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Acute traumatic disruption of the thoracic aorta: Emergency department management
ORIGINAL CONTRIBUTION
aortic disruption
A c u t e TraumaticDisruptionof the Thoracic Aorta: EmergencyDepartmentManagement From the Departments o f
Ralph L Warren, MD * ~
Study objective: Toevaluate the safety and effectiveness of
Surgery* and Emergency
Cary W Akins, MD ~
Services, t Massachusetts
Alasdair K T Conn, MD *~r
temporary IV antihypertensive therapy in patients with acute traumatic thoracic aortic disruption.
General Hospital, and Harvard
Alan D Hilgenberg, MD**
Medical School, Boston. ¢
Charles J McCabe, MD *~:
Received for publication
Design: Retrospective chart review of all patients treated for proven traumatic aortic disruption during the ten-year period of 1980 through 1989.
February 25, 1991. Revision
Setting:
received August 8, 1991.
center.
Accepted for publication October 30, 1991.
Emergency department of a large, urban, Level I trauma
Interventions: Preoperative IV 13-blockade and nitroprusside after initial resuscitation in hemodynamically stable patients. Rcsu|ts: Thirty-seven patients with angiographically proven aortic disruption were separated retrospectively into one of three groups. Group 1 (15 patients without preoperative antihypertensive therapy] had two deaths. Group 2 (15 patients treated for two to seven hours [mean, 3.8 hours] before surgery with antihypertensives) had one death. Group 3 (seven patients treated with antihypertensives for 24 hours to four months before surgery to allow recovery from associated severe injuries) had one death. There were no complications resulting from antihypertensive therapy. Conclusion: Temporary antihypertensive therapy appears to be safe and effective in patients with aortic disruption. [Warren RL, Akins CW, Conn AKT, Hilgenberg AD, McCabe CJ: Acute traumatic disruption of the thoracic aorta: Emergency department management. Ann EmergMedApri11992;21:391-396.]
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ANNALS OF EMERGENCY MEDICINE 21:,4 APRIL1992
THORACIC AORTA Warren et al
INTRODUCTION
Since the first descriptions of the n a t u r a l history of traumatic thoracic aortic disruption in 19471 and 19582 and the first surgical r e p a i r of this lesion in 1958, 3 it has become well established that urgent surgical r e p a i r is most often the treatment of choice. However, after Wheat and colleagues introduced the nonsurgical pharmacologic t h e r a p y for acute aortic dissection in 1965, a ~t was suggested that such treatment also could be used for t r a u m a t i c aortic tears. 5~9 The safety of this so-called "medical t h e r a p y " as a temporizing measure in patients with acute aortic tears who have contraindications to immediate surgical r e p a i r was subsequently demonstrated by Akins et al 1° as well as others. ~-13 Injuries to the aorta caused by blunt t r a u m a consist of transverse, usually circumferential, tears of the intima and varying amounts of media and adventitia.14-16 If the full thicknesses of media and adventitia are torn, as occurs in 80% to 85% of victims, 1'2"]7 immediate exsanguination and death result. If, on the other h a n d , the adventitia - - which provides most of the collagenous strength of the aortic wall does not tear, a p s e u d o a n e u r y s m is formed, and exsanguination is forestalled. This pseudoaneurysm, however, is inherently unstable and prone to unpredictable r u p t u r e . Not only is the wall of the p s e u d o a n e u r y s m greatly thinned, but because its diameter is greater than that of the uninjured aorta, the tension in this segment of thinned wall is greater (the law of Laplace). In the management of patients with aortic tears, therefore, it would seem p r u d e n t , if not m a n d a t o r y , to minimize the stresses on the attenuated and weakened aortic wall. The aortic intraluminal pressure, and especially the rate of rise of the aortic pressure wave (dP/dT),a'18 should be carefully controlled and if not actually lowered to less t h a n normal, at least prevented from increasing excessively. As in the pharmacologic treatment of aortic dissection, the d P / d t is best controlled by decreasing the force of left ventricular ejection with negative inotropic agents; the mean aortic pressure then is controlled with systemic a r t e r i a l vasodilators. Pure vasodilators, if used alone, increase r a t h e r than decrease the dP/dt because they lower diastolic pressure more than systolic pressure. 4'18 Medical treatment should always begin with negative inotropic agents, adding vasodilators as needed. With these considerations in mind, our a p p r o a c h in the emergency department since 1980 to the hemodynamically stable trauma patient suspected of having a torn thoracic aorta has included early placement of a right r a d i a l arterial pressure-monitoring catheter and aggressive control of cardiac contractility with ~-adrenergic blockade and of systemic blood pressure with nitroprusside. Ideally, this treatment is begun as soon as the diagnosis of aortic t e a r is suspected, even before aortography, and is continued until surgical control of the t o r n aorta is obtained. We conducted -
-
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our retrospective study to evaluate the safety and effectiveness of such therapy.
