Aortic Abdominal Aneurysm

Continued surveillance or elective repair.

Stacey Biggs BBiomedSc, s2148529

Course: 7208NSC Physiology Clinical Placement A

Convener: Mrs. Alison White

Due Date: 11 Sept 2015

1

Introduction

An Abdominal Aortic Aneurysm (AAA) is defined as a focal dilatation of the

abdominal aorta greater than 3.0cm or 1.5 times its original size [5]. The aortic

aneurysm is a full-thickness dilatation involving all layers of the artery wall. The

pathophysiology of aortic aneurysms can be characterized by four main events.

The first and most frequently documented event is the degeneration of the aortic

media and adventitia elastin and collagen by proteases, which comprises

metalloproteinases, plasmin and cathepsin S and K. The cause of this event is

largely debated but remains elucidated. The second recognized event is the

infiltration of the vessel wall by inflammatory cells, such as CD4-positive

lymphocytes and macrophages [5, 7]. Aneurysmal size has had a positive

association discovered with inflammatory markers such as C-reactive protein

(CRP) and interlueukin-6 (IL-6) [10]. Infiltration by inflammatory cells is thought to

be involved with the third event, which is apoptosis of vascular smooth muscles

resulting in thinning of the media layer [5, 7]. The fourth event in degeneration of

the arterial wall is neovascularization, which is considered to play a critical role in

development and rupture of an AAA [9].

Approximately 85% of all AAA’s are infrarenal and often involve the Common Iliac

Arteries (CIA) [7]. Only 5% of infrarenal AAA’s include the renal arteries [5]. Most

are asymptomatic with 30% of cases discovered when pulsatility of the abdomen

is felt, on palpation, during a routine physical examination. In addition to this,

auscultation of the abdomen may reveal the presence of a bruit however body

habitus is a major obstacle to accuracy in both circumstances [6]. Non-modifiable

risk factors include age, race, gender and family history. Men are 10 times more

likely to have an AAA with rates of prevalence increased from the age of 55 years

advancing by 10% between the ages of 65-79 years [10]. Modifiable risk factors

include hypertension, hyperlipidemia, atherosclerotic disease and tobacco use.

Smoking can increase the risk of developing an AAA by approximately 7% and is

associated with causing incremental increase in AAA growth by 0.4mm per year

[5, 6].

2

Case presentation

Patient C Characteristic

Age: 75yrs

Gender: Male

Relevant case history:

Hyperlipidaemia

Hypertension

Clinical diagnosed prostate cancer

Controlled schizophrenia

Socioeconomic background:

Patient C is a retired non-smoking gentleman living with his wife.

Clinical details as documented by treating physician:

The earliest documented report of Patient C’s AAA dated 6th February 2004 notes

an incidental finding of an asymptomatic 3.8cm abdominal aortic aneurysm.

Regular surveillance of the AAA was to be conducted with surgical repair to be

considered once the AAA was > 5cm.

The latest vascular surgeon report, dated 19th September 2014 reveals that

Patient C remains asymptomatic with ultrasound today measuring an infrarenal

AAA of 48mm X 51mm, which has grown 1mm over the previous 12 months.

He has good pulses in his femoral, dorsalis pedis and posterior tibial distally. He

has no sequelae of thrombus emboli or ischemic disease. On examination he

does have a prominent right popliteal artery for further investigation. Conservative

management is to continue with repeat duplex Aorto-iliac scan and duplex arterial

right leg in one year’s time.

3

Test requested

1. Aorto-Iliac Arterial Duplex Scan (Appendix 1 Worksheet/ Appendix 3

Report)

Duplex imaging of the Abdominal Aorta and Iliac arteries was performed using two-

dimensional (B-mode imaging system) spectral pulse wave Doppler and colour flow

imaging with a 4C (9-14MHz) curved linear array transducer. The patient was

positioned supine throughout the test. In Patient C’s case body habitus or

comorbidity did not require repositioning throughout the test from supine to either

right or left lateral decubitus, or perhaps virtually prone, as can commonly be

required. The Abdominal Aorta is viewed in transverse and longitudinal planes from

the celiac trunk distally past the iliac arteries. Assessment of both Aortic diameter

and basic structure is performed using B-mode imaging. Flow velocities and areas of

possible stenoses are evaluated using pulsed Doppler. Colour flow Doppler was

used to assess for branches and the extent of Mural thrombus present in the

aneurysmal sac [11].

