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Traumatic Aortic Injuries
Introduction
In the United States (US), trauma is the fourth leading cause of death in adults and the leading cause of death in children and adolescents. Traumatic aortic injuries are a rare but serious subset of traumatic emergencies, with potentially catastrophic consequences if not promptly recognized and managed. Traumatic aortic injuries are usually secondary to penetrating chest injuries, deceleration injuries, or blunt chest trauma. Traumatic aortic injuries range from aortic bruising to complete aortic transection, also known as an aortic rupture. Traumatic aortic injuries may manifest initially as a contained rupture or pseudoaneurysm, which may not elicit significant clinical symptoms. However, this relatively silent phase is transient, as the pseudoaneurysm progresses to uncontained rupture, leading to rapid exsanguination and, ultimately, death.
Occurring primarily as a result of blunt traumatic mechanisms, traumatic aortic injuries often present formidable challenges to healthcare professionals due to their elusive clinical manifestations and rapid progression to life-threatening complications. Despite their infrequent occurrence, traumatic aortic injuries are a significant contributor to morbidity and mortality in trauma patients, second only to traumatic brain injury. Trauma disproportionately affects the thoracic aorta at anatomical fixation points. Thoracic aortic injuries account for one-third of automobile accident fatalities; the prehospital mortality rate for such patients approaches 80%.[1]
Patients with a blunt traumatic aortic injury will exhibit a spectrum of presentations and severity levels, categorized into 3 main groups based on clinical outcomes. Between 80% and 85% of patients succumb to their injuries at the scene. Another subset presents alive but hemodynamically unstable, constituting 2% to 5% of cases; mortality rates range from 90% to 98%. The remaining patients, approximately 15% to 20%, present with hemodynamic stability, and the diagnosis of traumatic aortic injury is typically established within 4 to 18 hours after injury.[2][3] Despite advancements in trauma care, a significant proportion of patients with blunt aortic injury face high mortality rates in the hospital; the 24-hour mortality rate is 32% to 50%. However, many deaths may not be directly attributable to the aortic injury, as most of these patients have polytrauma.[4][5]
Traumatic aortic injuries can also occur as a result of penetrating trauma such as gunshot wounds and stabbings; these mechanisms of injury are much more likely to injure the abdominal aorta. While the survival rates from a penetrating traumatic aortic injury are slightly better than from a blunt force injury, the overall mortality still approximates 80%.
A high index of clinical suspicion, rapid diagnosis, and prompt management dictates the survival of patients with traumatic aortic injuries.[6][7][8] Injury mechanism and severity, clinical stability, and associated traumatic injuries all influence the timing and method of aortic repair.[9][10][11] The treatment of these injuries has dramatically shifted within the last 2 decades with the advent of endovascular treatments. Endovascular stent grafts are the mainstay of treatment, with fewer complications and improved morbidity and survival profiles compared to open surgical treatment.
Etiology
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Etiology
A traumatic aortic injury is characterized by damage to the vessel wall or rupture of the vessel secondary to penetrating or blunt force trauma.
Blunt Trauma
Blunt force trauma is the primary etiology of traumatic thoracic aortic injuries. Traumatic thoracic aortic rupture is usually associated with a sudden and rapid deceleration of the heart and the aorta within the thoracic cavity. Anatomically, the heart and great vessels (superior vena cava, inferior vena cava, pulmonary arteries, pulmonary veins, ascending aorta, and aortic arch) are mobile within the thoracic cavity and not fixed to the chest wall, unlike the descending aorta. Injury to the aorta during a sudden deceleration commonly originates near the terminal section of the aortic arch, also known as the isthmus. The aortic isthmus lies just distal to the origin of the left subclavian artery at the intersection of the mobile and fixed portions of the aorta. This anatomy creates a focus of shear stress during the deceleration mechanism, resulting in varying degrees of wall disruption. A mild disruption may cause an intimal tear, while more severe mechanisms may cause a complete aortic wall rupture. Patients who survive traumatic aortic injuries sustain either incomplete or noncircumferential lesions to the intima and media; the tunica adventitia and mediastinal pleura can prevent free rupture and death.
