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Penetrating injuries of the aortic arch and its branches
Penetrating Injuries of the Aortic Arch and Its Branches James W. Pate, MD, F. Hammond Cole, Jr, MD, William A. Walker, MD, and Timothy C. Fabian, MD Section of Cardiothoraac Surgery, University of Tennessee, and Elvis Presley Trauma Center, Memphis, Tennessee
Acute cardiac failure, pulmonary edema, and ischemia of the brain, cord, and other structures pose special problems with trauma to the aortic arch and its branches. Data on 93 such cases are reported. Diagnosis was made by clinical examination in hemodynamically unstable patients and led to immediate operation in 61.3%. Patients in stable condition had angiography, which localized the injury and allowed planning of incision and bypass shunts. In left subclavian artery injuries, anterior thoracotomy was best for proximal control regardless of wound entry sites; midline stemotomy with stemocleidomastoid extension was usually adequate for other
vessels. Flow was reestablished in all carotid injuries; there were no neurological complications. Temporary or permanent bypass shunts during periods of proximal aortic occlusion were valuable in decreasing cardiac afterload, maintaining circulation to the brain, and allowing an unhurried methodical approach to the hematoma. Occlusion of one or more venae cavae alleviated acute cardiac dilatation during brief periods of ascending aortic clamping. Associated trauma contributed to the high mortality.
P
to Y grafts to both carotid arteries before disturbing the hematoma or attempting repair. These injuries are uncommon [4,51; Rich and associates’ report [6] of 1,OOO arterial injuries from the Vietnam war includes only three innominate and eight subclavian artery injuries. The development of well-organized trauma systems is leading to increasing numbers of such victims of urban warfare reaching the treatment facility alive. To summarize our experience and arrive at reasonable recommendations, we are reporting our more recent experience of penetrating injuries to the aortic arch (from superior pericardial reflection to the aortic isthmus) and its branche-innominate, common carotid, and subclavian arterie-that we treated at their initial trauma episode during the 8 years ending September 1, 1992. Only carotid artery injuries that resulted from thoracic wounds or wounds of the base of the neck or supraclavicular spaces that passed into the thorax are included.
ulmonary edema, acute heart failure, and irreversible ischemia of the brain, spinal cord, kidneys, and viscera are special problems associated with control of exsanguinating hemorrhage from penetrating trauma to the aortic arch and its branches. Many injuries localized to the anterior surface of the arch or its branches (more than a centimeter distal to their origin) can be easily repaired by simple digital pressure or partial occlusion and suture, whereas more complex injuries involving the posterior surface of the arch or the origin of innominate or carotid arteries may require bypass techniques to avoid these potentially fatal complications. Surgical approaches should be directed at decreasing cardiac afterload and maintaining oxygenated blood flow to the brain and distal body. For these purposes, Symbas and Sehdeva [l], in 1970, reported the use of a temporary shunt from the ascending aorta to innominate artery for repair of a stab wound of the arch. This concept was extended in 1973 by DeMeester and associates [Z],who used a heparinized shunt from the ascending aorta to the femoral artery to maintain distal circulation and decompress the heart during repair of an arch injury. Rather than temporary shunts, the Houston group [3],in 1982, introduced the use of a permanent prosthetic bypass graft from the ascending aorta to the distal carotid or innominate artery before repair of the arch and innominate artery. In 1984, we adopted the routine use of both temporary and permanent bypass shunts for managing these injuries and expanded the use Presented at the Thirty-ninth Annual Meeting of the Southern Thoracic Surgical Association, Wesley Chapel, FL, Nov 5-7, 1992. Address reprint requests to Dr Pate, Department of Surgery, University of Tennessee, 956 Court Ave, Memphis, TN 38163.
0 1993 by The Society of Thoraac Surgeons
(Ann Thorac Surg 1993;55:586-92)
Material and Methods We reviewed the medical records of 93 consecutive patients who sustained penetrating injury (63.5% of which were gunshot wounds) of the aortic arch and its branches and were admitted to the Elvis Presley Trauma Center, Memphis (Table 1).Most patients (79.7%)were male; they had a median age of 26 years. Among the factors studied were age, mechanism of injury, hemodynamics, preoperative and postoperative neurological findings, associated trauma, diagnostic methods, anatomy of vascular injury, surgical exposure, use of shunts, and mortality. When there was evidence of massive or pulsatile bleeding or persistent hemodynamic instability, the patient was im0003-4975/93/$6.00
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Table 1. Clinical Outcomes of Entire Series Site Aorta
Innominate Carotid
Subclavian Total a
Number
Not
Resuscitated
27 6 31 29
9 (33.3%)
93 (100.0%)
Operated Patients Lived
Died
Total Survivors
...
11 (61.1%) 5 (83.3%) 25 (89.3%) 25 (86.2%)
7 (38.9%) 1(16.7%) 3 (10.7%) 4 (13.8%)
11” (40.7%) 5 (83.3%) 25 (80.6%) 25 (86.2%)
12 (12.9%)
66 (81.5%)
15 (18.5%)
66 (71.0%)
... 3 (9.7%)
Four deaths resulted from other injuries. Excluding these, sunrival related to the aortic arch injury alone for operated patients would have been 83.3%.
mediately operated on without further study. All patients
in stable condition demonstrating pulse deficit, major hematoma, widened mediastinum, or missile tracts thought to be near major arteries had aortograms for precise anatomical diagnosis and to plan surgical exposure and the possible use of shunts (”selective” operation). Operating rooms and an arteriographic suite are integral to the Trauma Center, thus avoiding unnecessary and dangerous transportation of these patients in critical condition.
Operative Technique The two basic incisions usually used were (1) midline sternotomy, with cervical extensions over one or both carotids when needed, and (2) an anterior left thoracotomy through the fourth intercostal space (with dislocation of cartilage) for exposure of the left subclavian artery. The latter incision was extended by partial median sternotomy, neck incision, and excision of half the clavicle, as required. Entrance wounds in the left supraclavicular fossa and associated with a left pneumothorax or hemothorax were assumed to be subclavian artery injuries for purposes of selecting the incision. When an arteriogram was available, the plan of the operation was based on the site of vascular injury. In the group having immediate operation, the operative approach was chosen based on suspected injury and the exact technique was modified as necessary after the chest was open. Injuries on the anterior surface of the arch or branches further than 1 cm away from the aorta were usually managed by digital pressure or tangential partial occlusion clamps and suture. Intermittent aortic occlusion, either partial or complete, and caval occlusion were useful adjuncts both for exposure and for decreasing blood pressure while suturing. For larger wounds and gunshot injuries, large felt pledgets or patches of prosthetic material were used. With involvement of the superior surface of the arch and origins of the innominate or carotid arteries, more complex procedures were usually considered necessary. When exposure of the concavity and posterior surface of the aorta was necessary, the pulmonary artery and aorta were separated by sharp incision, followed by division of the pericardial and fascia1 tissue from within the pericardium (Fig 1). Dissection of the concave and posterior surfaces of the arch from outside the pericardium is hazardous, as the fibrous layer of the pericardium
blends into and forms the aortic adventitia. Dissection from without leads to an apparent cleavage plane, which may actually be within the aortic wall [7]. Principles aimed at avoiding irreversible ischemic damage to vital organs or distension of the left ventricle were followed (Table 2). When practical, blood flow to the distal arterial bed was always reestablished. When a midline incision was used, the pericardium was immediately opened vertically, before the hematoma was entered. This allowed tapes to be easily placed around the cava(e) for cardiac inflow occlusion and around the ascending aorta for temporary partial occlusion while the repair was effected. While bleeding was controlled by the hematoma or by digital pressure, distal control of the carotid artery (or arteries) was obtained. When compromise of carotid flow was anticipated, shunts were established before disturbing the hematoma or bleeding site (Fig 2). This allowed both decompression of the aorta and left heart and flow to the brain during vascular repair. The proximal end of a graft or shunt was placed into the intrapericardial aorta and the other end was placed in the carotid artery distally, before the hematoma was entered. When grafts were used, they were left in situ as bypass grafts; temporary shunts were removed when the repair n
Fig I. Exposure of the concavity and posterior surface of the aortic arch begins with dissection from within the pericardium (see text).