2. Bilateral Peripheral Leg Arterial Duplex Scan (Appendix 2 Worksheet/

Appendix 4 Report)

Duplex imaging of the right leg arteries was performed using two-dimensional (B-

mode imaging system) spectral pulse wave Doppler and colour flow imaging with a

9L (4-10MHz) linear array transducer. The patient was positioned supine with a 20-

30 degree reverse Trendelenburg throughout the test. The subsequent imaging

evaluated clinical findings of a prominent right popliteal pulse with interest to

assessing for an aneurysm. The presence of vascular disease of the arteries can be

assessed for areas of stenosis and occlusion as well as dilatation. The worksheet in

appendix 2 illustrates observed pathological changes.

Interpretation of the test results

Aorto-Iliac Arterial Duplex Scan – Abdominal Aorta (Illustrated in appendix 1-

Report appendix 3)

The Infra-renal Aorta was significantly dilated to a maximal diameter of 50mm X

53mm from a baseline 23mm X 23mm. This is a 2mm increase over the last 12

4

months, which is consistent with growth rates represented in appendix 5.4. The neck

length measured at 78mm with a saccular length of 73mm. The walls of the AAA

were mildly calcific with evidence of mural thrombus and no associated flow

disturbances on Doppler sampling. Characteristics of mural thrombi are described as

a permanent dynamic interface with circulating blood components. Recent evidence

suggests that a relationship exists between the presence of mural thrombi and

evolution of aneurysmal dilation towards rupture. The extent of involvement of the

mural thrombus encompasses thinner arterial walls, increased elastolysis, a lower

density of smooth muscle cells in the media layer and a higher level of immune-

inflammatory of the adventitia [12]. Mural thrombi increases Patient C’s

predisposition to distal embolization [8].

Aorto-Iliac Arterial Duplex Scan – Iliac Arteries (Illustrated in appendix 1- Report

appendix 3)

Minor thickening of the right iliac artery was noted with no associated flow

disturbance on Doppler sampling. The right Common Iliac Artery (CIA) was ectatic

with a maximal diameter measured of 17mm. The right External Iliac Artery (EIA)

had a maximal diameter of 11mm. The left CIA and EIA were ectatic and measure

maximal diameters of 17mm and 15mm, respectively. Normal triphasic flow was

demonstrated bilaterally in the Iliac arteries on Doppler sampling. The CIA diameter

reference range of 1.1-1.4cm is considered normal [13]. A CIA diameter of

for men and for women is considered ectatic [2].

Right Leg Arterial Duplex Scan (Illustrated in appendix 2- Report appendix 4)

Minor plaque was observed in the common Femoral, Profunda Femoris, Superficial

Femoral and Popliteal arteries. Normal triphasic flow noted throughout on Doppler

sampling. The Femoro-Popliteal arteries showed evidence of ectasia but were not

aneurysmal. The Popliteal artery measured a maximum diameter of 11.0mm along

its length. The calf arteries demonstrated normal triphasic flow on Doppler sampling.

Patient C was investigated for right Popliteal artery aneurysm after a Popliteal

prominence was revealed on clinical examination. No evidence to support clinical

findings of prominent Popliteal artery aneurysm, however it was found to be ectatic.

Studies reveal 62% of patients with a Popliteal aneurysm will also have an AAA.

5

Dissimilarly to this only 14% of patients with an AAA will develop a Femoral or

Popliteal artery aneurysm. Hence justifying the need for further investigation when a

prominence is identified on clinical examination [5].

Management and treatment outcomes

Elective AAA repair should be considered in men with aneurysm 5.5cm or when

rate of expansion is 0.6cm-0.8cm per year [1, 10]. Duplex ultrasound on Patient C

revealed a 2mm growth in the last year of his AAA thus this measurement criteria in

isolation suggests continued management by surveillance. Conservative treatment

by risk modification is limited as the main modifiable risk factor and leading

contributor to AAA growth is smoking and Patient C is known to be a non-smoker.