Blunt traumatic aortic injuries are typically the result of high-energy impacts. Approximately 81% follow a motor vehicle crash, but motorcycle and aircraft crashes, automobile versus pedestrian collisions, serious falls of 3 meters or more, and crush injuries may also cause a traumatic aortic injury.[12][13][14]
Historically, traumatic aortic injuries were thought to be primarily associated with severe frontal or "head-on" vehicle crashes. However, recent hospital admissions data following a motor vehicle accident indicates that side-impact collisions carry a significant risk of aortic injury. The crash factors that correlate strongly with aortic injury and rupture include a vehicle velocity change of 20 or more miles per hour, direct impact on the patient's side of the automobile, and intrusion of the vehicle wall into the passenger compartment by 15 inches or greater.[15] Surprisingly, no correlation was found between using safety restraints like seatbelts and airbags and the incidence of traumatic aortic injury.[16][17]
Penetrating Trauma
Penetrating trauma is defined as a direct aortic puncture or laceration. These injuries can be broadly divided into high-velocity mechanisms, such as gunshots or other missiles, and low-velocity mechanisms, typically associated with sharp objects, such as knives, axes, and glass.[13]
A traumatic injury of the abdominal aorta is most frequently due to penetrating trauma; blunt abdominal aortic injuries comprise less than 1% of all blunt traumatic aortic injuries. The relative fixation of the abdominal aorta against the vertebral column predisposes it to injury from adjacent vertebral body fractures. The most commonly involved segments in traumatic abdominal aortic injuries are infrarenal (67%), suprarenal (33%), and extension from a thoracic aortic injury (25%).[18]
Epidemiology
Traumatic aortic injury is rare, occurring in less than 1% of all trauma patients.[19] In the US, the annual incidence of traumatic aortic injury is estimated between 7500 and 8000 cases. In a study of almost 500,000 patients with chest trauma, Sheehan et al reported only 1012 (approximately 0.25%) patients presented with a traumatic aortic injury.[20] Wu et al stated that in their trauma center, only 4 of 1250 (0.32%) of patients with a traumatic chest injury were eventually diagnosed with a traumatic aortic injury.[19]
However, despite its low incidence, traumatic aortic injury is second only to traumatic brain injury as the most common cause of death in patients with blunt-force trauma. While the reported incidence of traumatic aortic injury following motor vehicle accidents is less than 1%, these injuries are responsible for up to 33% of automobile collision fatalities.
A consensus among multiple studies shows that patients with a traumatic aortic injury are more likely to be men between the ages of 16, the onset of driving privileges in many parts of the US, and 50.[21] One study reported that approximately 70% of traumatic aortic injuries occurred in men, while 67% of patients were overweight or obese.[22] In an autopsy study of patients who experienced blunt thoracic trauma, the average age of the patients with a traumatic aortic injury was 43 years, and 71% were men; approximately 40% of these patients were intoxicated at the time of injury.[23]
Pathophysiology
The aorta originates near the upper border of the second or third sternocostal articulation on the right side and is positioned behind the ventricular outflow tract and pulmonary trunk. The right atrial appendage overlaps the aorta. As the aorta ascends, it arches over the pulmonary trunk, right pulmonary artery, and right main bronchus, posterior to the right second costal cartilage, the right lung, and the sternum. The aorta then passes posteriorly and to the left, arching over the left main bronchus and left pulmonary artery, reaching the left side of the T4 vertebral body. Superiorly, the aortic arch gives rise to 3 main branches: the brachiocephalic trunk, the left common carotid artery, and the left subclavian artery.
Apart from the fixed aortic root, the ascending aortic arch is relatively mobile. The aortic isthmus is where this moveable section of the aorta meets the fixed descending thoracic aorta, which abuts the posterior chest wall. This juncture is anchored by the ligamentum arteriosum, a remnant of the fetal ductus arteriosus, and this attachment amplifies shearing forces during sudden deceleration (see Image. Aortic Arch Anatomy). Research indicates that the isthmus displays diminished tensile strength under stress, making this portion of the aorta particularly vulnerable to traumatic injury.
