Katherine B. Harrington, MD, and Michael P. Fischbein, MD, PhD
Concept
- Presentation and classification of aortic dissections
- Initial treatment
- Medical versus surgical therapy
- Operative steps for repair
Chief complaint
“A 56 year-old man presents to the ED with sharp, tearing back pain. CT scan shows an aortic dissection extending from just distal to the left subclavian artery to the aortic bifurcation.”
Differential
The diagnosis, aortic dissection, is already known. The dissection must be classified into Type A vs. Type B, acute vs. chronic, and complicated vs. uncomplicated. Dissections are considered “acute” in the first 14 days after development of symptoms. After 14 days dissections are considered “chronic” as patients typically stabilize after this time and are managed under a different algorithm.
There are several anatomic classification schemes for describing aortic dissections. The Stanford system considers all dissections which involve the ascending aorta, i.e., the aorta proximal to the right innominate artery, to be Type A, and those which involve only the descending aorta, i.e., everything distal to the left subclavian, to be Type B dissections. The Debakey classification classifies dissections into three groups. Type I and II include the ascending aorta. In Type I it propagates at least to the aortic arch and often further distally, while Type II is confined to the ascending aorta. Type III originates in the descending aorta is further broken down into Type IIIa (descending thoracic aorta only) and Type IIIb (extending into abdominal aorta).
“Complicated” dissections are those with persistent pain, thoracoabdominal malperfusion (spinal, visceral, and extremity), impending rupture, or other life-threatening complications. The majority of Type B dissections are “uncomplicated.”
History and physical
The most common presenting symptom is abrupt onset, sharp, severe, chest or back pain. Patients tend to be significantly hypertensive when they present. Most patients have a history of long-standing hypertension. Social history should query amphetamine or cocaine use, both risk factors for dissection. A brief skeletal exam should assess for connective tissue disorders, especially in younger patients. A very thorough vascular exam should be documented. Pulse deficits are present in approximately 10% of patients.
Tests
- Initial CXR: mediastinal widening or abnormal aortic contour in 56% of patients.
- Laboratory: serum creatinine, liver function tests, and lactate (evaluate for renal or visercal malperfusion).
- Diagnostic procedures: computed tomographic angiographic scanning (CTA), transesophageal echocardiography, and magnetic resonance angiography. Study interpretation should include dissection classification, extent, primary intimal tear (PIT) location, and presence/absence organ malperfusion. Further information can also be acquired for possible endovascular stent graft insertion including the dimensions of descending aorta, size of true and false lumen, arch branch vessel anatomy, potential landing zones, and femoral/iliac dimensions for access.
Index scenario (additional information)
“Upon further questioning the patient’s pain started this morning. He continues to have severe pain even after his blood pressure is brought to appropriate levels and is requiring a large amount of narcotics.”
Treatment/management
As soon as acute aortic dissection is suspected, emergency medical therapy should be initiated and continued while the diagnostic procedures are performed. Medical treatment includes reduction of mean, peak, and rate of rise in arterial pressure (dP/dt) with both an intravenous (a) B-Blocker (esmolol, labetolol) and (b) vasodilator (nipride). Parenteral calcium channel antagonists, like diltiazem or nifedipine, that lower arterial blood pressure and left ventricular dP/dt can also be used.
For Type B dissections medical treatment results in equal if not better results than surgical repair. Current registry studies show medical management carries a 30-day mortality between 9-16% while surgical management yields an operative mortality of 27-32%, biased by the more complicated patients receiving intervention. Comparative retrospective studies which attempted to match risk adjusted cohorts have shown that long-term survival, as well as freedom from late aortic reintervention, is similar for both medically and surgically treated patients.
Currently, a “complication-specific” approach is recommended, reserving surgical or endovascular intervention on the descending aorta for those with complicated dissections. Other conditions that should prompt consideration of early intervention include extensive aortic arch involvement, expectations of poor medical compliance, and underlying connective tissue disorders.
After determining that an intervention is required, the surgeon must decide between an open versus endovascular approach. Endovascular stent grafts should be considered in patients who are older, poor operative risks (renal failure, COPD, poor cardiac function, acidotic from malperfusion), and have favorable anatomy. Younger patients, good surgical candidates, patients with connective tissue diseases, and patients with unfavorable endovascular stent graft anatomy receive a central aortic operation.