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was completed. Although available in the Trauma Center, cardiopulmonary bypass was used in only 1 patient (patient 3). When the injury involved the origin of the innominate or carotid artery, the bypass prosthetic graft was left in place permanently and the end of the carotid was oversewn. When the injury did not involve the origin of the branch vessel or continued hemorrhage was a problem, a temporary shunt (see Fig 2) with primary repair or interpositional prosthesis became the preferred technique; this was faster and led to use of less prosthetic material in the narrow confines of the thoracic inlet. The intrathoracic carotid was never ligated without bypass grafting. Primary repair was done when feasible [8].
Illustrative Cases Both the applications of these principles and some difficulties in their use are illustrated by the following three case reports. I. A man sustained a stab wound in the right supraclavicular space. Initial pulsatile bleeding was controlled by pressure. Aortogram revealed injury to the aortic arch at the base of the innominate and left carotid arteries. There was associated filling of the left innominate vein and superior vena cava. Repair involved bypass Y shunts to both common carotid arteries followed by brief, intermittent periods of aortic aoss-clamping and partial caval occlusion, while the aorta was repaired with pledgeted sutures (see Fig 2). The innominate veins were repaired by simple suture. There were no major complications.
PATIENT
PATIENT 2. This man had a gunshot wound to the left chest. Emergency anterolateral thoracotomy for massive bleeding revealed through-and-through wounds of the aortic arch. The anterior aortic wound and lung were repaired, while the posterior aortic wound was tampon-
Table 2 . Surgical Principles Used In Repair of Aortic Arch
Injuries
Princiule Local control Proximal control Distal control Maintain flow" From ventricle (1 min) To brain (5 min) To cord, viscera (30min) Prevent hypertensionof left ventricle, pulmonary veins, central veins, cerebrospinal fluid Exposure of injury site Reestablish distal circulation
Application Pressure only Intrapericardial Tapes: aorta, carotid($, & innominate Bypass shunts: ascending aorta to carotid(s) Arterial shunts and caval occlusion After proximal and distal control Repair or graft
.'Time of occlusion of arterial flow was kept below indicated times whenever feasible. Hypothermia allows some safe prolongation.
Fig 2 . (Patient 1 .) Bypass shunt from ascending aorta to carotid arteries is established before attempting suture of the arch. An injury to the posterior surface of the junction of the brachiocephalic wins and the caval tapes are not shown.
aded. A midline incision was necessary for adequate exposure of the posterior aortic wound. The pericardium between the aorta and pulmonary arteries was divided, followed by division of the posterior fascial attachments of the aorta. Exposure and repair of the posterior defect was done in intermittent steps by temporary tape occlusions of aortic branches, intrapericardial control of the aorta, and periods of venous inflow occlusion (Fig 3). Although the patient later died of complications of prolonged shock, this case is useful in emphasizing the necessity for exposure of the posterior arch from the midline. Had the location of the posterior wound been known before the necessary emergency thoracotomy, use of partial cardiopulmonary bypass may have been of benefit. This man sustained a stab wound in the right supraclavidar space with a hunting knife; an aortogram demonstrated a large aorto-left innominate vein fistula. The groin vessels were exposed as a midline thoracotomy was begun. Massive bleeding was encountered upon opening the supramanubrial fascial space; cannulation was performed and partial cardiopulmonary bypass was begun before the sternum was divided. Pressure controlled the hemorrhage while the pericardium was opened and the incision extended along the left carotid sheath. Ascending aorta, superior vena cava, and neck vessels were controlled with tapes. The left innominate vein was almost severed; it was divided, allowing visualization of the anterior and superior surfaces of an extensive aortic laceration (Fig 4). Full cardiopulmonary bypass through the right atrium was instituted with systemic PATIENT 3.
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A
m m
589
Fig 4. (Patient 3.) Large laceration of Left innominate vein and aorta, with functioning arteriovenous fistula. Repaired with hypothermic cardiopulmonary bypass.
temporary bypass shunts from the ascending aorta to the distal carotid arteries, but shunts were not used in either because of the inability to control hemorrhage without occlusion of the ascending aorta after the chest was opened. Repair of all major vein injuries has been our policy since 1964; however, this has not always been feasible without an intervening graft, which we did not use in the acute trauma setting. No caval ligation was done, although several cavae and innominate veins were sutured without problems.
Results B
Fig 3. (Patient 2.) (A) Exposure of gunshot wound on the posterior surface of arch, after dissection from within the pericardium and control of all branches. Caval tapes for inflow occlusion and distal aortic wound are not illustrated for clarity. ( B ) Completed repair using prosthetic patches.
Associated injury was present in most patients (Table 3) and accounted for several of the deaths. Fifty-seven patients (61.3%)were hemodynamically unstable; 12 of them (12.9%)died during attempted resuscitation before definitive operation (see Table 1). All had Table 3. Associated Injuries to Other Structures Injury to
hypothermia and with cold cardioplegia. The ascending and descending aorta were cross-clamped (at 25"C), and the aorta was dissected and repaired with pledgeted sutures. Aortic cross-clamp time was 19 minutes, followed by 15 minutes of unclamping and then another 22 minutes of reclamping. The patient made an uneventful recovery. Although this patient could have been handled as patient 2, cardiopulmonary bypass allowed a more controlled situation. Both patients could have benefited from
Major vein Trachea Esophagus Lung Spinal cord Bracheal plexus Heart Abdomen Total (includes other injuries)
Number
Percent
21 8 7 6 5 4 4
22.6 8.6 7.5 7.5 6.5 5.4 4.3 4.3
77
82.8
7
590
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injury of the aortic arch, proximal carotid artery, or both. The other 45 unstable patients were immediately operated on without angiograms. In the 36 patients in stable condition operation was delayed until angiography was performed. Arteriovenous fistulas were demonstrated in 4 of these. In 4 patients not having angiograms, the incision was suboptimal and stemotomy became necessary. Three of these had emergency anterolateral thoracotomies for relief of cardiac tamponade. Another patient with massive left hemothorax was explored through a left posterolateral thoracotomy, but exposure of the posterior arch was not possible and a midline thoracotomy became necessary (patient 2). All aortic injuries were repaired, usually with direct suture over felt pledgets, but on several occasions with prosthetic patches to avoid undue tension on the sutures. Digital pressure or partial occlusion clamps were usually adequate for control during repair. Of 18 patients who underwent operation, cardiopulmonary bypass was used in 1, aorto-carotid shunts in 3, and aorto-innominate shunts in 3. No such adjuncts were used in the other 11 patients, whose injuries were repaired without significant periods of carotid occlusion. Of the 18 patients who reached the operating room alive, 11 survived. Four patients died of other trauma: 1, of an extensive gunshot wound to the heart; 2, of abdominal injuries; and 1, of tracheal injury and asphyxia (see Table 1). Considering only the aortic injury (ie, hemorrhage, operating room deaths, cardiac malfunction, and neurologic complications), the injury-specific survival rate after surgical repair of aortic arch injuries themselves was 83.3%. All innominate artery injuries were repaired or bypassed; only 1 patient died, unrelated to hemorrhage or complications of the innominate artery injury. None had neurologic defects. Bypass shunts were used in 4 patients who had shunts from the ascending aorta, and 1 had a bypass shunt from carotid artery to carotid artery before the chest was entered. Three of the 31 patients with common carotid artery injury were agonal on arrival and definitive therapy was not possible before death. Two of the 28 patients operated on had obvious hemiplegia on admission; there was no improvement after operation. Twenty-six of the 28 patients survived to have carotid artery repairs. Bypass shunts, four permanent and one temporary, were used in these patients. No new or worsening neurologic symptoms developed in any patient after repair or grafting of the carotid artery. Two patients, both in profound shock, died on the operating table of associated injuries and could not be neurologically evaluated. Of patients with subcluviun artery injuries, half had primary repair; in 1the subclavian artery was ligated and in the others it was repaired using grafts. Distal arterial flow was good in all patients. Two patients who had major venous trauma had residual edema of the arm after ligation of subclavian veins; this slowly improved over many months. Concomitant brachial plexus injuries were crippling in 3. The only amputation was of a single finger.