However Patient C’s comorbidities of hypertension and hyperlipidaemia should

continue to be aggressively managed with antihypertensives and statins. There are

current debates to the additional benefit of statin use for reduction of AAA size.

Nonetheless statins have been shown to be useful as a threefold reduction in risk for

cardiovascular death after repair [7, 10].

At 75 years of age Patient C has been clinically diagnosed with prostate cancer for

which he has decided to take a watchful waiting approach. As the AAA is yet to

reach ≥5.5cm and expansion rates are consistent with predicted values the vascular

surgeon and Patient C may choose to take the same approach. As represented in

appendix 5.3 AAA between 5.0-5.9cm in diameter have an increased risk of rupture

by 1-10%. Taking this into consideration, with the increase in aneurysmal diameter to

twice that of the year before, surveillance of Patient C by Duplex ultrasound should

increase in frequency from 12 monthly to 3 monthly (appendix 5.1). This

recommendation is also reflected in, appendix 5.2, AAA surveillance intervals by

country.

Outcomes vary between asymptomatic and symptomatic presentations of patients

with AAA. Asymptomatic cases are often found incidentally on clinical examination

when a palpable abdominal mass is present. Symptomatic cases can present with a

pulsatile and painful abdomen, pain in the chest, lower back pain and scrotum. One

6

study reported mortality rates in symptomatic patients that undergo elective repair

are as high as 26% compared with asymptomatic patients with a 5%rate [10].

7

Discussion

Rupture of an AAA is highly lethal with an estimated incidence of sudden death in

>50% of cases. The high mortality rates can be attributed to patient failure to reach a

hospital in time as well as the level of surgical experience [10]. Emergency repairs

hold mortality rates as high as 50-80%. Whereas mortality rates in elective repair are

much lower at less than 5% in some cases [5]. Infrarenal AAA can rupture into the

peritoneal cavity (anteriorly) or retroperitoneum (posteriorly). Peritoneal rupture has

the highest mortality rate as it is commonly accompanied by haemodynamic

collapse. A posterior rupture into the retroperitoneum can occur without significant

blood loss and initially be haemodynamically stable. This occurs due to the

containment abilities of the psoas muscle, adjacent periaortic and perivertebral

tissue [1].

Surgical intervention of an AAA encompasses two main approaches of repair. The

first of which is an open repair requiring an abdominal flank incision, control of

vessels above and below the aneurysm whilst the aneurysmal sac is opened and

interposition of a synthetic graft is implemented. The second approach is an

endovascular repair (EVAR), which can be performed percutaneously under local

anaesthetic [7]. Patients 70 years and older, as in Patient C’s case, tend to do better

with open repair regardless of the 30-day mortality risk between 4-5%[6].

Common postoperative complications associated with elective repair include

myocardial ischaemia, mild renal insufficiency (occurs in 6%), pulmonary disease

(pneumonia 5%), lower extremity ischaemia and postoperative bleeding. EVAR is

significantly less invasive than open surgical repairs requiring fewer postoperative

days in hospital care, including ICU, and typically result in shorter patient recovery

periods. EVAR is initially offered to patient deemed unfit for open repair due to its

invasive nature but is dependent on anatomical structures. Failure of the EVAR to

exclude blood flow from the aneurysmal sac completely leads to endoleaks. In

addition to this the occasional report of endograft migration, aneurysmal rupture and

aneurysmal enlargement has raised questions regarding longevity. Thus it is seen

that where open repair has varied rates of complication following elective repair

EVAR requires more post-repair interventions. The long-term durability EVAR has

8

not been as well established as open repair [1, 8]. Nevertheless the curve of long-

term survival rates with either treatment approach appears to converge after 2-

3years [5].

