Chapter 26 - McGraw-Hill Professional

More documents

Recommendations

Info

492 Management of Specific Injuries SECTION 3 X ■ Follow-Up As discussed above, secondary sequelae in survivors of cardiac trauma include valvular abnormalities and intracardiac fistulas. 4 , 19 , 21 Early postoperative clinical examination and ECG findings are unreliable. 4 , 21 Thus, echocardiography is recommended during the initial hospitalization in all patients to identify occult injury and establish a baseline study. Because the incidence of late sequelae can be as high as 56%, follow-up echocardiography 3–4 weeks after injury has been recommended by 19 , 21 some. THORACIC GREAT VESSEL INJURY Injuries to the thoracic great vessels—the aorta and its brachiocephalic branches, the pulmonary arteries and veins, the superior and intrathoracic inferior vena cava, and the innominate and azygos veins—occur following both blunt and penetrating trauma. Exsanguinating hemorrhage, the primary acute manifestation, also occurs in the chronic setting when the injured great vessel forms a fistula involving an adjacent structure or when a post-traumatic pseudoaneurysm ruptures. Current knowledge regarding the treatment of injured thoracic great vessels has been derived primarily from experience with civilian injuries. Great vessel injuries have been repaired with increasing frequency, a phenomenon that has paralleled the development of techniques for elective surgery of the thoracic aorta and its major branches. A detailed understanding of normal and variant anatomy and structural relationships is important for the surgeon and any one who is a consultant to the surgeon in the evaluation of imaging studies. Venous anomalies are infrequent with the most common being absence of the left innominate vein and persistent left superior vena cava. Thoracic aortic arch anomalies are relatively common ( Table 26-3 ). Knowledge of such anomalies is essential for both open and catheter-based therapies. TABLE 26-3 Thoracic Aortic Anomalies Common origin of innominate and left carotid arteries (“bovine arch”) Ductus diverticulum Persistent left ductus arteriosus Aberrant takeoff of the right subclavian artery from the descending thoracic aorta Dextroposition of the thoracic aorta Coarctation of the thoracic aorta Origin of left vertebral artery off the aortic arch Pseudocoarction of the thoracic aorta (“kinked aorta”) Double aortic arch Right ductus arteriosus Persistent truncus arteriosus Cervical aortic arch (persistent complete third aortic arch) Absence of the internal carotid artery Cardio-aortic fistula ETIOLOGY AND PATHOPHYSIOLOGY More than 90% of thoracic great vessel injuries are due to penetrating trauma: gunshot, fragments, and stab wounds or therapeutic misadventures. 22 Iatrogenic lacerations of various thoracic great vessels, including the arch of the aorta, are reported complications of percutaneous central venous catheter placement. The percutaneous placement of “trocar” chest tubes has caused injuries to the intercostal arteries and major pulmonary and mediastinal vessels. Intra-aortic cardiac assist balloons can produce injury to the thoracic aorta. During emergency center resuscitative thoracotomy, the aorta may be injured during clamping if a crushing (nonvascular) clamp is used. Overinflation or migration of the Swan–Ganz balloon has produced iatrogenic injuries to pulmonary artery branches with resultant fatal hemoptysis; therefore, once a linear relationship has been established between the pulmonary artery diastolic pressure and the pulmonary capillary wedge pressure, further “wedging” may be unnecessary. Self-expanding metal stents have recently produced perforations of the aorta and innominate artery following placement into the esophagus and trachea, respectively. 23 The great vessels particularly susceptible to injury from blunt trauma include the innominate artery origin, pulmonary veins, vena cava, and, most commonly, the descending thoracic aorta. 24 Aortic injuries have caused or contributed to 10–15% of deaths following motor vehicle accidents for nearly 50 years. These injuries usually involve the proximal descending aorta (54–65% of cases), but often involve other segments—that is, the ascending aorta or transverse aortic arch (10–14%), the mid- or distal descending thoracic aorta (12%), or multiple sites (13–18%). The postulated mechanisms of blunt great vessel injury include (1) shear forces caused by relative mobility of a portion of the vessel adjacent to a fixed portion, (2) compression of the vessel between bony structures, and (3) profound intraluminal hypertension during the traumatic event. The atrial attachments of the pulmonary veins and vena cava and the fixation of the descending thoracic aorta at the ligamentum arteriosum and diaphragm enhance their susceptibility to blunt rupture by the first mechanism. At its origin, the innominate artery may be “pinched” between the sternum and the vertebrae during sternal impact. Blunt aortic injuries may be partial thickness—histologically similar to the intimal tear in aortic dissection—but most commonly are full thickness and therefore equivalent to a ruptured aortic aneurysm that is contained by surrounding tissues. The histopathological similarities between aortic injuries and nontraumatic aortic catastrophes suggest that similar therapeutic approaches be employed. Therefore, in hemodynamically stable patients with blunt aortic injuries, the concepts of permissive hypovolemia and minimization of arterial pressure impulse (d P /dT )—which are widely accepted in the treatment of aortic dissection and aneurysm rupture—should be considered. In opposition to patients with aortic intimal disease where the adventitia is the restraining barrier, with blunt injury to the descending thoracic aorta, it is the intact parietal pleura (not the adventitia) that contains the hematoma and prevents a massive hemothorax. True traumatic aortic dissection, with a longitudinal separation of the media extending along the length of the aorta, is extremely rare. 25 The use of the term “dissection” in the setting
