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Asian Cardiovasc Thorac Ann 2004;12:202-207
© 2004 Asia Publishing EXchange Ltd


ORIGINAL CONTRIBUTION

Factors Affecting Early Exsanguination and Death in Blunt Thoracic Aortic Trauma

Robert A Lancey, MD, A Thomas Pezzella, MD1, David A Phillips, MD2

University of Massachusetts Medical School, Division of Cardiac Surgery, Mary Imogene Bassett Hospital, New York, USA
1 St. Mary s Good Samaritan Hospital, Illinois, USA
2 University of Massachusetts Medical School, Department of Radiology, UMass Memorial Medical Center, Massachusetts, USA

For reprint information contact: Robert A Lancey, MD Tel: 1 607 547 4770 Fax: 1 607 547 4786 Email: robert.lancey{at}bassett.org Director, Division of Cardiac Surgery, Mary Imogene Bassett Hospital, 1 Atwell Road, Cooperstown, NY 13326, USA.


    ABSTRACT
 TOP
 ABSTRACT
 INTRODUCTION
 PATIENTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
The traditional approach to blunt thoracic aortic injuries has been expedient diagnosis and operative repair due to the significant risk of early exsanguination and death in initial survivors. Nonoperative management has been advocated in patients with multiple injuries to reduce the operative mortality. However, specific clinical parameters and diagnostic tests that may predict the risk of early exsanguination and death have yet to be identified. A retrospective analysis of 80 patients with these injuries was undertaken to identify factors associated with early exsanguination or death. Available aortograms were also examined and graded to determine their utility in predicting these outcomes. Early exsanguination and death were found to be associated with low systolic blood pressure on admission and with short duration from injury to diagnosis. Exsanguination was also associated with the total number of lesions in thoracic injuries, and mortality with age greater than 30 years. Aortographic appearance was not found to correlate with either outcome. Patients with blunt thoracic aortic injuries should continue to be managed expediently, with immediate surgical repair if not contraindicated by associated injuries, to avoid early rupture.


    INTRODUCTION
 TOP
 ABSTRACT
 INTRODUCTION
 PATIENTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Despite the delivery of expedient treatment, blunt thoracic aortic trauma continues to carry a significant mortality rate of over 30%, in large multi-institutional series of minority patients who survive to reach an acute care facility.1,2 Parmley and associates were the first to identify the significant early lethality of these injuries.3 The initial care of these patients thus has been focused on expeditious diagnosis and immediate surgical repair before exsanguination and death occur. Reports of elective delayed repair, however, have demonstrated survival rates of 80% or more.4

Although trauma grading systems have been developed for injuries to the liver and spleen to better plan the timing and need for operative intervention, such criteria have not been developed for blunt thoracic aortic injuries. No specific clinical parameters or diagnostic tests have been found to be associated with exsanguination and/or death, making it unclear which of these patients are at risk for early rupture and exsanguination.

This report retrospectively reviewed a 20-year experience with these injuries, examining diagnostic test results and clinical parameters to determine if they are associated with or can identify patients with partial disruption of the thoracic aortic wall are at high risk for early exsanguination and/or death.


    PATIENTS AND METHODS
 TOP
 ABSTRACT
 INTRODUCTION
 PATIENTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
UMass Memorial Medical Center is Level I trauma center where over 1500 trauma patients are seen annually, the majority are blunt injuries. From September 1978 to December 2001, 80 patients were diagnosed with acute blunt injuries to the thoracic aorta. Their medical records were retrospectively reviewed to obtain data on demographics, clinical presentation (admission and maximum systolic blood pressure, type and total number of lesions in thoracic and extrathoracic injuries, hours to diagnosis and to repair), diagnostic methods and results, management and outcomes.

A subset analysis was performed on 46 of these patients to determine the relationship of thoracic aortographic findings with both operative findings and outcomes. Reasons for exclusion from this subset were lack of aortogram for review, exsanguination prior to aortography, no aortogram performed prior to repair, nonoperative management, and inadequate description of findings in the operative note. Aortograms with LAO and RAO views were retrospectively evaluated by an interventional radiologist and a cardiothoracic surgeon who were not informed of the operative findings and outcomes.