Another suggested mechanism of traumatic aortic injury is the "water-hammer" effect, where a sudden impact leads to a simultaneous rise in intraaortic pressure and the formation of a high-pressure wave, causing significant strain and potential rupture at the arch. Additionally, the "osseous pinch" hypothesis posits that the aorta could be trapped between the bony structures of the chest wall and the vertebral column, resulting in rupture. However, most injuries probably arise from a combination of these mechanisms, acting in concert to cause trauma (see Image. Mechanisms of Traumatic Aortic Injuries).
Patients who initially survive a traumatic aortic injury are transiently shielded from aortic rupture and catastrophic hemorrhage by the aortic adventitia and surrounding mediastinal structures, akin to nontraumatic dissection pathology. However, delayed adventitial rupture may occur during hospitalization, and vigilance is warranted. The time course of aortic rupture is biphasic but unpredictable. The aortic intima and media rupture immediately following a traumatic injury. However, it is typically disruption of the outermost adventitial layer that leads to rapid clinical decline. Studies have revealed that the time interval between the disruption of the intima-media and adventitial rupture can vary from seconds to years.
Histopathology
At the cellular level, the aorta and the aortic arch are composed of 3 layers: the tunica intima, which surrounds the lumen and is composed of simple squamous epithelial cells; the tunica media, consisting of smooth cell muscles and elastic fibers; and the tunica adventitia, composed of loose collagen fibers.
History and Physical
Patients with a traumatic aortic injury frequently present a diagnostic challenge as there are no distinct signs or symptoms specific to an aortic injury. History taking should focus on the mechanism of injury, such as motor vehicle accidents or high-impact events, and any past medical history of conditions predisposing to aortic disease, such as hypertension, connective tissue disorders, or previous aortic pathology.
The aortic adventitia and surrounding mediastinal tissues may initially protect against aortic rupture following trauma. However, the accumulation of blood within the adventitia stretches the tissue and may cause the retrosternal chest pain commonly described by patients with a traumatic aortic injury. Symptoms such as dyspnea, cough, interscapular pain, and hoarseness stem from acute aortic expansion and dilation. Nonetheless, patients may be completely asymptomatic.
The physical examination may reveal hypotension, external evidence of chest trauma, a new heart murmur, and pseudocoarctation, characterized by upper extremity hypertension and hypotension in the lower extremities along with absent femoral pulses; psuedocoarctation may indicate a rupture involving the aortic arch. Associated traumatic injuries can include closed head injury, multiple rib fractures, flail chest, pulmonary contusion, myocardial contusion, blunt diaphragmatic rupture, splenic or liver damage, small bowel injury, intraabdominal bleeding, spinal cord injuries, fractures, upper extremity injury, and maxillofacial injury.
In the absence of specific clinical signs, the diagnosis of traumatic aortic injury often relies on high clinical suspicion and consideration of associated injuries that may distract from or complicate the diagnosis. Prompt recognition of a traumatic aortic injury is paramount, as delayed diagnosis and treatment can lead to catastrophic outcomes.
Evaluation
The evaluation of a suspected traumatic aortic injury comprises a comprehensive approach that includes clinical suspicion based on the mechanism and severity of the injury and diagnostic imaging studies. The possibility of aortic injuries should be considered and excluded in patients with a history of falls from heights or high-speed motor vehicle crashes.[24][25] Myriad imaging modalities are available and are often used in concert to confirm the diagnosis of a traumatic aortic injury.
Chest Radiography
Chest radiography is frequently the initial imaging modality for trauma patients due to its facility and availability. The sensitivity of chest radiography for aortic injury approximates 40%, making it unsuitable as an isolated screening tool.[26]
Chest radiographic findings suggestive of aortic injury include:
- Mediastinal widening of greater than 8 cm
- This finding has a reported sensitivity of 81% to 100% and a specificity of 60% for aortic injury.[27][28][29]
- The positive predictive value of a widened mediastinum on chest radiography is only 5%, and the negative predictive value is 99%. Therefore, a widened mediastinum may not represent aortic transection; its absence nearly confirms the lack of aortic pathology.[30]
- Loss of the normal shadow of the aortic knob
- Left apical pleural cap of fluid or blood
- Left pleural effusion
- Deviation or displacement of the trachea or esophagus to the right.