MATERIALS
AND
METHODS
T r a u m a patient management at the Massachusetts General Hospital is directed on a 24-hour basis by ED attending physicians and surgical residents and follows the guidelines of the American College of Surgeons regarding advanced t r a u m a life support. The diagnosis of aortic disruption is suspected on the basis of chest r a d i o g r a p h y and mechanism of i n j u r y and confirmed or ruled out by aortography. Diagnostic peritoneal lavage is used liberally to quickly detect i n t r a - a b d o m i n a l injuries. As soon as the diagnosis of thoracic aortic i n j u r y is suspected, the cardiac surgical and angiographic services are alerted, and a right r a d i a l arterial pressure-monitoring catheter is inserted. If the patient is hemodynamically stable, treatment with IV analgesics, p-blockade, and nitroprusside is begun. P r o p r a n o l o l or labetolol is given in sufficient quantities to lower the h e a r t rate to 60 + 5 and is followed by nitroprusside infusion as needed to keep systolic blood pressure between 90 and 100 mm Hg. We reviewed the records of all patients t r e a t e d at the Massachusetts General Hospital for acute thoracic aortic disruption secondary to blunt t r a u m a from J a n u a r y 1, 1980, through December 31, 1989. Of the 43 patients identified, at immediate emergency thoracotomy the diagnosis of aortic disruption was made in six, the diagnosis of p r e a r rival cardiac a r r e s t was made in four, and the diagnosis of p r o f o u n d persistent hypotension was made in two. All six died and are not considered f u r t h e r in this report. Thirty-seven patients survived long enough to undergo diagnostic aortography, and they constituted the study population. There were 31 men and six women (age range, 16 to 70 years; mean, 36 years). Motor vehicle accidents were the cause of i n j u r y in 35 (95%): 30 were occupants (19 drivers and 11 passengers) of automobiles, two were pedestrians struck by cars, and three were motorcyclists. Two patients fell from a height of m o r e than 20 ft. Almost all patients h a d associated m a j o r injuries. Mean I n j u r y Severity Score (ISS) was 39: 51% experienced i n t r a c r a n i a l injury; 65%, p u l m o n a r y injury; 38%, i n t r a - a b d o m i n a l injury; 35%, pelvic injury; and 65%, m a j o r extremity fracture. Only six of the 37 patients a r r i v e d at our institution directly from the accident scene, whereas 31 (84%) were t r a n s f e r r e d from other hospitals. All 37 patients h a d a b n o r m a l chest r a d i o g r a p h s , although three h a d initial chest r a d i o g r a p h s that were normal. The most common chest film findings were widened mediastinum (97%), rib fractures (51%), indistinct aortic knob (38%), left h e m o t h o r a x and/or p n e u m o t h o r a x (38%), and deviation of the t r a c h e a and/or nasogastric tube to the right (14%). Eight patients h a d chest computed tomography perlb
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THORACIC AORTA Warren et al
formed at the referring hospital, and all showed mediastinal and/or aortic abnormalities. The site of the aortic tear was in the region of the aortic isthmus in 35 patients (95%) and the ascending aorta in two (5%). Surgical r e p a i r was carried out in 34 of the 37. Six patients underwent l a p a r o t o m y before thoracotomy, all with grossly positive peritoneal lavage, and four patients underwent l a p a r o t o m y immediately after thoracotomy. Of the 32 operated patients with isthmus tears, 19 (59%) were r e p a i r e d without aortic bypass. In the other 13 (41%), a 9mm Gott shunt (TDMAC-heparin shunt, a flexible plastic catheter with the internal surface coated with h e p a r i n , thus obviating the need for systemic heparinization) was used to bypass the i n j u r e d aortic segment during cross-clamping. Three of the 37 patients - - all with isthmus tears - - did not undergo surgical repair. One of them exsanguinated before surgery in the induction room. One, who was being treated nonsurgicaUy because of severe associated injuries, died of r e s p i r a t o r y failure unrelated to the aortic tear. The third patient was managed entirely nonsurgically because of an associated high thoracic cord transection. The 37 patients were s e p a r a t e d retrospectively into one of three groups (Table). Group 1 (15 patients) underwent urgent surgical r e p a i r without surgical antihypertensive therapy; these patients were considered hemodynamically unstable, with either low or labile (episodes of low r a t h e r than high) blood pressure. Group 2 (15 patients) had surgical antihypertensive t h e r a p y ; these patients h a d stable normal or high blood pressure after p r i m a r y resuscitation and evaluation. Group 3 (seven patients) was treated with p h a r macologic antihypertensive t h e r a p y as the p r i m a r y t h e r a p y to stabilize other severe injuries that p r o h i b i t e d immediate surgery. Mean age of the patients in group i was 42 years, and mean ISS was 38. One patient in the group had l a p a r o t o m y before and three had l a p a r o t o m y after thoracotomy. Mean time between i n j u r y and thoracotomy in this group was 7.0 hours (excluding two patients who had diagnosis of aortic injury delayed for three and 3.5 days, followed by surgical r e p a i r in both cases within three hours of diagnosis).
Table.
Description of patient groups and outcomes No. of Patielwl~ Group*
No. of
Mean Age
No. of
With
Patients
(yr)
Mean ISS
Deaths (%)
Paraplegia 1
1
15
42
38
2 (13)
2
15
32
32
1 (7)
1
3
7
35
54
1 (14)
1
*Group I, immediate surgical repair and no preoperative antihypertensive therapy (hemodynamically unstable); group 2, immediate surgical repair with preoperative antihypertensive therapy {hemodynamically stable); group 3, deJayed surgical repair (one indefinitery) with primary interval antihypertensive therapy (initial or persistent centraindication to surgery).
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Mean age of patients in group 2 was 32 years, and mean ISS was 32. The d u r a t i o n of pharmacologic t h e r a p y was two to seven hours (mean, 3.8 hours). One patient in this group h a d l a p a r o t o m y before and one had l a p a r o t o m y after thoracotomy. Mean time between i n j u r y and thoracotomy was 8.7 hours (again excluding two who had diagnosis delayed for 24 and 48 hours, followed by medical t h e r a p y for three and six hours, respectively, before thoracotomy). Mean age of the seven patients in group 3 was 35 years, and mean ISS was 54. Medical treatment was begun with IV #-blockade and nitroprusside and maintained with oral agents if surgery was delayed beyond several days. F o u r of these seven patients had grossly positive peritoneal lavage and l a p a r o t o m y before aortography. The indications for delay of surgery were as follows: Three patients had severe i n t r a c r a n i a l central nervous system injury, which improved with time so that aortic r e p a i r was u n d e r t a k e n after 24 hours, 52 days, and four months. One patient had acute renal and r e s p i r a t o r y insufficiency after l a p a r o t o m y at the referring hospital and was treated medically for three days to allow adequate improvement of these two systems. One patient, whose diagnosis was delayed 26 days after injury and whose aortic tear was complicated by limited distal aortic dissection and m y o c a r d i a l ischemia, was stabilized medically for 12 days to ensure optimum c a r d i o p u l m o n a r y condition for surgery. One patient had severe b i l a t e r a l p u l m o n a r y contusions that prevented safe thoracic surgery; this patient died (the only death in group 3). One patient had a T3 vertebral fracture/dislocation with high spinal cord transection and was managed entirely nonsurgically.
