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Acute Traumatic Aortic Disruption
Definition
Acute traumatic aortic disruption is rupture of all or part of the aortic wall, usually occurring as a result of blunt trauma. A theoretical sequence of injury involves initial rupture of the intimal and medial layers. After a period of unpredictable duration, rupture of the adventitial layer occurs. Patients are considered to have acute disruption when it occurs within 14 days of injury. Chronic traumatic aortic disruptions and posttraumatic aneurysms (pseudoaneurysms) are discussed in Chapter 26 .
Paraplegia as a complication of aortic surgery, and grafts used to replace or exclude the aorta, are also discussed in this chapter.
Historical Note
Although the lethal nature of acute traumatic aortic disruption had been recognized for centuries and was noted by Strassmann in 1947, data supporting lethality of traumatic disruption and temporal relationships between trauma and subsequent death were delineated by Parmley and colleagues in 1958. The first report of successful repair of traumatic disruption of the thoracic aorta apparently was by Dshanelidze in 1923 (cited by Clarke and colleagues ). In 1957, Gerbode and colleagues reported successful repair of such an injury, as did Klassen and colleagues in 1958 (according to Passaro and Pace and Vasko and colleagues ). In 1998, Kato and colleagues at Stanford University reported successful treatment of three patients with acute traumatic aortic disruption using endovascular stent-grafts constructed from modified Z stents covered with woven polyester or expanded polytetrafluoroethylene (PTFE) graft material and deployed through a delivery sheath from a peripheral artery.
Morphology
Upper Descending Thoracic Aorta
Traumatic aortic disruptions occur most commonly in the upper descending thoracic aorta at or near the aortic isthmus. In the study of Parmley and colleagues, 45% of disruptions occurred at this site. In a more recent multicenter study by the American Association for the Surgery of Trauma (AAST) reported by Demetriades and colleagues, 82 (74%) of 110 acute aortic injuries occurred in this location. Occasionally, the disruption may occur at the origin of the left subclavian artery and extend proximally to involve the distal portion of the aortic arch.
A traditional view has been that with abrupt deceleration of the thorax, such as occurs in a high-speed vehicular accident in which the body is thrown against a near-stationary object, the ligamentum arteriosum and intercostal arteries anchor the upper descending thoracic aorta to the thorax, as do the thoracic exits of the brachiocephalic vessels. These structures decelerate with the thorax, but the distal end of the aortic arch and most proximal part of the descending thoracic aorta continue to move forward. Aortic disruption tends to develop at the interface between these two areas, although the sum of the forces involved and directions of their effects are complex. The force needed to produce rupture is equivalent to an intravascular pressure of 2500 mmHg.
There are other theories regarding the mechanism of blunt aortic injury ( Fig. 24-1 ). Aortic rupture from a sudden increase in intraabdominal pressure may explain the association between blunt aortic injury and diaphragmatic rupture. A “water-hammer” effect, which involves simultaneous occlusion of the aorta and a sudden elevation in blood pressure, and the “osseous pinch” effect from entrapment of the aorta between the anterior chest wall and the vertebral column have also been postulated. Most injuries probably involve a combination of forces.
Disruption can be complete, including aortic adventitia and mediastinal pleura. If the deceleration forces are less severe, the mediastinal pleura and the adventitia are spared. With lower initial velocity or less rapid deceleration, the mediastinal pleura and adventitia remain intact, while a fracture develops in a portion of the circumference of the aorta, usually posteriorly.
If the person survives the immediate post-disruption period, the periaortic hematoma begins to liquefy about 2 weeks after the traumatic event. It is gradually absorbed or evacuated into the aorta, and a false aneurysm (pseudoaneurysm) develops. The false aneurysm may remain stable for a long period and even calcify, but it can enlarge and rupture.
Ascending Aorta
Disruption of the ascending aorta is uncommon (10% of isolated cases of disruption without other major visceral injuries reported by Parmley and colleagues and 3.6% [4 of 111 patients] reported by Demetriades and colleagues ). Again, the mechanism is sudden deceleration, which is apt to be severe in unrestrained drivers who strike the steering wheel. Cammack and colleagues showed that vertical forces of deceleration tend to lead to rupture of the ascending aorta and arch, and horizontal forces to rupture of the descending aorta. Disruption occurs most commonly in the distal portion of the ascending aorta, near the origin of the brachiocephalic trunk. Less commonly, it is in the proximal portion of the ascending aorta. As in the upper descending thoracic aorta, disruption may be complete or partial.