Computed Tomography Angiography
Computed tomography angiography (CTA) has replaced traditional angiography and transesophageal echocardiography (TEE) as the chosen diagnostic imaging modality when evaluating blunt thoracic aortic injury. CTA has an 86% to 100% sensitivity and 40% to 100% specificity for detecting aortic injuries. Most experts agree that a negative CTA may prevent the need for angiography. Therefore, CTA is recommended for patients following high-speed accidents to exclude aortic injury.
CTA findings indicative of traumatic aortic injury include:
- Pseudoaneurysm formation
- Intimal flap
- Luminal filling defects due to intimal flap or clot
- Periaortic hematoma formation
- Abnormal aortic contour
- Extravasation of contrast; active extravasation of injected contrast medium suggests active hemorrhage and necessitates immediate thoracotomy.
Angiography
Angiography, also known as aortography, may be indicated in cases of suspected aortic trauma when CTA is contraindicated, unavailable, or when there is a high suspicion of aortic injury despite inconclusive findings with other imaging modalities. Angiography may also be used as a confirmatory test when other imaging studies suggest aortic injury but are not definitive. Fabian et al reported that angiography had a sensitivity of 100%, a specificity of 97%, a negative predictive value of 97%, and a positive predictive value of 97% for aortic injury; other studies show similar findings.[28][31]
The angiographic abnormalities indicative of traumatic aortic injury include but are not limited to:
- Dissection, typically visualized as an intimal flap or double lumen within the aorta.
- Pseudoaneurysm, seen as a focal outpouching of the aortic wall.
- Active extravasation or a direct visualization of contrast dye leaking from the aorta, indicating active hemorrhage.
Transesophageal Echocardiography
Transesophageal echocardiography (TEE) can be performed quickly at the bedside, making it useful for hemodynamically unstable patients with suspected aortic injuries. TEE provides real-time diagnostic imaging of the aorta.
Other Imaging Modalities
Intravascular ultrasonography and magnetic resonance imaging (MRI) may be used in specific cases of suspected traumatic aortic injury but are less frequently employed than chest radiography or CTA.
Aortic Injury Grading Classification System
Traumatic aortic injuries encompass a spectrum of severity, reflecting varying degrees of damage to the integrity of the aortic wall. Careful consideration of the injury's severity, the hemodynamic stability of the patient, and any concurrent injuries is crucial when selecting an imaging approach. Timely diagnosis and grading of the injury are essential for guiding treatment strategies and optimizing patient outcomes. The grades of injury correspond to the degree of aortic wall disruption present, with higher grades indicating greater damage and usually necessitating acute intervention (see Image. Aortic Injury Grading Classification). The grading system is valuable in determining the urgency and approach to a traumatic aortic injury. The grading scale classification is:
Traumatic aortic injury grading scale
- Grade I: Intimal tear
- Intimal tears may be observed with CTA or intravascular ultrasound; angiography may fail to identify an intimal tear.
- Grade II: Intramural hematoma or dissection
- These injuries may affect the contour of the aorta.
- Grade III: Pseudoaneurysm
- These affect the aortic contour and are observed with all imaging modalities.
- Grade IV: Complete rupture of the aortic wall [32]
Treatment / Management
Several factors, including aortic injury severity, patient hemodynamic stability, and the presence of concomitant injuries, dictate the management and treatment of a traumatic aortic injury. While grade I injuries are often managed medically, grade II-IV injuries typically require repair to rectify the aortic defect. Although prompt repair of the aortic injury is ideal, other injuries the patient has sustained may require more urgent attention and take priority.