RESULTS Of 37 patients with angiographically proven thoracic aortic disruption, four died, yielding an overall mortality of 11%. Mean age of the survivors was 34 years, and mean ISS was 39, whereas mean age and ISS of the patients who died were 55 years and 38, respectively. The outcomes with respect to preoperative antihypertensive treatment are shown (Table). The three groups in our study are not directly c o m p a r a b l e as representing similar patients undergoing different treatments; rather, they were t r e a t e d differently b e c a u s e of their differing presenting clinical conditions. In group 1, there were two deaths, both occurring after surgery. Both patients h a d very difficult i n t r a o p e r a t i v e courses, including cardiac a r r e s t at induction of anesthesia; in addition, they were two of the oldest patients in the series (66 and 70 years). In group 2 there was one death. This patient died in the operating room; after two hours of medical treatment and eight hours after injury, he suddenly awoke in the induction room and became acutely hypertensive, resulting in free r u p t u r e of his a o r t a and exsanguination. Thus, death
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THORACIC AORTA Warren et al
resulted from inadequate blood pressure control r a t h e r than from failure of adequate antihypertensive treatment. In group 3 there was one death. This patient had severe bilateral pulmonary contusions, which prevented safe thoracic surgery after his initial emergency l a p a r o t o m y and splenectomy; he died two days after i n j u r y of r e s p i r a t o r y failure. One patient was managed completely nonsurgically because of a high spinal cord transection and survived. The remaining five patients underwent successful surgical r e p a i r of their aortic tears (all in the region of the isthmus) from one day to four months after injury. The occurrence of postoperative paraplegia was related more to intraoperative than to p r e o p e r a t i v e factors. Of the 32 operated patients with isthmus tears, three developed postoperative paraplegia, one case in each of groups 1, 2, and 3, for an overall incidence of 9%. Nineteen of the 32 patients (59%) were r e p a i r e d without aortic bypass, with one instance of postoperative paraplegia. Mean aortic crossclamp time among these nonshunted patients was 33 minutes (median, 27 minutes; range, 20 to 55 minutes). The crossclamp time for the patient who became paraplegic was 50 minutes; this patient's surgery was difficult because of obesity, bleeding from a large mediastinal hematoma, and the presence of a persistent left s u p e r i o r vena cava. In 13 of the 32 patients (41%), a Gott shunt was used to bypass the injured aortic segment during cross-clamping, with two cases of postoperative paraplegia. These two p a t i e n t s ' aortic cross-clamp times were 80 and 90 minutes because of intraoperative difficulties and were the two longest cross-clamp times in the entire operated group. Mean aortic cross-clamp time among the Gott-shunted patients was 51 minutes (median, 45 minutes; range, 26 to 90 minutes). There were no identifiable complications of p r e o p e r a t i v e antihypertensive therapy such as documented excessive decrease in blood pressure or sequelae thereof, including stroke, myocardial ischemia, or renal insufficiency. Nor were there any evident difficulties with hypotension resulting from induction of anesthesia in these patients. We know of no complications of antihypertensive t h e r a p y in t r a u m a patients with suspected aortic i n j u r y but subsequent negative aortography. Even though the three groups are not directly comparable, some useful conclusions can be drawn. F i r s t , because the pharmacologically treated patients h a d no greater morbidity or mortality than the u n t r e a t e d patients, the aggressive antihypertensive t h e r a p y used is safe. Second, the natural history of unrepaired traumatic aortic tears has been estimated to yield a mortality rate of approximately 1% p e r hour during the first 48 hours after injury. 1,2 Therefore, the fact that the treated groups had no greater mortality than the untreated group despite their significantly longer time between injury and surgical r e p a i r suggests that the therapy is effective.
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DISCUSSION
The 15% to 20% of patients with blunt aortic disruption who survive long enough to reach an ED alive do so only because the aortic adventitia a r o u n d the tear has remained intact. T h a t the damaged aortic wall is prone to r u p t u r e is evidenced by the fact that less than 5% of u n t r e a t e d patients with t r a u m a t i c aortic tears will live long enough t o enter the chronic aneurysm group. 1"2J9-21 W h a t is most impressive is that at more than 50% of operations, the torn ends of the intima and media are found to be s e p a r a t e d by several centimeters; all that stands between the patient's survival and exsanguination is a r a t h e r tenuous m e m b r a n e of adventitia. Urgent surgical r e p a i r of aortic disruption is solidly established as the treatment of choice: Survival of 75% to 90% of operated patients can be expected. 22-25 Although many points of controversy remain concerning the ideal surgical r e p a i r technique, 22-26 a separate p r o b l e m is that the majority of patients with aortic disruption who die do so before surgery, usually because of sudden aortic r u p t u r e and exsanguination. 22-25'27-29 There is no way to predict whether or when an aorta will r u p t u r e , nor is there any method, short of surgical repair, of strengthening the i n j u r e d aortic segment. However, a means of decreasing the likelihood of r u p t u r e before surgery by minimizing the hemodynamic stress on the pseudoaneurysm is available, and its use as a temporizing measure in patients otherwise unable to undergo surgical r e p a i r has been r e p o r t e d in several series. 1°-13 To our knowledge, our study is the first description of the use of aggressive antihypertensive therapy begun in the ED to t r e a t all hemodynamically stable patients with thoracic aortic disruption in an effort to prevent r u p t u r e before surgical control can be obtained. This study was neither randomized nor prospective; it is very unlikely for many reasons (including numbers of patients, heterogeneity of associated injuries, and the emergency n a t u r e of the injuries) that such a statistically desirable study will ever be done. A second shortcoming of this study is that solid p r o o f of the effectiveness of antihypertensive t h e r a p y in decreasing mortality and/or m o r b i d i t y was not obtainable because of the lack of records of detailed blood pressure (and other hemodynamic) measurements taken before and after antihypertensive treatment; this, in t u r n , was due p r i m a r i l y to the emergency, often "middle of the night" n a t u r e of the patients' p r e o p e r a t i v e courses. Nevertheless, we believe that it is justified to infer that aggressive p r e o p e r a t i v e antihypertensive t h e r a p y can be used safely in the management of acute traumatic thoracic aortic disruption. In addition, we believe that the survival of all patients in our study who were treated with adequate pharmacologic blood pressure control for periods ranging from two hours to four months suggests that such treatment is effective. •
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THORACIC AORTA W a r r e n et al
Optimal hemodynamic control of the patient with an aortic tear consists of more than just IV antihypertensive medications. Provision of adequate analgesia and/or sedation, for both injuries already present and procedures such as placement of nasogastric tubes and u r i n a r y and vascular catheters, is very important. The patient should be in an ]CU with continuous circulatory and r e s p i r a t o r y monitoring. F u r t h e r m o r e , the presence of true " p s e u d o c o a r c t a t i o n " - - u p p e r extremity hypertension with diminished femoral pulses - - i n 5% to 25 % of patients 24'3°'3] may r e p r e s e n t a theoretical relative contraindication to antihypertensive t h e r a p y because it might critically reduce renal and spinal cord perfusion. We are not advocating medical t h e r a p y over surgical therapy for aortic tears, nor do we recommend anything other than immediate involvement of the thoracic surgical team. The aortic i n j u r y should be r e p a i r e d when the risk-to-benefit ratio is optimized, a judgment that requires experience and individualized care. Most patients with aortic tears have other major, and potentially fatal, injuries. Several of the most recent reports on aortic t r a u m a 27-29 deal with the optimal prioritization of treatment of all the injuries: evacuation of i n t r a c r a n i a l hematomas, control of i n t r a - a b d o m i n a l hemorrhage, and so on. The pharmacologic control of hemodynamic stresses on the i n j u r e d and weakened aortic wall is meant to be used only in patients who are hemodynamically stable after resuscitation to prevent the r u p t u r e of the tenuous covering of the aortic t e a r while other necessary procedures are p e r f o r m e d or until conditions comprising contraindications to immediate surgical r e p a i r (eg, severe head injury, estabhshed sepsis or likely development of septicemia, or severe right p u l m o n a r y contusion t°) are treated successfully.
