abdominal aortic aneurysm - wikipedia, the free encyclopedia

8/3/2019 Abdominal Aortic Aneurysm - Wikipedia, The Free Encyclopedia

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Abdominal aortic aneurysm

Classification and external resources

CT reconstruction image of an abdominal aortic aneurysm

ICD-10 I71.3 (http://apps.who.int/classifications/apps/icd/icd10online/?

gi70.htm+i713) , I71.4

(http://apps.who.int/classifications/apps/icd/icd10online/?

gi70.htm+i714)

ICD-9 441.3 (http://www.icd9data.com/getICD9Code.ashx?

icd9=441.3) , 441.4

(http://www.icd9data.com/getICD9Code.ashx?icd9=441.4)

OMIM 100070 (http://omim.org/entry/100070)

DiseasesDB 792 (http://www.diseasesdatabase.com/ddb792.htm)

MedlinePlus 000162

(http://www.nlm.nih.gov/medlineplus/ency/article/000162.htm)

eMedicine med/3443 (http://www.emedicine.com/med/topic3443.htm)emerg/27 (http://www.emedicine.com/emerg/topic27.htm#)

radio/1 (http://www.emedicine.com/radio/topic1.htm#)

MeSH D017544 (http://www.nlm.nih.gov/cgi/mesh/2011/MB_cgi?

field=uid&term=D017544)

Abdominal aortic aneurysmFrom Wikipedia, the free encyclopedia

Abdominal aortic aneurysm (also

known as AAA, pronounced "triple-

a") is a localized dilatation(ballooning) of the abdominal aorta

exceeding the normal diameter by

more than 50 percent, and is the

most common form of aortic

aneurysm. Approximately 90

percent of abdominal aortic

aneurysms occur infrarenally (below

the kidneys), but they can also occur

pararenally (at the level of the

kidneys) or suprarenally (above thekidneys). Such aneurysms can

extend to include one or both of the

iliac arteries in the pelvis.

Abdominal aortic aneurysms occur

most commonly in individuals

between 65 and 75 years old and

are more common among men and

smokers. They tend to cause no

symptoms, although occasionallythey cause pain in the abdomen and

back (due to pressure on

surrounding tissues) or in the legs

(due to disturbed blood flow). The

major complication of abdominal

aortic aneurysms is rupture, which is

life-threatening, as large amounts of

blood spill into the abdominal cavity,

and can lead to death within

minutes.[1]

Mortality in the hospital is60% to 90%.

Surgery is recommended when the

aneurysm is large enough (>5.5 cm

in diameter) that the risk of surgery

(1% to 6%) is less than the risk of

rupture. In open surgery, the surgeon opens the abdomen and stitches in a replacement section of artery; in

endovascular surgery the surgeon feeds the replacement section through the patient's artery and replaces it from

inside.

Search


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There is moderate evidence to support screening in individuals with risk factors for abdominal aortic aneurysms

(e.g., males 65).

Contents

1 Classification

2 Signs and symptoms3 Causes

4 Pathophysiology

5 Diagnosis

6 Screening

7 Management

7.1 Conservative

7.2 Medication

7.3 Surgery

8 Prognosis9 Epidemiology

10 History

11 Research

11.1 Risk assessment and experimental models

11.2 Prevention and treatment

12 References

Classification

Abdominal aortic aneurysms are commonly divided according to their size and symptomatology. An aneurysm is

usually defined as an outer aortic diameter over 3 cm (normal diameter of the aorta is around 2 cm).[2] If the outer

diameter exceeds 5.5 cm, the aneurysm is considered to be large.[3] A ruptured AAA is a clinical diagnosis

involving the presence of the triad of abdominal pain, shock and a pulsatile abdominal mass. If these conditions are

present, indicating AAA rupture, no further clinical investigations are needed before surgery.[4]

Signs and symptoms

The vast majority of aneurysms are asymptomatic. However, as abdominal aortic aneurysms expand, they may

become painful and lead to pulsating sensations in the abdomen or pain in the chest, lower back, or scrotum.[5] Th

risk of rupture is high in a symptomatic aneurysm, which is therefore considered an indication for surgery. The

complications include rupture, peripheral embolization, acute aortic occlusion, and aortocaval (between the aorta

and inferior vena cava) or aortoduodenal (between the aorta and the duodenum) fistulae. On physical examination

a palpable abdominal mass can be noted. Bruits can be present in case of renal or visceral arterial stenosis.[6]

The clinical manifestation of ruptured AAA usually includes excruciating pain of the lower back, flank, abdomen

and groin. The bleeding usually leads to a hypovolemic shock with hypotension, tachycardia, cyanosis, and altered


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A plate from Gray's Anatomy with

yellow lines depicting the most

common infrarenal location of the

AAA.

mental status. The mortality of AAA rupture is up to 90%. 6575% of

patients die before they arrive at hospital and up to 90% die before they

reach the operating room.[7] The bleeding can be retroperitoneal or

intraperitoneal, or the rupture can create an aortocaval or aortointestinal

(between the aorta and intestine) fistula.[8] Flank ecchymosis

(appearance of a bruise) is a sign of retroperitoneal hemorrhage, and is

also called Grey Turner's sign.[6]

Causes

The exact causes of the degenerative process remain unclear. There are,

however, some theories and well defined risk factors.