Other Sites
Disruptions can occur in the lower thoracic aorta (often in association with spinal fractures) and in the aortic arch and abdominal aorta.
Clinical Features And Diagnostic Criteria
Pathophysiology
When complete disruption occurs that includes the investing mediastinal pleura or pericardium, hemorrhage is free and exsanguinating, and death occurs instantly or within a few minutes. When the tear involves all layers of the aortic wall but the mediastinal pleura remains intact, a large amount of blood escapes into the retropleural tissues, and signs and symptoms of hemorrhagic shock appear. Usually under such circumstances, some blood or plasma passes through the mediastinal pleura to produce a left hemothorax or pleural fluid collection. When the adventitia of the aorta remains essentially intact, a smaller extravasation of blood occurs, and the mediastinal hematoma is less extensive. The aortic adventitia is more likely to remain intact when the tear does not involve the entire circumference of the aortic wall.
Clinical Features
Persons with acute traumatic aortic disruptions frequently have other severe injuries, including liver and spleen lacerations with intraabdominal hemorrhage, and head injuries. Such injuries have their own clinical features and diagnostic criteria that may affect management of the aortic disruption (see Indications for Operation later in this chapter).
Those who survive to reach the hospital may be in profound hemorrhagic shock if a large mediastinal extravasation has occurred or if there has been extensive intraabdominal or extremity bleeding. Some patients, however, are hemodynamically stable after initial resuscitative measures, and a few show no signs of hemodynamic instability. In such patients, upper body hypertension is common. Some patients in whom other trauma is not severe complain of interscapular back pain, but pain is generally not a major part of the presentation.
Evidence of impaired blood flow beyond the disruption is uncommon. However, a small number of patients with acute disruption of the descending thoracic aorta who reach the hospital alive have paraplegia or paraparesis (2.6%; CL 2.2%-3.0%, of the 1742 patients in the meta-analysis of von Oppell and colleagues ). Rarely, patients have severe lower body and leg ischemia.
Diagnostic Imaging
Chest Radiography
The chest radiograph is usually abnormal, but with variable findings. There may be opacification of the left hemothorax and rightward shift of the mediastinum resulting from massive collection of fluid in the left pleural space. These features are not diagnostic of aortic disruption, because bleeding after trauma may come from intercostal or pulmonary vessels, cardiac and pericardial rupture, or traumatic rupture of the left hemidiaphragm with intrathoracic splenic rupture.
Commonly the radiograph shows only diffuse upper mediastinal widening ( Fig. 24-2 ), which in the setting of a severe injury strongly suggests upper descending aortic disruption. However, rightward shift of the trachea, blurring of the normally sharp outline of the upper descending thoracic aorta, and opacification of the usually clear space between it and the pulmonary trunk may be evident; all these findings suggest aortic disruption.
Computed Tomography
Computed tomography (CT) has been evaluated as a screening examination to detect aortic injury in patients with blunt chest trauma. In the early years of its use, time required to perform the study (60-70 minutes) in patients who often were severely injured, low sensitivity and positive predictive value, and lack of demonstrated cost effectiveness limited its utility. It is, however, essential for managing patients with associated head trauma and for assessing presence of intraabdominal and retroperitoneal injuries.
Now, helical CT of the thorax can be performed more rapidly than conventional CT, and its sensitivity for detecting blunt aortic injury equals that of aortography (discussed later). In trauma centers, it is currently the most widely used technique to diagnose traumatic aortic disruption. Findings indicative of aortic disruption include extravasation of contrast, intimal flaps, mural thrombus, paraaortic hematoma, wall thickening, pseudoaneurysm, and pseudocoarctation ( Fig. 24-3 ). Advantages of helical CT over other imaging techniques include its wide availability, speed of performance, sensitivity, and relatively low cost.
