Abdominal Aortic Aneurysm_ an Illustrated Narrative Review

8/19/2019 Abdominal Aortic Aneurysm_ an Illustrated Narrative Review

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12/1/2016 Abdominal aortic aneurysm: an illustrated narrative review

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Abstract

Keywords

Introduction

Discussion

Conclusion Acknowledgements

References

Figures and tables

doi:10.1016/S0161-4754(02)54111-7

Journal of Manipulative and Physiological

Therapeutics

Volume 26, Issue 3, March 2003, Pages 184–195

Review of the literature

Abdominal aortic aneurysm: an illustrated narrative review ☆

Colin M Crawford, BAppSc (Chiro)a, , , Kristin Hurtgen-Grace, DCb, Ernest Talarico, BAppSc (Chiro)c,

John Marley, MD, MBChB, FRACGPd

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Abstract

Objective

To present a descriptive review of abdominal aortic aneurysm (AAA), including a review

of risk factors for and case finding in AAA for chiropractors as primary contact health care

practitioners.

Data sources

Clinical and scientific literature identified through various sources including MEDLINE

and citation tracking.

Data synthesis

Selective narrative review of relevant literature.

Results

AAA may be asymptomatic; however, back pain is a common presenting feature. Risk

factors include male gender, increasing age, cigarette smoking, hypertension, chronic

obstructive airway disease, claudication, and AAA in a first-degree relative. AAA should

be considered in the differential diagnosis of older white patients, especially males, with

low back pain. Estimated prevalence for AAAs in older males is in the order of 3% to 5%;

rupture accounts for 1.7% of deaths in men aged 65 to 75 years. Elective surgical

resection of AAAs (prior to rupture) offers a low operative mortality and good prognosis.

Conclusion

AAA should be considered in the differential diagnosis of older patients presenting withlow back pain and those with risk factors for AAA. Chiropractors, as primary contact

health care practitioners, have a responsibility to refer patients suspected of having AAA

for appropriate imaging and, where indicated, vascular surgical opinion.

Keywords

Abdominal Aneurysm; Chiropractic; Diagnosis; Low Back Pain

Introduction

Low back pain is the most common disabling musculoskeletal symptom.1 It is the second

most common reason prompting patients to seek care from physicians 2 and the

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predominant presenting complaint to chiropractors.3 and4 While most back pain may be

of “mechanical” origin,5 careful consideration must be given to other causes, especially in

an aging population. Abdominal aortic aneurysm (AAA) is a significant cause of low back

pain and an important cause of preventable death in the older person. 6 Unlike coronary

artery disease and cerebrovascular disease, the incidence of AAA dramatically

increased over the 3 decades to 19897 and may be rising. AAA should therefore be

considered in the differential diagnosis of an older patient with low back pain, particularly

in those patients with known risk factors for AAA.

“A significant number of lives might be saved…if clinicians (especially rheumatologists

and orthopedic surgeons) were made more aware of this possibility.” 8 The quote by

Duthie8 applies equally to chiropractors purporting primary contact status as it does to

general and specialist medical practitioners. This article reviews pathology and

pathogenesis, epidemiology and screening, clinical presentation and assessment,

imaging, case finding,9, 10 and11 natural history, and management of AAA.

Discussion

Pathology and pathogenesis

An aneurysm is a pathologic, irreversible12 dilatation of a segment of a blood vessel,13

caused by a congenital or acquired weakness.14 Aneurysms are classified according to

their site, configuration, and etiology.14 Seventy-five percent of abdominal aortic

aneurysms are located below the renal arteries in the distal abdominal aorta. 13 AAAs are

usually ovoid swellings affecting the entire circumference of a segment of the distal aorta

and are described as fusiform. 14 A saccular aneurysm is an eccentric, localized

distended sac affecting only part of the circumference of the arterial wall ( Fig 1). 15

Fig 1.

Cadaveric specimen of lower abdominal aorta and iliac bifurcation demonstrating saccular aneurysms, the

lower of which extends, as a fusiform aneurysm, into right proximal iliac artery. Horizontal metal marker

approximately 2.5 c m below intercristal (iliac crest) line. A, Pin in lumbosacral disk; B, pin in L4-5 disk; C ,

pin in L3-4 disk; D, pin (head) at origin of inferior mesenteric artery; E , pin in L2-3 disk. Right renal artery

(small arrow ). Unmarked pin in L1-2 disk. Left psoas muscle (arrow ). Incidentally, this cadaver has an

anomalous inferior vena cava (not shown here). (Man, white, aged 68 years; cause of death: congestive

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heart f ailure, also chronic obstructive airway disease.)