A grading system based on the degree of subadventitial hematoma (SAH) present on both LAO and RAO views in the aortograms was formulated, with a score of 0 assigned for absence of SAH; 1 for hematoma on only one side of the aorta; and 2 for hematoma on both sides. The aortographic scores were added to obtain a combined score. Patients were then classified into three grades: grade A for a score of 0 (no hematoma), grade B for a total score of 1–3 (partial circumferential hematoma) and grade C for a total score of 4 (circumferential hematoma). The grades were then compared to operative findings, specifically to the extent of the hematoma (either localized at the area of injury or extensive, throughout the mediastinum) and to the degree of disruption of the intima and media (less than 120 degrees, 120–240 degrees, or greater than 240 degrees). The grading system was also examined for its relationship to outcome using exsanguination and/or death as end points.

The association of death or exsanguination with categorical variables was analyzed using the chi-square test, and for association with continuous variables; a comparison of means and the Student’s t-test were used. All variables found to predict death with a p-value of < 0.05 were then entered into a logistic regression analysis. The relationships between death and exsanguination and the assigned grades of aortic injury by thoracic aortography was conducted using Fisher’s Exact test.


    RESULTS
 TOP
 ABSTRACT
 INTRODUCTION
 PATIENTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
There were 62 male and 18 female patients with a mean age of 37.2 years, ranging from 14 to 86 years (Figure 1Go). Seventy-five (93.7%) were victims of motor vehicle accidents, three were injured in falls, and two were pedestrians struck by automobiles. The disruption occurred at the isthmus in 71 (87.7%) patients, at the ascending aorta or arch in 7 (8.6%), and at the descending aorta in 3 (3.7%), including one patient with disruptions both at the ascending and descending aorta.



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Figure 1. Incidence and mortality rates of blunt thoracic aortic injury by age.

 
Admission chest roentgenograms were performed on 76 of the 80 patients. The most common finding was mediastinal widening, followed by loss of aortic knob contour and apical capping. With presence of apical capping on admission, the chest X-Ray was found to be significantly associated with mortality, but none of the findings were significantly associated with exsanguination (Table 1Go). Diagnosis was confirmed by emergency aortography in 69 patients, by thoracic computed tomography (CT) scanning in 3, and by transesophageal echocardiography (TEE) in 1. Injury was first noted during emergency thoracotomy for remaining 7 patients. The average time from injury to diagnosis was 7.9 hours (mean, 5 hours).


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Table 1. Admission Chest Radiographic Findings in Patients with Blunt Thoracic Aortic Injury
 
The mean systolic blood pressure (SBP) on admission was 121 mm Hg (range, 0 to 200 mm Hg), and the mean maximum preoperative SBP was 143.7 mm Hg (range, 0 to 225 mm Hg). Three patients had an initial SBP less than 70 mm Hg. Of the 27 patients with a maximum SBP of 160 mm Hg or greater, only 2 (7.41%) exsanguinated. Of the remaining 53 patients with a maximum SBP less than 160 mm Hg, 10 (18.87%) exsanguinated (Figure 2Go). There was no significant difference in time from injury to exsanguination between the two groups.



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Figure 2. Association of exsanguination with admission and maximum systolic blood pressure (in mm Hg) in patients with blunt thoracic aortic trauma (adm SBP = admission systolic blood pressure; max SBP = maximum systolic blood pressure).

 
Additional intrathoracic injuries were identified in 48 patients (average, 1.05 per patient) and none were found to be significantly associated with exsanguination (Table 2Go). Extrathoracic injuries were found in 69 patients, an average of 2.0 per patient (Table 3Go). Neither the number nor the type of extrathoracic injuries were found to correlate with exsanguination and death.