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Comment This retrospective, uncontrolled analysis of a group of patients with a broad spectrum of major injuries and of varying clinical status precludes meaningful statistical analysis. Although the general policies of Table 2 were in use during this series, they could not always be followed. Even with 27 years' experience with similar injuries [9] before this series, details of surgical management still changed during this period. Simplification of incisions and more use of bypass shunts were the major evolutional changes during these 8 years. Pulse deficits were of little diagnostic help in these patients; they were noted in only a few patients with firearm injuries of the subclavian artery. Hematomas of the base of the neck or gross arterial bleeding were of no aid in identifying the site of vascular injury. Unilateral hemothorax was usually of help in delineating the injury. The major indication for aortogram was known or suspected wound entry into the mediastinum or base of the neck. When the patient was in stable condition, aortograms were of great help, not only in diagnosis, but especially in planning the operation. In the selective group, we routinely did esophagograms only in those whose entry wound was in the base of the neck. Most of these patients were too uncooperative, either from trauma, drugs, or alcohol, to safely have an esophagogram. Of the seven esophageal injuries, six were repaired at initial operation and one was not diagnosed until serious postoperative infection occurred. About a fourth of all patients had simultaneous major venous injuries, and an arteriovenous fistula was demonstrated in 4 of the 36 patients (11.1%) who had arteriograms. If the same incidence were true in those patients who did not have an arteriogram, one could expect as many as nine or ten fistulas. A significant correlation of arch injuries and arteriovenous fistulas has also been noted by others [7]. Large vein-ways in the legs, an arterial catheter in the right radial artery, and the use of autotransfusion devices are important basics in the management of these patients. In previous years we frequently used a Sauerbruch incision for exposure of the innominate and subclavian arteries; its use has steadily diminished. A midline sternotomy with sternocleidomastoid extensions was usually adequate for the innominate artery; a posterolateral thoracotomy served for most of the left subclavian artery injuries resulting from thoracic wounds. However, wounds of the base of the neck involving the left subclavian arteries and extending into the thorax are usually best managed by anterior thoracotomy for proximal control of the artery, a supraclavicular incision with division of the sternocleidomastoid muscle, and clavicular resection as needed for distal control and repair. A full Sauerbruch incision may be necessary if still further exposure is needed. The issue of ligation versus reconstruction of the carotid artery has received much attention in the literature. In 1974,it was demonstrated [lo] that repair of the intrathoracic carotid artery could be associated with massive
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cerebral infarction. By 1991, it had become obvious that about half of the deaths after innominate and carotid injuries were due to cerebral infarction caused by ischemic, not reperfusion, infarction [Ill. Our experience leads us to recommend bypass shunts from the intrapericardial aorta to one or both carotid arteries before exposing the bleeding site when injury to innominate or intrathoracic carotid artery is known or strongly suspected. Only about 20% of patients have a “normal” circle of Willis; preoperative and intraoperative shock and hypoxia contribute to cerebral ischemia, and there is high probability of prolonged occlusion of the carotid artery during dissection and vascular repair. Fabian and associates’ [8] recent extensive review of the literature and their experience with a large series of carotid injuries led to conclusions that (1) there is no valid reason to avoid carotid artery reconstruction, (2) there are some patients in whom other impairments (eg, alcohol, drugs, shock) prevent proper preoperative neurological evaluation, (3) there are some patients with neurologic defects whose condition may actually improve after revascularization, and (4) patients with preoperative neurologic defects are seldom, if ever, harmed by reconstruction. None of the patients in this series had worsening neurologic status after flow was reestablished. The fear of “hemorrhagic infarct” of the brain after reestablishing carotid artery flow seems misfounded. A careful study of the use of shunts has not been possible because of the rarity of these injuries. A recent report [12] of 30 years’ experience with the use of shunts in 31 patients with penetrating (24) and blunt (7) injuries of the innominate artery, however, leaves little doubt that this should now be the accepted method of management. There is a widespread aversion to the use of systemic heparinization in the severely injured patient. In this series of penetrating trauma, we used systemic heparin in doses of about 100 to 150 U/kg, while temporary shunts were in use or when a patient‘s carotid artery was occluded. We have used full systemic heparinization (300 U/kg initial dose) in more than 100 cases of blunt injury of the thoracic aorta or carotid artery. Most of these patients had concomitant injuries, including head, liver, or spleen disruptions. We have been unable, in spite of prospective critical observation, to demonstrate clear deleterious effects of short-term heparinization, except in patients with severe pulmonary contusions. Others have reported similar experiences [131. During brief periods of aortic occlusion, the left ventricular afterload abruptly rises. Ventricular dilatation and resultant damage to the myocardium is a real threat. Continuous observation of the electrocardiogram and heart is necessary during these periods. Bradycardia usually occurs as the heart dilates. When a heartbeat drops to 50/min or electrocardiographic signs of ischemia evolve, the occlusion should be released as quickly as possible. In our clinical experience, and in the literature, the deleterious effects on the heart seem to be ameliorated by simultaneous caval occlusion. We have confirmed this in the animal laboratory (Van Voorst and Pate; unpublished results). Theoretically, the beneficial effects of caval occlu-
591
sion should extend to the lungs and cerebrospinal fluid pressure. Hypovolemia, as suggested by the work of Martin and associates [14], is probably beneficial until repair is complete. Elevated central venous pressure results in elevated cerebrospinal fluid pressure with consequent decrease in blood flow to the central nervous system. With aortic occlusion resulting in such an increase in cerebrospinal fluid pressure, superimposed on decreased carotid blood flow during clamping, cerebral ischemia is increased on the clamped side and unilateral cerebral edema on the unclamped side might be expected. Hypovolemia, again, might help prevent this effect. Essentially all of these patients remained on mechanical ventilation for more than 24 hours and most showed varying evidence of pulmonary dysfunction. Shock and massive intravenous fluids are major factors in the disturbed physiology, but the rise in pulmonary venous pressure with partial aortic occlusion certainly might contribute. Again, brief periods of caval occlusion or hypovolemia should be of value in alleviating pulmonary damage. Robicsek and Matos-Cruz [15] recently used electrically induced ventricular fibrillation for these purposes. Postoperative paraplegia, which occurs in up to 35% of cases of occlusion at the distal arch required for repair of traumatic rupture of the aorta, was not recognized in these patients with penetrating wounds. This is probably due to the fact that periods of proximal aortic occlusion long enough to produce cord damage resulted in fatal cardiac dilatation or cerebral ischemia. Although patient 3 had a favorable outcome after the use of cardiopulmonary bypass, we believe that most patients (91/93) were more expeditiously managed by the use of arterial bypass shunts and brief caval and aortic occlusion. Retrospectively, in only 2 patients, both with large through-and-through gunshot wounds of the arch, do we believe that cardiopulmonary bypass would have been of value. In both patients necessity for prompt control of the hemorrhage precluded use of cardiopulmonary bypass, even though only 30 to 45 minutes are needed for its set-up. We thank Jean Distretti, RN, Service Manager, and her staff in the Data Processing Unit of the Elvis Presley Trauma Center for their valuable contribution in data collecting and tabulation.
