Cath Lab Digest

Introduction
Blunt thoracic aortic injuries (BTAIs) due to a deceleration trauma are highly lethal and remain a therapeutic challenge. BTAIs represent only 10% of all thoracic vascular traumas and usually involve the isthmic portion of the aorta, but up to 80% of patients with acute rupture die at the scene of injury or before reaching the operating room.^1,2 In fact, for patients who survive, prognosis is still poor, because even in a properly-monitored unit, there is a 30% mortality rate within the first six hours and up to a 50% mortality rate within the first twenty-four hours.^3,4 Thus, considerable attention is paid to rapid diagnosis and treatment.

Over the past decades, open surgical repair has been the standard method of treatment since the first description of traumatic injury of the aorta.¹ However, BTAI is rarely a simple injury and patients have severe co-morbidities, making immediate conventional repair problematic, including thoracotomy, one-lung ventilation and anticoagulation. Early postoperative mortality is still reported to range from 7.7–28%.^5-9 More recently, several reports have highlighted excellent results using an endovascular approach for chronic traumatic ruptures of the descending thoracic aorta.^10,11 The main advantages of the endovascular technique include the absence of thoracotomy, aortic cross-clamping and fully intraoperative heparinization.

We report our ongoing experience with emergency SG treatment for the management of patients with BTAI.

Materials and Methods
In the last three years, 35 patients underwent endovascular repair of descending thoracic aorta, including 7 patients (20%) with BTAI after a road-traffic accident (RTA). All were male patients with a median age of 26 years (mean: 26.8 ± 9.2; range 18–45). Glasgow Coma Score (GCS) and injury severity scores (ISS) were 8 ± 5 (range 3–15; median 6) and 42.7 ± 29 (range 4–75; median 50), respectively.

Since 2001, every patient admitted to the Emergency Departement (ED) with suspected BTAI was evaluated for endovascular repair (EVAR). The management team included a senior vascular surgeon and an interventional radiologist. In addition, other personnel (e.g., anesthesiologist, anesthesiology nurses, emergency department staff) were involved as appropriate for both standard management and endovascular approach of acute thoracic aortic rupture. Our protocol involved accepted steps for acute aortic rupture, including blood samples for routine laboratory studies and cross-matched, purified red blood cells, central venous and bladder catheters, a peripheral 14-G vein access, and radial artery cannulation for invasive blood pressure (BP) control. Feasibility for emergency endovascular repair (eEVAR) was assessed, if and when cardiocirculatory stability was present. Assessment was via CT-angiography (CT-A) with 3D reconstructions, carried out with the senior surgeon and the interventional radiologist to immediately confirm the feasibility of the endovascular approach, and an anesthesiologist to control the cardiocirculatory and airway support. CT-A was used to confirm the diagnosis of acute thoracic aortic rupture, assess the feasibility of the endovascular procedure, measure the morphological dimensions, exclude alternative intra-thoracic disease, and complete trauma staging. During the CT-A, the operating room staff was notified. Acute traumatic rupture is defined as disruption of the aortic wall with blood outside the adventitia and mediastinal hematoma (contained rupture) or hemothorax documented by preoperative CT-A.

Location of aortic injury involved the aortic isthmus in all patients, and originated 0.5–4 cm (mean: 1.5 ± 0.5 cm) from the origin of the left subclavian artery (LSA). We detected two kinds of lesions (Figure 1): a contained circular/semi-circumferential transection (n = 5) and a localized intimal disruption (n = 2). All lesions extended 4 to 6 cm (mean: 4.4 ± 0.7) from the origin of the LSA. Suitable morphology for EVAR also included no marked tortuosity or stenosis of the aorto-iliac arteries.

Six out of 7 patients (85.7%) were treated within 48 hours from the RTA. Delay between the RTA and EVAR ranged between 2 hours and 22 days (median: 15). The long delay was mostly due to hemodynamically stable patients (3 cases) who underwent SG placement two days after surgical treatment of concomitant life-threatening lesions. In 4 cases (57%), the procedure was done on the same day as the event because of a severe hemorrhagic shock. The remaining 3 patients were treated between 24 and 72 hours from admission.

Repairs were performed in the operating room with the patient under general anesthesia and endotracheal intubation. A cell-saver system and cardiopulmonary bypass were available in the event that surgical conversion was needed. Inventory of various devices is kept in the operating room to allow for such urgent cases without delay. The fluoroscopic machine (Isocentric mobile C-arm, Siemens, Munich, Germany) was positioned opposite to the first operator; patients were prepared and draped for either femoral arteriotomy or retroperitoneal iliac artery approach, and emergency left thoracotomy. We used autotransfusion (Compact-Dideco®, Modena, Italy) and a fluid protocol [5%-mannitol, dopamine (3g/kg/min) plus N-acetylcysteine (600 mg i.v.)] against the ischemic-related delivery of free-radicals and the renal damage due to the contrast medium. Every patient received a short-term antibiotic prophylaxis with vancomycin (1 gr b.i.d.).