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Table 2. Incidence of Intrathoracic Injuries in Blunt Thoracic Aortic Trauma
 

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Table 3. Incidence of Extrathoracic Injuries in Blunt Thoracic Aortic Trauma
 
Operative repair was completed in 62 patients, 91.9% with an interposition graft and the remainder with primary repair. Spinal cord protection was provided by left heart bypass (53.1%), with a heparin-bonded shunt (29.7%), and cardiopulmonary bypass (12.5%). In 3 patients (4.7%), a clamp-and-sew technique was employed. The median time from diagnosis to repair was 2 hours, and from injury to repair was 6 hours. A total of 18 patients did not undergo operative repair due to severe accompanying injuries, or exsanguination and death prior to repair, or intraoperative death (Table 4Go).


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Table 4. Timing of Death in Patients with Blunt Thoracic Aortic Trauma
 
For the subset comparison of aortography with intraoperative findings and outcomes, 44 of the injuries were in the proximal descending aorta at the isthmus and the remaining 2 were in the ascending aorta, arch, or mid-descending aorta. In 25% of patients, the hematoma appeared circumferential, and no hematoma was visible in 1 patient. In the remaining 72.7%, it appeared partial circumferential. Intraoperatively, the hematoma was found localized to the site of injury in 15 patients, and a diffuse spread beyond the area of injury was in 26 patients. The operative note did not specify the extent of the hematoma in 5 patients. The extent of subadventitial division was found to be less than 120 degrees in 7 patients, from 120 to 240 degrees in 13 patients, and greater than 240 degrees in 20 patients, which includes 14 patients with total circumferential disruption of the intima. In 7 patients the operative description was inadequate to determine the extent of separation. Neither the extent of the hematoma nor the subadventitial disruption was found to correlate with each other or with the assigned grades of hematoma by aortographic analysis, or with exsanguination or death.

A total of 28 patients died for an overall mortality rate of 35%. For those who underwent operative repair, the mortality rate was 22.7%. Free rupture and exsanguination occurred in 15 patients, with one survivor. The average time from injury to exsanguination was 4.2 hours (mean, 3 hours), two-thirds of exsanguination occurred in less than four hours and none was more than ten hours after injury (Table 4Go). Exsanguination was found to be significantly associated with low SBP on admission, short duration from injury to diagnosis, number of additional intrathoracic injuries, and death (Table 5Go).


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Table 5. Factors Associated with Exsanguination in Blunt Thoracic Aortic Trauma
 
Factors found significantly to correlate with mortality were age greater than 30 years, low admission SBP, the presence of apical capping on the chest X-Ray, short duration both from injury to diagnosis and diagnosis to repair, and exsanguination (Table 6Go). Those 50 years and older had an odds of death that was 43 times of those under 50 years when mean time to diagnosis was controlled (p = 0.003).


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Table 6. Factors Associated with Mortality in Blunt Thoracic Aortic Trauma
 

    DISCUSSION
 TOP
 ABSTRACT
 INTRODUCTION
 PATIENTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Trauma to the thoracic aorta is estimated to be responsible for one-quarter of trauma deaths and is present in almost two-thirds of motor vehicle fatalities,5 with 80% to 95% of deaths occurring within the first hour after injury.6 Hartford and associates noted that nearly half died at the scene or before arrival to the hospital, and of the initial survivors, nearly two-thirds died within 24 hours of admission, 81% from aortic injuries.7

Although traditional management has emphasized expeditious diagnosis and early operative intervention, the risk of operation for some may be prohibitive due to accompanying injuries. Intracranial trauma and pulmonary contusions may be aggravated by operative repair.8 Clinical scenarios in which early surgery may be contraindicated include extensive intracerebral hemorrhage, a Glasgow Coma Scale score of less than 6, inability to support the patient with single-lung ventilation, the requirement for inotropic support, or marked coagulopathy. Delay may also be warranted in the presence of an unstable high cervical spine fracture, extensive pulmonary contusions, significant cardiac injury or infarct, or massive intra-abdominal hemorrhage. Many reports have documented successful delayed operations in these settings,4,8 and some have suggested that serial diagnostic studies be performed in lieu of surgery, with operative repair reserved for those with expanding pseudoaneurysms.9

Despite reports of successful management of patients with delayed repair or non-operative treatment, anatomic disruption of the intima and media may lead to chronic expansion of a pseudoaneurysm and early acute rupture in significant numbers of initial survivors. Mattox noted that patients with early hemodynamic instability have a high mortality rate, with death often occurring in the first 2 to 4 hours after injury, even when an operation is undertaken immediately.10 Patients who survive the first few hours may be self-selected by virtue of a more well-contained periaortic hematoma, possibly from either less disruption of the intima and media or from greater adventitial strength.