F u r t h e r prospective studies to confirm our impressions are warranted. •
REFERENCES 1. Strassman6: Traumatic rupture of the aorta. Am HeartJ 1947;33:508-515. 2. Parmley LF, Mattingly TW, Manion WC, Jahnke EJ: Nonpenetratingtraumatic injury of the aorta. Circulation1958;17:1086-1101. 3. Passare E, Pace WG: Traumatic rupture of the aorta. Surgery1959;46:787-791. 4. Wheat MW, Palmer RF, Bartley TD, et al: Treatment of dissecting aneurysms of the aorta without surgery. J Thorac CardiovascSurg 1965;50:364-373. 5. Aronstam EM, 6omez AC, O'ConnellTJ, et al: Recent surgical and pharmacologic experience with acute dissecting and traumatic aneurysms. J ThoracCardiovascSurg 1970;59:231-238. 6. Worrnan LW: In discussion: Allen TW, Reul 6J, Morton JR, et al: Surgical management of aortic trauma. J Trauma1972;12:862-868. 7. Kirsh MM, Behrendt DM, Orringer MB, et al: The treatment of acute traumatic rupture of the aorta: A ten-year experience. Ann Surg 1976;184:308-316. 8. Shaw RK, Ariyan S, Krant SM, et al: Modification in the treatment of the multiple injury patient. J Trauma1977;17:630-633. 9. Pezzella AT, Todd EP, Dillon ML, et al: Early diagnosis and individualized treatment of blunt thoracic aortic trauma. Am Surg 1978;44:699-703. 10. Akins CW, Buckley MJ, Daggett WM, et al: Acute traumatic disruption of the thoracic aorta: A ten-year experience. Ann ThoracSurg 1981;31:305-309. 11. Stiles QR, Cohlmia GS, Smith JH, et al: Management of injuries of the thoracic and abdominal aorta. Am J Surg 1985;150:132-140. 12. Fisher RG, Oria RA, Mattox KL, et al: Conservativemanagementof aortic lacerations due to blunt trauma. J Trauma1990;30:1562-1566. 13. Walker WA, Pate JW: Medical managementof acute traumatic rupture of the aorta. Ann ThoracSurg 1990;50:965-967. 14. Lundevall J: The mechanism of traumatic rupture of the aorta. Acta Pathol Microbiol Scand 1984;62:34-46. 15. Sevitt S: The mechanisms of traumatic rupture of the thoracic aorta. BrJ Surg 1977;64:186-173. 16. Moar J J: Traumatic rupture of the thoracic aorta: An autopsy and histopathological study. S Afr Mud J 1985;67:383-385.
CONCLUSION
To prevent p r e o p e r a t i v e r u p t u r e of the angiographically proven torn thoracic aorta in stable patients with blunt t r a u m a , pharmacologic reduction of hemodynamic stresses on the i n j u r e d aorta was instituted in patients in the ED and continued until surgical control of the a o r t a was obtained. Over a ten-year period, 15 patients were t r e a t e d with temp o r a r y (less than eight hours) and seven with prolonged (one day to four months in six patients and indefinitely in one patient) aggressive antihypertensive therapy, reducing the force of left ventricular ejection and lowering the mean systemic blood pressure. Of these 22 patients, two died - one from documented i n a d e q u a t e antihypertensive t h e r a p y and one from associated injuries u n r e l a t e d to either the aortic tear or the antihypertensive treatment. We conclude that aggressive preoperative antihypertensive t h e r a p y begun in the ED is safe and may be effective in the management of patients with b l u n t t r a u m a t i c thoracic aortic disruption.
17. Greendyke RM: Traumatic rupture of the aorta: Special reference to automobile accidents. JAMA 1966;195:527-530. 18. Milnor WR: Hemodynamics.Baltimore, Williams & Wilkins, 1982. 19. Bennett DE, Cherry JK: The natural history of traumatic aneurysms of the aorta, Surgery1967;61:518-523. 20. MoCollum CH, 6raham JM, Noon GP, et al: Chronic traumatic anaurysms of the thoracic aorta: An analysis of fifty patients. J Trauma1979;19:248-252. 21. Finkelrneier BA, Mentzer RM, Kaiser DL, et al: Chronic traumatic thoracic aneurysm Influence of operative treatment on natural history: An analysis of reported cases, 1950 - - 1980.J Thorac CardiovascSurg 1982;84:257-266. 22. Pate JW: Traumatic rupture of the aorta: Emergencyoperation. Ann ThoracSurg 1985;39:531-537. 23. Mattox KL, Holzman M, Pickard LR, et al: Clan]p/repair:A safe technique for treatment of blunt injury to the descending thoracic aorta. Ann ThoracSurg 1985;40:456-482. 24. Merrill WH, Lee RB, HammonJW, et al: Surgical treatment of acute traumatic tear of the thoracic aorta. Ann Surg 1988;207:899-708. 25. Hess PJ, Howe HR, Robicsek F, et al: Traumatic tears of the thoracic aorta: Improved results using the Biomedicus pump. Ann ThoracSurg 1989;48:6-9. 26. Mattex KL: Fact and fiction about managementof aortic transection (editorial). Ann ThoracSurg 1989;48:1-2.
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27.ClarkDE, Zeiger MA, Wallace KL, et al: Blunt aortic trauma: Signs of high risk. J Trauma1990;30:701-705. 28.TownsendRN, Co]ella J J, Diamond DL: Traumatic rupture of the aorta - - Critical decisionsfor trauma surgeons. J Trauma 1990;30:1169-1174.
Address for reprints: Ralph L Warren, MD, Department of Emergency Services, Massachusetts General Hospital, Fruit Street, Boston, Massachusetts 02114.
29.RichardsonJD, Wilson ME, Miller FB: The widened mediastinum: Diagnostic and therapeutic priorities. Ann Surg 1990;211:731-737. 30.SyrnbasP: Cardiothoracic Trauma. Philadelphia, WB Saunders, 1989, p 195-196. 3I. SturmJT, Parry JF, Olson FR, et al: Significance of symptoms and signs in patients with traumatic aortic rupture. Ann Emerg Med 1984;13:876-878.