Transesophageal Echocardiography
Transesophageal echocardiography (TEE) is a highly effective method for imaging the proximal ascending aorta, distal aortic arch, and descending thoracic aorta. Its characteristic finding is presence of a mobile mural flap ( Fig. 24-4 ). Two studies comparing TEE with aortography or with findings at operation or autopsy in 101 and 32 patients, respectively, have demonstrated a sensitivity of 91% and 100% and a specificity of 100% and 98%, respectively. A more recent prospective comparison of TEE to helical CT demonstrated a sensitivity, specificity, negative predictive value, and positive predictive value of 93%, 100%, 99%, and 100%, respectively, for TEE, compared with 73%, 100%, 95%, and 100% for helical CT. TEE can be performed with minimal risk in the emergency room, intensive care unit, or operating room and can be carried out simultaneously with other diagnostic or therapeutic procedures. It requires less than 30 minutes to complete and provides, in addition to images of the aorta, information about ventricular function and wall motion. It can detect presence of cardiac valvar lesions and pericardial fluid. A limitation is that the distal ascending aorta and brachiocephalic trunk cannot be imaged clearly because of interposition of the column of air in the distal trachea and right bronchus between the probe in the esophagus and the aorta. Thus, presence of a tear in these locations cannot be excluded. In centers with extensive experience, TEE can be used as the primary diagnostic imaging technique in patients with blunt chest trauma.
Aortography
Until recently, aortography has been the definitive diagnostic study for acute aortic disruption ( Fig. 24-5 ), the imaging modality against which all subsequently developed imaging techniques have been compared. Its specificity approaches 100%, and prevalence of false positives and false negatives is low. The procedure is associated with some risk, is time consuming, and requires a skilled interventional radiology team. Up to 90% of studies performed to determine presence of aortic disruption are negative.
With increasing use of CT as the primary diagnostic imaging study, aortography is being used less frequently. In a multicenter study by the AAST, it was used to screen for traumatic aortic disruption in only 8.3% of 193 patients treated during a 26-month interval in 2005-2007, as compared with 87% of 274 patients treated during a 30-month interval in 1994 to 1996.
Magnetic Resonance Imaging
Magnetic resonance imaging (MRI) provides excellent images of vascular structures in the thoracic aorta and provides diagnostic accuracy similar to aortography. Its use in the acute trauma patient is limited because of the confining nature of the scanners and the time required to obtain images.
Natural History
Risk of death, generally from massive intrathoracic hemorrhage, is greatest immediately after the injury. As time passes, the instantaneous risk of death (hazard function) decreases, but the patient remains at risk of death from hemorrhagic shock over the next several days ( Fig. 24-6 ). Shock may be secondary either to initial blood loss into a large mediastinal hematoma or to renewed bleeding into the adventitia and mediastinal pleura as arterial blood pressure rises after the initial period of hypotension. Probability of survival for at least 4 hours after the accident is not improved with certainty by rapid transport from accident scene to hospital. About 40% to 50% of persons die within 48 hours of the traumatic event.
Instantaneous risk of death in surgically untreated patients begins to level off about 7 days after injury (see Fig. 24-6 ). Most patients who survive this long without treatment survive much longer. However, a low constant risk of death from hemorrhage persists because of propensity of the false aneurysm (see Morphology earlier in this chapter) to rupture even years later. It has been estimated that even after 10 years, 20% of patients with this type of traumatic false aneurysm will die of rupture within the subsequent 5 years.
Technique Of Operation
Preoperative Management
When a presumptive diagnosis of acute traumatic aortic disruption or other major vascular injury is made based on an abnormal chest radiograph, hemodynamic monitoring and medical therapy are instituted before diagnostic imaging (CT, TEE, or aortography) is performed. In hemodynamically stable patients, medical therapy should include intravenous infusion of a vasodilator (usually sodium nitroprusside) to avoid hypertension, limitation of intravenous fluid infusion once the systolic arterial blood pressure exceeds 90 to 100 mmHg, and administration of a β-adrenergic antagonist when heart rate exceeds 80 to 90 beats/min. This therapy should be continued while diagnostic studies and any surgical procedures, if indicated, are performed.