A true aneurysm involves all 3 layers of the vessel wall. Pseudoaneurysms involve

disruption of the intimal and medial layers, with the dilatation lined by adventitia and

sometimes by a perivascular clot.13 A dissecting aneurysm is, in fact, a dissecting

hematoma in which hemorrhage into the media separates the layers of the vessel. 14

In studies of anatomical specimens, the diameter of the inferior aspect of the normal

abdominal aorta was less than 15 mm (Fig 2). Radiological studies have found the

diameter of the normal abdominal aorta to measure, on average, 19 mm.16 Despite these

established standards, a consensus definition of AAA does not exist.17 An increase in

diameter of 50% is one accepted criterion for defining an abdominal aortic aneurysm. 12

Other definitions include an infrarenal aorta measurement of 30 mm or more17, 18 and19 or

a ratio of infrarenal to suprarenal diameters greater than 1.5:1.17

Fig 2.

Normal lower abdominal aorta, iliac bifurcation (arrow ) and right (R ) and left (L) iliac arteries in a cadaveric

specimen (Man, white, aged 68 years).

Traditionally, AAAs have been associated with atherosclerotic disease and frequently

referred to as atherosclerotic aneurysms. However, it appears that atheroscleroticchanges may be secondary to abdominal aortic aneurysms rather than being primary. 7

Epidemiological characteristics and genetic risk factors are different in patients with AAA

compared to those with stenosing arterial disease.20 The lower abdominal aorta depends

on diffusion of nutrients from the aortic lumen, because vasa vasorum are deficient in this

part of the aorta.12 Impaired diffusion through damaged intima, atherosclerotic plaques

and overlying thrombi, and vessel wall vibration may further weaken the aortic media and

facilitate the development of infrarenal abdominal aortic aneurysm. 12 and20

Histologically, the aneurysmal aortic wall contains inflammatory infiltrate and

inflammatory mediators, which may contribute to the destruction and weakening of the

aortic media. In patients undergoing surgery for AAA, the aneurysm is considered to be

inflammatory in about 3% to 10% of cases. 20 and21 Traditionally, inflammatory

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aneurysms have been viewed as a distinct clinical and pathological entity caused by an

autoimmune response to components of the aortic wall. 20 Inflammatory AAAs are

characterized by a triad of thickened aneurysm wall, extensive perianeurysmal and

retroperitoneal fibrosis, and dense adhesions of adjacent abdominal organs.21 Intense

inflammatory cell infiltrate often extends beyond the aortic wall into surrounding

tissues.20 Recent evidence suggests that although inflammatory AAAs arise from the

same stimuli responsible for noninflammatory AAAs, they represent one extreme of an

inflammatory spectrum.21

Many factors, acting over time, contribute to the pathogenesis of abdominal aortic

aneurysm. Elastin and collagen are important structural components of the aortic wall.

Elastin is easily stretched and provides the elastic recoil of large arteries, while aortic

collagen is coiled such that the initial load in the aorta is borne by elastin. As the vessel

continues to stretch, collagen fibers become load bearing. Aortic collagen has a tensile

strength more than 20 times greater than that of elastin but cannot extend beyond a small

proportion of its original length before structural damage occurs. Initially, destruction of

elastin shifts the load of pulsatile blood flow in the lower aorta from elastin to collagen.

Part of the marked stiffness or inelasticity of dilated or aneurysmal vessels is attributable

to the loss of elastin. Years of pulsatile blood flow through the degenerated vessel wall

exacerbate the process, and the collagen is continuously exposed to the expansile force

of intraluminal blood pressure. The extent of dilatation and subsequent rupture depends

on the properties of the collagen and the net effect of collagen degradation, turnover, and

remodeling.20

Familial clustering of AAA suggests a genetic basis to this disease. Inherited defects in

elastin and collagen might weaken the aortic wall, or genetic variables may increase

enzymatic destruction of vessel wall constituents.20 Both X-linked and autosomal

dominant modes of inheritance have been suggested.22 and23

Certain heritable diseases of connective tissue have an association with AAA, including

Marfan syndrome and Ehlers-Danlos syndromes (EDS). Marfan syndrome results from a

mutation in the gene that codes for fibrillin, a family of connective tissue proteins that

serve as scaffolding for the deposition of elastin during embryonic development. This

genetic mutation weakens the aortic media and dilatation occurs, resulting in a high

incidence of dissecting aneurysms, especially in the ascending aorta. The EDS are a

rare group of disorders characterized by hyperelasticity and fragility of the skin, jointhypermobility, and a bleeding diathesis. EDS IV is associated with a tendency to

spontaneous rupture of large arteries.24

Cigarette smoking has been strongly associated with the presence of AAA, death from

rupture, and aneurysm expansion rates. The mechanism is thought to be enhancement

of proteolytic enzyme degradation of the aortic wall by gaseous and blood-borne

products of tobacco combustion.20 and25 The only prophylactic advice that appears

useful is cessation of smoking.26

Hypertension is associated with increased prevalence and increased risk of rupture.