The value of conservative treatment by surveillance continues to be maintained in

the presence of surgical risk and varied long term survival rates. Studies have

determined that until the infrarenal AAA diameter exceeds 5.5cm it carries a

9

10

References

1. Arko, F., Smith, S., & Zarins, C. 2007, "Repair of Infrarenal Abdominal

Aortic Aneurysms", ACS Surgery: Principles and Practice, pp. 1-12.

2. Arunkumar Mistry, K., Bashir, O. & et al. 2015, “Iliac artery aneurysm”,

Radiopedia viewed 09 September 2015, via radiopedia database.

3. Bown, M.J., Sweeting, M.J., Brown, L.C., Powell, J.T., Thompson, S.G. &

RESCAN Collaborators 2013, "Surveillance Intervals for Small Abdominal

Aortic Aneurysms: A Meta-analysis", JAMA, vol. 309, no. 8, pp. 806-813.

4. Grant SW, Sperrin M, Carlson E. & National Library of Medicine 2015,

Calculating when elective abdominal aortic aneurysm repair improves

survival for individual patients: development of the Aneurysm Repair

Decision Aid and economic evaluation, NIHR Journals Library.

5. Jacob, A.D., Barkley, P.L., Broadbent, K.C. & Huynh, T.T.T. 2015,

"Abdominal aortic aneurysm screening", Seminars in roentgenology, vol.

50, no. 2, pp. 118-126.

6. Keisler, B. & Carter, C. 2015, "Abdominal aortic aneurysm", American

Family Physician, vol. 91, no. 8, pp. 538.

7. Kent, K.C. 2014, "Clinical practice. Abdominal aortic aneurysms", The New

England journal of medicine, vol. 371, no. 22, pp. 2101.

8. Robinson, D., Mees, B., Verhagen, H. & Chuen, J. 2013, "Aortic aneurysms:

Screening, surveillance and referral", Australian Family Physician, vol. 42,

no. 6, pp. 364-369.

11

9. Sano, M., Sasaki, T., Hirakawa, S., Sakabe, J., Ogawa, M., Baba, S., Zaima,

N., Tanaka, H., Inuzuka, K., Yamamoto, N., Setou, M., Sato, K., Konno, H.

& Unno, N. 2014, "Lymphangiogenesis and Angiogenesis in Abdominal

Aortic Aneurysm: e89830", PLoS One, vol. 9, no. 3.

10. Skow, G. 2011, "Abdominal aortic aneurysm", Journal of Men's Health, vol.

8, no. 4, pp. 306-312.

11. Stickley, S. & Meier, G. 2013, " The Role of Color Duplex Ultrasound in Patients with Abdominal Aortic Aneurysms and Peripheral Aneurysms",

Noninvasive Vascular Diagnosis: A Practical Guide to Therapy, Springer-

Verlag London.

12. Thrush, A. & Hartshorne, T. 2005, Peripheral vascular ultrasound: how,

why, and when, 2nd edn, Churchill Livingstone, New York; Edinburgh.

13. Touat, Z., Ollivier, V., Dai, J., Huisse, M., Bezeaud, A., Sebbag, U.,

Palombi, T., Rossignol, P., Meilhac, O., Guillin, M. & Michel, J. 2006,

"Renewal of Mural Thrombus Releases Plasma Markers and Is Involved in

Aortic Abdominal Aneurysm Evolution", The American Journal of

Pathology, vol. 168, no. 3, pp. 1022-1030.

12

Appendix 1 – Aorto-Iliac Arterial Duplex Worksheets (August 2015)

13

Appendix 2 – Right Leg Peripheral Arterial Duplex Worksheets

14

Appendix 3 – Report – Aorto-Iliac Arterial Duplex Scan (August 2015)

15

Appendix 4 – Report - Peripheral Leg Arterial Duplex Scan

16

Appendix 5 5.1 Suggested surveillance for patients with stable AAA [8]

5.2 Abdominal Aortic Aneurysm Surveillance Intervals by Country [3]

5.3 Risk of rupture for AAA [8]

Reprinted from AUSTRALIAN FAMILY PHYSICIAN VOL. 42, NO. 6, JUNE 2013 365

growth and rupture have been promising in animal models, these benefits

have not been consistently reproduced in human studies. 21,22 Optimal

cardiovascular risk factor management should include smoking cessation,

a statin, antiplatelet and antihypertensive agents to improve life

expectancy by reducing cardiovascular mortality. In addition to preventing

aneurysm related mortality, screening for AAA will identify patients with

small aneurysms who are at increased risk of cardiovascular events and

who will benefit from cardiovascular risk management.