Repair of Acute Traumatic Aortic Disruption of Upper Descending Thoracic Aorta
Operative Strategies
Open operative repair has been the standard surgical treatment of traumatic aortic disruption of the descending thoracic aorta for more than 50 years. Development and recent widespread availability of endovascular stent-grafts have dramatically altered management. The first patients with traumatic aortic disruption of the descending thoracic aorta treated this way were reported by Kato and colleagues in 1997. The technique is now widely used in trauma centers throughout the world. A prospective multicenter study by the AAST reported by Demetriades and colleagues compared the methods of definitive repair of traumatic aortic disruption in two time intervals: 1994-1996 (274 patients, 50 participating centers) and 2005-2007 (193 patients, 18 participating centers) ( Table 24-1 ). In the latter interval, 65% of patients were treated with stent-grafts. Although there are no randomized trials comparing endovascular stent-grafting with open repair, ease of insertion, reduced operative time, and reduction in major postoperative complications are attractive features of the technique that have led to increasing use.
Table 24-1
Methods of Definitive Repair of Blunt Thoracic Aortic Injuries (American Association for the Surgery of Trauma)
Modified from Demetriades and colleges.
| Repair Method | Study Interval | |
|---|---|---|
| 1994-1996 n = 207 a No. (%) |
2005-2007 n = 193 No. (%) |
|
| Open | 207 (100) | 68 (35) |
| Endovascular | 0 (0) | 125 (65) |
Open Repair
Spinal cord ischemic injury resulting in paraplegia or paraparesis is a devastating complication of surgical repair, and the optimal technique for avoiding injury to the spinal cord during open repair remains arguable (see detailed discussion in “ Paraplegia after Aortic Clamping ” under Special Situations and Controversies later in this chapter). In their meta-analysis, von Oppell and colleagues noted that the mean number of patients with acute traumatic aortic disruption admitted to any unspecified center was 2.6 per year (range 0.2-10.7 patients). The centers in most of the reports (39 of 60 with data suitable for analysis) treated fewer than this mean number of patients per year. Thus, annual experience with this condition is limited in all but a few centers. With simple aortic clamping, von Oppell and colleagues found that the earliest reported case of paraplegia occurred after a clamp time of 24 minutes; if clamp time extended to 34 minutes, cumulative risk of paraplegia increased to 18%. At 60 minutes, risk approached 80%, and at 120 minutes, 100%. In contrast, when distal aortic perfusion was used, the earliest paraplegia occurred after a clamp time of 34 minutes, and risk of paraplegia at 120 minutes was approximately 18% ( P < .0001) ( Fig. 24-7 ).
![Figure 24-7, Risk of paraplegia according to duration (minutes) of aortic clamping in patients undergoing surgical repair of acute traumatic disruption of the descending thoracic aorta. Blue line depicts 137 patients with no augmentation of distal perfusion (simple aortic clamp group). Red line depicts 153 patients with augmentation of distal perfusion. Analyses derived by product limit survival meta-analysis of patients selected from articles published in the English language literature between 1972 and July 1992. Shaded areas indicate one standard error bands. (*Clamp time [31 minutes] of earliest evident difference between the two groups [ P < .05; Fisher's exact test]; ** P < .00001 cumulative risk for augmented distal perfusion group compared with simple aortic clamp group [Mantel-Cox].)](https://storage.googleapis.com/dl.dentistrykey.com/clinical/AcuteTraumaticAorticDisruption/6_3s20B9781416063919000243.jpg "Figure 24-7, Risk of paraplegia according to duration (minutes) of aortic clamping in patients undergoing surgical repair of acute traumatic disruption of the descending thoracic aorta. Blue line depicts 137 patients with no augmentation of distal perfusion (simple aortic clamp group). Red line depicts 153 patients with augmentation of distal perfusion. Analyses derived by product limit survival meta-analysis of patients selected from articles published in the English language literature between 1972 and July 1992. Shaded areas indicate one standard error bands. (*Clamp time [31 minutes] of earliest evident difference between the two groups [ P < .05; Fisher's exact test]; ** P < .00001 cumulative risk for augmented distal perfusion group compared with simple aortic clamp group [Mantel-Cox].)")