References 1. Symbas PN, Sehdeva JS. Penetrating wounds of the thoracic aorta. Ann Surg 1970;171:441-50. 2. DeMeester TR, Cameron JL, Gott VL. Repair of a throughand-through gunshot wound of the aortic arch using a heparinized shunt. Ann Thorac Surg 1973;16:193-8. 3. Graham JM, Feliciano DV, Mattox KL, Beall AC Jr. Innominate vascular injury.J Trauma 1982;22:&17-55. 4. Timberlake GA, Kerstein MD, McSwain NE Jr. Penetrating thoracic aortic injuries: rare but potentially salvageable sequelae of urban warfare. South Med J 1989;82:97&2. 5. Cheek RC, Pope JC, Smith HF, Britt LG, Pate JW. Diagnosis and management of major vascular injuries: a review of 200 operative cases. Am Surg 1975;41:755-60.
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6. Rich NM, Baugh JH, Hughes CW. Acute arterial injuries of Vietnam: lo00 cases. J Trauma 1970;10359-68. 7. Rasaretnam R, Tissera W. Penetrating wound of the arch of
the aorta. Injury 1980;12:14!b7. 8. Fabian CF, George SM Jr, Croce MA, Mangiante EC, Voeller GR, Kudsk KA. Carotid artery trauma: management based on mechanism of injury. J Trauma 1990;30:953-63. 9. Pate JW, Casini M. Penetrating wounds of the neck: explore or not? Am Surg 1980;463&43. 10. Stallone RJ, Ecker RR, Samson PC. Management of major acute thoracic vascular injuries. Am J Surg 1974;128:248. 11. George SM Jr, Croce MA, Fabian TC, et al. Cervicothoraac arterial injuries: recommendations for diagnosis and management. World J Surg 1991;15:13440.
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12. Johnston RH,Wall MJ, Mattox KL. Innominate artery trauma: a 30 year experience. J Vasc Surg (in press). 13. Cemaianu AC, Cilley JH Jr, Baldino WA, Spence RK, DelRossi AJ. Determinants of outcome in lesions of the thoracic aorta in patients with multiorgan system trauma. Chest 1992;101:331-5. 14. Martin RR, Bickell WH, Pepe PE, Burch JM, Mattox KL. Prospective evaluation of preoperative fluid resuscitation in hypotensive patients with penetrating truncal injury: a preliminary report. J Trauma 1992;33:354-61. 15. Robicsek F, Matos-Cruz M. Artificially induced ventricular fibrillation in the management of through-and-through penetrating wounds of the aortic arch: a case report. Surgery 1991;11054&5.
DISCUSSION D R HOOSHANG BOLOOKI (Miami, FL):I enjoyed this presen-
tation very much and had the privilege of reading the manuscript earlier. I would like to congratulate Dr Pate and associates for doing admirable work on these very ill patients. This series of 93 patients actually is one of the largest reported series in the world literature. We have had an experience similar to this but not in as many patients. We have our experience summarized in a chapter in a book titled Trauma Management edited by the late Dr Kreis [l]. We entirely agree with your recommendations in managing this injury. The points that you bring up, and I think they should be reemphasized, are mainly three. First, control the bleeding as fast as you can; second, establish blood flow distally if at all possible and do not just tie off the artery; third, during hypotension periods either incidentally (or because of clamping the vena cava, as you have suggested, and it is a very good idea) continue to work aiming at control of bleeding specifically around the aorta itself and the aortic arch. In other words, use the hypotensive periods to the patient’s advantage by controlling the major branches of the arch. I think it is important to note, as you are indicating, that the farther away the injury is from the arch the greater is the need for a shunt or some kind of bypass. Conversely, for injuries on the aortic arch, especially around the arch or behind the arch, heart-lung bypass is needed. There is no doubt that a heart-lung machine is used in a small number of these patients. It is used more often when angiography delineates the lesion and the operation is planned. In fact, we have lost some patients due to central or arch injuries because we did not have an angiogram. Such a study cannot be done in a patient who is bleeding out, as you indicated already, and as a result one does not know the extent or location of the injury. I think it is important to do a very good physical examination, especially if the injury is a day or two old. A systolic murmur is an important finding because that would allow for better patient management and work-up. The murmur may point to the presence of an arteriovenous fistula. An angiogram, whenever possible, is an invaluable guide to location of injury and hence the method of management. I have three questions. First, what would you do with an enlarging mediastinal hematoma if the patient is in stable condition and the aorta is intact? Would you explore it or leave it alone and treat the patient conservatively?Second, if there is an acute brain injury (or mild stroke) due to a carotid lesion (cut-off by a flap or by external pressure but without acute carotid bleeding)
would you reestablish the blood flow to the distal carotid artery, or if the neurologic dysfunction is not serious would you wait and intervene at a later time, say a few weeks? Third, around the aortic arch there are many nerves, especially the phrenic, vagus, and recurrent laryngeal. I have had at times problems with these patients after I have done a successful operation on the arch in that they have been respirator dependent. Have you had any problems with that, and what special maneuvers do you use to idenhfy these nerves in the bulk of the hematoma? I thank you again for a fine presentation and congratulateyou for good work.
DR PATE: I appreciate your comments, Dr Bolooki. First, a
mediastinal hematoma in a patient in stable condition is a definite indication for aortography; most of the time, a major vascular injury will be seen. When an aortogram cannot be obtained, consideration must be given to surgical exposure. In relation to aortic injuries, we cannot answer the question about completed strokes because, even though this is a very large series, we had too few strokes. There is a lot of information in the literature in relation to neck injuries. As far back as 1974, it was known that revascularizationof the carotid artery could result in hemorrhagicinfarction. By 1991, it was obvious that about half of the deaths after carotid trauma were due to cerebral infarction, usually ischemic. The fear of reperfusion infarction after carotid injury repair is probably based on a myth. An occasional patient will show some improvement after reconstruction. Confusing the issue is the fact that many of these patients are in shock or under the influence of alcohol or drugs and cannot be evaluated preoperatively. Yes, circulation should always be reestablished regardless of neurological findings. Most of the time, the phrenic nerve can be identified by feel as the hematoma displaces it medially and anteriorly. The reasons for the difficulty in getting a patient off the ventilator place us in the area of opinion rather than facts-I could preach a sermon. Most of these patients are ”drowned” during the resuscitation process with 18 to 20 L of crystalloid. They have many reasons for difficulty in weaning. I do not believe this is unique to phrenic or recurrent nerve injury.