The initial resuscitation of a trauma patient is based on Advanced Trauma Life Support principles of airway, breathing, circulation, disability, and everything else, known as the ABCs of trauma. Any life-threatening condition identified during this assessment should be immediately treated.[33][34][35] Once the patient is stabilized clinically, endovascular or open repair of an identified traumatic aortic injury should be planned as indicated. In a select few cases, evidence suggests potential benefits of delayed repair in terms of overall mortality, albeit with increased complications and prolonged intensive care unit and hospital stays.[36][37] (B2)
Initial Management of a Traumatic Aortic Injury
Following a traumatic aortic injury, medical therapy is paramount in stabilizing patients and mitigating further progression of aortic injury. Aggressive blood pressure control is a cornerstone of management; the preferred intervention is an intravenous beta blocker such as labetalol or esmolol to reduce heart rate and minimize tension on the compromised aortic wall. Additionally, intravenous vasodilators alleviate shear forces acting on the aortic wall.
Indications for Operative Repair
Operative repair is warranted in unstable patients and those with contrast extravasation on CTA, a rapidly expanding mediastinal hematoma, or penetrating aortic injury. Additionally, patients with significant blood return from chest tubes warrant operative aortic repair. Operative repair is required for grades II-IV traumatic aortic injuries. However, nonoperative management is suggested for grade I aortic injuries because intimal hemorrhage may heal spontaneously with and without a partial intimal tear. Operative repairs may be performed via either an open or endovascular technique.
Endovascular repair
The most significant advancement in managing traumatic thoracic aortic injuries has been the widespread adoption of stent grafting, known as thoracic endovascular aortic repair (TEVAR). Endovascular abdominal aortic repair (EVAR) is mainly employed when treating nontraumatic abdominal aortic aneurysms but has also been adopted in some traumatic injury cases. TEVAR and EVAR are innovative approaches that achieve aortic repair by delivering and placing an endograft through the femoral arteries, effectively covering the damaged portion of the aorta and halting further blood loss. Endovascular treatment has emerged as the preferred method for aortic repair, boasting improved perioperative outcomes compared to traditional open surgery.[38] Studies have consistently demonstrated a reduction in mortality rates with endovascular repair; the mortality rate of endovascular repair is 7.2% compared to 23.5% with open surgery. Moreover, studies of patients undergoing TEVAR demonstrate a significantly lower incidence of postoperative complications such as spinal cord ischemia, paraplegia, stroke, and acute kidney injury.[39][40](B2)
The need for repeat interventions following TEVAR in the trauma setting is 1.8%, underscoring the efficacy of this method.[41] As TEVAR and EVAR gain universal acceptance and stent-graft devices continue to evolve, the incidence of complications and the burden of perioperative morbidity and mortality have notably diminished. Since the US Food and Drug Administration approved the first thoracic stent-graft device in 2005, introducing aortic stent grafts has revolutionized surgical strategies for traumatic aortic injury, and endovascular repair has superseded traditional open repair in many clinical scenarios. However, specific anatomical challenges, such as inadequate proximal landing zones or suboptimal femoral artery access sites, may still limit the widespread applicability of endovascular repair.
The TEVAR procedure is typically performed in a hybridized endovascular suite operating room equipped with fixed angiographic imaging and full surgical capabilities if conversion to an open procedure is required. Following anesthesia induction and groin preparation, bilateral common femoral artery access is established using the Seldinger technique. A wire and catheter are advanced to the aortic root to identify the injury via aortogram. A suitable stent-graft device is selected and positioned over a wire. Due to the curvature of the aortic arch, covering the ostium of the left subclavian artery is necessary to achieve adequate apposition at the graft landing zone in 40% of patients.[42] In these cases, delayed carotid subclavian bypass may be indicated. Following stent placement, postdeployment balloon angioplasty may be employed, followed by completion angiography to assess for endoleak. Successful procedures conclude with femoral arteriotomy closure, anesthesia emergence, or transfer for further resuscitation. (B2)
Following TEVAR and EVAR, surveillance is critical to monitor the condition of the repaired aorta. A CTA is typically performed 1, 6, and 12 months after TEVAR or EVAR and annually after that. These regular evaluations help ensure the ongoing health and integrity of the repaired aorta and facilitate the early detection of potential complications.
