Blunt Thoracic Aortic Injury and Contemporary Management Strategy

Thoracic aortic injury (TAI) is a leading cause of death in blunt chest trauma. Motor vehicle collisions are the commonest cause, and most patients die before receiving medical attention. Survivors who make it to the hospital also typically have other debilitating injuries with high morbidity. It is imperative to understand the nature of these injuries and implement current management strategies to improve patient outcomes. A literature review on contemporary management strategies on blunt thoracic aortic injuries was performed to evaluate the available evidence using online databases (PubMed and Google Scholar). We found that there has been an improved survival owing to the current advancement in diagnostic modalities, the use of contrast-enhanced computed tomography angiography, and contemporary management techniques with an endovascular approach. However, careful assessment of patients and a multidisciplinary effort are necessary to establish an accurate diagnosis. Minimal aortic injuries (intimal tear and aortic hematoma) can be managed medically with careful monitoring of disease progression with imaging. Endovascular approaches and delayed intervention are key strategies for optimal management of high-grade TAI.

A Technique for Safe Redo Sternotomy in Patients with Aortic Proximity to the Sternum

The risk of redo sternotomy is greatly elevated in the setting of aortic proximity to the sternum. Current strategies to avoid catastrophic neurologic injury upon sternal reentry include establishment of peripheral bypass with the use of deep hypothermia and low-flow bypass, both of which may increase risk of neurologic complications. Here, we describe a technique for safe sternal reentry and illustrate its successful use in a patient with close proximity of the aorta to the sternum. With this technique, peripheral cardiopulmonary bypass is established prior to sternal reentry via cannulation of the right axillary artery and femoral vein, and the patient is cooled as the innominate artery is dissected, mobilized, and controlled. This permits the rapid institution of selective antegrade cerebral perfusion (SACP) in the event of aortic injury during sternal reentry. Once the innominate artery is isolated and SACP is initiated, one can safely complete the redo sternotomy, dissection, and distal ascending aortic cross-clamping to continue the operation without interruption in cerebral blood flow. This technique offers a safe approach in select patients and should be utilized in similar high-risk cases.

Thoracic Endovascular Aortic Repair for Iatrogenic Injury of the Thoracic Aorta

Purpose: Address iatrogenic injury to the descending thoracic aorta by breached spinal screws through a novel approach of concomitant spinal screw removal and thoracic endovascular repair (TEVAR) placement. Case Report: A 36-year-old female with idiopathic scoliosis underwent T4 to L3 bilateral pedicle instrumentation with spinal fusion and correction of scoliosis deformity. Ten months post-operative, she continued to complain of mid-thoracic pain; computed tomography (CT) angiography revealed protrusion of the left T5 and T6 transpedicular screws into her descending thoracic aorta by 3 and 5 mm, respectively. She was taken to the odds ratio (OR) in a combination case with vascular and neurosurgery. Positioned in the right lateral decubitus position, TEVAR was successfully deployed while neurosurgery concurrently removed the invading spinal screws via posterior spinal exposure. Neurosurgery then completely revised the spinal hardware during the same operation. The patient progressed well throughout the remainder of her hospital stay and was discharged on postoperative day 4. Two-year angiography demonstrated a well-placed TEVAR with no extravasation or aortic abnormality. Conclusions: In the setting of iatrogenic aortic injury due to pedicle screws, concomitant TEVAR and spinal screw removal is a safe and feasible treatment option that allows for spinal reconstruction to occur without multiple trips to the operating room.

Aortic Impingement in Displaced Traumatic Spine Fracture with Complete Spinal Cord Transection: A Case Report

Aortic impingement associated with traumatic thoracic spinal fractures is a rare and potentially lethal complication that creates management challenges in an already complex clinical problem. Traumatic aortic injury is one of the leading causes of death in blunt trauma. Magerl divided thoracic and lumbar fractures into 3 categories; the primary focus of this report, type C fractures, describes rotational injury and is one of the less common types, especially associated with aortic impingement as such. In this case, a young man was admitted following a near-fatal fall resulting in blunt force trauma to the midthoracic region. Emergency CT revealed a type C complete transection at the level of T11 and a grade I aortic injury. Definitive fixation of the spinal injury was delayed in favor of preventing further vascular injury by prioritizing the securing of hemodynamic stability. In traumatic thoracolumbar injuries, blunt traumatic aortic injury is often managed conservatively. However, blunt thoracic aortic injury is one of the leading causes of death from trauma, and each case requires its own case-by-case multidisciplinary management. In this occasion, management of the vascular insult was paramount to ensuring patient survival and favorable outcome.

Neuraminidase 1 Exacerbating Aortic Dissection by Governing a Pro-Inflammatory Program in Macrophages

Inflammation plays an important role in aortic dissection (AD). Macrophages are critically involved in the inflammation after aortic injury. Neuraminidases (NEUs) are a family of enzymes that catalyze the cleavage of terminal sialic acids from glycoproteins or glycolipids, which is emerging as a regulator of macrophage-associated immune responses. However, the role of neuraminidase 1 (NEU1) in pathological vascular remodeling of AD remains largely unknown. This study sought to characterize the role and identify the potential mechanism of NEU1 in pathological aortic degeneration. After β-aminopropionitrile monofumarate (BAPN) administration, NEU1 elevated significantly in the lesion zone of the aorta. Global or macrophage-specific NEU1 knockout (NEU1 CKO) mice had no baseline aortic defects but manifested improved aorta function, and decreased mortality due to aortic rupture. Improved outcomes in NEU1 CKO mice subjected to BAPN treatment were associated with the ameliorated vascular inflammation, lowered apoptosis, decreased reactive oxygen species production, mitigated extracellular matrix degradation, and improved M2 macrophage polarization. Furthermore, macrophages sorted from the aorta of NEU1 CKO mice displayed a significant increase of M2 macrophage markers and a marked decrease of M1 macrophage markers compared with the controls. To summarize, the present study demonstrated that macrophage-derived NEU1 is critical for vascular homeostasis. NEU1 exacerbates BAPN-induced pathological vascular remodeling. NEU1 may therefore represent a potential therapeutic target for the treatment of AD.