A comparable protective effect of distal aortic perfusion was demonstrated in a subsequent meta-analysis by Jahromi and colleagues and in a single institution by Katz and colleagues. Taken together, these findings strongly suggest that distal aortic perfusion, achieved either by partial cardiopulmonary bypass (CPB) and mild hypothermia or by left atrial–to–distal arterial bypass, should be used for most patients with acute traumatic aortic disruption undergoing open repair. Simple aortic clamping should be reserved for patients in whom anticipated clamp time is less than 20 to 25 minutes (although this is not always predictable) and for patients with life-threatening hemorrhage.
An arterial catheter is inserted in the patient's right arm to monitor blood pressure; nasopharyngeal and bladder or rectal thermistors are placed for temperature measurement. If not already in place, a Swan-Ganz catheter is inserted for measurement of pulmonary artery pressure and cardiac output. A double-lumen endotracheal tube is inserted whenever possible. At least one large-bore needle must be securely in position in a peripheral vein. The patient is placed in a right lateral decubitus position, but with hips rolled back toward a supine position so that the left femoral vessels are accessible ( Fig. 24-8, A [inset]). Facilities are organized for aspirating shed blood from the thorax in a sterile manner, washing and compacting red blood cells, and rapidly returning them to the patient.
A left posterolateral incision is made, and the thorax is entered through either the fourth intercostal space or the bed of the resected fifth rib. The rib spreader is positioned and opened in stages over several minutes, and the opening into the thorax anteriorly and posteriorly is lengthened with scissors. As soon as the rib spreader has been partially opened, unclotted blood and clots are removed from the thorax, taking great care not to exacerbate the bleeding by disturbing the mediastinal hematoma. Usually there is no active bleeding into the pleural space (persons with such bleeding usually have not survived to this point), but if it is occurring, immediate control is obtained by digital pressure.
Once the rib spreader has been positioned, the lung is covered with a moist laparotomy pad and retracted anteriorly with a malleable retractor held by an assistant. The mediastinal pleura is still undisturbed, and at this point a decision is made about the technique that will be used for spinal cord protection during aortic clamping (see previous text and “ Paraplegia after Aortic Clamping ” under Special Situations and Controversies later in this chapter).
A synthetic aortic tube graft is then selected (see “ Grafts for Use in Aortic Surgery ” under Special Situations and Controversies later in this chapter), as are clamps for aortic control. A few stay sutures are placed along the mediastinum behind the hilum of the lung and held anteriorly by clamps, which replace the malleable retractor.
The mediastinal pleura is opened adjacent to the hematoma at three points: (1) over the mid-descending thoracic aorta, (2) over the aortic arch, and (3) over the left subclavian artery (see Fig. 24-8, A-B ). Dissection is carried around the aorta and subclavian artery at these three sites so that clamps can be placed. Tapes can be placed around the vessels, but they are not necessary and generally should be avoided. If accessible, the vagus nerve—identified as it descends over the aorta—is protected. When the hematoma is small and general condition of the patient is good, dissection is carried along the anterior surface of the aorta toward the hematoma from below, and down the aortic arch and the subclavian artery from above. The aortic arch is usually dissected circumferentially between the left carotid and left subclavian arteries (see Fig. 24-8, B ).
When the hematoma is extensive or the hemodynamic state is unstable, dissection is not performed until the clamps are in place. When this dissection has been accomplished, clamps are placed in a preliminary manner, one across the aortic arch between the left carotid and left subclavian arteries, one across the subclavian artery, and one on the descending thoracic aorta ( Fig. 24-8, C ). With this maneuver, reasonable control of bleeding can be established, although there may be bleeding retrogradely into the aorta from intercostal arteries above the distal aortic clamp. After the clamps are placed, dissection is carried toward the hematoma from the distal clamp, and this clamp is expeditiously moved proximally as far as possible to allow blood from the distal aorta to perfuse as many intercostal arteries as possible. The surgeon must recognize that clamping the distal aortic arch rather than aorta beyond the left subclavian artery causes a greater increase in left ventricular afterload and also decreases collateral flow to the lower body and spinal cord from the left subclavian artery. Thus, whenever possible, the clamps on the arch and left subclavian artery should be replaced with one on the aorta just beyond the left subclavian artery ( Fig. 24-8, D ).
