Ascending aortic aneurysms are the most common (~60%) thoracic aortic aneurysm (TAA) followed by aneurysms of the descending aorta (~35%) and of the transverse aortic arch (< 10%). Most descending TAAs begin just distal to the orifice of left subclavian artery.7
Most TAA are clinically silent; with nontraumatic TAAs detected as incidental findings on chest imaging obtained for other purposes. A minority of patients may present with chest discomfort or pain that intensifies with aneurysm expansion or rupture, aortic valvular regurgitation, congestive heart failure, compression of adjacent structures (recurrent laryngeal nerve, left main-stem bronchus, esophagus, superior vena cava), erosion into adjacent structures (esophagus, lung, airway), or distal embolization.
Chest X-ray reveals widened mediastinum or an enlarged calcific aortic shadow. Traumatic aneurysms may be associated with skeletal fractures. MR or CT imaging with intravenous (IV) contrast provides precise estimation of the size and extent of aneurysms and facilitates surgical planning (refer to Figure 56–2 for CT evidence of a contained TAAA rupture). Echocardiography may be useful in evaluating aneurysms involving the aortic arch.
Contained thoracoabdominal aortic aneurysm rupture.
Options include open repair and thoracic endovascular aneurysm repair (TEVAR). Surgical management varies based on type and location of TAA. Repair of proximal arch aneurysms requires cardiopulmonary bypass and circulatory arrest. Ascending and transverse arches are repaired through a median sternotomy incision. Descending and thoraco-AAAs (TAAAs) are approached through a left posterolateral thoracotomy or thoracoabdominal incision.
Endovascular management of descending TAA: Because of the considerable morbidity and mortality associated with surgical repair of descending thoracic aneurysms, the endovascular approach to aneurysm exclusion is preferred for isolated descending thoracic aneurysms. Newer technologies are being developed for management of TAAA.
Both open surgical repairs and EVAR are associated with a wide variety of complications ranging from major organ system dysfunction to procedure specific localized complications carrying significant morbidity and mortality.
Cardiac derangements manifest as fatal arrhythmias and myocardial infarction. Myocardial infarction is the most common cause of death following major vascular surgery. Troponin I is a consistent predictor of increased cardiac events and increased mortality following vascular surgery.
Respiratory compromise requiring mechanical ventilation might be needed as a complication secondary to cases with significant intraoperative hemorrhage with ensuing fluid shifts and noncardiogenic pulmonary edema. Respiratory complications are also common due to a history of smoking, COPD, and heart failure.
Acute renal insufficiency negatively impacts hospital length of stay and mortality, with an incidence of 1% to 23% post-EVAR (lower compared to that of open repair).8 The likely pathophysiology of AKI in EVAR is complex with multiple probable implicated mechanisms—contrast-induced nephropathy, renal microembolization, and acute tubular necrosis. Among the several preventive strategies for AKI, hydration is the mainstay of prevention as it ameliorates the effect of contrast and oxidative stress and increases renal perfusion. Hydration is of crucial importance in ruptured EVAR to correct the associated hypovolemia and decrease the effect of the pronounced oxidative stress onto the kidney. One may also consider the use of NAC or bicarbonate (there is a need for further rigorous clinical trials and studies to validate these 2 measures). Again, these are very relevant in ruptured AAAs where oxidative stress is more significant.
Abdominal compartment syndrome (ACS) is defined by the World Society of Abdominal Compartment Syndrome as intra-abdominal pressure greater than 20 mm Hg with new organ dysfunction. Intra-abdominal hypertension (IAH) is defined as intra-abdominal pressure greater than 12 mm Hg. ACS results in significant cardiac, renal, and respiratory compromise. It is suggested that large retroperitoneal hematoma and diffuse visceral edema postoperatively contribute to the development of IAH/ACS. Intra-abdominal hypertension is noted to be an important risk factor for colonic hypoperfusion and ensuing ischemic colitis after ruptured AAA repair.9 Monitoring of IAP may be associated with improved mortality postruptured AAA repair treated with open surgery or EVAR.10
Intra-abdominal pressures are measured by intermittent or continuous bladder pressure measurement with urethral catheterization. The definitions of the WSACS are used as the diagnostic criteria for both IAH and ACS.
The major pathophysiologic consequences of ACS are listed as follows:
Decreased preload—compression of IVC
Increased afterload—aortic impedance, decreased stroke volume
Decreased extra thoracic compliance—increased shunt fraction, dead space, transalveolar pressures
Hypoperfusion—hepatic, splanchnic dysfunction
Increased transmitted intracerebral pressure
Cessation of renal filtration gradient
Successful outcomes depend on early recognition and management to reduce IAH. Decompressive laparotomy should be used if conservative treatments fail or if the clinical picture warrants decompression (see Table 56–1 for medical management of IAH).