Reference 1. Bolooki H. Thoracic vascular trauma. In: Kreis DJ, Gomez GA,
eds. Trauma management. Boston: Little, Brown, 1989:
238-301.
Acute cardiac failure, pulmonary edema, and ischemia of the brain, cord, and other structures pose special problems with trauma to the aortic arch and its branches. Data on 93 such cases are reported. Diagnosis was made by clinical examination in hemodynamically unstable patients and led to immediate operation in 61.3%. Patients in stable condition had angiography, which localized the injury and allowed planning of incision and bypass shunts. In left subclavian artery injuries, anterior thoracotomy was best for proximal control regardless of wound entry sites; midline stemotomy with stemocleidomastoid extension was usually adequate for other
vessels. Flow was reestablished in all carotid injuries; there were no neurological complications. Temporary or permanent bypass shunts during periods of proximal aortic occlusion were valuable in decreasing cardiac afterload, maintaining circulation to the brain, and allowing an unhurried methodical approach to the hematoma. Occlusion of one or more venae cavae alleviated acute cardiac dilatation during brief periods of ascending aortic clamping. Associated trauma contributed to the high mortality.
P
to Y grafts to both carotid arteries before disturbing the hematoma or attempting repair. These injuries are uncommon [4,51; Rich and associates’ report [6] of 1,OOO arterial injuries from the Vietnam war includes only three innominate and eight subclavian artery injuries. The development of well-organized trauma systems is leading to increasing numbers of such victims of urban warfare reaching the treatment facility alive. To summarize our experience and arrive at reasonable recommendations, we are reporting our more recent experience of penetrating injuries to the aortic arch (from superior pericardial reflection to the aortic isthmus) and its branche-innominate, common carotid, and subclavian arterie-that we treated at their initial trauma episode during the 8 years ending September 1, 1992. Only carotid artery injuries that resulted from thoracic wounds or wounds of the base of the neck or supraclavicular spaces that passed into the thorax are included.
ulmonary edema, acute heart failure, and irreversible ischemia of the brain, spinal cord, kidneys, and viscera are special problems associated with control of exsanguinating hemorrhage from penetrating trauma to the aortic arch and its branches. Many injuries localized to the anterior surface of the arch or its branches (more than a centimeter distal to their origin) can be easily repaired by simple digital pressure or partial occlusion and suture, whereas more complex injuries involving the posterior surface of the arch or the origin of innominate or carotid arteries may require bypass techniques to avoid these potentially fatal complications. Surgical approaches should be directed at decreasing cardiac afterload and maintaining oxygenated blood flow to the brain and distal body. For these purposes, Symbas and Sehdeva [l], in 1970, reported the use of a temporary shunt from the ascending aorta to innominate artery for repair of a stab wound of the arch. This concept was extended in 1973 by DeMeester and associates [Z],who used a heparinized shunt from the ascending aorta to the femoral artery to maintain distal circulation and decompress the heart during repair of an arch injury. Rather than temporary shunts, the Houston group [3],in 1982, introduced the use of a permanent prosthetic bypass graft from the ascending aorta to the distal carotid or innominate artery before repair of the arch and innominate artery. In 1984, we adopted the routine use of both temporary and permanent bypass shunts for managing these injuries and expanded the use Presented at the Thirty-ninth Annual Meeting of the Southern Thoracic Surgical Association, Wesley Chapel, FL, Nov 5-7, 1992. Address reprint requests to Dr Pate, Department of Surgery, University of Tennessee, 956 Court Ave, Memphis, TN 38163.
0 1993 by The Society of Thoraac Surgeons
(Ann Thorac Surg 1993;55:586-92)
Material and Methods We reviewed the medical records of 93 consecutive patients who sustained penetrating injury (63.5% of which were gunshot wounds) of the aortic arch and its branches and were admitted to the Elvis Presley Trauma Center, Memphis (Table 1).Most patients (79.7%)were male; they had a median age of 26 years. Among the factors studied were age, mechanism of injury, hemodynamics, preoperative and postoperative neurological findings, associated trauma, diagnostic methods, anatomy of vascular injury, surgical exposure, use of shunts, and mortality. When there was evidence of massive or pulsatile bleeding or persistent hemodynamic instability, the patient was im0003-4975/93/$6.00
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587
Table 1. Clinical Outcomes of Entire Series Site Aorta
Innominate Carotid
Subclavian Total a
Number
Not
Resuscitated
27 6 31 29
9 (33.3%)
93 (100.0%)
Operated Patients Lived
Died
Total Survivors
...
11 (61.1%) 5 (83.3%) 25 (89.3%) 25 (86.2%)
7 (38.9%) 1(16.7%) 3 (10.7%) 4 (13.8%)
11” (40.7%) 5 (83.3%) 25 (80.6%) 25 (86.2%)
12 (12.9%)
66 (81.5%)
15 (18.5%)
66 (71.0%)
... 3 (9.7%)
Four deaths resulted from other injuries. Excluding these, sunrival related to the aortic arch injury alone for operated patients would have been 83.3%.
mediately operated on without further study. All patients
in stable condition demonstrating pulse deficit, major hematoma, widened mediastinum, or missile tracts thought to be near major arteries had aortograms for precise anatomical diagnosis and to plan surgical exposure and the possible use of shunts (”selective” operation). Operating rooms and an arteriographic suite are integral to the Trauma Center, thus avoiding unnecessary and dangerous transportation of these patients in critical condition.
Operative Technique The two basic incisions usually used were (1) midline sternotomy, with cervical extensions over one or both carotids when needed, and (2) an anterior left thoracotomy through the fourth intercostal space (with dislocation of cartilage) for exposure of the left subclavian artery. The latter incision was extended by partial median sternotomy, neck incision, and excision of half the clavicle, as required. Entrance wounds in the left supraclavicular fossa and associated with a left pneumothorax or hemothorax were assumed to be subclavian artery injuries for purposes of selecting the incision. When an arteriogram was available, the plan of the operation was based on the site of vascular injury. In the group having immediate operation, the operative approach was chosen based on suspected injury and the exact technique was modified as necessary after the chest was open. Injuries on the anterior surface of the arch or branches further than 1 cm away from the aorta were usually managed by digital pressure or tangential partial occlusion clamps and suture. Intermittent aortic occlusion, either partial or complete, and caval occlusion were useful adjuncts both for exposure and for decreasing blood pressure while suturing. For larger wounds and gunshot injuries, large felt pledgets or patches of prosthetic material were used. With involvement of the superior surface of the arch and origins of the innominate or carotid arteries, more complex procedures were usually considered necessary. When exposure of the concavity and posterior surface of the aorta was necessary, the pulmonary artery and aorta were separated by sharp incision, followed by division of the pericardial and fascia1 tissue from within the pericardium (Fig 1). Dissection of the concave and posterior surfaces of the arch from outside the pericardium is hazardous, as the fibrous layer of the pericardium
blends into and forms the aortic adventitia. Dissection from without leads to an apparent cleavage plane, which may actually be within the aortic wall [7]. Principles aimed at avoiding irreversible ischemic damage to vital organs or distension of the left ventricle were followed (Table 2). When practical, blood flow to the distal arterial bed was always reestablished. When a midline incision was used, the pericardium was immediately opened vertically, before the hematoma was entered. This allowed tapes to be easily placed around the cava(e) for cardiac inflow occlusion and around the ascending aorta for temporary partial occlusion while the repair was effected. While bleeding was controlled by the hematoma or by digital pressure, distal control of the carotid artery (or arteries) was obtained. When compromise of carotid flow was anticipated, shunts were established before disturbing the hematoma or bleeding site (Fig 2). This allowed both decompression of the aorta and left heart and flow to the brain during vascular repair. The proximal end of a graft or shunt was placed into the intrapericardial aorta and the other end was placed in the carotid artery distally, before the hematoma was entered. When grafts were used, they were left in situ as bypass grafts; temporary shunts were removed when the repair n
Fig I. Exposure of the concavity and posterior surface of the aortic arch begins with dissection from within the pericardium (see text).