Open surgical repair
Open repair via left posterolateral thoracotomy remains a management option for traumatic aortic injuries, particularly when anatomical constraints preclude an endovascular repair. The patient is positioned laterally and flexed to optimize visualization of the aorta. After exposing the aorta and aortic arch, clamps are applied distally, and a tube graft is sewn into place proximally and distally. Special attention is given to incorporating the adventitia into the repair to bolster the strength of the aortic wall. Interrupting aortic flow necessitates cardiac bypass via left heart bypass or full cardiopulmonary bypass. Left heart bypass is typically achieved by cannulating the left inferior pulmonary vein and the distal thoracic aorta, ensuring continued perfusion to vital organs, the spinal cord, and lower extremities. If proximal clamping is unfeasible, full cardiopulmonary bypass via the femoral artery and vein cannulation may be necessary, although systemic anticoagulation poses challenges in polytrauma patients. Open repair of a thoracic aortic injury is conducted under mild hypothermia (32-34 °C) to mitigate risks associated with aortic manipulation.
Despite technological advancements and refinements in surgical techniques, open aortic injury repair is associated with significant surgical risks, including high rates of morbidity and mortality.[43] Mortality rates approximate 24%, and the risk of paraplegia is estimated at 19%.[44] While open repair is a valuable option in cases where endovascular repair is impractical, ongoing research is essential to delineate the optimal approach for each patient, considering anatomical suitability and overall clinical condition.
Differential Diagnosis
Potential alternate diagnoses to consider in a patient with a suspected traumatic aortic injury encompass a range of conditions causing chest pain and cardiovascular instability. The differential diagnosis of traumatic aortic injury includes but is not limited to:
Aortic dissection: is secondary to an intimal tear and the formation of a false lumen within the vessel wall. Aortic dissection can present with hemodynamic instability and severe chest pain that may or may not radiate to the back.
Acute coronary syndrome: includes myocardial infarction and unstable angina that can mimic the radiating chest pain of traumatic aortic injury. Electrocardiogram (ECG) changes and cardiac enzyme levels can help differentiate between the 2 conditions.
Pulmonary embolism: may present with sudden chest pain, shortness of breath, and hemodynamic instability. Pulmonary embolism can be mistaken for traumatic aortic injury, especially when the embolism leads to acute aortic dilatation. This diagnosis must be considered, particularly in patients with risk factors such as recent surgery, immobility, or a history of deep vein thrombosis.
Thoracic spine injury: fractures or dislocations of the thoracic spine can cause severe back pain that may radiate to the chest or shoulders. Imaging studies such as CT or MRI can help confirm the diagnosis.
Esophageal conditions: esophageal spasms can cause severe, squeezing chest pain that may mimic the pain associated with a traumatic aortic injury. Esophageal rupture can cause severe chest pain and dysphagia and often occurs in the context of forceful vomiting or esophageal instrumentation. Gastroesophageal reflux disease (GERD) can cause chest pain that may mimic cardiac-related pain.
Anxiety or panic disorder: may manifest with symptoms such as chest pain, palpitations, and shortness of breath.
Musculoskeletal pain: noncardiac causes of chest pain, such as rib fractures, muscle strain, or costochondritis, can present with chest discomfort that may be mistaken for a traumatic aortic injury.
Pneumothorax: a spontaneous or tension pneumothorax can present with sudden-onset chest pain and respiratory distress. Patients may have decreased breath sounds or tracheal deviation. A pneumothorax can be diagnosed with chest radiography or CT.
Pericarditis: pericardial inflammation can cause chest pain. Patients with pericarditis may have an audible friction rub or ECG changes such as diffuse ST-segment elevation or PR depression.
Pleuritis: pleural inflammation can cause sharp chest pain exacerbated by deep breathing or coughing and is commonly associated with viral infections, pneumonia, or connective tissue diseases.
