Type Iv Thoracoabdominal, Infrarenal, and Pararenal Aortic Aneurysms



Type Iv Thoracoabdominal, Infrarenal, and Pararenal Aortic Aneurysms


Marc L. Schermerhorn

April E. Nedeau



Background

Since the first description of abdominal aortic aneurysms (AAAs) by the 16th-century anatomist Vesalius, the history of this disease has reflected the remarkable progress of vascular surgery. Prior to the development of modern surgical techniques, successful outcomes were rare. Dubost, in 1951, began placing aortic homografts to repair AAA with unacceptable rates of degeneration, calcification, and poor patency rates. In 1967, DeBakey developed the first synthetic graft made out of velour, a knitted elastic textile, and together with Creech and colleagues popularized the current standard surgical procedure, “endoaneurysmorrhaphy with intraluminal graft placement.” This surgical technique remained essentially unchanged for nearly 40 years, until Parodi and colleagues in 1991 reported the first clinical use of endovascular stent graft placement for AAA repair in humans.

The etiology of aneurysms has been historically attributed to atherosclerosis in the majority of cases; however, in recent years researchers have shown that complex molecular and inflammatory interactions and hemodynamic and structural changes within the aortic wall play a significant role. Aneurysmal degeneration of the aortic wall results from destruction of structural matrix proteins and apoptosis of medial smooth muscle cells (SMCs). It is therefore more accurately defined as a degenerative process. The etiology of initial aortic wall injury is unknown, but the combination of genetic polymorphism and environmental insult is probable. Approximately 15% of patients diagnosed with AAA, unrelated to a concomitant connective tissue disorders, have a family history of the disease. Familial inheritance patterns of aneurysm development suggest a genetic component that is supported by genome-wide linkage studies. Susceptibility loci on chromosomes 19q13 and 4q31 have been identified and correspond to genes that express inflammatory cytokines, such as interleukin-15, and proteins that regulate apoptosis. LRP3 is another candidate gene that has generated interest and encodes for low-density lipoprotein (LDL) receptor–related protein-3. LRP1 is a gene in the same family and its knockout mice develop both aneurysms and atherosclerosis.

Atherosclerosis, mechanical stress, and infection make the aortic wall more susceptible to injury, which exposes endothelial antigens and initiates an inflammatory response. Both in vivo studies in mice and examination of human aneurysm specimens in vitro suggest that the initial production of inflammatory cytokines and influx of polymorphonuclear leukocytes is followed by a transition to a chronic inflammatory state, mediated by macrophages and T cells. Macrophage-mediated proteolysis via secretion of matrix metalloproteinases (MMPs), as well as cysteine proteases of the cathepsin family, has been implicated as a key part of the pathophysiology. The secretion and activation of MMP-2, MMP-9, and, perhaps more significantly, the expression of macrophage cell surface MT1–MMP result in the degradation of elastin in the aortic wall media. The degradation of elastin compromises structural integrity and releases by-products or elastin degradation peptides (EDPs) that perpetuate the process by stimulating monocyte chemotaxis. Natural killer cells are also elevated in the circulation of patients with AAAs and have increased cytotoxicity toward aortic SMCs, which are depleted in explanted specimens. The capability to regenerate and remodel the extracellular matrix during ongoing proteolytic destruction may therefore be limited by the depletion of SMCs, resulting in end-stage disease and rupture.

Other well-known factors include chronic dissections, Marfan’s and Ehlers–Danlos syndromes, mycotic aneurysms, Takayasu’s disease, and pseudoxanthoma elasticum. Chlamydia pneumoniae has been found in the AAA wall, indicating a possible infectious origin.


Epidemiology

Largely a disease of white elderly men, the reported incidence is 3 to 117 per 100,000 person-years when based on rates of repair. However, when screening programs are in place, the incidence can be as much as 3.5 per 1,000 person-years in a UK study. In men, AAAs begin to occur after age 50, whereas the onset in women is around 60 years of age. The male-to-female ratio is approximately 5:1. Prevalence may be more accurate than incidence, now that large ultrasound screening studies have been performed, ranging from 3% to 10% for AAA
>3 cm, and 1.4% for AAA >4 cm in patients older than 50. The prevalence of AAAs, in a given population, depends on associated risk factors including older age, male gender, smoking, positive family history, white race, hypertension, hypercholesterolemia, peripheral vascular occlusive disease, and coronary artery disease (Table 1). However, these risk factors are more likely to be markers of the disease, rather than independent predictors. Age, gender, and smoking seem to have the largest independent impact on AAA prevalence. The risk of rupture also increases with age and ranges from 1 to 21 per 100,000 person-years. Overall mortality after rupture is approximately 80%, with three-fourths occurring outside the hospital.