Heart and Thoracic Vascular Injuries 493 TABLE 26-4 Groups of Patients with Thoracic Aortic Injury Group Description Time to Diagnosis Location of Death Mortality (%) Cause of Death 1 2 3 Dead/dying at scene Unstable during transport Stable 60 min 1–6 h 4–18 h Scene/EMS EMS/EC ICU 100 96 5–30 Bleeding Multisystem trauma CNS injury CHAPTER 26 X of aortic trauma should be equally rare, being used only in a few appropriate cases. Similarly, the terms “aortic transection” and “blunt aortic rupture” should be used only when describing specific injuries, that is, full-thickness lacerations involving either the entire or partial circumference, respectively. Increasingly, patients with thoracic great vessel injury have associated head, abdominal, and extremity injury. Often preexisting medical conditions are present, such as diabetes, hypertension, coronary artery disease, or cirrhosis. These patients are also on a large variety of medications, often aspirin, warfarin, or other platelet inhibitors. These interfere with the clotting mechanism and adaptations in treatment must be made. PATIENT CLASSIFICATION Three distinctly different groups of patients with thoracic aortic trauma exist ( Table 26-4 ). The epidemiology of aortic injury is changing, due to rapid accident notification and emergency medical system (EMS) transport. The mortality statistics reveal that those whose cause of death is exsanguinating hemorrhage almost all die within the first 0–2 hours of injury. Those who die in the emergency department, operating room, or intensive care unit (ICU) within 2–4 hours of injury often have extensive multisystem injury with hemorrhage often being from sites other than the thoracic aorta. Hemodynamically stable patients who are subsequently found to have aortic injury but who die most often have central nervous system injury as the cause of their injury. It is this later group in whom the diagnosis is made by the trauma team, and therefore amenable to appropriate screening, diagnostic, and therapeutic considerations. INITIAL EVALUATION ■ Prehospital Management Interventions often performed by paramedics during transport include judicious intravenous fluid administration and endotracheal intubation when indicated. 26 Though seldom seen, pneumatic anti-shock garment (PAST) application in patients with thoracic great vessel injuries statistically increases the chance of death in both adult and pediatric populations. 27 The PAST elevate blood pressure by increasing afterload and are equivalent to placing a cross-clamp distal to the potential injury—a clearly counterproductive maneuver. Similarly, in patients with acute thoracic great vessel injuries, excessive fluid resuscitation with the goal of increasing blood pressure to normal or supernormal levels increases the incidence of mortality, ARDS, and other postoperative complications. 28 ■ Emergency Center Evaluation History In cases of penetrating thoracic trauma, information regarding the length of a knife, the firearm type and number of rounds fired, and the patient’s distance from the firearm is sought from the patient or accompanying persons. Unfortunately, this is frequently unavailable and unreliable. Although the head-on motor vehicle collision is often considered the typical mechanism for blunt aortic injury, recent epidemiological data reveal that up to 50% of cases occur following side-impact collisions. Blunt aortic injuries have also been reported following equestrian accidents, blast injuries, auto-pedestrian accidents, crush injuries, and falls from heights of 30 ft or more. 29 In addition to information involving the mechanism of injury, the emergency transport personnel can provide medical information important in evaluating the potential for a thoracic great vessel injury, such as the amount of hemorrhage at the scene, the extent and location of damage to the vehicle, any history of intermittent paralysis following the accident, and hemodynamic instability during transport. Physical Examination On arrival to the emergency center, each patient is given a rapid, thorough examination. External signs of penetrating or blunt trauma are noted. With an intrapericardial vascular injury, the classic signs of pericardial tamponade (distended neck veins, pulsus paradoxus, muffled heart sounds, elevated central venous pressure) may be present but not uniformly. Clinical findings associated with thoracic great vessel injury include: 1. Hypotension 2. Upper extremity hypertension 3. Unequal blood pressures or pulses in the extremities (upper extremity from innominate or subclavian injury, or lower extremity from pseudocoarctation syndrome) 4. External evidence of major chest trauma (e.g., steering wheel imprint on chest) 5. Expanding hematoma at the thoracic outlet 6. Intrascapular murmur 7. Palpable fracture of the sternum 8. Palpable fracture of the thoracic spine 9. Left flail chest
Page 1 and 2: 485 CHAPTER 26 Heart and Thoracic V
Page 3 and 4: Heart and Thoracic Vascular Injurie
Page 7: Heart and Thoracic Vascular Injurie
Page 27: Heart and Thoracic Vascular Injurie

Chapter 26 - McGraw-Hill Professional

You also want an ePaper? Increase the reach of your titles

Delete template?

Save as template?