Dissection now continues toward the site of disruption, staying in the periaortic tissue plane (see Fig. 24-8, C ). At some point the hematoma is entered, and blood and clot are evacuated rapidly. Usually there will be some bleeding into the field from the intercostal arteries between the disruption and distal clamp. This blood should be aspirated through a system that returns blood to the patient. Alternatively, the bleeding intercostal arteries can be occluded with bulldog clamps (see Fig. 24-8, D ). They should not be ligated or oversewn (see “ Paraplegia after Aortic Clamping ” under Special Situations and Controversies later in this chapter); the aorta can often be tailored to preserve their origins.
When disruption involves only part of the circumference of the aorta, direct repair can often be made with interrupted pledgeted everting mattress sutures or a simple whip stitch of 4-0 or 5-0 polypropylene ( Fig. 24-8, E ). Although Fontan and colleagues report being always able to make a direct repair with partial or complete disruption, this method is considered advisable only if the tissues are of good quality. Otherwise, a segment of the tube graft already selected is anastomosed to the two ends of the aorta using a 4-0 or 5-0 polypropylene suture ( Fig. 24-8, F-G ). The distal clamp is released, anastomotic bleeding between the sutures is secured with fine interrupted sutures, and the proximal clamp is slowly removed. Disruptions that involve the middle or lower descending thoracic aorta are repaired in a similar fashion after obtaining proximal and distal control of the aorta.
For patients in shock resulting from massive intra-thoracic hemorrhage, full cardiopulmonary bypass and hypothermic circulatory arrest permits salvage of the shed blood in the pleural space and mediastinum and eliminates the need for mediastinal dissection of placement of clamps proximal and distal to the aortic tear. Kawahito and Adachi utilized this technique in 10 patients with hemorrhagic shock and major associated injuries. Nine of the patients were discharged from the hospital without complications.
After repair is completed and any devices used for distal aortic perfusion have been removed, as much of the mediastinal pleura as possible is closed over the operative site. One intercostal drainage catheter is positioned posteriorly and inferiorly in the chest cavity, and another anteriorly and superiorly. The incision is closed after making certain the lung has been reexpanded and the catheters are attached to a suction apparatus.
Endovascular Stent-Grafting
Endovascular stent-grafting should be performed under general anesthesia in a standard cardiovascular operating room with a C-arm fluoroscopy unit, or in a “hybrid” operating room with a fluoroscopy unit designed for endovascular surgery. The operating team must be prepared to convert to an open procedure if necessary, and a cardiopulmonary perfusion team should be available on standby.
Access to the aorta is established through a common femoral, external iliac, or common iliac artery. If the common femoral artery is large enough to admit the sheath necessary for deployment of the endovascular stent-graft (EVSG), the procedure can be performed percutaneously or through a small incision in the groin area. If the femoral artery is not of suitable size, access is obtained through a small extraperitoneal incision in a lower quadrant of the abdominal wall to expose the external or common iliac artery. An 8- or 10-mm segment of collagen- or gelatin-impregnated polyester graft is sutured end-to-side to the artery and is used as a conduit through which the graft is deployed. Only low-dose heparinization (2500-5000 units) is required.
Appropriate flexible guidewires are advanced under fluoroscopic guidance into the ascending aorta, and the sheath through which the EVSG will be inserted is passed over the guidewire and positioned in the abdominal aorta. The diameter of the aorta proximal and distal to the site of the tear is determined from a previously obtained CT angiogram (or alternatively, using TEE or intravascular ultrasound), and the appropriate-sized EVSG is selected. The diameter of the graft is 10% to 15% greater than the diameter of the aorta. In general, 2 cm of aorta proximal and distal to the site of disruption is essential for proper sealing of the graft. This may require covering the orifice of the left subclavian artery. Length of the graft should only be long enough to ensure an adequate seal, thus avoiding unnecessary coverage of adjacent intercostal arteries. Once the graft is deployed, angiography or CT imaging is performed to assess adequacy of the seal and to be certain that the left carotid artery has not been compromised ( Fig. 24-9 ). If the left subclavian artery is covered and there is evidence postoperatively of compromised circulation to the left arm, a left carotid–to–left subclavian artery bypass graft with simultaneous embolization of the proximal left subclavian artery, or left subclavian artery transposition to left carotid artery, should be performed.
