Microbiol Scand 1964;62:29-33 16. Hartford JM, Fayer RL, Shaver TE, et al: Transection of the thoracic aorta: Assessment of a trauma system. Am J Surg 1986; 151:224-229 17. Parmley LF, Mattingly TW, Manion WC, et al: Non-penetrating traumatic injury of the aorta. Circulation 1958;17:1086-1101 18. Applebaum A, Karp RB, Kirklin JW: Surgical treatment for closed thoracic aortic injuries. J Torac Cardiovasc Surg 1976;71: 458-460 19. Voigt GE, Wilfert K: Mechanisms of injuries to unrestrained drivers in head-on collisions. SAE Report No.: 690811. Warrendale, PA, Society of Automotive Engineers, Inc., 1969 20. Moffat RC, Roberts VL, Berkas EM: Blunt trauma to the thorax: Development of pseudoaneurysms in the dog. J Trauma 1966;6:666-680 21. Louhimo I: Heart injury after blunt thoracic trauma. An experimental study on rabbits. Acta Chit Scand 1968;380:1-60 (suppl) 22. Sevitt S: The mechanisms of traumatic rupture of the thoracic aorta. Br J Surg 1977;64:166-173 23. Zehnder MA: Delayed post-traumatic rupture of the aorta in a young healthy individual after closed injury. Angiology 1956;7:252267 24. Crass JR, Cohen AM, Motta AO, et al: A proposed new mechanism of traumatic aortic rupture: The osseous pinch. Radiology 1990;176:645-649 25. Cohen AM, Crass JR, Thomas HA, et al: CT evidence for the "osseous pinch" mechanism of traumatic aortic injury. A JR Am J Roentgenol 1992;159:271-274 26. Lundevall J: The mechanism of traumatic rupture of the aorta. Acta Pathol Microbiol Scand 1964;62:34-46