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was completed. Although available in the Trauma Center, cardiopulmonary bypass was used in only 1 patient (patient 3). When the injury involved the origin of the innominate or carotid artery, the bypass prosthetic graft was left in place permanently and the end of the carotid was oversewn. When the injury did not involve the origin of the branch vessel or continued hemorrhage was a problem, a temporary shunt (see Fig 2) with primary repair or interpositional prosthesis became the preferred technique; this was faster and led to use of less prosthetic material in the narrow confines of the thoracic inlet. The intrathoracic carotid was never ligated without bypass grafting. Primary repair was done when feasible [8].
Illustrative Cases Both the applications of these principles and some difficulties in their use are illustrated by the following three case reports. I. A man sustained a stab wound in the right supraclavicular space. Initial pulsatile bleeding was controlled by pressure. Aortogram revealed injury to the aortic arch at the base of the innominate and left carotid arteries. There was associated filling of the left innominate vein and superior vena cava. Repair involved bypass Y shunts to both common carotid arteries followed by brief, intermittent periods of aortic aoss-clamping and partial caval occlusion, while the aorta was repaired with pledgeted sutures (see Fig 2). The innominate veins were repaired by simple suture. There were no major complications.
PATIENT
PATIENT 2. This man had a gunshot wound to the left chest. Emergency anterolateral thoracotomy for massive bleeding revealed through-and-through wounds of the aortic arch. The anterior aortic wound and lung were repaired, while the posterior aortic wound was tampon-
Table 2 . Surgical Principles Used In Repair of Aortic Arch
Injuries
Princiule Local control Proximal control Distal control Maintain flow" From ventricle (1 min) To brain (5 min) To cord, viscera (30min) Prevent hypertensionof left ventricle, pulmonary veins, central veins, cerebrospinal fluid Exposure of injury site Reestablish distal circulation
Application Pressure only Intrapericardial Tapes: aorta, carotid($, & innominate Bypass shunts: ascending aorta to carotid(s) Arterial shunts and caval occlusion After proximal and distal control Repair or graft
.'Time of occlusion of arterial flow was kept below indicated times whenever feasible. Hypothermia allows some safe prolongation.
Fig 2 . (Patient 1 .) Bypass shunt from ascending aorta to carotid arteries is established before attempting suture of the arch. An injury to the posterior surface of the junction of the brachiocephalic wins and the caval tapes are not shown.
aded. A midline incision was necessary for adequate exposure of the posterior aortic wound. The pericardium between the aorta and pulmonary arteries was divided, followed by division of the posterior fascial attachments of the aorta. Exposure and repair of the posterior defect was done in intermittent steps by temporary tape occlusions of aortic branches, intrapericardial control of the aorta, and periods of venous inflow occlusion (Fig 3). Although the patient later died of complications of prolonged shock, this case is useful in emphasizing the necessity for exposure of the posterior arch from the midline. Had the location of the posterior wound been known before the necessary emergency thoracotomy, use of partial cardiopulmonary bypass may have been of benefit. This man sustained a stab wound in the right supraclavidar space with a hunting knife; an aortogram demonstrated a large aorto-left innominate vein fistula. The groin vessels were exposed as a midline thoracotomy was begun. Massive bleeding was encountered upon opening the supramanubrial fascial space; cannulation was performed and partial cardiopulmonary bypass was begun before the sternum was divided. Pressure controlled the hemorrhage while the pericardium was opened and the incision extended along the left carotid sheath. Ascending aorta, superior vena cava, and neck vessels were controlled with tapes. The left innominate vein was almost severed; it was divided, allowing visualization of the anterior and superior surfaces of an extensive aortic laceration (Fig 4). Full cardiopulmonary bypass through the right atrium was instituted with systemic PATIENT 3.
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A
m m
589
Fig 4. (Patient 3.) Large laceration of Left innominate vein and aorta, with functioning arteriovenous fistula. Repaired with hypothermic cardiopulmonary bypass.
temporary bypass shunts from the ascending aorta to the distal carotid arteries, but shunts were not used in either because of the inability to control hemorrhage without occlusion of the ascending aorta after the chest was opened. Repair of all major vein injuries has been our policy since 1964; however, this has not always been feasible without an intervening graft, which we did not use in the acute trauma setting. No caval ligation was done, although several cavae and innominate veins were sutured without problems.
Results B
Fig 3. (Patient 2.) (A) Exposure of gunshot wound on the posterior surface of arch, after dissection from within the pericardium and control of all branches. Caval tapes for inflow occlusion and distal aortic wound are not illustrated for clarity. ( B ) Completed repair using prosthetic patches.
Associated injury was present in most patients (Table 3) and accounted for several of the deaths. Fifty-seven patients (61.3%)were hemodynamically unstable; 12 of them (12.9%)died during attempted resuscitation before definitive operation (see Table 1). All had Table 3. Associated Injuries to Other Structures Injury to
hypothermia and with cold cardioplegia. The ascending and descending aorta were cross-clamped (at 25"C), and the aorta was dissected and repaired with pledgeted sutures. Aortic cross-clamp time was 19 minutes, followed by 15 minutes of unclamping and then another 22 minutes of reclamping. The patient made an uneventful recovery. Although this patient could have been handled as patient 2, cardiopulmonary bypass allowed a more controlled situation. Both patients could have benefited from
Major vein Trachea Esophagus Lung Spinal cord Bracheal plexus Heart Abdomen Total (includes other injuries)
Number
Percent
21 8 7 6 5 4 4
22.6 8.6 7.5 7.5 6.5 5.4 4.3 4.3
77
82.8
7
590
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injury of the aortic arch, proximal carotid artery, or both. The other 45 unstable patients were immediately operated on without angiograms. In the 36 patients in stable condition operation was delayed until angiography was performed. Arteriovenous fistulas were demonstrated in 4 of these. In 4 patients not having angiograms, the incision was suboptimal and stemotomy became necessary. Three of these had emergency anterolateral thoracotomies for relief of cardiac tamponade. Another patient with massive left hemothorax was explored through a left posterolateral thoracotomy, but exposure of the posterior arch was not possible and a midline thoracotomy became necessary (patient 2). All aortic injuries were repaired, usually with direct suture over felt pledgets, but on several occasions with prosthetic patches to avoid undue tension on the sutures. Digital pressure or partial occlusion clamps were usually adequate for control during repair. Of 18 patients who underwent operation, cardiopulmonary bypass was used in 1, aorto-carotid shunts in 3, and aorto-innominate shunts in 3. No such adjuncts were used in the other 11 patients, whose injuries were repaired without significant periods of carotid occlusion. Of the 18 patients who reached the operating room alive, 11 survived. Four patients died of other trauma: 1, of an extensive gunshot wound to the heart; 2, of abdominal injuries; and 1, of tracheal injury and asphyxia (see Table 1). Considering only the aortic injury (ie, hemorrhage, operating room deaths, cardiac malfunction, and neurologic complications), the injury-specific survival rate after surgical repair of aortic arch injuries themselves was 83.3%. All innominate artery injuries were repaired or bypassed; only 1 patient died, unrelated to hemorrhage or complications of the innominate artery injury. None had neurologic defects. Bypass shunts were used in 4 patients who had shunts from the ascending aorta, and 1 had a bypass shunt from carotid artery to carotid artery before the chest was entered. Three of the 31 patients with common carotid artery injury were agonal on arrival and definitive therapy was not possible before death. Two of the 28 patients operated on had obvious hemiplegia on admission; there was no improvement after operation. Twenty-six of the 28 patients survived to have carotid artery repairs. Bypass shunts, four permanent and one temporary, were used in these patients. No new or worsening neurologic symptoms developed in any patient after repair or grafting of the carotid artery. Two patients, both in profound shock, died on the operating table of associated injuries and could not be neurologically evaluated. Of patients with subcluviun artery injuries, half had primary repair; in 1the subclavian artery was ligated and in the others it was repaired using grafts. Distal arterial flow was good in all patients. Two patients who had major venous trauma had residual edema of the arm after ligation of subclavian veins; this slowly improved over many months. Concomitant brachial plexus injuries were crippling in 3. The only amputation was of a single finger.