Hypertension may be related directly to pathogenesis or may merely exacerbate the

effect of blood flow forces on an already weakened aortic wall. 20 A recent study found a

low incidence of AAAs in elderly patients with treated, uncomplicated hypertension and

concluded that uncomplicated hypertension by itself was not an indication for

screening.27

AAA is uncommon before 50 years of age. Normal aging is associated with alterations in

the structure and, consequently, the mechanical properties of the aortic wall. Thus, the

aging aorta may be less able to withstand the force of pulsatile blood flow, resulting in

aneurysmal dilatation.20

The different processes involved in the pathogenesis of AAA are integrated

diagrammatically in Figure 3. Their relative importance may vary from one patient to

another.20



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Fig 3.

Pathogenesis of abdominal aortic aneurysm. Reproduced with permission of the Editors of the British

Journal of Surgery.20

Epidemiology and risk factors

AAA is 10 times more common in 65- to 75-year-old men compared to women of the

same age. This is in contrast to the male-to-female ratio for atherosclerotic disease,

which is closer to 2:1. The gender-related difference in AAA diminishes to about 3:1 in the

85- to 89-year-old age group.25 The prevalence of aneurysms greater than 4.0 cm in

diameter in men aged between 65 and 75 years is approximately 3%. Other studies have

estimated the prevalence of unsuspected aortic aneurysm to be 5.4%. 28 Studies have

reported prevalence rates of 12% to 33% in first-degree relatives.12 and17

Abdominal aortic aneurysm (with elective repair or rupture) is the 10th to 13th leading

cause of death in the United States.7 The death rate for AAA (rupture) in the United

Kingdom peaks at 65 to 75 years of age; rupture accounts for 1.7% of all deaths in men in

this age group in the United Kingdom. Death from AAA in England and Wales showed a

progressive and continuing increase over a 30-year period to 1988. 25 and29 The

increased prevalence of aneurysm has paralleled the pattern of tobacco addiction, which

rose during the period 1916 to 1948; a cohort effect with a 40-year time lag has been

suggested to explain this observation.25 Increased awareness of abdominal aortic

aneurysms, screening programs, and the aging population are also thought to have

contributed to an increase in the incidence of asymptomatic AAAs. In a study in the

United States, white men had higher age-adjusted death rates for aortic aneurysm than

black men. The age-specific rates were similar or higher in black men under age 65

years. Black women had higher rates than white women under age 65 years, similar

rates at ages 65 to 84 years, and lower rates above 85 years.30

Correlation between hypertension and cigarette smoking and the development of AAA

was found in studies reviewed by Reilly and Tilson.7 However, a substantial number of

patients without hypertension or a history of smoking develop abdominal aortic

aneurysms.7 The presence of chronic obstructive pulmonary (airway) disease,

independent of smoking, was found to be predictive of rupture of aortic aneurysm. 31

Reilly and Tilson7 concluded that further research is needed to look at the clinical

expression of the disease and the interplay of environmental factors, such as smoking,

against a background of defined genetic risk. Claudication was the only cardiovascular

complication independently associated with the presence of AAA in a study of

predominantly white men presenting to a hypertension clinic.27

The mean body mass index (weight in kg/height in m 2)10 in men and women with

aneurysms was not significantly greater than that of normal subjects in an Italian study. 32

However, a North American study found height to be related to the presence of aortic

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aneurysms and a positive association between body weight and aneurysms.33 This

study documented the strong association of cardiovascular risk factors and measures of

clinical and subclinical atherosclerosis, cardiovascular disease, and prevalence of

aneurysms.