Table 1 Independent Risk Factors for Detecting an Unknown ≥4-cm Diameter AAA During Ultrasound Screening
































































Risk factor Odds ratio 95% CI
Increased Risk    
Smoking history 5.1 4.1–6.2
Family history of AAA 1.9 1.6–2.3
Older age (per 7-yr interval) 1.7 1.6–1.8
Coronary artery disease 1.5 1.4–1.7
High cholesterol 1.4 1.3 to 1.6
COPD 1.2 1.1–1.4
Height (per 7-cm interval) 1.2 1.1–1.3
Decreased Risk    
Abdominal imaging within 5 yr 0.8 0.7–0.9
Deep vein thrombosis 0.7 0.5–0.8
Diabetes mellitus 0.5 0.5–0.6
Black race 0.5 0.4–0.7
Female gender 0.2 0.1–0.5
CI, confidence interval; COPD, chronic obstructive pulmonary disease.


Diagnosis

Most aneurysms are asymptomatic at the time of diagnosis and are found incidentally during diagnostic imaging performed for other reasons, most commonly with abdominal computed tomography (CT) scan, ultrasound, or magnetic resonance imaging (MRI). With physical examination alone, the diagnosis is made in 29% for AAAs 3.0 to 3.9 cm, 50% for AAAs 4.0 to 4.9 cm, and 75% for AAAs 5.0 cm or larger. Although a focused physical examination detected 50% of 3.5- to 6-cm-diameter AAAs, these had all been missed during a nonfocused examination. The positive predictive value of physical examination is 15% for an AAA >3.5 cm. Occasionally, patients present with symptoms, most frequently pain, related to aortic expansion or compression of adjacent structures. When ruptured, patients may present with intense back or flank pain, abdominal distention, hypovolemia, or shock. Pain may occasionally radiate to the groin, mimicking an incarcerated hernia.


Classification

Operative management of AAA is dependent on its anatomic features. There are three major types of aneurysms involving the abdominal aorta: (a) infrarenal aneurysms, which refers to aneurysmal degeneration of the aorta below the renal arteries with an adequate neck for clamp placement below the renal arteries; (b) pararenal aneurysms, which are subclassified as: juxtarenal, which refers to aneurysmal degeneration below the level of the renal arteries without an adequate neck for an infrarenal clamp, necessitating clamp placement above one or both renal arteries to obtain proximal control while the graft is sutured to the infrarenal aorta; or suprarenal, which involves renal artery reimplantation or bypass, due to aneurysm involvement of the renal artery origin; (c) type IV thoracoabdominal aneurysms (TAAAs), which involve the entire abdominal aorta from the diaphragm to the aortic bifurcation.


Surgical Decision Making


Rupture Risk

Treatment of the AAA is dictated by both aneurism size and symptomatology. In an asymptomatic patient, it is imperative to evaluate the individual’s rupture risk, operative risk, and life expectancy. Currently, the best predictor of rupture is aneurysm diameter. Randomized control trials have demonstrated the safety of ultrasound surveillance until AAA diameter exceeds 5.5 cm, and for the majority of patients this is the appropriate course. The United Kingdom Small Aneurysm Trial (UKSAT) and the Aneurysm Detection and Management (ADAM) trial both demonstrated no benefit to early surgery for small 4.0- to 5.5-cm aneurysms. Although the annual rupture risk under surveillance was 1.0% (UKSAT) and 0.6% (ADAM), it was less than the risk of operative mortality in the early surgical groups (5.6% for UKSAT and 2.2% for ADAM). In the UKSAT, fatal rupture occurred in 5% of men and 14% of women undergoing surveillance, suggesting that a lower threshold in women may be appropriate.

The decision to treat must be individualized, as there are other factors that increase rupture risk independent of aneurysm diameter. Rupture risk is increased by female gender, smoking status, rapid expansion (>1 cm/year), hypertension, chronic obstructive pulmonary disease (COPD), family history, eccentric shape, and onset of symptoms or tenderness to palpation of the aorta. Operative risk and life expectancy must also be considered.