1993;55586-92
Comment This retrospective, uncontrolled analysis of a group of patients with a broad spectrum of major injuries and of varying clinical status precludes meaningful statistical analysis. Although the general policies of Table 2 were in use during this series, they could not always be followed. Even with 27 years' experience with similar injuries [9] before this series, details of surgical management still changed during this period. Simplification of incisions and more use of bypass shunts were the major evolutional changes during these 8 years. Pulse deficits were of little diagnostic help in these patients; they were noted in only a few patients with firearm injuries of the subclavian artery. Hematomas of the base of the neck or gross arterial bleeding were of no aid in identifying the site of vascular injury. Unilateral hemothorax was usually of help in delineating the injury. The major indication for aortogram was known or suspected wound entry into the mediastinum or base of the neck. When the patient was in stable condition, aortograms were of great help, not only in diagnosis, but especially in planning the operation. In the selective group, we routinely did esophagograms only in those whose entry wound was in the base of the neck. Most of these patients were too uncooperative, either from trauma, drugs, or alcohol, to safely have an esophagogram. Of the seven esophageal injuries, six were repaired at initial operation and one was not diagnosed until serious postoperative infection occurred. About a fourth of all patients had simultaneous major venous injuries, and an arteriovenous fistula was demonstrated in 4 of the 36 patients (11.1%) who had arteriograms. If the same incidence were true in those patients who did not have an arteriogram, one could expect as many as nine or ten fistulas. A significant correlation of arch injuries and arteriovenous fistulas has also been noted by others [7]. Large vein-ways in the legs, an arterial catheter in the right radial artery, and the use of autotransfusion devices are important basics in the management of these patients. In previous years we frequently used a Sauerbruch incision for exposure of the innominate and subclavian arteries; its use has steadily diminished. A midline sternotomy with sternocleidomastoid extensions was usually adequate for the innominate artery; a posterolateral thoracotomy served for most of the left subclavian artery injuries resulting from thoracic wounds. However, wounds of the base of the neck involving the left subclavian arteries and extending into the thorax are usually best managed by anterior thoracotomy for proximal control of the artery, a supraclavicular incision with division of the sternocleidomastoid muscle, and clavicular resection as needed for distal control and repair. A full Sauerbruch incision may be necessary if still further exposure is needed. The issue of ligation versus reconstruction of the carotid artery has received much attention in the literature. In 1974,it was demonstrated [lo] that repair of the intrathoracic carotid artery could be associated with massive
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Ann Thorac Surg 1993;55:5&92
cerebral infarction. By 1991, it had become obvious that about half of the deaths after innominate and carotid injuries were due to cerebral infarction caused by ischemic, not reperfusion, infarction [Ill. Our experience leads us to recommend bypass shunts from the intrapericardial aorta to one or both carotid arteries before exposing the bleeding site when injury to innominate or intrathoracic carotid artery is known or strongly suspected. Only about 20% of patients have a “normal” circle of Willis; preoperative and intraoperative shock and hypoxia contribute to cerebral ischemia, and there is high probability of prolonged occlusion of the carotid artery during dissection and vascular repair. Fabian and associates’ [8] recent extensive review of the literature and their experience with a large series of carotid injuries led to conclusions that (1) there is no valid reason to avoid carotid artery reconstruction, (2) there are some patients in whom other impairments (eg, alcohol, drugs, shock) prevent proper preoperative neurological evaluation, (3) there are some patients with neurologic defects whose condition may actually improve after revascularization, and (4) patients with preoperative neurologic defects are seldom, if ever, harmed by reconstruction. None of the patients in this series had worsening neurologic status after flow was reestablished. The fear of “hemorrhagic infarct” of the brain after reestablishing carotid artery flow seems misfounded. A careful study of the use of shunts has not been possible because of the rarity of these injuries. A recent report [12] of 30 years’ experience with the use of shunts in 31 patients with penetrating (24) and blunt (7) injuries of the innominate artery, however, leaves little doubt that this should now be the accepted method of management. There is a widespread aversion to the use of systemic heparinization in the severely injured patient. In this series of penetrating trauma, we used systemic heparin in doses of about 100 to 150 U/kg, while temporary shunts were in use or when a patient‘s carotid artery was occluded. We have used full systemic heparinization (300 U/kg initial dose) in more than 100 cases of blunt injury of the thoracic aorta or carotid artery. Most of these patients had concomitant injuries, including head, liver, or spleen disruptions. We have been unable, in spite of prospective critical observation, to demonstrate clear deleterious effects of short-term heparinization, except in patients with severe pulmonary contusions. Others have reported similar experiences [131. During brief periods of aortic occlusion, the left ventricular afterload abruptly rises. Ventricular dilatation and resultant damage to the myocardium is a real threat. Continuous observation of the electrocardiogram and heart is necessary during these periods. Bradycardia usually occurs as the heart dilates. When a heartbeat drops to 50/min or electrocardiographic signs of ischemia evolve, the occlusion should be released as quickly as possible. In our clinical experience, and in the literature, the deleterious effects on the heart seem to be ameliorated by simultaneous caval occlusion. We have confirmed this in the animal laboratory (Van Voorst and Pate; unpublished results). Theoretically, the beneficial effects of caval occlu-
591
sion should extend to the lungs and cerebrospinal fluid pressure. Hypovolemia, as suggested by the work of Martin and associates [14], is probably beneficial until repair is complete. Elevated central venous pressure results in elevated cerebrospinal fluid pressure with consequent decrease in blood flow to the central nervous system. With aortic occlusion resulting in such an increase in cerebrospinal fluid pressure, superimposed on decreased carotid blood flow during clamping, cerebral ischemia is increased on the clamped side and unilateral cerebral edema on the unclamped side might be expected. Hypovolemia, again, might help prevent this effect. Essentially all of these patients remained on mechanical ventilation for more than 24 hours and most showed varying evidence of pulmonary dysfunction. Shock and massive intravenous fluids are major factors in the disturbed physiology, but the rise in pulmonary venous pressure with partial aortic occlusion certainly might contribute. Again, brief periods of caval occlusion or hypovolemia should be of value in alleviating pulmonary damage. Robicsek and Matos-Cruz [15] recently used electrically induced ventricular fibrillation for these purposes. Postoperative paraplegia, which occurs in up to 35% of cases of occlusion at the distal arch required for repair of traumatic rupture of the aorta, was not recognized in these patients with penetrating wounds. This is probably due to the fact that periods of proximal aortic occlusion long enough to produce cord damage resulted in fatal cardiac dilatation or cerebral ischemia. Although patient 3 had a favorable outcome after the use of cardiopulmonary bypass, we believe that most patients (91/93) were more expeditiously managed by the use of arterial bypass shunts and brief caval and aortic occlusion. Retrospectively, in only 2 patients, both with large through-and-through gunshot wounds of the arch, do we believe that cardiopulmonary bypass would have been of value. In both patients necessity for prompt control of the hemorrhage precluded use of cardiopulmonary bypass, even though only 30 to 45 minutes are needed for its set-up. We thank Jean Distretti, RN, Service Manager, and her staff in the Data Processing Unit of the Elvis Presley Trauma Center for their valuable contribution in data collecting and tabulation.