Clinical presentation and examination

Abdominal aortic aneurysm is usually asymptomatic until rupture or size draws the

attention of the patient or physician to it.25 A feeling of fullness or pulsations in the

abdomen may be early symptoms.34 In one review of 528 patients with aneurysms, 91%

had symptoms at their first presentation; the most common symptoms at firstpresentation were abdominal pain and backache. Only 48 of the 528 patients in this study

were completely asymptomatic, with an aneurysm found at examination for another

complaint.35 The clinician should consider the possibility of rupture of an AAA in a male

patient over the age of 60 years who presents with sudden onset back and/or loin pain 8

with shock and/or syncope.12 In addition, patient characteristics which may raise clinical

suspicion of AAA include being a current smoker or with a significant smoking history,

increased weight, a history of myocardial infarction,6 and claudication.27 As discussed

above, a strong familial occurrence of AAA should also raise diagnostic suspicion, as

should the presence of hypertension.7

Clinically, the abdominal aorta may be located anteriorly in the midline between a point

2.5 cm above the transpyloric plane and a point slightly inferior and a little to the left of the

umbilicus. The transpyloric plane is an imaginary horizontal plane located midway

between the xiphisternal joint and the umbilicus. The aortic bifurcation into the common

iliac arteries occurs just to the left of the midpoint of the line joining the highest points of

the iliac crests (intercristal line) (Fig 1, Fig 2 and Fig 6).36 Appleberg12 highlights the need

to palpate specifically for abdominal aneurysm. The examination should be conducted

with the supine patient’s knees raised and the abdomen relaxed. 37 The technique

involves deep and careful palpation with the palms down, to the left of the midline,

keeping the hands steady in one position until the aortic pulse is felt, and then carefully

evaluating the transverse extent of the expansile pulse with the pads of the index

fingers.12 and37 Physical findings may include a tender,38 palpable, pulsatile abdominal

mass35 with abdominal bruit.34

It is important to recognize that abdominal palpation for the detection of abdominal aortic

aneurysms has low overall sensitivity (ie, high false-negatives).6 One study, the purpose

of which was inter alia “to determine the accuracy of physical examination in AAA

detection,”6(p1753) found that abdominal palpation detected only half of 18 previously

unsuspected aneurysms in 201 patients. This study found that abdominal girth was an

important factor in detecting AAA by physical examination. No AAA was missed on

palpation by the study team, comprising staff internists, when the girth was less than 100

cm. In 109 subjects with a girth of 100 cm or greater, only 3 of 12 AAAs were palpable. 6

Five patients in this study with AAAs who had a definite pulsatile mass detected by

palpation had, on chart review, abdominal examinations recorded as negative by their

primary care physicians. The authors of this study did not comment specifically on

interexaminer or intraexaminer reliability of abdominal examination findings. A later study

found fair to good interobserver mean pair agreement and kappa scores for the presence

or not of AAA. It found high sensitivity for diagnosis of abdominal aortic aneurysms large

enough to warrant elective intervention in patients who did not have a large abdominal

girth and good sensitivity in patients with a large girth if the aorta was palpable. 37

Unusual clinical presentations

Unusual clinical presentations of AAA may result from chronic contained rupture,

inflammatory aneurysm, aortovenous fistula, and atheroembolism. These manifestations

may complicate surgery and raise operative morbidity and mortality.38 A chronic

contained rupture may, in addition to abdominal or low back pain, cause pressure effects

resulting in jaundice from common bile duct compression or in ureteral obstruction,

femoral neuropathy, or extension of the hematoma into the femoral sheath, simulating a

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groin hernia.38

So-called inflammatory aneurysms (see comments above) may result in adhesions

involving structures such as the duodenum, inferior vena cava, and left renal vein. Two

thirds or more of patients with inflammatory aneurysms are symptomatic at the time of

presentation; common symptoms include abdominal, flank, and/or back pain; anorexia;

weight loss; and elevated erythrocyte sedimentation rate.21 and38

Aortocaval and aortorenal vein fistulas result from rupture of an AAA into the inferior vena

cava or the left renal vein. Clinical presentation includes high-output heart failure,

cardiomegaly, a palpable abdominal mass, audible continuous bruit, hypotension,

oliguria, and abdominal and back pain.38

Infected aneurysms are rare and may result from superimposed infection or arise

secondarily from an infection. Clinically, infected aneurysms may present with the

sudden appearance of a pulsatile mass or recent enlargement of a known AAA in

combination with fever or recent febrile illness.38

Atheroembolism from an abdominal aortic aneurysm to 1 or both of the lower extremities

is a well-documented occurrence.38 Thrombus within the lumen of the aneurysm or

cholesterol debris from within the intima of the wall can be the source of macroemboli or

microemboli, respectively. Macroembolism presents with symptoms and signs of large-

vessel occlusion and sudden ischemia of the lower limbs. Small-vessel occlusion

resulting from microemboli presents as slowly evolving livedo reticularis, painful cyanotic

toes, and palpable pedal pulses. Microembolism has been termed blue toe syndrome

because of the characteristic cyanosis of the toes; if both lower extremities are involved,

an AAA or other aortic source should be considered. 38

Other unusual complications of AAAs include recurrent ischemic myelopathy and/or

paraparesis. Ischemic spinal cord lesions may present with bladder incontinence, a

mixture of upper and lower motor neuron lower limbs signs, and patchy sensory loss. 39