Operative steps
Goals – patients with acute Type B aortic dissection is graft replacement of a limited segment of the descending thoracic aorta, hopefully including the site of the PIT, to restore flow to the true lumen and obliterate flow to the false lumen.
- After insertion of a double-lumen endobronchial tube, and often a lumbar intrathecal catheter for cerebrospinal fluid drainage, patients with acute Type B dissections are explored through a left posterolateral thoracotomy through the third or fourth intercostal space, providing access to the transverse arch and proximal descending aorta. Alternatively, a second entry point into the 7th intercostal space may provide access to the distal thoracic aorta.
- Full cardiopulmonary bypass with antegrade perfusion is preferred. Arterial cannulation strategies include the following: perfusion into the arch, left subclavian artery, left common carotid artery, right subclavian artery, left ventricular apex and across the aortic valve, or femoral artery (perfuse true lumen). Venous return can be accomplished with central venous cannulation via the femoral vein or retrograde cannulation through the main pulmonary artery.
- Hypothermic circulatory arrest is utilized to perform an open proximal anastomosis. Most Type B dissection tears originate at the origin of the subclavian artery; clamping between the left common carotid and left subclavian arteries may be utilized, but frequently results in insufficient length for a proximal anastomosis. If left ventricular distension occurs during systemic cooling and subsequent ventricular fibrillation, the left heart may need to be decompressed with a vent via the left superior pulmonary vein or left ventricular apex. During hypothermic circulatory arrest, myocardial protection is from systemic hypothermia only.
- The phrenic and vagus nerves are identified and dissected free from the transverse arch, with special attention paid to the recurrent laryngeal nerve near the ligamentum and along the posterior proximal aortic neck. The transverse arch, proximal descending thoracic aorta, left subclavian artery, and distal aortic anastomotic site are circumferentially dissected.
- The primary goal is to replace only a short segment of aorta to redirect flow into the true lumen. This strategy allows one to stay above T7 and therefore prevents the need to re-implant intercostal arteries.
- When the goal hypothermic temperature is achieved (18-22° C core temperature), the pump is turned off, and the proximal descending aorta opened. An appropriately sized woven double velour Dacron graft is selected and sewn proximally to undissected aorta with an open technique taking care to excise the entire PIT. If the dissection extends into the arch (retrograde from the PIT), incorporate both the aortic intima and adventitia while performing the anastomosis to obliterate the false lumen. The left subclavian artery may need to be individually reimplanted if the PIT is very close or proximal to the left subclavian artery. Carefully identify the recurrent laryngeal nerve along the proximal aortic neck, especially while transecting the aorta along the posterior wall (common site of nerve injury while performing proximal anatomosis).
- Resume arterial flow to the head and heart slowly (about 500-700 mL/hr) either through the axillary or a perfusion cannula inserted directly into the graft. Replace the cross clamp on the graft after taking care to evacuate any air trapped in the heart or ascending aorta.
- Proximal intercostals arteries (above T7) are oversewn to eliminate steal of blood from the spinal cord.
- The distal anastomosis is also performed with an open technique under circulatory arrest, taking care to incorporate both aortic layers and obliterate the false lumen. Distally, intima and adventitia may occasionally be reapproximated with a Teflon felt media or adventitial bolster. Proximal cross-clamp is released, air is evacuated both proximally and distally prior to tying the sutures, and both anastomoses checked for hemostasis. Systemic rewarming is commenced approximately 10 minutes after reperfusion to allow oxygen debt reversal. After warming to 35-36˚ C, CPB is discontinued. Transesophageal echo should be used to assure perfusion of the true lumen at the level of the diaphragm.
Potential questions/alternative scenarios
“Post-operatively the patient has a rising lactate and creatinine…”
Visceral malperfusion postoperatively should be monitored with urine output and serial lactates/ABGs. Malperfusion results when a dissection compromises blood flow to end-organs and occurs in approximately 21% of dissections. Two pathophysiological mechanisms of malperfusion are commonly described: dynamic and static branch malperfusion. Dynamic branch compromise is the more common mechanism of malperfusion (80%) and occurs when the true lumen is narrowed or compressed due to the majority of flow occurring in the false lumen- this should be alleviated by open repair. Static branch malperfusion occurs when the dissection flap or intimal tear extends into a branch vessel ostium, leading to mechanical obstruction of flow from the intimal intussusception. This may be treated percutaneously with balloon septal fenestration and uncovered stenting in collaboration with an interventional radiologist.