Table 56–1Medical management of intra-abdominal hypertension. ||Download (.pdf) Table 56–1Medical management of intra-abdominal hypertension.
|Conservative Medical Management of Elevated Intra-abdominal Hypertension Include |
|Insertion of gastric and rectal decompressive tubes |
|Administration of promotilic/kinetic GI agents |
|Percutaneous drainage of fluid collections |
|Optimize sedation and analgesia |
|Consider neuromuscular blockade |
|Consider using reverse Trendelenburg position |
|Remove abdominal constrictive bandages/dressings |
|Prevention of positive fluid balance after initial resuscitation |
|Diuresis or ultrafiltration |
|Use of hypertonic crystalloids or colloids to expand intravascular compartment |
|Goal directed resuscitation |
|Successful outcome depends on early recognition, early conservative treatment to reduce IAH and decompression laparotomy if ACS develops. |
Hypertension—Even brief episodes of hypertension can disrupt suture lines in open surgery and can precipitate bleeding or pseudoaneurysm formation. At the same time, hypotension, after TAA repair, can lead to spinal cord ischemia. Hence it is a delicate, fine balancing act in these cases to maintain mean arterial blood pressure between 80 and 100 mm Hg. Use of IV nitroprusside, IV beta blockers, or IV calcium channel blockers in cases of hypertension in the first 24 to 48 hours may be needed.
Spinal cord ischemia (SCI)—Surgical and endovascular repair of thoracoabdominal aneurysm is associated with a significant risk of spinal cord ischemia at the rate of 5% to 21%.11 More common with TAAA and TAA than with AAA, but can occasionally be seen with high AAA or AAA in the setting of prior TAA. The etiology is likely multifactorial involving interference with cord blood supply, prolonged intraoperative hypotension, extended aortic cross-clamping time and aortic embolization. None of these are, however, solely responsible for SCI. The spinal cord depends on more than the artery of Adamkiewicz for perfusion; it relies on a complex network of flow from the vertebral arteries, intercostal arteries, lumbar arteries, and hypogastric arteries. Classical symptoms are lower extremity sensory and motor deficits with bowel/bladder incontinence with conservation of vibration and proprioception sense. SCI can also be seen after TEVAR. The subset of this population that remain at a higher risk are as follows: prior history of aortic surgery, a previous stent graft placement, aortic graft covering more than 20 cm, aortic graft covering the subclavian artery without revascularization, and graft placement in the high-risk zone between T8 and T12.
All patients at a high risk for spinal cord ischemia should be strongly considered for prophylactic CSF drainage with a CSF lumbar catheter placed in the preoperative period to optimize spinal cord perfusion.12 CSF is drained to achieve target pressures of 10 to 12 mm Hg. The MAP is maintained between 80 and 100 mm Hg to optimize the spinal cord perfusion pressure13 (MAP – CSF pressure = spinal cord perfusion pressure).
However, patients who develop clinical features suggestive of cord ischemia should have prompt elevation of the blood pressure to maintain mean arterial pressures between 80 and 100 mm Hg using crystalloids, colloids or even vasopressors such as phenylephrine. These patients should then have an emergent CSF drain placed if a preoperative drain is not in place.
Acutely, an initial 20 cc of CSF is drained and opening pressure should be checked. Subsequently 10 cc of CSF is drained every 1 hour to achieve a target spinal fluid pressure of 10 to 12 mm Hg. Careful monitoring of the CSF pressures with intermittent drainage should be done in the ICU to minimize the risk of subdural hematoma. Overaggressive drainage can result in intracranial hemorrhage and/or herniation (see Table 56–2 for management of spinal cord ischemia).
Table 56–2Management of spinal cord ischemia. ||Download (.pdf) Table 56–2Management of spinal cord ischemia.
|Management of Spinal Cord Ischemia |
|Symptoms of acute spinal cord ischemia (lower extremity sensory/motor deficits or bowel/bladder incontinence) |
|Maintain MAP between 80-100 mm Hg (with crystalloids/colloids/pressures) |
|Place emergent lumbar CSF catheter |
|Drain 20 cc CSF and check opening pressure |
|Subsequently drain 10 cc/h until you achieve opening pressure of 10-12 mm Hg |
Optimizing spinal cord perfusion has been shown to result in marked clinical improvement if implemented early.