Tobacco smoking: Greater than 90% of people who develop

an AAA have smoked at some point in their life.[9]

Genetic influences: The influence of genetic factors is highly

probable. The high familial prevalence rate is most notable in

male individuals.[10] There are many theories about the exact genetic disorder that could cause higher

incidence of AAA among male members of the affected families. Some presumed that the influence of

alpha 1-antitrypsin deficiency could be crucial, some experimental works favored the theory of X-linke

mutation, which would explain the lower incidence in heterozygous females. Other theories of genetic

etiology have also been formulated.[6] Connective tissue disorders, such as Marfan syndrome and

Ehlers-Danlos syndrome, have also been strongly associated with AAA.[8] Both relapsing polychondrit

and pseudoxanthoma elasticum may cause abdominal aortic aneurysm.[11]

Atherosclerosis : The AAA was long considered to be caused by atherosclerosis, because the walls o

the AAA are frequently affected heavily. However, this theory cannot be used to explain the initial defe

and the development of occlusion, which is observed in the process.[6]

Other causes: Other causes of the development of AAA include: infection, trauma, arteritis, cystic

medial necrosis (m. Erdheim).[8]

Pathophysiology

The most striking histopathological changes of aneurysmatic aorta are seen in tunica media and intima. These

include accumulation of lipids in foam cells, extracellular free cholesterol crystals, calcifications, thrombosis, and

ulcerations and ruptures of the layers. There is an adventitial inflammatory infiltrate.[8] However, the degradation o

tunica media by means of proteolytic process seems to be the basic pathophysiologic mechanism of the AAAdevelopment. Some researchers report increased expression and activity of matrix metalloproteinases in individual

with AAA. This leads to elimination of elastin from the media, rendering the aortic wall more susceptible to the

influence of the blood pressure.[6] There is also a reduced amount of vasa vasorum in the abdominal aorta

(compared to the thoracic aorta); consequently, the tunica media must rely mostly on diffusion for nutrition which

makes it increasingly susceptible to damage.[12]

Hemodynamics affect the development of AAA. It has a predilection for the infrarenal aorta. The histological

structure and mechanical characteristics of infrarenal aorta differ from those of the thoracic aorta. The diameter

decreases from the root to the bifurcation, and the wall of the abdominal aorta also contains a lesser proportion of


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elastin. The mechanical tension in abdominal aortic wall is therefore higher than in the thoracic aortic wall. The

elasticity and distensibility also decline with age, which can result in gradual dilatation of the segment. Higher

intraluminal pressure in patients with arterial hypertension markedly contributes to the progression of the

pathological process.[8] Suitable hemodynamics conditions may be linked to specific Intraluminal Thrombus (ILT)

patterns along the aortic lumen, which in turn may affect AAA's development.[13]

Diagnosis

An abdominal aortic aneurysm is usually diagnosed by physical exam, ultrasound, or CT. Plain abdominal

radiographs may show the outline of an aneurysm when its walls are calcified. However, this is the case in less than

half of all aneurysms. Ultrasonography is used to screen for aneurysms and to determine the size of any present.

Additionally, free peritoneal fluid can be detected. It is noninvasive and sensitive, but the presence of bowel gas or

obesity may limit its usefulness. CT scan has a nearly 100% sensitivity for aneurysm and is also useful in

preoperative planning, detailing the anatomy and possibility for endovascular repair. In the case of suspected

rupture, it can also reliably detect retroperitoneal fluid. Alternative less often used methods for visualization of the

aneurysm include MRI and angiography.

An aneurysm ruptures if the mechanical stress (tension per area) exceeds the local wall strength; consequently, peawall stress (PWS) [14] and peak wall rupture risk (PWRR) [15] have been found to be more reliable parameters

than diameter to assess AAA rupture risk. Medical software allows computing these rupture risk indices from

standard clinical CT data and provides a patient-specific AAA rupture risk diagnosis.[16]

A rupture AAA with an

open arrow making the

aneurysm and the closed

arrow the free blood in

the abdomen

Sagittal CT image of an

AAA.

Biomechanical AAA

Rupture risk prediction.

An axial contrast

enhanced CT scan

demonstrating an

abdominal aortic

aneurysm of 4.8 by 3.8

cm


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Ultrasound image of a

normal abdominal aorta

measuring 1.9 cm in

diameter.

The faint outline of the

calcified wall of a AAA

as seen on plain X-ray

CT image of an AAA

40,8 mm.

