In general, the management of vascular injury can be categorized into surgical or medical. Surgery can be approached via an open or endovascular modality. The mainstays of medical management are supportive care, anticoagulation, and hemodynamic control.
Preoperatively, transesophageal echocardiography may be performed to assess the extent and type of injury and anti-impulse therapy with short-acting β blockade and potentially vasodilatory drugs should be started. Anti-impulse therapy has been shown to reduce in-hospital aortic rupture rates without adversely affecting the outcome of other injuries.
Conventional open repair of contained aortic rupture, elective aneurysm treatment, or traumatic aortic disruption with interposition grafting is the standard with which all other management strategies should be compared. Traditionally, simple aortic cross-clamping has been used, but more contemporary practice using extracorporeal lower body perfusion techniques lower the rate of paraplegia, which is as high as 30% with simple "clamp and sew" techniques with cross-clamp times longer than 30 minutes. Paradoxically, it is possible that young trauma victims have not developed significant vascular collateral flow and, therefore, are thought to be at higher risk of organ dysfunction distal to the aortic clamp site.
The spinal cord blood supply is through the anterior and posterior spinal arteries. The anterior two-thirds of the spinal cord is supplied by the anterior spinal artery arising from radicular and medullary branches of the posterior intercostal arteries off the aorta. The anterior spinal artery is well developed in the upper thorax and receives collateral flow from the left vertebral artery and the internal mammary artery through the intercostals, whereas in the lower thorax and abdomen, it is more dependent on collateral flow that it receives from the intercostals and lumbar arteries at these levels. The artery of Adamkiewicz comes off the aorta at approximately the level of the first lumbar vertebra (with much variation around T8 to L4) and is essential for the blood supply to the spinal cord in at least 25% of patients. Risk factors for postoperative paraplegia include increased cross-clamp time, the length of the aorta excluded, low distal perfusion pressure, systemic hypotension, the number of intercostal arteries ligated, increased body temperature, and increased cerebrospinal fluid pressure.
In addition to lower-body perfusion, several adjunctive measures can be used to reduce the risk of spinal cord ischemia during the management of thoracic aortic surgery, such as motor or somatosensory evoked potentials, lumbar cerebrospinal fluid drainage, and hypothermia. These modalities should certainly be considered in the perioperative care of these patients. Aside from the spinal cord, organ beds distal to the cross-clamp are also affected, most notably the mesentery, the kidneys, and the lower extremities. Monitoring of renal function, acid-base, liver enzymes, creatine kinase, arterial lactate, and serial examinations of the abdomen and lower extremities along with a low index of suspicion for abdominal compartment syndrome should be considered in the postoperative care plan.
Thoracic Endovascular Aortic Repair (TEVAR)
There are currently many reports of the efficacy of TEVAR for acute traumatic aortic disruption. Experience gleaned from the selective use of TEVAR in the repair of thoracic aortic aneurysms in high-risk patients has transformed the management of traumatic thoracic aortic injuries. Endovascular repair is the preferred management modality in many institutions. Although the long-term durability of these grafts in this younger subset of trauma patients is unknown, the accepted risk of chronic complications is offset by the benefits afforded by a less-invasive, less time-consuming technique where the added potential morbidity of an open repair is avoided.26
Complications occurring after TEVAR include endoleak, stent-graft collapse, stroke, embolization, bronchial obstruction, migration, paralysis, dissection, or rupture. Endoleaks are categorized as type I (leak around the proximal or distal end of the graft); type II (leak from an artery excluded by the graft that perfuses the vessel in a retrograde fashion between the wall of the aorta and the graft); type III (leak between modular components); and type IV (failure of graft integrity).
Three days after undergoing endovascular graft repair of the proximal descending aorta, the patient appears to be doing well. He is extubated, and his lumbar spinal drain has been removed. Over the course of the next 12 hours, he develops a metabolic acidosis as well as hypotension, requiring vasopressor therapy and volume resuscitation. The nurse informs you that the patient has had three episodes of melena.