Early rupture occurs in significant numbers of patients who initially survive to be hospitalized.2 In Duhaylongsod’s series of over 100 patients, 17 suffered fatal ruptures after admission, 88% occurred in less than 4 hours.11 Other reports have documented mortality rates of 30% to 44% from exsanguination prior to operative intervention.12,13 In a large multi-center analysis, exsanguination was found to be responsible for nearly two-thirds of the deaths, 46% occurring less than 4 hours after presentation and 84% in less than 8 hours.2 Differentiating between those who require emergency versus urgent or elective repair based on diagnostic tests or clinical parameters is difficult. We found aortographic appearance not to be predictive of operative findings, exsanguination or death, suggesting that the extent of the periaortic hematoma does not solely contribute to the risk of rupture. Other factors, such as the degree of tensile strength of the adventitia, may play a more important role. Despite its lack of prognostic utility, aortography remains the gold standard for diagnosing blunt thoracic aortic injuries due to its superb specificity and sensitivity in identifying these injuries.

Certain clinical findings have been found to be associated with exsanguination, such as left hemothorax, pseudocoarctation effect, and/or a left supraclavicular hematoma, a triad of "grossly widened mediastinum", hemothorax, and transient hypotension.14 Their clinical usefulness in predicting exsanguination though is limited by low sensitivity and specificity.

Although a direct correlation has been demonstrated between mortality and delays of more than 3 hours from injury to repair in stable patients,12 others have found no difference in time to diagnosis or treatment between survivors and non-survivors, and no effect of delays in treatment on exsanguination and death.14 We found early diagnosis and repair were both associated with death and exsanguination. This finding is probably due to early exsanguination resulting in earlier identification of the injury rather than the reverse.

The use of beta-blockers to prevent exsanguination in patients with blunt thoracic aortic injuries was initially suggested by Hilgenberg,15 and others have documented the benefits of hypotensive therapy in preventing rupture.16 We however found no correlation between hypertension and exsanguination; but low SBP on admission was associated with death and exsanguination, as reported by Eddy and associates.12

Advanced age was found to be associated with mortality though not with exsanguination. Others have noted higher mortality rates in the elderly for blunt thoracic trauma in general and specifically for those with aortic injuries.2,17 Higher mortality rates with operative repair have also been noted in those over 55 years of age.18 Factors contributing to this relationship may be the greater pliability of the thoracic wall in younger patients and the lack of physiologic reserve in elderly patients subjected to severe multiple injuries.

A limitation of our study was the number of aortograms available for examination. As most centers see an average of 2.5 patients with these injuries annually, a prospective multi-institutional approach to defining predictive factors for exsanguination in these patients may be more promising. Advances in diagnostic techniques may also help to identify those at risk for exsanguination. Helical CT scanning, for instance, has shown early promise in defining mediastinal anatomy and diagnosing aortic trauma.19

One-half of the deaths in our series were due to exsanguination, with nearly two-thirds of these events occurring in the first four hours after injury, and all but one who exsanguinated expired. Thus, our approach to patients with blunt thoracic aortic trauma continues to be an aggressive one. The early high mortality of initial survivors and our inability to accurately identify patients who are at greatest risk for exsanguination argues against a shift towards nonoperative management in all patients with such injuries. Patients with severe concomitant injuries may not be candidates for immediate surgery and will require close medical management and monitoring, in general this nonoperative approach should be an exception rather than the rule of early management after injury to avoid lethal rupture.


