Thoracic Aortic Aneurysm




Abstract


Morbidity and mortality related to thoracic aortic aneurism repair remains high despite advances in endovascular and open techniques. TAA patients are older, carry multiple comorbidities, and present with unique pathologic anatomy. Careful consideration of each patient’s anatomy, surgical plan, and risk profile can help the anesthesiologist optimize a patient’s outcome. Intraoperative and immediate postoperative management have a major impact on nearly all patient outcomes.




Keywords

aortic aneurysm, dissection, paraplegia, renal failure, TAAA

 




Case Synopsis


An 80-year-old man with previous abdominal aortic aneurysm (AAA) repair presents with abrupt-onset back pain starting 1 hour ago. He is alert, diaphoretic, tachycardic, and hypertensive. He is given oxygen, nitroglycerin, and morphine. He was found to have a dissecting thoracoabdominal aortic aneurysm (TAAA) on a computed tomography (CT) scan. There is absence of blood flow to the left kidney. Large peripheral intravenous access was placed, and with blood pressure control his pain resolved. He has multiple medical problems including hypertension, chronic obstructive pulmonary disease (COPD), chronic kidney disease, and diabetes.




Problem Analysis


Definition


Serious aortic disease falls into four categories: aneurysm, dissection, rupture, and coarctation. Coarctation, narrowing of the aorta, is typically a pediatric disease recognized and treated before adulthood. Recurrent stenosis and proximal aneurysm may require intervention in adulthood. Arteritis, atherosclerosis, and trauma may rarely give rise to acquired coarctation.


Congenital diseases that contribute to aortic pathology are the inherited connective tissue disorders: Marfan, Ehlers Danlos, and Loyes Dietz syndromes and others. These diseases weaken the aortic wall structure producing aneurysm, dissection, and rupture. Other diseases associated with TAAA include hypertension, smoking, polycystic kidney disease, steroid use, and arteritis (syphilis, giant cell, Behçet disease). Aneurysm is usually defined as an aortic dilation to a diameter greater than 4.5 cm or more than twice its normal size. Aneurysms may be true, if they contain all three layers (intima, media, adventitia), or false. Aneurysms are classified by the Crawford classifications ( Fig. 79.1 ). TAAA is a progressive disease with a growth rate of 0.05 to 0.3 cm per year depending on the size and cause. As aneurysms grow, wall tension and risk of rupture increase via the law of LaPlace. Aneurysms occur following half of acute dissections.




Fig. 79.1


Crawford classification of aortic aneurysms.

From Norris EJ, Frank SF: Anesthesia for vascular surgery. In Miller RD, editor: Anesthesia, 5th ed. Philadelphia, Churchill Livingstone, 2000, p 1870.


Aortic dissection is a disruption in the aortic wall such that blood is pumped from the true lumen into a false lumen created within the medial or adventitial layers. If the lesion extends through the adventitial layer, an aortic rupture has occurred. This false channel is separated from the true lumen by an intimal flap. Without an outflow track, any blood entering the false lumen causes the dissection to extend. As the false lumen grows, it compresses the true lumen, and may disrupt blood flow to branch arteries.


Dissections are defined by the DeBakey and Stanford classifications ( Fig. 79.2 ). Rupture or dissection is the eventual result of progressive aneurysm. Dissections may be simple or complicated. Complicated dissection produces malperfusion to organs or limbs, or unrelenting pain despite control of hemodynamics.




Fig. 79.2


DeBakey (types I, II, IIIA, and IIIB) and Stanford (types A and B) classifications of aortic dissection.

From Ibe R, Baig K, Chukwuemeka A: Surgery of the thoracic aorta. Surgery [Oxford] 30[1]:28-31, 2012.


Aortic rupture, with or without previous aneurysm, is seen spontaneously, with vigorous activity, or with deceleration injury. Iatrogenic rupture may occur during reparative manipulation or rarely from manipulation of the airway during intubation. Aortic rupture represents failure of the entire thickness of the aorta such that blood is pumped directly into the adjacent space. Rupture is frequently fatal but may be contained before exsanguination by adjacent structures, hematoma, or rising compartment pressures.


Recognition


Rapid and specific diagnosis can be lifesaving. Untreated, the mortality rate is 1% per hour and 50% at 48 hours. Missed diagnosis may occur in up to 38% of acute aortic presentations because of its rarity and variable symptoms that mimic more common diseases (coronary artery disease, cholecystitis, pyelonephritis). Presenting symptoms of dissection are listed in Table 79.1 . Patients rarely present classically with ripping, migratory back pain, hypotension, and malperfusion syndromes. Many aneurysms are found incidentally. Large thoracic aneurysms may present with hoarseness, dysphagia, dyspnea, or arrhythmia.