References 1. Symbas PN, Sehdeva JS. Penetrating wounds of the thoracic aorta. Ann Surg 1970;171:441-50. 2. DeMeester TR, Cameron JL, Gott VL. Repair of a throughand-through gunshot wound of the aortic arch using a heparinized shunt. Ann Thorac Surg 1973;16:193-8. 3. Graham JM, Feliciano DV, Mattox KL, Beall AC Jr. Innominate vascular injury.J Trauma 1982;22:&17-55. 4. Timberlake GA, Kerstein MD, McSwain NE Jr. Penetrating thoracic aortic injuries: rare but potentially salvageable sequelae of urban warfare. South Med J 1989;82:97&2. 5. Cheek RC, Pope JC, Smith HF, Britt LG, Pate JW. Diagnosis and management of major vascular injuries: a review of 200 operative cases. Am Surg 1975;41:755-60.
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6. Rich NM, Baugh JH, Hughes CW. Acute arterial injuries of Vietnam: lo00 cases. J Trauma 1970;10359-68. 7. Rasaretnam R, Tissera W. Penetrating wound of the arch of
the aorta. Injury 1980;12:14!b7. 8. Fabian CF, George SM Jr, Croce MA, Mangiante EC, Voeller GR, Kudsk KA. Carotid artery trauma: management based on mechanism of injury. J Trauma 1990;30:953-63. 9. Pate JW, Casini M. Penetrating wounds of the neck: explore or not? Am Surg 1980;463&43. 10. Stallone RJ, Ecker RR, Samson PC. Management of major acute thoracic vascular injuries. Am J Surg 1974;128:248. 11. George SM Jr, Croce MA, Fabian TC, et al. Cervicothoraac arterial injuries: recommendations for diagnosis and management. World J Surg 1991;15:13440.
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12. Johnston RH,Wall MJ, Mattox KL. Innominate artery trauma: a 30 year experience. J Vasc Surg (in press). 13. Cemaianu AC, Cilley JH Jr, Baldino WA, Spence RK, DelRossi AJ. Determinants of outcome in lesions of the thoracic aorta in patients with multiorgan system trauma. Chest 1992;101:331-5. 14. Martin RR, Bickell WH, Pepe PE, Burch JM, Mattox KL. Prospective evaluation of preoperative fluid resuscitation in hypotensive patients with penetrating truncal injury: a preliminary report. J Trauma 1992;33:354-61. 15. Robicsek F, Matos-Cruz M. Artificially induced ventricular fibrillation in the management of through-and-through penetrating wounds of the aortic arch: a case report. Surgery 1991;11054&5.
DISCUSSION D R HOOSHANG BOLOOKI (Miami, FL):I enjoyed this presen-
tation very much and had the privilege of reading the manuscript earlier. I would like to congratulate Dr Pate and associates for doing admirable work on these very ill patients. This series of 93 patients actually is one of the largest reported series in the world literature. We have had an experience similar to this but not in as many patients. We have our experience summarized in a chapter in a book titled Trauma Management edited by the late Dr Kreis [l]. We entirely agree with your recommendations in managing this injury. The points that you bring up, and I think they should be reemphasized, are mainly three. First, control the bleeding as fast as you can; second, establish blood flow distally if at all possible and do not just tie off the artery; third, during hypotension periods either incidentally (or because of clamping the vena cava, as you have suggested, and it is a very good idea) continue to work aiming at control of bleeding specifically around the aorta itself and the aortic arch. In other words, use the hypotensive periods to the patient’s advantage by controlling the major branches of the arch. I think it is important to note, as you are indicating, that the farther away the injury is from the arch the greater is the need for a shunt or some kind of bypass. Conversely, for injuries on the aortic arch, especially around the arch or behind the arch, heart-lung bypass is needed. There is no doubt that a heart-lung machine is used in a small number of these patients. It is used more often when angiography delineates the lesion and the operation is planned. In fact, we have lost some patients due to central or arch injuries because we did not have an angiogram. Such a study cannot be done in a patient who is bleeding out, as you indicated already, and as a result one does not know the extent or location of the injury. I think it is important to do a very good physical examination, especially if the injury is a day or two old. A systolic murmur is an important finding because that would allow for better patient management and work-up. The murmur may point to the presence of an arteriovenous fistula. An angiogram, whenever possible, is an invaluable guide to location of injury and hence the method of management. I have three questions. First, what would you do with an enlarging mediastinal hematoma if the patient is in stable condition and the aorta is intact? Would you explore it or leave it alone and treat the patient conservatively?Second, if there is an acute brain injury (or mild stroke) due to a carotid lesion (cut-off by a flap or by external pressure but without acute carotid bleeding)
would you reestablish the blood flow to the distal carotid artery, or if the neurologic dysfunction is not serious would you wait and intervene at a later time, say a few weeks? Third, around the aortic arch there are many nerves, especially the phrenic, vagus, and recurrent laryngeal. I have had at times problems with these patients after I have done a successful operation on the arch in that they have been respirator dependent. Have you had any problems with that, and what special maneuvers do you use to idenhfy these nerves in the bulk of the hematoma? I thank you again for a fine presentation and congratulateyou for good work.
DR PATE: I appreciate your comments, Dr Bolooki. First, a
mediastinal hematoma in a patient in stable condition is a definite indication for aortography; most of the time, a major vascular injury will be seen. When an aortogram cannot be obtained, consideration must be given to surgical exposure. In relation to aortic injuries, we cannot answer the question about completed strokes because, even though this is a very large series, we had too few strokes. There is a lot of information in the literature in relation to neck injuries. As far back as 1974, it was known that revascularizationof the carotid artery could result in hemorrhagicinfarction. By 1991, it was obvious that about half of the deaths after carotid trauma were due to cerebral infarction, usually ischemic. The fear of reperfusion infarction after carotid injury repair is probably based on a myth. An occasional patient will show some improvement after reconstruction. Confusing the issue is the fact that many of these patients are in shock or under the influence of alcohol or drugs and cannot be evaluated preoperatively. Yes, circulation should always be reestablished regardless of neurological findings. Most of the time, the phrenic nerve can be identified by feel as the hematoma displaces it medially and anteriorly. The reasons for the difficulty in getting a patient off the ventilator place us in the area of opinion rather than facts-I could preach a sermon. Most of these patients are ”drowned” during the resuscitation process with 18 to 20 L of crystalloid. They have many reasons for difficulty in weaning. I do not believe this is unique to phrenic or recurrent nerve injury.
Reference 1. Bolooki H. Thoracic vascular trauma. In: Kreis DJ, Gomez GA,
eds. Trauma management. Boston: Little, Brown, 1989:
238-301.