Paraparesis may result from anterior spinal artery syndrome, which presents as a

varying degree of muscle weakness and dissociated sensory loss of pain with sparing of

proprioception.40

Imaging

There are numerous modalities available for imaging the aorta; each has strengths andweaknesses. Variations in individual cases, equipment availability, technical expertise,

and surgeon preference all influence imaging modality selection.41

Abdominal aortic aneurysms are frequently noted on frontal (anterior-posterior [AP]) (Fig

4), lateral (Fig 5), and oblique low back plain film radiographs. Most AAAs occur between

the renal arteries and the iliac bifurcation; that is, between the L2 and L4 vertebral levels,

respectively. In the frontal (AP) projection, an AAA is usually seen on the left side of the

spine and appears as a soft tissue density demarcated by a thin, curvilinear rim of

continuous or discontinuous calcification. On the lateral view, collimation may prevent

the anterior margin from being visualized. At times on the lateral view, the only indication

of AAA may be a horizontally oriented calcified plaque.19 Calcification is noted in 55% to

85% of AAAs41 and42; in the remainder, a soft tissue density may be identifiable. Erosion

of the anterior margins of the vertebral bodies (Oppenheimer erosions) may be noted

with inflammatory and saccular (Fig 1 and Fig 6) aneurysms and those involving

contained rupture.19 and43

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Fig 4.

Antero-posterior lumbo-pelvic (AP LP) plain film radiograph: Curvilinear rim of discontinuous calcif ication of

the wall of AAA (large arrows); maximum transverse diameter 8.5 cm. Bilateral iliac artery calcification

(seen clearly on right side only–small arrow ).

Fig 5.

Lateral lumbosacral (LAT LS) plain film radiograph: Horizontally oriented calcified plaque on the superior

margin of AAA (arrows) just anterior to the L3 vertebral body.

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Fig 6.

Anterior-posterior (AP) radiograph of cadaveric specimen in Figure 1. A, Pin in lumbosacral disk; B, pin in

L4-5 disk; C , pin in L3-4 disk; D, pin (head) in origin of inferior mesenteric artery; E , pin in L2-3 disk; F , pin

in L1-2 disk. Right proximal iliac artery aneurysm (small arrows). Larger arrow at level of aortic bifurcation.

Ultrasound scanning is currently the most practical and accurate way of detecting

abdominal aortic aneurysms in large numbers of people 17 and44 and has become the

most commonly used method of screening.41, 44, 45 and46 Ultrasound enables diagnostic

confirmation, evaluation of size, and monitoring of progression.44 Measurements of

AAAs from ultrasound correlate within 3 mm of surgical specimens.41 Diagnostic

ultrasound may show thrombus (Fig 7), periaortic abnormalities, dissections, and the

cephalic and caudal extent of the lesion.41 Diagnostic limitations of ultrasound include

difficulties imaging obese patients and those with abundant overlying bowel gas.41 The

renal arteries can only rarely be visualized directly and inferences regarding suprarenal

extension of an AAA can only be made from the relationship of the aneurysm to the

superior mesenteric artery.41 Graham and Chan44 studied ultrasound screening for

clinically occult AAA and concluded that the false-negative results for the ultrasound

detection of AAAs was probably low, suggesting that ultrasound scanning was a

sensitive procedure for the diagnosis of AAA. The specificity and positive predictive value

of ultrasound have been shown to be 100%,6 and thus, this modality is optimal for

screening and follow-up in noncomplicated cases.41 Clinical suspicion of AAA should

lead to confirmation with ultrasound.19

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Fig 7.

Ultrasound of a l arge AAA. The t ransverse diameter of this AAA measures 7.91 cm ; intraluminal diameter

is 4.73 cm. Intraluminal clot is clearly visible. (Courtesy of Sulzer Vascutek, Australia.)

Computed tomography (CT) accurately demonstrates the size and craniocaudal extent

of an abdominal aortic aneurysm and is usually able to detect intraluminal thrombus. CT

also enables visualization of the retroperitoneum, allowing detection of aneurysmal leak,

ureteral obstruction, perianeurysmal fibrosis, and other unusual causes of abdominal or

back pain.41 Postinfusion CT scans facilitate differentiation of the patent lumen of the

aneurysm from surrounding intraluminal thrombus (Fig 8). CT scanning is the modality of

choice for postsurgical repair evaluation of AAAs.41 However, CT scanning of AAAs

requires exposing the patient to ionizing radiation and the administration of contrast

material.47

Fig 8.