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aortic disruption
A c u t e TraumaticDisruptionof the Thoracic Aorta: EmergencyDepartmentManagement From the Departments o f
Ralph L Warren, MD * ~
Study objective: Toevaluate the safety and effectiveness of
Surgery* and Emergency
Cary W Akins, MD ~
Services, t Massachusetts
Alasdair K T Conn, MD *~r
temporary IV antihypertensive therapy in patients with acute traumatic thoracic aortic disruption.
General Hospital, and Harvard
Alan D Hilgenberg, MD**
Medical School, Boston. ¢
Charles J McCabe, MD *~:
Received for publication
Design: Retrospective chart review of all patients treated for proven traumatic aortic disruption during the ten-year period of 1980 through 1989.
February 25, 1991. Revision
Setting:
received August 8, 1991.
center.
Accepted for publication October 30, 1991.
Emergency department of a large, urban, Level I trauma
Interventions: Preoperative IV 13-blockade and nitroprusside after initial resuscitation in hemodynamically stable patients. Rcsu|ts: Thirty-seven patients with angiographically proven aortic disruption were separated retrospectively into one of three groups. Group 1 (15 patients without preoperative antihypertensive therapy] had two deaths. Group 2 (15 patients treated for two to seven hours [mean, 3.8 hours] before surgery with antihypertensives) had one death. Group 3 (seven patients treated with antihypertensives for 24 hours to four months before surgery to allow recovery from associated severe injuries) had one death. There were no complications resulting from antihypertensive therapy. Conclusion: Temporary antihypertensive therapy appears to be safe and effective in patients with aortic disruption. [Warren RL, Akins CW, Conn AKT, Hilgenberg AD, McCabe CJ: Acute traumatic disruption of the thoracic aorta: Emergency department management. Ann EmergMedApri11992;21:391-396.]
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INTRODUCTION
Since the first descriptions of the n a t u r a l history of traumatic thoracic aortic disruption in 19471 and 19582 and the first surgical r e p a i r of this lesion in 1958, 3 it has become well established that urgent surgical r e p a i r is most often the treatment of choice. However, after Wheat and colleagues introduced the nonsurgical pharmacologic t h e r a p y for acute aortic dissection in 1965, a ~t was suggested that such treatment also could be used for t r a u m a t i c aortic tears. 5~9 The safety of this so-called "medical t h e r a p y " as a temporizing measure in patients with acute aortic tears who have contraindications to immediate surgical r e p a i r was subsequently demonstrated by Akins et al 1° as well as others. ~-13 Injuries to the aorta caused by blunt t r a u m a consist of transverse, usually circumferential, tears of the intima and varying amounts of media and adventitia.14-16 If the full thicknesses of media and adventitia are torn, as occurs in 80% to 85% of victims, 1'2"]7 immediate exsanguination and death result. If, on the other h a n d , the adventitia - - which provides most of the collagenous strength of the aortic wall does not tear, a p s e u d o a n e u r y s m is formed, and exsanguination is forestalled. This pseudoaneurysm, however, is inherently unstable and prone to unpredictable r u p t u r e . Not only is the wall of the p s e u d o a n e u r y s m greatly thinned, but because its diameter is greater than that of the uninjured aorta, the tension in this segment of thinned wall is greater (the law of Laplace). In the management of patients with aortic tears, therefore, it would seem p r u d e n t , if not m a n d a t o r y , to minimize the stresses on the attenuated and weakened aortic wall. The aortic intraluminal pressure, and especially the rate of rise of the aortic pressure wave (dP/dT),a'18 should be carefully controlled and if not actually lowered to less t h a n normal, at least prevented from increasing excessively. As in the pharmacologic treatment of aortic dissection, the d P / d t is best controlled by decreasing the force of left ventricular ejection with negative inotropic agents; the mean aortic pressure then is controlled with systemic a r t e r i a l vasodilators. Pure vasodilators, if used alone, increase r a t h e r than decrease the dP/dt because they lower diastolic pressure more than systolic pressure. 4'18 Medical treatment should always begin with negative inotropic agents, adding vasodilators as needed. With these considerations in mind, our a p p r o a c h in the emergency department since 1980 to the hemodynamically stable trauma patient suspected of having a torn thoracic aorta has included early placement of a right r a d i a l arterial pressure-monitoring catheter and aggressive control of cardiac contractility with ~-adrenergic blockade and of systemic blood pressure with nitroprusside. Ideally, this treatment is begun as soon as the diagnosis of aortic t e a r is suspected, even before aortography, and is continued until surgical control of the t o r n aorta is obtained. We conducted -
-
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our retrospective study to evaluate the safety and effectiveness of such therapy.
