Abdominal Aortic Aneurysm Presenting as Back Pain to a Chiropractic Clinic: A Case Report

Pathophysiology of Aneurysm 

Abdominal aortic aneurysm represents a common chronic degenerative disease of the aortic wall.2 The incidence of AAA worldwide is increasing, especially among the older population. Historically, the most frequent cause of AAA was atherosclerotic changes in the vessel wall.1 Newer theories suggest that AAA development involves several factors that decrease the integrity of the anatomical structure of the aortic wall. Degenerative vascular disease accounts for more than 90% of all infrarenal AAA.

The fundamental histopathologic change in the AAA is the degeneration of the arterial media. The media consist of closely packed layers of smooth muscle cells in association with elastin and collagen. Elastin provides elasticity to the vessel wall, although collagen provides the mechanical strength, and limits the amount of distension and prevents disruption. Chronic inflammation and enzymatic degradation of elastic lamellae and extracellular matrix proteins constitute the most prominent pathophysiological characteristic of AAA.2, 4 There is mounting evidence that matrix metalloproteinases (MMPs) are the predominant proteinases in the AAA wall. These enzymes therefore represent a potential target for therapeutic intervention to modify vascular pathology.

In AAA, the media of the aortic wall thin, and only fragments of smooth muscle cells, collagen, and elastin fibers remain. There is 36% elastin in the normal aortic wall, whereas the aneurysmal wall has only 8%.1 There is also a reduction of collagen content in the media of the aneurysmal wall. Abnormal proteolytic enzymes are responsible for elastin and collagen synthesis and degradation. Several types of cells are competent at producing elastases; in humans, however, only the polymorphonuclear neutrophils and macrophages can produce elastases in large quantities. Elastases and collagenase are part of an enzyme complex secreted in inflammatory conditions. Plasmin is a part of that complex and plays an important role as an activator of proelastases and procollagenases. A parietal thrombus within the aneurysmal wall is a rich source of plasmin. In addition, plasmin increases the effects of a sublesional dose of elastase and the production of an aneurysm. Leukocyte accumulation in the aneurysmal tissue is presumed to be stimulated by secretion of specific cytokines such as interleukin (IL) 8 and monocyte chemoattaractant protein–1, which have been detected by immunocytochemistry in the AAA.4, 5, 6, 7 Other proinflammatory cytokines such as IL-1, IL-6, tumor necrosis factor α and interferon-γ are also detected in AAA tissue. Similarly, plasmin potentiates the degrading activity of extracellular matrix, induced by macrophages and T lymphocytes via MMPs.2 The extent of proteolytic activity of these proteinases also depends on the presence of endogenous inhibitors such as tissue inhibitors of metalloproteinases and α2-macroglobulin. Angiotensin II has also recently been cited as a mediator of AAA.8 Other pathogenic theories focus on the role of trace metals and an inflammatory response in the media and adventitia. Abnormalities in trace metals such as copper and zinc are also related because they are necessary for the maturation of collagen and elastin.5

The natural history of AAA is to expand and rupture.9 Abdominal aortic aneurysm rupture occurs when the hemodynamic forces within an aneurysm exceeds the aortic wall strength. Size, measured by diameter, is the best predictor of aneurysm rupture. It is estimated that rupture risk increases exponentially with size. Initial aneurysm size, hypertension, and chronic obstructive pulmonary disease (COPD) are independently predictive of AAA rupture. Absolute aneurysmal diameter is a more accurate predictor than the ratio of the aneurysm diameter to the proximal aorta. Diastolic blood pressure is a more accurate predictor than systolic blood pressure. Chronic obstructive pulmonary disease is the most influential risk factor. It may be related to a possible increase in systemic proteinase activity, affecting both pulmonary and aortic connective tissue.9 Smoking history or current smoking status is not a direct predictor of aneurysm rupture, but it may be related to increased risk of COPD, which, in turn, is related with increased risk of rupture of AAA. There is an increase in prevalence of AAA in first-degree relatives. However, there is no clear-cut evidence that this familial AAA has higher rupture risk. The shapes of aneurysm range from cylindrical to saccular, with varying degrees of eccentricity. There is an unproven clinical opinion suggesting that the eccentric saccular has a higher rupture risk than the diffuse cylindrical aneurysm.10 The thickness of thrombus within the aneurysm is related with the expansion of the aneurysm but not with the rupture of AAA. Thrombus within the aneurysm contains plasmin, which, in turn, can activate MMPs; this could explain the relationship between increased thrombus thickness and increased aneurysm expansion rate.2 The rapid expansion rate of aneurysm is presumed to increase rupture risk, but the absolute diameter of an aneurysm can also influence the expansion rate of an AAA. An aneurysm measuring 3 to 6 cm can expand by 10% of its diameter per year. Increasing pulse pressure is associated with an increased AAA expansion rate.