    REFERENCES
 TOP
 ABSTRACT
 INTRODUCTION
 PATIENTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 

  1. von Oppell UO, Dunne TT, De Groot MK, Zilla P. Traumatic aortic rupture: twenty-year metaanalysis of mortality and risk of paraplegia. Ann Thorac Surg 1994;58:585–93.[Abstract]

  2. Fabian TC, Richardson JD, Croce MA, Smith JS Jr, Rodman G Jr, Kearney PA, et al. Prospective study of blunt aortic injury: Multicenter Trial of the American Association for the Surgery of Trauma. J Trauma 1997;42:374–83.[Medline]

  3. Parmley LF, Mattingly TW, Manion WC, Jahnkey EJ Jr. Non-penetrating traumatic injury of the aorta. Circulation 1958;17:1086–101.[Medline]

  4. Akins CW, Buckley MJ, Daggett W, McIlduff JB, Austen WG. Acute traumatic disruption of the thoracic aorta: a ten year experience. Ann Thorac Surg 1981;31:305–9.[Abstract]

  5. Moar JJ. Traumatic rupture of the thoracic aorta. An autopsy and histopathological study. S Afr Med J 1985;67:383–5.[Medline]

  6. Williams JS, Graff JA, Uku JM, Steinig JP. Aortic injury in vehicular trauma. Ann Thorac Surg 1994;57:726–30.[Abstract]

  7. Hartford JM, Fayer RL, Shaver TE, Thompson WM, Hardy WR, Roys GD, et al. Transection of the thoracic aorta: assessment of a trauma system. Am J Surg 1986;151:224–9.[Medline]

  8. Soots G, Warembourg H Jr, Prat A, Roux JP. Acute traumatic rupture of the thoracic aorta: place of delayed surgical repair. J Cardiovasc Surg (Torino) 1989;30:173–7.[Medline]

  9. Galli R, Pacini D, Di Bartolomeo R, Fattori R, Turinetto B, Grillone G, et al. Surgical indications and timing of repair of traumatic ruptures of the thoracic aorta. Ann Thorac Surg 1998;65:461–4.[Abstract/Free Full Text]

  10. Mattox KL. Red River anthology. J Trauma 1997;42:353–68.[Medline]

  11. Duhaylongsod FG, Glower DD, Wolfe WG. Acute traumatic aortic aneurysm: the Duke experience from 1970 to 1990. J Vasc Surg 1992;15:331–43.[Medline]

  12. Eddy AC, Rusch VW, Marchioro T, Ashbaugh D, Verrier ED, Dillard D. Treatment of traumatic rupture of the thoracic aorta; A 15 year experience. Arch Surg 1990;125:1351–6.[Abstract/Free Full Text]

  13. Hunt JP, Baker CC, Lentz CW, Rutledge RR, Oller DW, Flowe KM, et al. Thoracic aorta injuries: management and outcome of 144 patients. J Trauma 1996;40:547–56.[Medline]

  14. Simon BJ, Leslie C. Factors predicting early in-hospital death in blunt thoracic aortic injury. J Trauma 2001;51:906–11.[Medline]

  15. Hilgenberg AD, Logan DL, Akins CW, Buckley MJ, Daggett WM, Vlahakes GJ, et al. Blunt injuries of the thoracic aorta. Ann Thorac Surg 1992;53:233–9.[Abstract]

  16. Pate JW, Fabian TC, Walker W. Traumatic rupture of the aortic isthmus: an emergency? World J Surg 1995;19:119–26.[Medline]

  17. Sturm JT, Billiar TR, Dorsey JS, Luxenberg MG, Perry JF Jr. Risk factors for survival.following surgical treatment of traumatic aortic rupture. Ann Thorac Surg 1985;39:418–21.[Abstract]

  18. Camp PC Jr, Rogers FB, Shackford SR, Leavitt BJ, Cobean RA, Clark DE. Blunt traumatic thoracic aortic lacerations in the elderly: an analysis of outcome. J Trauma 1994;37:418–25.[Medline]

  19. Downing SW, Sperling JS, Mirvis SE, Cardarelli MG, Gilbert TB, Scalea TM, et al. Experience with spiral computed tomography as the sole diagnostic method for traumatic aortic rupture. Ann Thorac Surg 2001;72:495–502.[Abstract/Free Full Text]




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