Many patients are under the misapprehension that a diagnosis of

small AAA prohibits them from physical activity, or overseas travel.

There is no evidence that physical activity leads to aneurysm rupture.

The role of imaging

A number of imaging modalities are available for the assessment of

AAA. Ultrasound is a relatively cheap, non-invasive, widely available

and reliable tool for detecting and measuring AAAs. It is the modality

of choice for screening and surveillance.

Computed tomography angiography (CTA) is fast, reproducible

and accurately depicts aneurysm morphology. It is the investigation

of choice when considering potential surgical repair, and enables

multiplanar analysis. Limitations include the need for high doses of

intravenous iodinated contrast (potentially harmful in patients with

renal impairment), and the use of ionising radiation.

Magnetic resonance angiography has limited utility in AAA.

Digital subtraction angiography has largely been replaced by CTA for

preoperative planning. It is now predominantly reserved for therapeutic

purposes and is utilised during endovascular aneurysm repair (EVAR) to

accurately position the stent graft before deployment.

In AAA surveillance imaging, the most relevant dimension is the

maximum transverse diameter, ideally perpendicular to the line of

flow. Aneurysm length is often reported, but is not relevant, except in

planning for surgical repair. The presence of mural thrombus is also

generally not relevant unless the aorta is critically stenosed or there is

evidence of distal embolisation.

demonstrated to reduce aneurysm related mortality in four large trials,

including one performed in Western Australia.2–5,12 Considerable

variation exists between international screening protocols, with

concerns over value and effectiveness.13,14 Cost effectiveness may

be increased by screening those at particularly increased risk of AAA,

such as men with a history of smoking, or patients with atherosclerotic

risk factors or a family history of AAA. More rigorous risk scoring

systems are being explored.15

First degree family members of patients with a diagnosed AAA

are at higher lifetime risk of developing a AAA of up to 20%, 16–18

however, the genetic mechanisms for this are unclear.19 Previous

recommendations have included screening for men and women over 50

years of age with a family history of AAA.20

The majority of AAAs detected with screening are below the

threshold for elective repair. The management of patients with small

AAA most importantly includes cardiovascular risk management

with lifestyle advice, smoking cessation, pharmacotherapy (anti-

hypertensives, statins, beta-blockers), and ongoing aneurysm

surveillance. Suggested surveillance intervals are listed in Table 3,

although local protocols may vary based on accessibility to imaging,

patient preference and logistical factors.

While pharmacological interventions such as doxycycline, beta-

blockers, statins and angiotensin pathway inhibitors to reduce AAA

Ta b le 1. AAA r isk fa ct ors

Advancing age

Male gender

Smoking

Family history

Atherosclerosis

Hypertension

Hypercholesterolaemia

Other vascular aneurysm

Ta b le 2. 12 m on t h AAA ru p t u re r isk b y d ia m et er

AAA diameter (cm) Rupture risk (%/year)

3.0–3.9 0%

4.0–4.9 1%

5.0–5.9 1–10%

6.0–6.9 10–22%

>7.0 30–50%

Ta b le 3. Su g g est ed AAA su rveilla n ce in t erva ls

AAA diameter (cm) Surveillance interval (months)

3.0–3.9 24

4.0–4.5 12

4.6–5.0 6

>5.0 3

Figure 1. Anatomical reference terms for aor tic segments

Image cour tesy Cook Medical, Bloomington NH, USA

Ascending aorta, aortic root

Visceral segment suprarenal aorta

Iliac segment

Infrarenal aorta

Supra-aortic trunks and aortic arch

Descending thoracic aorta (distal to left subclavian artery)

Reprinted from AUSTRALIAN FAMILY PHYSICIAN VOL. 42, NO. 6, JUNE 2013 365

growth and rupture have been promising in animal models, these benefits

have not been consistently reproduced in human studies. 21,22 Optimal

cardiovascular risk factor management should include smoking cessation,

a statin, antiplatelet and antihypertensive agents to improve life

expectancy by reducing cardiovascular mortality. In addition to preventing

aneurysm related mortality, screening for AAA will identify patients with

small aneurysms who are at increased risk of cardiovascular events and

who will benefit from cardiovascular risk management.