Clinical Diagnosis 

Abdominal aortic aneurysm occurs most frequently in elderly white men, with the onset at around 50 years of age for men and 60 years for women. The incidence progressively increases with age, reaching a peak at around 80 years. Abdominal aortic aneurysm is 5 times more common in men than in women and is more frequent in smokers and patients with hypertension, coronary artery disease, COPD, or hyperlipidemia (Fig 4). Abdominal aortic aneurysm also has a higher prevalence in first-degree family members.11, 12

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Fig 4. Risk factors associated with developing abdominal aortic aneurysm.

The clinical manifestations of AAA differ by 3 categories of clinical presentation (ie, asymptomatic, symptomatic, and rupture). Approximately 66% to 75% of AAA are asymptomatic. This asymptomatic AAA can be diagnosed during a routine physical examination by palpation of a pulsatile abdominal mass located at or slightly above the umbilicus in the epigastrium. Abdominal aortic aneurysm should be suspected when peripheral aneurysms are found because at least one third of patients with femoral or popliteal artery aneurysm will have an AAA.6, 7, 13 The incidental diagnosis of an asymptomatic AAA is often made from a radiographic examination for another condition. This was the case in our patient with low back pain who underwent lumbar spine radiography.

In symptomatic AAA, patients frequently report vague abdominal pain, usually located in the epigastrium that may radiate to back, flank, or groin. Symptoms in patients with known AAA require emergent evaluation to rule out rupture. Other symptoms result from the compression of an AAA on adjacent structures, distal embolization from intraluminal thrombus, and aortic occlusion due to thrombosis of aneurysm.

Rupture is the most lethal clinical presentation of AAA. The triad of symptoms associated with ruptured AAA is sudden onset of severe abdominal pain, hypotension, and presence of a pulsatile mass. Abdominal pain is usually constant and is not altered by a change in position. If bleeding occurs in the peritoneal cavity, rapid, massive hemorrhage often occurs followed by cardiovascular collapse and death.

Although most patients with rupture of an AAA present acutely, some cases are known to be delayed for weeks or months before detection. In these cases, the rupture occurs into the retroperitoneal space, where it may be contained without further leakage. Characteristically, these patients have continuous, chronic back pain, and the pain may radiate to the groin and scrotum. Several complications are caused by the retroperitoneal hematoma, such as sciatic neuropathy and compression of retroperitoneal structures. Although they may have survived with a “stable” rupture for long periods, they remain at risk for progression to frank hemorrhage at any time. There are several atypical presentations of AAA, with or without rupture. These atypical presentations include the following: chronic contained rupture, aneurysm dissection, inflammatory aneurysm, aortovenous or aortoenteric fistula, and embolic complications. These complications of AAA are uncommon and are usually only discovered because they were included in the differential.

Dissection of the abdominal aorta can occur, but this is rare, because fewer than 4% of aortic dissections begin in the abdominal aorta.13 These can occur without the presence of AAA. Coincidentally, the symptom complex produced by abdominal aortic dissection is similar to AAA rupture, and the difference may be recognized during the workup for AAA rupture or detected at surgery.

Diagnostic Imaging 

Abdominal aortic aneurysm is an incidental finding on lumbar spine or kidney-ureter-bladder radiography. In the presence of atherosclerotic disease of an abdominal aorta, this finding includes a loss of parallelism with fusiform or sacular dilation of an abdominal aorta, measuring 3.8 cm or higher.14 Atherosclerotic disease of an abdominal aorta makes it easier to see this aneurysmal dilation. In the absence of atherosclerotic disease of the abdominal aorta, this finding includes a soft tissue mass density with displacement of the bowel.

Ultrasonography is the preferred method for the initial evaluation of a suspected AAA.15 It is noninvasive, readily available, and a cost-effective choice for the initial evaluation and follow-up for aneurysm. It also provides accuracy in size measurement to within 5 mm. Conversely, US cannot provide information about surrounding vascular anatomy and structures, which is important for operative planning. On the other hand, contrast-enhanced CT, angiography, magnetic resonance imaging, and magnetic resonance angiography provide detailed information of AAA and the surrounding anatomy.

Computed tomographic scan examination is best for the preoperative assessment of AAA. It gives an accurate measurement of the aneurysm and also provides a better understanding of the relationship of the AAA with the surrounding anatomy. Advances in 3-dimensional and saggital reconstruction provide even more detailed images with excellent resolution. Like US, CT scans are readily available but the main disadvantages are complications from contrast agent exposure and higher costs.