After satisfactory deployment of the EVSG has been confirmed, the sheath and guidewires are removed, and the artery through which they were inserted is repaired with a 5-0 or 6-0 polypropylene suture. If a graft was used for access, it is excised, leaving a small remnant attached to the artery that is oversewn with a 5-0 or 6-0 polypropylene suture.
Repair of Acute Traumatic Disruption of Ascending Aorta
When the ascending aorta is disrupted, preparations are made for standard CPB as the patient is being transferred to the operating room (see “Preparation for Cardiopulmonary Bypass” in Section III of Chapter 2 ).
In the operating room, the usual peripheral and monitoring devices are placed. After the patient is anesthetized and intubated, one member of the surgical team performs a median sternotomy while another exposes a common femoral artery and vein in the groin. The pericardium is opened just enough to expose the right atrial appendage. No dissection should be performed in the region of the hematoma. If there is active bleeding, control is obtained with digital pressure.
The patient is heparinized and the femoral artery cannulated. A single right atrial venous cannula is placed (see Cardiopulmonary Bypass Established by Peripheral Cannulation in Section III of Chapter 2 ) and CPB established. If the right atrium is not accessible, a long cannula is inserted from a common femoral vein (preferably the right) and positioned with its tip in the middle of the right atrium. Body temperature is reduced by cooling the perfusate (see “Technique in Adults” in Section IV of Chapter 2 ). As this is being done, the thymus gland is divided, the pericardium is opened more widely, and the pericardial reflection is carefully dissected away from the hematoma over the distal portion of the ascending aorta. If massive hemorrhage occurs, perfusion flow is reduced to 0.5 L · min −1 · m −2 until enough of the aorta can be dissected to place an aortic occlusion clamp beyond the site of disruption. If the tear does not involve the brachiocephalic trunk, this clamp is placed just proximal to its origin from the aorta, although the clamp may have to be angled so that it excludes more of the undersurface of the aortic arch. Once this clamp is positioned, full CPB flow may be resumed and perfusate temperature stabilized at 28°C to 32°C.
After this clamp has been placed, the aorta is opened and cardioplegic solution is administered directly into the ostia of the coronary arteries using perfusion cannulae (see “Perfusion of Individual Coronary Arteries” in Chapter 3 ). Alternatively, or as an adjunctive measure, cardioplegic solution can be infused retrogradely into the coronary sinus (see “Technique of Retrograde Infusion” in Chapter 3 ). A venting catheter is placed into the left ventricle, either through a purse-string suture in the right superior pulmonary vein or through the opened aorta.
The area of disruption is dissected carefully. Usually there has been sufficient damage to the aorta that a tube graft is required for reconstruction of aortic continuity (see “ Grafts for Use in Aortic Surgery ” under Special Situations and Controversies later in this chapter). Repair is made by the technique described for graft interposition for descending thoracic aortic disruptions (see previous text). After the anastomosis is completed, the clamp on the aorta is released. Aortic root reperfusion is begun, and the remainder of the procedure is completed (see “De-airing the Heart” in Section III of Chapter 2 ).
If the disruption clearly involves the brachiocephalic trunk or aortic arch, or if it is unclear whether the brachiocephalic trunk is involved, no dissection or manipulation of the aorta and hematoma is begun until the patient has been cooled by the perfusate to a nasopharyngeal temperature below 18°C. Then, with the patient in moderate Trendelenburg position, CPB is discontinued, an aortic clamp is placed across the uninvolved proximal portion of the aorta, cardioplegic solution is administered through a previously placed aortic infusion cannula, and the aorta is opened at the area of disruption without placing a clamp distally. Repair is accomplished by the technique used to repair aortic arch aneurysms (see “Replacement of Aortic Arch” under Technique of Operation in Chapter 26 ). When disruption involves the origin of the brachiocephalic trunk or left carotid artery, the damaged segment is resected and an appropriately sized collagen- or gelatin-impregnated woven polyester graft is sutured to the normal artery distally and to the aortic arch proximally, or to the graft that has replaced the aortic arch and ascending aorta.