Many patients are under the misapprehension that a diagnosis of

small AAA prohibits them from physical activity, or overseas travel.

There is no evidence that physical activity leads to aneurysm rupture.

The role of imaging

A number of imaging modalities are available for the assessment of

AAA. Ultrasound is a relatively cheap, non-invasive, widely available

and reliable tool for detecting and measuring AAAs. It is the modality

of choice for screening and surveillance.

Computed tomography angiography (CTA) is fast, reproducible

and accurately depicts aneurysm morphology. It is the investigation

of choice when considering potential surgical repair, and enables

multiplanar analysis. Limitations include the need for high doses of

intravenous iodinated contrast (potentially harmful in patients with

renal impairment), and the use of ionising radiation.

Magnetic resonance angiography has limited utility in AAA.

Digital subtraction angiography has largely been replaced by CTA for

preoperative planning. It is now predominantly reserved for therapeutic

purposes and is utilised during endovascular aneurysm repair (EVAR) to

accurately position the stent graft before deployment.

In AAA surveillance imaging, the most relevant dimension is the

maximum transverse diameter, ideally perpendicular to the line of

flow. Aneurysm length is often reported, but is not relevant, except in

planning for surgical repair. The presence of mural thrombus is also

generally not relevant unless the aorta is critically stenosed or there is

evidence of distal embolisation.

demonstrated to reduce aneurysm related mortality in four large trials,

including one performed in Western Australia.2–5,12 Considerable

variation exists between international screening protocols, with

concerns over value and effectiveness.13,14 Cost effectiveness may

be increased by screening those at particularly increased risk of AAA,

such as men with a history of smoking, or patients with atherosclerotic

risk factors or a family history of AAA. More rigorous risk scoring

systems are being explored.15

First degree family members of patients with a diagnosed AAA

are at higher lifetime risk of developing a AAA of up to 20%, 16–18

however, the genetic mechanisms for this are unclear.19 Previous

recommendations have included screening for men and women over 50

years of age with a family history of AAA.20

The majority of AAAs detected with screening are below the

threshold for elective repair. The management of patients with small

AAA most importantly includes cardiovascular risk management

with lifestyle advice, smoking cessation, pharmacotherapy (anti-

hypertensives, statins, beta-blockers), and ongoing aneurysm

surveillance. Suggested surveillance intervals are listed in Table 3,

although local protocols may vary based on accessibility to imaging,

patient preference and logistical factors.

While pharmacological interventions such as doxycycline, beta-

blockers, statins and angiotensin pathway inhibitors to reduce AAA

Ta b le 1. AAA r isk fa ct ors

Advancing age

Male gender

Smoking

Family history

Atherosclerosis

Hypertension

Hypercholesterolaemia

Other vascular aneurysm

Ta b le 2. 12 m on t h AAA ru p t u re r isk b y d ia m et er

AAA diameter (cm) Rupture risk (%/year)

3.0–3.9 0%

4.0–4.9 1%

5.0–5.9 1–10%

6.0–6.9 10–22%

>7.0 30–50%

Ta b le 3. Su g g est ed AAA su rveilla n ce in t erva ls

AAA diameter (cm) Surveillance interval (months)

3.0–3.9 24

4.0–4.5 12

4.6–5.0 6

>5.0 3

Figure 1. Anatomical reference terms for aor tic segments

Image cour tesy Cook Medical, Bloomington NH, USA

Ascending aorta, aortic root

Visceral segment suprarenal aorta

Iliac segment

Infrarenal aorta

Supra-aortic trunks and aortic arch

Descending thoracic aorta (distal to left subclavian artery)

17

5.4 Growth rates for AAA [10]