Prognosis
Despite advancements in trauma care, traumatic aortic injuries secondary to blunt or penetrating trauma continue to have a dismal prognosis.[45] The prognosis for these injuries will vary with the injury location and severity, promptness of diagnosis and treatment, presence of associated injuries, type of management employed, and the patient's overall health.
Approximately 80% of patients with a blunt traumatic aortic injury die before reaching the hospital. Of those who survive the initial injury to reach medical care, free aortic rupture is fatal in 95% to 100% of cases; less severe aortic injuries have a mortality rate of 18% to 80%.[42][46] Patients who die with a traumatic aortic injury have high injury severity scores, indicative of severe polytrauma. Risk factors for aortic-related mortality include higher injury severity scores and higher grades of injury.[42]
A review of penetrating traumatic aortic injuries by Demetriades et al. demonstrated an overall mortality of 80.6%, 87.5% for gunshot injuries, and 64.7% for knife injuries. This same review revealed that patients with abdominal aortic injuries were 3 times more likely to survive than those with thoracic aortic injuries (23.9% vs 7.7%).[45]
Blunt and penetrating traumatic aortic injuries present significant risks and require timely intervention; penetrating injuries may have a better prognosis than blunt injuries, provided appropriate treatment is administered promptly. Early recognition, swift transport to a trauma center, and multidisciplinary management involving vascular surgeons, trauma surgeons, and other specialists are essential for optimizing outcomes for patients with any traumatic aortic injury.
Complications
Medical Complications of a Traumatic Aortic Injury
The complications of a traumatic aortic injury can be life-threatening if not promptly recognized and managed. Additionally, delayed complications of traumatic aortic injuries, such as pseudoaneurysm formation or late-onset aortic dissection, may present days to weeks after the initial injury. A high index of suspicion, surveillance, and monitoring are essential to detect and manage these complications, which include but are not limited to:
Aortic rupture: occurs when a complete tear or disruption of the aortic wall leads to a massive hemorrhage into the mediastinum or pleural space. Aortic rupture can rapidly result in hypovolemic shock and death if not treated urgently.
Aortic dissection: an aortic intimal tear secondary to a traumatic injury can create a false lumen within the vessel wall. Aortic dissection can propagate along the length of the aorta, compromising blood flow to vital organs and subsequent ischemia, or can induce catastrophic aortic rupture.
Aortic aneurysm: a localized dilation or bulging of the aortic wall can be prone to rupture, especially if it enlarges over time or if there is ongoing trauma to the weakened vessel wall.
Hemothorax: a severe traumatic aortic injury can cause bleeding into the pleural space, and the accumulation of blood can compromise lung function and lead to respiratory distress if not drained promptly.
Organ ischemia: severe thoracoabdominal aortic injuries can disrupt blood flow to abdominal organs and the lower extremities, leading to ischemic bowel, kidney failure, or limb ischemia if not promptly addressed.
Spinal cord injury: traumatic injuries to the thoracic or thoracoabdominal segments of the aorta can lead to spinal cord ischemia or infarction secondary to interruption of blood flow to the anterior spinal cord, resulting in neurologic deficits or paralysis. Paraplegia is a severe complication of a traumatic aortic injury.
Complications Following Surgical Repair of a Traumatic Aortic Injury
All surgical interventions carry some risk of bleeding, infection, or injury to surrounding tissues. The endografts, or endovascular stent grafts, commonly utilized when repairing a traumatic aortic injury present risks unique to endovascular repair. Preliminary data suggests that 18% of endovascular repairs have a graft-related complication, which may include:
Endoleak: occurs when blood leaks around the endograft, either through incomplete sealing at the proximal or distal attachment sites (type I endoleak), through branch vessels (type II endoleak), through fabric tears or defects in the graft material (type III endoleak), or due to graft migration or kinking. Endoleaks can lead to persistent pressurization of the aneurysm sac, increasing the risk of rupture in the weeks to months following placement. The incidence of endoleak is minimized with proper sizing of the stent graft to the aorta.
Migration: can occur when the device moves from its original placement within the aorta. Migration can lead to endoleaks, device misalignment, or compromise of branch vessel perfusion.