MATERIALS
AND
METHODS
T r a u m a patient management at the Massachusetts General Hospital is directed on a 24-hour basis by ED attending physicians and surgical residents and follows the guidelines of the American College of Surgeons regarding advanced t r a u m a life support. The diagnosis of aortic disruption is suspected on the basis of chest r a d i o g r a p h y and mechanism of i n j u r y and confirmed or ruled out by aortography. Diagnostic peritoneal lavage is used liberally to quickly detect i n t r a - a b d o m i n a l injuries. As soon as the diagnosis of thoracic aortic i n j u r y is suspected, the cardiac surgical and angiographic services are alerted, and a right r a d i a l arterial pressure-monitoring catheter is inserted. If the patient is hemodynamically stable, treatment with IV analgesics, p-blockade, and nitroprusside is begun. P r o p r a n o l o l or labetolol is given in sufficient quantities to lower the h e a r t rate to 60 + 5 and is followed by nitroprusside infusion as needed to keep systolic blood pressure between 90 and 100 mm Hg. We reviewed the records of all patients t r e a t e d at the Massachusetts General Hospital for acute thoracic aortic disruption secondary to blunt t r a u m a from J a n u a r y 1, 1980, through December 31, 1989. Of the 43 patients identified, at immediate emergency thoracotomy the diagnosis of aortic disruption was made in six, the diagnosis of p r e a r rival cardiac a r r e s t was made in four, and the diagnosis of p r o f o u n d persistent hypotension was made in two. All six died and are not considered f u r t h e r in this report. Thirty-seven patients survived long enough to undergo diagnostic aortography, and they constituted the study population. There were 31 men and six women (age range, 16 to 70 years; mean, 36 years). Motor vehicle accidents were the cause of i n j u r y in 35 (95%): 30 were occupants (19 drivers and 11 passengers) of automobiles, two were pedestrians struck by cars, and three were motorcyclists. Two patients fell from a height of m o r e than 20 ft. Almost all patients h a d associated m a j o r injuries. Mean I n j u r y Severity Score (ISS) was 39: 51% experienced i n t r a c r a n i a l injury; 65%, p u l m o n a r y injury; 38%, i n t r a - a b d o m i n a l injury; 35%, pelvic injury; and 65%, m a j o r extremity fracture. Only six of the 37 patients a r r i v e d at our institution directly from the accident scene, whereas 31 (84%) were t r a n s f e r r e d from other hospitals. All 37 patients h a d a b n o r m a l chest r a d i o g r a p h s , although three h a d initial chest r a d i o g r a p h s that were normal. The most common chest film findings were widened mediastinum (97%), rib fractures (51%), indistinct aortic knob (38%), left h e m o t h o r a x and/or p n e u m o t h o r a x (38%), and deviation of the t r a c h e a and/or nasogastric tube to the right (14%). Eight patients h a d chest computed tomography perlb
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formed at the referring hospital, and all showed mediastinal and/or aortic abnormalities. The site of the aortic tear was in the region of the aortic isthmus in 35 patients (95%) and the ascending aorta in two (5%). Surgical r e p a i r was carried out in 34 of the 37. Six patients underwent l a p a r o t o m y before thoracotomy, all with grossly positive peritoneal lavage, and four patients underwent l a p a r o t o m y immediately after thoracotomy. Of the 32 operated patients with isthmus tears, 19 (59%) were r e p a i r e d without aortic bypass. In the other 13 (41%), a 9mm Gott shunt (TDMAC-heparin shunt, a flexible plastic catheter with the internal surface coated with h e p a r i n , thus obviating the need for systemic heparinization) was used to bypass the i n j u r e d aortic segment during cross-clamping. Three of the 37 patients - - all with isthmus tears - - did not undergo surgical repair. One of them exsanguinated before surgery in the induction room. One, who was being treated nonsurgicaUy because of severe associated injuries, died of r e s p i r a t o r y failure unrelated to the aortic tear. The third patient was managed entirely nonsurgically because of an associated high thoracic cord transection. The 37 patients were s e p a r a t e d retrospectively into one of three groups (Table). Group 1 (15 patients) underwent urgent surgical r e p a i r without surgical antihypertensive therapy; these patients were considered hemodynamically unstable, with either low or labile (episodes of low r a t h e r than high) blood pressure. Group 2 (15 patients) had surgical antihypertensive t h e r a p y ; these patients h a d stable normal or high blood pressure after p r i m a r y resuscitation and evaluation. Group 3 (seven patients) was treated with p h a r macologic antihypertensive t h e r a p y as the p r i m a r y t h e r a p y to stabilize other severe injuries that p r o h i b i t e d immediate surgery. Mean age of the patients in group i was 42 years, and mean ISS was 38. One patient in the group had l a p a r o t o m y before and three had l a p a r o t o m y after thoracotomy. Mean time between i n j u r y and thoracotomy in this group was 7.0 hours (excluding two patients who had diagnosis of aortic injury delayed for three and 3.5 days, followed by surgical r e p a i r in both cases within three hours of diagnosis).
Table.
Description of patient groups and outcomes No. of Patielwl~ Group*
No. of
Mean Age
No. of
With
Patients
(yr)
Mean ISS
Deaths (%)
Paraplegia 1
1
15
42
38
2 (13)
2
15
32
32
1 (7)
1
3
7
35
54
1 (14)
1
*Group I, immediate surgical repair and no preoperative antihypertensive therapy (hemodynamically unstable); group 2, immediate surgical repair with preoperative antihypertensive therapy {hemodynamically stable); group 3, deJayed surgical repair (one indefinitery) with primary interval antihypertensive therapy (initial or persistent centraindication to surgery).
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Mean age of patients in group 2 was 32 years, and mean ISS was 32. The d u r a t i o n of pharmacologic t h e r a p y was two to seven hours (mean, 3.8 hours). One patient in this group h a d l a p a r o t o m y before and one had l a p a r o t o m y after thoracotomy. Mean time between i n j u r y and thoracotomy was 8.7 hours (again excluding two who had diagnosis delayed for 24 and 48 hours, followed by medical t h e r a p y for three and six hours, respectively, before thoracotomy). Mean age of the seven patients in group 3 was 35 years, and mean ISS was 54. Medical treatment was begun with IV #-blockade and nitroprusside and maintained with oral agents if surgery was delayed beyond several days. F o u r of these seven patients had grossly positive peritoneal lavage and l a p a r o t o m y before aortography. The indications for delay of surgery were as follows: Three patients had severe i n t r a c r a n i a l central nervous system injury, which improved with time so that aortic r e p a i r was u n d e r t a k e n after 24 hours, 52 days, and four months. One patient had acute renal and r e s p i r a t o r y insufficiency after l a p a r o t o m y at the referring hospital and was treated medically for three days to allow adequate improvement of these two systems. One patient, whose diagnosis was delayed 26 days after injury and whose aortic tear was complicated by limited distal aortic dissection and m y o c a r d i a l ischemia, was stabilized medically for 12 days to ensure optimum c a r d i o p u l m o n a r y condition for surgery. One patient had severe b i l a t e r a l p u l m o n a r y contusions that prevented safe thoracic surgery; this patient died (the only death in group 3). One patient had a T3 vertebral fracture/dislocation with high spinal cord transection and was managed entirely nonsurgically.