Angiography provides excellent images of the surrounding vascular anatomy, but it is not a good test in the initial diagnosis and measurement of the aneurysm. In the presence of intraluminal thrombus, the distribution of contrast is prevented and gives a false impression about the size of AAA.

Manipulation Contraindication and AAA 

Abdominal aortic aneurysm of a significant size is a relative to absolute contraindication for high-velocity, low-amplitude (HVLA) manipulation within the area of pathology.16 There is no published evidence, however, that HVLA manipulation may cause rupture of an AAA. In addition, there is no evidence that abdominal palpation will trigger aneurysmal rupture. Lastly, it is not known whether postoperative repair of an AAA also constitutes a contraindication to HVLA. An appropriate referral should be made for further imaging and consultation with a vascular surgeon for the comanagement of patients with AAA.

Treatment and Complications 

Prevention is better than cure, and it is also better for the health care economy. Risk factors associated with the development of an AAA are of 2 types: modifiable and nonmodifiable (Fig 4). Diet, nutrition counseling, exercise, and lifestyle modification can reduce modifiable risk factors such as hypertension, diabetes, smoking, and hyperlipidemia.17, 18, 19

Patients are considered for elective repair when the risk of rupture of an AAA is greater than the risk of surgery. An elective surgery is recommended when an AAA is 5 cm or larger in a patient with a reasonable life expectancy and low or modifiable risk factors. Elective repair can be done successfully with a 2% to 5% mortality rate. Emergency repair of an intact AAA has an approximately 18% mortality rate because of insufficient time to perform a careful evaluation of concurrent medical conditions.1, 6, 7, 13 Elective repair of an AAA can be done as a conventional surgical repair or endovascular repair.

Traditional surgical repair for asymptomatic AAAs involves exposure of the abdominal aorta, aortic and iliac clamping, and replacement of the aneurysmal segment with a prosthetic graft. Graft replacement is an effective, durable procedure, and most hospitals report a 30-day mortality of approximately 5%.7, 13 One of the major developments in vascular surgery over the past 5 years has been the introduction of endovascular repair of aneurysms. This technique uses an endoprosthesis, which is delivered through the femoral arteries, to exclude an aneurysm from the circulation. The endograft is secured to the normal-caliber aorta and iliac arteries using metallic expandable stents and relies on subsequent thrombosis of the aneurysm to eliminate the risk of rupture. Endovascular repair has several theoretical advantages over conventional surgery, and early evidence suggests that endovascular surgery is better for patients with comorbidities, who would be at high risk for conventional surgery.20 We refer readers to relevant references for detailed information about risk factors, surgical management, and complications of elective surgical repair of the AAA, as these topics exceed the scope of this article.1, 6, 7, 12, 20

Pharmacologic treatment aiming to delay or even prevent expansion of a small asymptomatic AAA is a new treatment option. Drug therapy with 60% efficacy, good compliance, and tolerability lengthens the interval between diagnosis and need for surgery for up to 5 years in patients with AAA sized less than 4 cm. Doxycycline, a synthetic tetracycline derivative with antibiotic and anti-MMP properties, is a promising medical agent.2 Doxycycline nonselectively inhibits MMPs by binding to the active zinc site and to the inactive calcium site causing conformational changes and loss of enzymatic activity. Another option is to target the inflammatory response to interrupt the MMP pathway. Inflammatory cells in the adventitia and media of aortic wall release MMPs and proinflammatory cytokines (IL-1, IL-6, tumor necrosis factor α, and interferon-γ) that induce MMPs expression in AAA. Nonsteroidal anti-inflammatory drugs (NSAIDs), such as indomethacin, reduce cytokine release in aortic explants and prevent elastase-induced AAA in rats.9, 21 NSAIDs may have favorable effects on the aneurysmal wall by reducing both the inflammatory and proteolytic processes. In a case control study, NSAIDs halved the rate of AAA expansion, suggesting a potentially effective treatment. β-Blockers (propranolol) may slow down the expansion rate of aneurysm by the reduction in blood pressure, cardiac contractility, and direct effect on aortic wall connective tissue strength.9, 21 Several researchers have examined the effects of synthetic MMP inhibitors on experimental models of AAA.2 Marimastat is a competitive inhibitor of MMP-2, whereas Batimastat (BB-94) and RS132908 are broad-spectrum MMP inhibitors, which reduce matrix degradation and suppress the expansion of AAA in animal models. HMG-CoA reductase inhibitors (statins), besides their cholesterol-lowering effects, also suppress the expression of various inflammatory molecules including MMPs.