“The patient wakes up and is not able to move his/her legs.”
Paraplegia is a significant risk of any descending thoracic aortic repair (both open and endovascular). Dissection patients have an increased risk, although short segment replacement mitigates this somewhat. Patients with prexisting AAA repair have a higher risk. Pre-operative lumbar drain placement is commonly done, but not required. If it was not done pre-operatively in this patient, it needs to be placed now. If pre-existing, the amount of drainage should be increased and every effort should be made to get the ICP to less than 10, if not as low as possible. However, caution should be used in draining more than 20 mL per hour due to the risk of subdural hemorrhage. MAP should be increased to > 80-90 mmHg with neosynephrine or vasopressin to increase spinal cord perfusion pressure. Several adjunct strategies, such as a naloxone drip may be used, but no data support its benefit. There is no benefit to high dose steroid treatment.
“A similar patient presents but there is no visible flap, just hematoma within the wall of descending thoracic aorta.”
Intramural hematomas (IMH) and penetrating aortic ulcers (PAU) are pathological variants of the classic aortic dissection. Importantly, in contrast to the dissection, neither IMH nor PAU has blood flow down a false lumen. IMH likely results following aortic vasa vasorum rupture, causing hemorrhage into the aortic media. PAU originates from an intimal lesion (ruptured atherosclerotic plaque) that penetrates the aortic media and results in a variable amount of IMH. IMH is treated similarly to a dissection. Emergent anti-impulse therapy should be initiated.
“A patient with a previously uncomplicated Type B dissection several years ago returns with pain and a descending thoracic aorta that has now grown to 7 cm.”
All patients with acute Type B dissections should have serial CT scans at 3 months, 6 months, and then yearly to monitor for aneursymal development of the dissection. Surgical intervention for chronic Type B dissections may be considered for both symptomatic patients (pain, mesenteric ischemia) and asymptomatic patients (rapidly expanding or > 6 cm aneurysmal aortic dissections). The techniques utilized are identical to those for an acute Type B dissection, although the extent of resection is usually greater (remove all enlarged aorta) (Refer to descending aneurysm section). Importantly, prior to performing the distal anastomosis, a “tongue” of chronic dissection flap is excised from the aorta- a “flap septectomy,” allowing blood flow into both true and false lumens distally (visceral or iliac arteries may originate from either true or false lumens). Surgical resections distal to T-7 may require reimplantation of large intercostal arteries to avoid spinal cord ischemia.
Pearls/pitfalls
- Type B dissections involve the descending aorta. Current management for acute dissections involves aggressive anti-impulse blood pressure therapy with a beta blocker and vasodilator.
- Surgical or endovascular management is generally reserved for “complicated” dissections: those with persistent pain, refractory hypertension, thoracoabdominal malperfusion (spinal, visceral, and extremity), impending rupture, or other life-threatening complications.
- Endovascular stent grafting is reserved for elderly or non-operative candidates. Younger patients or those with connective tissue disorder should reccieve an open central aortic operation, if indicated.
- The goal of surgical treatment is graft replacement of a short segment of the descending thoracic aorta, including the site of the PIT, to restore flow to the true lumen and obliterate flow to the false lumen.
- Circulatory arrest with axillary cannulation is the simplest way to deal with the proximal and distal anastamosis.
Suggested readings
- Hagan PG, Nienaber CA, Isselbacher EM et al. The International Registry of Acute Aortic Dissection (IRAD): new insights into an old disease. JAMA 2000 February 16;283(7):897-903.
- Umana JP, Lai DT, Mitchell RS et al. Is medical therapy still the optimal treatment strategy for patients with acute Type B aortic dissections? J Thorac Cardiovasc Surg 2002 November;124(5):896-910.
- Suzuki T, Mehta RH, Ince H et al. Clinical profiles and outcomes of acute Type B aortic dissection in the current era: lessons from the International Registry of Aortic Dissection (IRAD). Circulation 2003 September 9;108 Suppl 1:II312-II317.
- Ehrlich MP, Dumfarth J, Schoder M et al. Midterm results after endovascular treatment of acute, complicated Type B aortic dissection. Ann Thorac Surg 2010 November;90(5):
1444-8.