RESULTS Of 37 patients with angiographically proven thoracic aortic disruption, four died, yielding an overall mortality of 11%. Mean age of the survivors was 34 years, and mean ISS was 39, whereas mean age and ISS of the patients who died were 55 years and 38, respectively. The outcomes with respect to preoperative antihypertensive treatment are shown (Table). The three groups in our study are not directly c o m p a r a b l e as representing similar patients undergoing different treatments; rather, they were t r e a t e d differently b e c a u s e of their differing presenting clinical conditions. In group 1, there were two deaths, both occurring after surgery. Both patients h a d very difficult i n t r a o p e r a t i v e courses, including cardiac a r r e s t at induction of anesthesia; in addition, they were two of the oldest patients in the series (66 and 70 years). In group 2 there was one death. This patient died in the operating room; after two hours of medical treatment and eight hours after injury, he suddenly awoke in the induction room and became acutely hypertensive, resulting in free r u p t u r e of his a o r t a and exsanguination. Thus, death
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resulted from inadequate blood pressure control r a t h e r than from failure of adequate antihypertensive treatment. In group 3 there was one death. This patient had severe bilateral pulmonary contusions, which prevented safe thoracic surgery after his initial emergency l a p a r o t o m y and splenectomy; he died two days after i n j u r y of r e s p i r a t o r y failure. One patient was managed completely nonsurgically because of a high spinal cord transection and survived. The remaining five patients underwent successful surgical r e p a i r of their aortic tears (all in the region of the isthmus) from one day to four months after injury. The occurrence of postoperative paraplegia was related more to intraoperative than to p r e o p e r a t i v e factors. Of the 32 operated patients with isthmus tears, three developed postoperative paraplegia, one case in each of groups 1, 2, and 3, for an overall incidence of 9%. Nineteen of the 32 patients (59%) were r e p a i r e d without aortic bypass, with one instance of postoperative paraplegia. Mean aortic crossclamp time among these nonshunted patients was 33 minutes (median, 27 minutes; range, 20 to 55 minutes). The crossclamp time for the patient who became paraplegic was 50 minutes; this patient's surgery was difficult because of obesity, bleeding from a large mediastinal hematoma, and the presence of a persistent left s u p e r i o r vena cava. In 13 of the 32 patients (41%), a Gott shunt was used to bypass the injured aortic segment during cross-clamping, with two cases of postoperative paraplegia. These two p a t i e n t s ' aortic cross-clamp times were 80 and 90 minutes because of intraoperative difficulties and were the two longest cross-clamp times in the entire operated group. Mean aortic cross-clamp time among the Gott-shunted patients was 51 minutes (median, 45 minutes; range, 26 to 90 minutes). There were no identifiable complications of p r e o p e r a t i v e antihypertensive therapy such as documented excessive decrease in blood pressure or sequelae thereof, including stroke, myocardial ischemia, or renal insufficiency. Nor were there any evident difficulties with hypotension resulting from induction of anesthesia in these patients. We know of no complications of antihypertensive t h e r a p y in t r a u m a patients with suspected aortic i n j u r y but subsequent negative aortography. Even though the three groups are not directly comparable, some useful conclusions can be drawn. F i r s t , because the pharmacologically treated patients h a d no greater morbidity or mortality than the u n t r e a t e d patients, the aggressive antihypertensive t h e r a p y used is safe. Second, the natural history of unrepaired traumatic aortic tears has been estimated to yield a mortality rate of approximately 1% p e r hour during the first 48 hours after injury. 1,2 Therefore, the fact that the treated groups had no greater mortality than the untreated group despite their significantly longer time between injury and surgical r e p a i r suggests that the therapy is effective.
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DISCUSSION
The 15% to 20% of patients with blunt aortic disruption who survive long enough to reach an ED alive do so only because the aortic adventitia a r o u n d the tear has remained intact. T h a t the damaged aortic wall is prone to r u p t u r e is evidenced by the fact that less than 5% of u n t r e a t e d patients with t r a u m a t i c aortic tears will live long enough t o enter the chronic aneurysm group. 1"2J9-21 W h a t is most impressive is that at more than 50% of operations, the torn ends of the intima and media are found to be s e p a r a t e d by several centimeters; all that stands between the patient's survival and exsanguination is a r a t h e r tenuous m e m b r a n e of adventitia. Urgent surgical r e p a i r of aortic disruption is solidly established as the treatment of choice: Survival of 75% to 90% of operated patients can be expected. 22-25 Although many points of controversy remain concerning the ideal surgical r e p a i r technique, 22-26 a separate p r o b l e m is that the majority of patients with aortic disruption who die do so before surgery, usually because of sudden aortic r u p t u r e and exsanguination. 22-25'27-29 There is no way to predict whether or when an aorta will r u p t u r e , nor is there any method, short of surgical repair, of strengthening the i n j u r e d aortic segment. However, a means of decreasing the likelihood of r u p t u r e before surgery by minimizing the hemodynamic stress on the pseudoaneurysm is available, and its use as a temporizing measure in patients otherwise unable to undergo surgical r e p a i r has been r e p o r t e d in several series. 1°-13 To our knowledge, our study is the first description of the use of aggressive antihypertensive therapy begun in the ED to t r e a t all hemodynamically stable patients with thoracic aortic disruption in an effort to prevent r u p t u r e before surgical control can be obtained. This study was neither randomized nor prospective; it is very unlikely for many reasons (including numbers of patients, heterogeneity of associated injuries, and the emergency n a t u r e of the injuries) that such a statistically desirable study will ever be done. A second shortcoming of this study is that solid p r o o f of the effectiveness of antihypertensive t h e r a p y in decreasing mortality and/or m o r b i d i t y was not obtainable because of the lack of records of detailed blood pressure (and other hemodynamic) measurements taken before and after antihypertensive treatment; this, in t u r n , was due p r i m a r i l y to the emergency, often "middle of the night" n a t u r e of the patients' p r e o p e r a t i v e courses. Nevertheless, we believe that it is justified to infer that aggressive p r e o p e r a t i v e antihypertensive t h e r a p y can be used safely in the management of acute traumatic thoracic aortic disruption. In addition, we believe that the survival of all patients in our study who were treated with adequate pharmacologic blood pressure control for periods ranging from two hours to four months suggests that such treatment is effective. •
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Optimal hemodynamic control of the patient with an aortic tear consists of more than just IV antihypertensive medications. Provision of adequate analgesia and/or sedation, for both injuries already present and procedures such as placement of nasogastric tubes and u r i n a r y and vascular catheters, is very important. The patient should be in an ]CU with continuous circulatory and r e s p i r a t o r y monitoring. F u r t h e r m o r e , the presence of true " p s e u d o c o a r c t a t i o n " - - u p p e r extremity hypertension with diminished femoral pulses - - i n 5% to 25 % of patients 24'3°'3] may r e p r e s e n t a theoretical relative contraindication to antihypertensive t h e r a p y because it might critically reduce renal and spinal cord perfusion. We are not advocating medical t h e r a p y over surgical therapy for aortic tears, nor do we recommend anything other than immediate involvement of the thoracic surgical team. The aortic i n j u r y should be r e p a i r e d when the risk-to-benefit ratio is optimized, a judgment that requires experience and individualized care. Most patients with aortic tears have other major, and potentially fatal, injuries. Several of the most recent reports on aortic t r a u m a 27-29 deal with the optimal prioritization of treatment of all the injuries: evacuation of i n t r a c r a n i a l hematomas, control of i n t r a - a b d o m i n a l hemorrhage, and so on. The pharmacologic control of hemodynamic stresses on the i n j u r e d and weakened aortic wall is meant to be used only in patients who are hemodynamically stable after resuscitation to prevent the r u p t u r e of the tenuous covering of the aortic t e a r while other necessary procedures are p e r f o r m e d or until conditions comprising contraindications to immediate surgical r e p a i r (eg, severe head injury, estabhshed sepsis or likely development of septicemia, or severe right p u l m o n a r y contusion t°) are treated successfully.