CT scan with contrast in the patent lumen (small arrow ) of a typical AAA; thrombus (large arrow ).

The multiplanar display capability of magnetic resonance imaging (MRI) can

demonstrate the features discussed above without the need for contrast; it allowsaccurate measurement, isolates flow abnormalities, identifies clot, and allows

assessment of visceral involvement.19 MRI is noninvasive and reduces the need for

angiography (Fig 9). MRI may be contraindicated in patients requiring respirators or

monitoring equipment. Gadolinium-enhanced magnetic resonance angiography (MRA)

is a variation of standard magnetic resonance imaging, utilizing a paramagnetic contrast

agent. This modality provides anatomic information for aortic reconstructive surgery

without the contrast-related renal toxicity or catheterization-related complications

attending conventional arteriography.48 Further, the advantages of MR angiography

include the lack of ionizing radiation and need for iodinated contrast material and its

ability to image the entire abdomen and pelvis, as well as the thorax and lower

extremities if necessary.49

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Fig 9.

MRI scans and aortograms of large infrarenal AAA in a 67-year-old man. A, Oblique coronal 2-dimensional

(time-of-flight) magnetic resonance (MR) angiogram demonstrates the widest dimension of the AAA. B,

Three-dimensional (maximum intensity projection) MR angiogram reconstructed from multiple 2-

dimensional sect ions shows the AA A s tarting below the renal arteries (white arrows) and extending into

both iliac arteries (black arrows). C, Conventional aortogram helps confirm the iliac artery extension of the

AAA. D, Targeted (maximum intensity projection) image helps confirm normal proximal renal arteries

(arrows) reconstructed from 2-dimensional MR angiograms. E, Conventional aortogram helps confirm

patent renal arteries. Reproduced with permission of the Editors of Radiology and the authors. 67

Angiography is used to evaluate the state of the renal arteries and other vessels in the

iliac artery system in patients with AAA12 (Fig 9, C and E ). It is the gold standard for

demonstrating visceral-branch involvement and vascular anatomy. 41 However,

angiography may underdemonstrate the size and extent of the thrombus-filled

aneurysm, as only the lumen is demonstrated.41 The use of angiography may alter the

surgical approach utilized in up to 25% of cases. 19

Natural history

Most AAAs continue to enlarge progressively.12 Small aneurysms increase in transverse

diameter by up to 5 mm per year 31 and50; the anteroposterior diameter increases by an

average of 2.2 mm per year.31 Large aneurysms expand more rapidly than smaller

ones.12 and50 The risk of rupture increases significantly as the size of the aneurysm

increases, with a 43% risk of rupture within 12 months of aneurysms greater than 6 cm. 51

Patients with aneurysms less than 5 cm also run the risk of rupture in 2% to 32.9% of

cases.12

The nonoperative mortality of ruptured abdominal aortic aneurysm is 100%. The

operative mortality of ruptured aneurysm is around 50%; survival prospects are

enhanced by admittance to a specialist surgical unit (ie, by surgical skill) and relate

inversely to increasing severity and duration of preoperative hypotension.25 In a

retrospective review of 528 cases, the mortality rate for acute presentations, as opposed

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to rupture, was 19%.35 Over the 3 decades to 1988, the mortality for elective AAA

surgery progressively fell to less than 3%.25 Some centers claim an elective mortality as

low as 1.4%.25 Age is not an indication to forego surgery; safe aneurysm repair is

possible for many patients over 80 years of age. 52

Role of screening

Screening is the presumptive identification of unrecognized disease or defect by the

application of tests, examinations, or other procedures which can be applied rapidly.53

To qualify as a target for a screening program, a disorder needs to be fairly prevalent and

detectable by tests that are inexpensive, accurate, acceptable to patients, and treatablewith low risk.54 Screening procedures also need to be both sensitive and

specific.44Sensitivity refers to “positivity in disease,” 55(p81) or the proportion of patients

with the target disorder who have a positive test. Specificity refers to the ability of a test to

correctly identify those patients without the target disorder (ie, “negativity in health”).55(p82)

In one study of patients with girth measurement of less than 100 cm, no AAA was missed

on abdominal palpation,6 suggesting high sensitivity of abdominal palpation in this group.

This degree of sensitivity was not obtained with “routine” examinations, and the study

concluded that the examination needed to be directed specifically toward AAA detection.