Endograft limb occlusion: occlusion of the branch vessels or visceral arteries arising from the aorta due to the positioning of the endograft limbs can lead to ischemia of affected organs, such as the kidneys, intestines, and spinal cord; spinal cord ischemia can result in paraplegia and occurs in 5% to 10% of patients.[14][47][48][49][50][51] Considerations for minimizing the risk of spinal cord ischemia include the length of time of aortic clamping, the length of covered stent-graft, level of stent-graft deployment, duration of hypotension, distal aortic pressure, and the number of ligated intercostal branches. Several adjunctive measures have been enlisted to decrease the risk of spinal cord ischemia. Placement of a lumbar CSF drain, corticosteroid administration, and induction of hypothermia have been described to minimize the risk of spinal cord ischemia.[52] A less common neurologic complication is stroke secondary to left subclavian coverage.
Infection: occurs less frequently than with open surgical repair, but can lead to sepsis. Infection may be related to intraoperative contamination, hematogenous seeding, or erosion of adjacent structures.
Thrombosis: within the endograft or its branches can cause acute limb ischemia or compromised blood flow to vital organs.
Device fracture or component degradation: the long-term durability of endografts is still being studied, and these complications can lead to endoleaks or device failure.
Access site complications: such as femoral artery injury, hematoma, pseudoaneurysm formation, or access site infection are well-documented.
Deterrence and Patient Education
Implementation of educational strategies to raise awareness of traumatic aortic injuries and their potential prevention includes:
Road Safety Education
Educate patients about the importance of safe driving practices, including adherence to speed limits, wearing seat belts properly, and avoiding distracted driving behaviors such as texting or using mobile phones while operating a vehicle. Emphasize the risks associated with reckless driving and the potential for severe injuries in the event of a collision.
Workplace Safety Training
Provide comprehensive safety training programs to minimize the risk of traumatic injuries for individuals working in high-risk occupations such as construction, manufacturing, or transportation. This may include proper handling of machinery, use of personal protective equipment, and adherence to established safety protocols.
Fall Prevention
Educate patients, particularly older adults, about fall prevention strategies to reduce the risk of blunt trauma resulting from falls. This may involve ensuring adequate lighting, removing hazards at home, using assistive devices such as handrails or grab bars, and participating in strength and balance exercises to improve stability.
Violence Prevention
Raise awareness about the dangers of interpersonal violence and provide resources for conflict resolution and anger management. Encourage individuals to seek help if they are in abusive situations and promote community initiatives aimed at reducing violence and promoting peaceful resolution of conflicts.
Enhancing Healthcare Team Outcomes
When managing traumatic aortic injuries, a multidisciplinary team approach involving physicians, advanced practitioners, nurses, pharmacists, and other health professionals is essential for optimizing patient-centered care, improving outcomes, ensuring patient safety, and enhancing team performance. Physicians, including trauma surgeons, vascular surgeons, and interventional radiologists, possess the expertise to promptly diagnose TAIs, assess injury severity, and determine the most appropriate treatment strategy. Advanced practitioners play a vital role in assisting with patient evaluation, conducting preoperative assessments, and providing postoperative care under the supervision of physicians. Nurses are instrumental in monitoring patients, administering medications, managing hemodynamic stability, and coordinating care throughout the treatment continuum. Pharmacists contribute by ensuring medication safety, optimizing drug therapy, and educating patients and healthcare providers about medication management and potential drug interactions.
Effective interprofessional communication is paramount, facilitating the exchange of crucial information, shared decision-making, and coordinated care planning among team members. Care coordination efforts by case managers, social workers, and other health professionals help streamline the patient's journey from initial evaluation and diagnosis through treatment, rehabilitation, and follow-up care, ensuring continuity and comprehensive support for the patient and their family. By leveraging the interprofessional team's diverse skills, responsibilities, and expertise, healthcare professionals can deliver high-quality, patient-centered care that maximizes outcomes, promotes patient safety, and enhances overall team performance in managing TAIs.
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