F u r t h e r prospective studies to confirm our impressions are warranted. •
REFERENCES 1. Strassman6: Traumatic rupture of the aorta. Am HeartJ 1947;33:508-515. 2. Parmley LF, Mattingly TW, Manion WC, Jahnke EJ: Nonpenetratingtraumatic injury of the aorta. Circulation1958;17:1086-1101. 3. Passare E, Pace WG: Traumatic rupture of the aorta. Surgery1959;46:787-791. 4. Wheat MW, Palmer RF, Bartley TD, et al: Treatment of dissecting aneurysms of the aorta without surgery. J Thorac CardiovascSurg 1965;50:364-373. 5. Aronstam EM, 6omez AC, O'ConnellTJ, et al: Recent surgical and pharmacologic experience with acute dissecting and traumatic aneurysms. J ThoracCardiovascSurg 1970;59:231-238. 6. Worrnan LW: In discussion: Allen TW, Reul 6J, Morton JR, et al: Surgical management of aortic trauma. J Trauma1972;12:862-868. 7. Kirsh MM, Behrendt DM, Orringer MB, et al: The treatment of acute traumatic rupture of the aorta: A ten-year experience. Ann Surg 1976;184:308-316. 8. Shaw RK, Ariyan S, Krant SM, et al: Modification in the treatment of the multiple injury patient. J Trauma1977;17:630-633. 9. Pezzella AT, Todd EP, Dillon ML, et al: Early diagnosis and individualized treatment of blunt thoracic aortic trauma. Am Surg 1978;44:699-703. 10. Akins CW, Buckley MJ, Daggett WM, et al: Acute traumatic disruption of the thoracic aorta: A ten-year experience. Ann ThoracSurg 1981;31:305-309. 11. Stiles QR, Cohlmia GS, Smith JH, et al: Management of injuries of the thoracic and abdominal aorta. Am J Surg 1985;150:132-140. 12. Fisher RG, Oria RA, Mattox KL, et al: Conservativemanagementof aortic lacerations due to blunt trauma. J Trauma1990;30:1562-1566. 13. Walker WA, Pate JW: Medical managementof acute traumatic rupture of the aorta. Ann ThoracSurg 1990;50:965-967. 14. Lundevall J: The mechanism of traumatic rupture of the aorta. Acta Pathol Microbiol Scand 1984;62:34-46. 15. Sevitt S: The mechanisms of traumatic rupture of the thoracic aorta. BrJ Surg 1977;64:186-173. 16. Moar J J: Traumatic rupture of the thoracic aorta: An autopsy and histopathological study. S Afr Mud J 1985;67:383-385.
CONCLUSION
To prevent p r e o p e r a t i v e r u p t u r e of the angiographically proven torn thoracic aorta in stable patients with blunt t r a u m a , pharmacologic reduction of hemodynamic stresses on the i n j u r e d aorta was instituted in patients in the ED and continued until surgical control of the a o r t a was obtained. Over a ten-year period, 15 patients were t r e a t e d with temp o r a r y (less than eight hours) and seven with prolonged (one day to four months in six patients and indefinitely in one patient) aggressive antihypertensive therapy, reducing the force of left ventricular ejection and lowering the mean systemic blood pressure. Of these 22 patients, two died - one from documented i n a d e q u a t e antihypertensive t h e r a p y and one from associated injuries u n r e l a t e d to either the aortic tear or the antihypertensive treatment. We conclude that aggressive preoperative antihypertensive t h e r a p y begun in the ED is safe and may be effective in the management of patients with b l u n t t r a u m a t i c thoracic aortic disruption.
17. Greendyke RM: Traumatic rupture of the aorta: Special reference to automobile accidents. JAMA 1966;195:527-530. 18. Milnor WR: Hemodynamics.Baltimore, Williams & Wilkins, 1982. 19. Bennett DE, Cherry JK: The natural history of traumatic aneurysms of the aorta, Surgery1967;61:518-523. 20. MoCollum CH, 6raham JM, Noon GP, et al: Chronic traumatic anaurysms of the thoracic aorta: An analysis of fifty patients. J Trauma1979;19:248-252. 21. Finkelrneier BA, Mentzer RM, Kaiser DL, et al: Chronic traumatic thoracic aneurysm Influence of operative treatment on natural history: An analysis of reported cases, 1950 - - 1980.J Thorac CardiovascSurg 1982;84:257-266. 22. Pate JW: Traumatic rupture of the aorta: Emergencyoperation. Ann ThoracSurg 1985;39:531-537. 23. Mattox KL, Holzman M, Pickard LR, et al: Clan]p/repair:A safe technique for treatment of blunt injury to the descending thoracic aorta. Ann ThoracSurg 1985;40:456-482. 24. Merrill WH, Lee RB, HammonJW, et al: Surgical treatment of acute traumatic tear of the thoracic aorta. Ann Surg 1988;207:899-708. 25. Hess PJ, Howe HR, Robicsek F, et al: Traumatic tears of the thoracic aorta: Improved results using the Biomedicus pump. Ann ThoracSurg 1989;48:6-9. 26. Mattex KL: Fact and fiction about managementof aortic transection (editorial). Ann ThoracSurg 1989;48:1-2.
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27.ClarkDE, Zeiger MA, Wallace KL, et al: Blunt aortic trauma: Signs of high risk. J Trauma1990;30:701-705. 28.TownsendRN, Co]ella J J, Diamond DL: Traumatic rupture of the aorta - - Critical decisionsfor trauma surgeons. J Trauma 1990;30:1169-1174.
Address for reprints: Ralph L Warren, MD, Department of Emergency Services, Massachusetts General Hospital, Fruit Street, Boston, Massachusetts 02114.
29.RichardsonJD, Wilson ME, Miller FB: The widened mediastinum: Diagnostic and therapeutic priorities. Ann Surg 1990;211:731-737. 30.SyrnbasP: Cardiothoracic Trauma. Philadelphia, WB Saunders, 1989, p 195-196. 3I. SturmJT, Parry JF, Olson FR, et al: Significance of symptoms and signs in patients with traumatic aortic rupture. Ann Emerg Med 1984;13:876-878.
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