The caution given by Appleberg12 is worthy of reiteration, namely, the need for deep and

careful palpation specifically for AAA (see above). In the Oxford Screening Programme

for AAA in men aged 65 to 74 years, the sensitivity and positive predictive value of

abdominal palpation for epigastric and/or infraumbilical midline pulsations were poor,

while specificity was over 90%.28 Overall, abdominal palpation has been reported to

have low sensitivity in detecting AAA.6 and56 Except in a small number of patients,

therefore, abdominal palpation fails to meet the requirements for a screening tool.

On the other hand, ultrasound screening meets the criteria to be considered an

acceptable screening test for the detection of AAA, including acceptable sensitivity and

specificity.6 and44 A recent prospective study supported annual screening using serial

ultrasound for small aneurysms (2.5 to 3.9 cm) and 6-month screening for those

measuring 4.0 cm or greater.50 Arguably, with high mortality rates associated with

surgical repair of ruptured AAAs and the low mortality rate associated with elective repair

of aneurysms, obese males over the age of 55 years with hypertension, coronary artery

disease, cerebrovascular disease, or peripheral artery disease56 should be routinely

screened with ultrasound.44 Patients, especially men with chronic obstructive airway

disease, or those who are first-degree relatives of a known aneurysm patient, should also

undergo screening.26 and54 As smoking is a significant risk factor, the screening of

smokers in the 65- to 80-year-old age group may also constitute a cost-effective

strategy.26 and54 Recently, a study concluded that uncomplicated hypertension by itself

was not an indication for screening but recommended screening for AAA in elderly white

patients with claudication.27

The introduction of the Oxford Screening Programme nationally (in the United Kingdom)

a decade ago was estimated to prevent potentially some 6000 unnecessary deaths. 28 A

study in Gloucestershire (United Kingdom) demonstrated a significant reduction in

number of deaths from all aortic aneurysm-related causes in the screened portion of themale population.57 In one study, 45 male patients aged 55 years or older, with a waist

measurement greater than 101 cm and no abdominal aortic aneurysm detected on

clinical examination, were referred to a tertiary referral center. In addition, these patients

had at least one of the following conditions: hypertension, coronary artery disease,

cerebrovascular disease, and peripheral vascular disease. Subsequent ultrasonography

(ultrasound) revealed 6 aneurysms, giving a detection rate of 13%. 44 Existing evidence

seems to favor screening at least for men aged 65 to 7554 or 60 to 80,58 but the costs and

benefits of more general screening have not been calculated. 54

The findings of a recent study indicate that a second screening, approximately 4 years

after the initial examination, is of little practical value, mainly because the AAAs detected

are small. Screening after 8 years may provide total yields similar to those seen in initial

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screening. Further, this study found that rescreening only those subjects with an

infrarenal aortic diameter of 2.5 cm or greater on initial examination would have missed

more than two thirds of new AAAs.59

Management

Surgical resection of abdominal aortic aneurysm was first described in 1952. Discussion

of the various repair options is outside the scope of this report; interested readers are

referred to other sources, including the editorial by Ernst. 60 Appropriate management of

patients with clinically suspected or diagnosed AAA by primary contact health

practitioners is referral for imaging studies and/or surgical opinion. Surgery is indicated incases of both small and large AAAs 25, 31 and52 (Fig 10 and Fig 11). As discussed above,

patients with small aneurysms run a risk of rupture, which may be as high as 9.5%. With

large AAAs, the risk of rupture is between 60% and 80%.44 The operative mortality from

elective surgery has progressively fallen to less than 3%. Thus, the risk of death without

surgery, even with small aneurysms, is significant. Naturally, other significant medical

problems need to be considered in making the decision to operate. 44 The authors of a

retrospective study of 1000 consecutive elective AAA repairs concluded that pulmonary

and renal disease did not, and should not, pose a significant risk for elective infrarenal

AAA replacement, although cardiac dysfunction and coronary artery disease increased

morbidity and mortality.61 The long-term survival of a patient undergoing surgical

resection and repair of an AAA with an artificial graft who survives the immediate

postoperative period is comparable to that in persons who never had an AAA.58

Collinemphatically states that “any doctor who .. does not refer the problem to a vascular

surgeon should be aware that he may willfully be condemning his (sic) patient to a totally

preventable premature death.”25 and67

Fig 10.

Operative v iew of AA A and bifurcation into the iliac arteries (bottom of f igure) seen through a long midline

incision. (Courtesy of Sulzer Vascutek, Australia.)