TABLE 79.1

Signs and Symptoms of Acute Dissection
































Diagnosis Postmortem b 28%
Neurologic Paraplegia a 3%
Syncope b 13%
Pain free b 6%
Cardiovascular Chest/back pain a 85%
Hypotension a Type A: 27%
Type B: 3%
Abdominal pain only b 5%
Renal Acute kidney injury a 60%

a Gallo A, Davies RR, Coe MP, et al: Indications, timing, and prognosis of operative repair of aortic dissections. Semin Thorac Cardivasc Surg 17:224-235, 2005.


b Tsai TT, Trimarchi S, Nienaber CA: Acute aortic dissection: perspectives from the International Registry of Acute Aortic Dissection (IRAD). Eur J Vasc Endovasc Surg 37:149-159, 2009.



Imaging is an important tool for rapid and specific diagnosis. Acute management requires information about anatomic extent, localization, perfusion of branch arteries, effusions, rupture, and tamponade. Demonstration of an intimal flap is diagnostic for dissection. Noninvasive imaging has replaced aortography for diagnosis. Currently, contrast CT is the tool of choice because it is noninvasive, fast, and available in most centers. Magnetic resonance imaging (MRI) does have incrementally greater specificity than CT imaging but is not universally available, takes longer, and has increased cost. Widened mediastinum on chest x-ray is neither sensitive nor specific to dissection but may help raise the index of suspicion in symptomatic patients. Transesophageal echocardiography (TEE) holds specificity on par with CT and MRI. TEE is frequently used intraoperatively to locate the proximal flap, to assess operational success, to identify correct wire-guided access of the true aortic lumen for distal circulatory support devices (DCS), and to guide hemodynamic management. Transthoracic echocardiography is not well suited for diagnosis of TAAA.


Risk Assessment


At baseline patients carry multiple comorbidities ( Table 79.2 ). In nearly every reported series there is a theme that older, sicker patients, with hemodynamic instability at any point perioperatively, perfusion deficits on presentation, and those in need of emergent or prolonged operations do much worse than the overall data suggest. Crawford II and III patients tend to be older, with more extensive disease and comorbidity, and have the worst outcomes. Annual risk of rupture increases with size from 5% at 4 cm, 6% at 5 cm, and then exponentially to 14% at 6 cm.



TABLE 79.2

TAAA/Dissection Baseline Demographics
















































Transient ischemic attack a 15%
Stroke b 5%
Intracranial hemorrhage b 2%
Male c 66%
Hypertension a , c , d 70%–80%
Prior computed tomography surgery c 16%–21%
Prior dissection or aneurysm with repair c , e 2%–25%
Coronary artery disease a , c , d 40%–70%
Coronary artery bypass graft or stenting a 33%
Recent cocaine c 0.5%–37%
Hyperlipidemia a 43%
Smoking a 63%
Chronic obstructive pulmonary disease a , d 33%–41%
Chronic renal failure (Creatinine ≥1.5) a , d 14%–18%
Diabetes mellitus a , c 4%–7%

a Kulik A, Castner CF, Kouchoukos NT: Outcomes after thoracoabdominal aortic aneurysm repair with hypothermic circulatory arrest. J Thorac Cardiovasc Surg 141:953-960, 2011.


b Estrera AL, Miller CC, Goodrick J, et al: Update on outcomes of acute type B aortic dissection. Ann Thorac Surg 83:S842-S845, 2007.


c Tsai TT, Trimarchi S, Nienaber CA: Acute aortic dissection: perspectives from the International Registry of Acute Aortic Dissection (IRAD). Eur J Vasc Endovasc Surg 37:149-159, 2009.


d Hnath JC, Mehta M, Taggert JB, et al: Strategies to improve spinal cord ischemia in endovascular thoracic aortic repair: outcomes of a prospective cerebrospinal fluid drainage protocol. J Vasc Surg 48:836-840, 2008.


e Baril DT, Carroccio A, Ellozy SH, et al: Endovascular thoracic aortic repair and previous or concomitant abdominal aortic repair: is the increased risk of spinal cord ischemia real? Ann Vasc Surg 20:188-194, 2006.

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Feb 18, 2019 | Posted by in ANESTHESIA | Comments Off on Thoracic Aortic Aneurysm
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