Operative Risk

Patients with AAA are elderly and most carry significant comorbidities, which put them at increased risk for complications, including myocardial infarction, bleeding, cerebrovascular accidents, and pulmonary complications. Blankensteijn found that mean operative mortality was 8% and 7.4% in population-based prospective and retrospective studies, respectively, whereas for hospital-based studies it was only 3.8%. Others have reported rates for elective repair of 5% (review by Hallin), 5.6% (UKSAT trial), and 5.3% (Medicare data). The operative mortality for open surgical repair has remained stable since 1980s. However, individual comorbid conditions have been identified as independent predictors for operative mortality, with renal failure, heart failure, and older age being the strongest predictors (Table 2). Standard preoperative evaluation should include an electrocardiogram (ECG), complete blood counts, coagulation panel, chemistries including liver and renal function, and a chest X-ray. According to individual risk factors, evaluation may include a cardiac stress testing and pulmonary function testing with arterial blood gases. Smoking cessation decreases the rate of pulmonary complications. Patients with suprarenal and type IV aortic aneurysms are understandably at a
higher risk than patients with infrarenal aneurysms due to visceral ischemia and increased alterations in cardiovascular physiology. Several risk assessment models are available to predict operative mortality after AAA repair (see Giles et al.).








Table 2 Predictors of Mortality after Endovascular and Open AAA Repair



























































Variable OR 95% CI Pvalue
Open repair (vs. EVAR) 3.2 2.7–3.8 <0.0001
Age (vs. 67–70 yr)      
    71–75 yr 1.2 0.9–1.6 .34
    76–80 yr 1.9 1.4–2.5 <0.0001
    80 yr 3.1 2.4–4.2 <0.0001
Female 1.5 1.3–1.8 <0.0001
Dialysis dependent renal failure 2.6 1.5–4.6 <0.001
Chronic renal insufficiency 2.0 1.6–2.6 <0.0001
Congestive heart failure 1.7 1.5–2.1 <0.0001
Vascular disease (peripheral arterial or cerebrovascular disease) 1.3 1.2–1.6 <0.0001
OR, odds ratio; CI, confidence interval.


Life Expectancy

The primary goal of AAA repair is to prolong life; therefore, the patient’s life expectancy must be considered and discussed with the patient before recommending repair. It is not surprising that the same comorbid conditions that increase the patient’s operative risk also shorten life expectancy. However, patients with short life expectancy may benefit if the risk of rupture is exceedingly high. Patients with AAA have been found to have a decreased life expectancy compared with age- and sex-matched controls. Predictors of late death after successful AAA repair include age, gender, continued smoking, renal, pulmonary, and cardiac disease. Table 3 shows US census data from 1998 that have been adjusted to reflect the life expectancy of an average patient surviving elective AAA repair.








Table 3 Estimating Life Expectancy

















































Age-, Sex,- and Race-Related Life Expectancy for Patients with AAA (yr)
Age Male Female
White Black White Black
60 12 11 14 13
65 11 10 12 11
70 9 8 10 10
75 8 7 9 8
80 6 6 7 6
85 and over 4 4 5 5


Impact of Endovascular Repair

Endovascular aneurysm repair (EVAR) has been associated with decreased perioperative morbidity, mortality, and hospital length of stay, making it a more appealing option for patients who were considered high risk for open repair. Randomized control trials, such as Dutch randomised endovascular aneurysm repair (DREAM), EVAR-1, and more recently open versus endovascular repair (OVER), have demonstrated a lower perioperative morbidity and mortality with EVAR compared with open repair. This perioperative advantage persists as a decrease in late aneurysm-related deaths although there was no significant difference in overall survival at 2 and 4 years. These findings of perioperative mortality and morbidity advantage with EVAR as well as similar late survival were confirmed in US Medicare patients. AAA-related reintervention is more likely after EVAR than open repair due to endoleak, migration, kinking, or thrombosis. The majority of these reinterventions are minor and can be performed as a minimally invasive procedure although occasionally conversion to open repair is required. Late rupture while rare after both EVAR and open repair is more common after EVAR. Lifelong surveillance is therefore required after endovascular repair. However, complications of open surgical repair requiring reintervention, including anastomotic pseudoaneurysm and hemorrhage, graft-enteric fistula, colon ischemia, graft thrombosis, and infection have also been reported and are not insignificant. Additionally, complications of laparotomy that are not graft related, such as abdominal wall hernia and bowel obstruction, are seen more commonly after open repair and may offset the increased AAA-related reinterventions associated with EVAR.

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Aug 2, 2016 | Posted by in GENERAL SURGERY | Comments Off on Type Iv Thoracoabdominal, Infrarenal, and Pararenal Aortic Aneurysms
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