Figure options

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Fig 11.

Operative v iew of AA A graft replacement. AAA graft replacement secured in place; the original aneurysm

sac is now sutured over the front of the graft in order to prevent aortoenteric fistula. (Courtesy of Sulzer

Vascutek, Australia.)

Chiropractors are, by training and legislation, primary contact health care practitioners.

Inherent in such status is the responsibility to consider conditions other than mechanical

back pain in patients presenting with spinal pain and putative spinal dysfunction in

patients presenting for so-called chiropractic maintenance care62 or wellness care.

Approximately 80% of patients presenting for chiropractic care do so for

neuromusculoskeletal pain, with low back pain being the predominant presenting

complaint.3 and4 With the aging population44 noted in western countries and with certain

groups of older patients, who until recently may have been denied access to chiropractic

care, now gaining access (for example, Australian armed services’ veterans through

recognition of chiropractic services by the Department of Veterans’ Affairs), chiropractors

need to be cognizant of AAA and vigilant in assessing their older patients for the

possibility inter alia of AAA. This involves not only circumstances where an abdominal

aortic aneurysm is the cause of the presenting back pain 63 but also case finding involving

the consideration of unrelated, intercurrent illnesses (eg, AAA) in presenting patients9

due to the presence of known risk factors.

Should a patient with risk factors associated with AAA present to a chiropractor, referral

for imaging (usually ultrasound) with subsequent vascular surgical opinion, where

appropriate, is required.64 and65 In Australia, referral is usually via the patient’s general

medical practitioner. Should an aneurysm present fortuitously on radiographic

examination, such referral is also mandatory. Patients known to have an abdominal

aortic aneurysm should be warned of the importance of characteristic symptoms of

rupture and the necessity for immediate attention should they arise. 12

It is not known whether an AAA is a definite contraindication to chiropractic manipulation

per se, although large AAAs are considered so.66 Further, it is not known if the forces

utilized in spinal manipulation are of sufficient magnitude to cause rupture of an AAA or if

patient positioning required for low back spinal manipulation/adjustment66 is such that

the risk of rupture of an AAA is increased by such positioning. Referral should be made

Figure options

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1

2

3

4

5

6

for further assessment because of the risk of spontaneous rupture and the high mortality

associated with rupture. Consideration should also be given to the relatively low surgical

mortality rate should surgery be indicated and the possibility that the AAA is the cause of

low back pain when this is the presenting complaint. Delay in referring an at-risk patient in

order to offer a trial of therapy may be indefensible morally, clinically, and in a

medicolegal context.

Conclusion

AAA should be considered in the differential diagnosis of older patients presenting with

low back pain. The possibility of abdominal aortic aneurysm should also be considered inasymptomatic, at-risk patients. Patients at risk for AAA include male patients over the

age of 65 years, with a history of smoking, hypertension, chronic obstructive airway

disease, claudication, and a first-degree relative with an AAA. Elective surgery offers a

cure with low operative mortality. Chiropractors, as primary contact practitioners, have a

responsibility to refer patients suspected of having AAA for appropriate imaging and,

where indicated, for a vascular surgical opinion.

Acknowledgements

The authors would like to thank and acknowledge the assistance of the following: Dr

Dennis Middendorp, DC (RMIT, Melbourne, Australia) for assistance with clinical details;

Dr Antony M. Hatton, BAppSc-Chiropractic, MSc, kindly reviewed the section on

pathology and pathogenesis; Roy Webb, MSc, Alex Zabobonin, MD, and Peter

Cauwenbergs, DC, PhD (CMCC, Toronto, Canada) for preparation and anatomic

orientation of the cadaveric specimen (Fig 1 and Fig 2); and Renata Lumsden, BSc,

MRT(R) and Lynda Tanner, MRT(R) (CMCC Radiology Department, Toronto, Canada)

who radiographed the specimen (Fig 6). Thanks also to Liz Holden, RN, of Sulzer

Vascutek (Australia) who kindly provided and granted permission to reproduce the

original slides of Fig 7, Fig 10 and Fig 11. The permission of the Editors of the British

Journal of Surgery to reproduce the diagram in Figure 3 and the permission of the Editors

of Radiology and the Authors to reproduce the diagnostic imaging in Figure 9 are

appreciated. Bryan Groulx and Michael Craven (Media Services, CMCC, Toronto,

Canada) provided assistance with reproduction of the figures for publication. The

Division of Graduate Studies & Research at CMCC provided financial assistance.

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Financial assistance was provided by The Division of Graduate Studies and Research

at Canadian Memorial Chiropractic College.

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