Special Features Of Postoperative Care
Postoperative care is that usually given after other major cardiovascular operations (see Chapter 5 ). Many patients have systemic hypertension early postoperatively, and particular care is taken to control it. Associated injuries are managed appropriately.
Results
Survival
Early (Hospital) Death
Many patients who would otherwise have died survive after repair of acute traumatic aortic disruption, but the proportion surviving varies according to the particular circumstances. Associated severe injuries decrease probability of survival. Paradoxically, rapid transport systems between accident site and hospital, although giving the patient a potentially better chance to survive, may actually decrease the proportion of surgical survivors, because more severely injured patients reach the hospital.
Open Operation
VonOppell and colleagues performed a meta-analysis of 88 articles published in English between 1972 and 1992 related to surgical management of acute aortic disruption in which sufficient information was available to permit estimation of mortality and prevalence of paraplegia. Of 1742 patients who reached the hospital alive, 179 (10%) died before surgical intervention. An additional 61 patients (3.5%) exsanguinated despite emergency thoracotomy for profound hemodynamic deterioration. Ten patients were managed without operation. Intraoperative deaths occurred in 111 patients (6.7%), and an additional 201 patients (11.5%) died in the postoperative period. Thus, overall mortality for patients who arrived at the hospital alive was 32% ( Table 24-2 ). Of 1492 patients who reached the operating room in a presumably stable hemodynamic state, mortality was 21%. This mortality ranged from 0% to 54% in individual institutions.
Table 24-2
Meta-analysis of Patients Reaching Hospital Alive or Operating Room in Stable Condition after Acute Traumatic Disruption of Descending Thoracic Aorta a
| Variable | No. | Reaching Hospital (% of 1742 Patients) | Reaching Operating Room (% of 1492 Patients) |
|---|---|---|---|
| Mortality | |||
| Preoperative | 179 | 10.3 | — |
| Emergency thoracotomy | 61 | 3.5 | — |
| Intraoperative | 117 | 6.7 | 7.8 |
| Postoperative | 201 | 11 | 14 |
| T otal | 558 | 32 (CL 31-33) | 21 (CL 20-22) |
| Paraplegia | |||
| Preoperative | 46 | 2.6 | — |
| Postoperative (new) | 147 | 8.4 | 9.9 |
| T otal | 193 | 11 (CL 10-12) | 9.9 (CL 90-11) |
Key: CL, 70% confidence limits.
In a more recent analysis, Demetriades and colleagues reported a 24% early mortality rate among 68 patients treated between 2005 and 2007 in 18 trauma centers. In a meta-analysis of 17 retrospective cohort studies from 2003 to 2007 involving 369 patients treated with open repair, 30-day mortality was 20% (72 patients; CL 17%-22%). It ranged from 0% to 50% in individual centers.
Endovascular Stent-Grafting
In the study of Demetriades and colleagues noted previously, early mortality for 125 patients treated concurrently by EVSG was 7.2% (9 patients; CL 4.9%-10%). In the meta-analysis of 17 retrospective cohort studies by Xenos and colleagues, 30-day mortality for 220 patients treated concurrently by EVSG was 7.9% (18 patients; CL 6.1%-10.0%). It ranged from 0% to 25% in individual centers.
Time-Related Survival
Long-term survival of patients discharged after open repair is excellent. Long-term results after EVSG are unknown.
Modes of Death
Most deaths occur in the postoperative period (see Table 24-2 ). Principal modes of intraoperative death are hemorrhagic shock and cardiac failure. Modes of postoperative death are central nervous system injury and organ failure (lung, kidney, liver).
Risk Factors for Premature Death
A higher Injury Severity Score (ISS) and older age appear to be important risk factors for increased hospital mortality. Surgical technique is not a risk factor for hospital mortality.
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