Screening

A clinical practice guideline by the U.S. Preventive Services Task Force "recommends one-time screening forabdominal aortic aneurysm (AAA) by ultrasonography in men age 65 to 75 years who have ever smoked".[17][18]

This is a grade B recommendation.[19] A re-analysis of the meta-analysis estimated a number needed to screen of

approximately 850 patients.[20]

The largest of the randomized controlled trials on which this guideline was based studied a screening program that

consisted of[21]:

Screening men ages 6574 years (not restricted to ever smokers). 'Men in whom abdominal aortic aneurysms

(> or =3 cm in diameter) were detected were followed-up... Patients with an aortic diameter of 3044 cm

were rescanned at yearly intervals, whereas those with an aortic diameter of 4554 cm were rescanned at 3monthly intervals ... Surgery was considered on specific criteria (diameter > or =5.5 cm, expansion > or =1 cm

per year, symptoms)'.

This trial reported significant short[21] (number needed to screen after 4 years of approximately 590 to prevent

nonfatal ruptured AAA plus AAA-related deaths[22]) and long term[23] (number needed to screen after 7 years of

approximately 280 to prevent nonfatal ruptured AAA plus AAA-related deaths) benefit and cost effectiveness.[24

Subsequent randomized controlled trials also found benefit:

number needed to screen after 4 years of 300[25]

number needed to screen after and after 7 years of 563 (calculation

(http://medinformatics.uthscsa.edu/calculator/calc.shtml?calc_rx_2x2.shtml?

a=47.0&b=2898&c=54.0&d=2991&row1total=2945&row2total=3045) ).[26]

In the U.S., effective January 1, 2007, provisions of the SAAAVE Act (Screening Abdominal Aortic Aneurysm

Very Efficiently) now provide a free, one-time, ultrasound AAA screening benefit for those qualified seniors. Men

who have smoked at least 100 cigarettes during their life, and men and women with a family history of AAA qualif

for the one-time ultrasound screening. Enrollees must visit their healthcare professional for their Welcome to

Medicare physical within six months of enrollment in order to qualify for the free screening. The Welcome to

Medicare Physical Exam must be completed within the first six months of Medicare eligibility, but there is no


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published time limit thereafter for completion of the AAA screening. Providers who perform the physical and orde

the AAA screening need to document the AAA risk factors.

Management

The treatment options for asymptomatic AAA are conservative management, surveillance with a view to eventual

repair, and immediate repair. There are currently two modes of repair available for an AAA: open aneurysm repai

(OR), and endovascular aneurysm repair (EVAR). An intervention is often recommended if the aneurysm growsmore than 1 cm per year or it is bigger than 5.5 cm. [9] Repair is also indicated for symptomatic aneurysms.[27]

Conservative

Conservative management is indicated in patients where repair carries a high risk of mortality and in patients where

repair is unlikely to improve life expectancy. The mainstay of the conservative treatment is smoking cessation.

Surveillance is indicated in small asymptomatic aneurysms (less than 5.5 cm) where the risk of repair exceeds the

risk of rupture. As an AAA grows in diameter the risk of rupture increases. Surveillance until the aneurysm has

reached a diameter of 5.5 cm has not been shown to have a higher risk as compared to early intervention.[28][29]

Medication

No medical therapy has been found to be effective at decreasing the growth rate or rupture rate of asymptomatic

AAAs.[27] Blood pressure and lipids should however be treated like in any atherosclerotic condition.[2] Studies

have suggested possible protective effects of therapy with angiotensin converting enzyme inhibitors,[30] beta-

blockers,[2] and statins.[31]

Surgery

Surgery for an abdominal aortic aneurysm is known as AAA surgery or AAA repair. The threshold for repair vari

slightly from individual to individual, depending on the balance of risks and benefits when considering repair versus

ongoing surveillance. The size of an individual's native aorta may influence this, along with the presence of

comorbidities that increase operative risk or decrease life expectancy.[27]

Open repair

Open repair is indicated in young patients as an elective procedure, or in growing or large, symptomatic or rupture

aneurysms. It was the main surgical intervention used from the 1950s until other procedures developed.

Endovascular repair

Main article: Endovascular aneurysm repair

Endovascular repair first became practical in the 1990s and although it is now an established alternative to open

repair, its role is yet to be clearly defined. It is generally indicated in older, high-risk patients or patients unfit for

open repair. However, endovascular repair is feasible for only a proportion of AAAs, depending on the

morphology of the aneurysm. The main advantages over open repair are that there is less peri-operative mortality,

less time in intensive care, less time in hospital overall and earlier return to normal activity. Disadvantages of


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Abdominal aortic endoprosthesis, CT

scan, original aneurysm marked in

blue.

AAA Size (cm) Growth rate (cm/yr)[39] Annual rupture risk (%)[40]

3.0-3.9 0.39 0

4.0-4.9 0.36 0.5-5

5.0-5.9 0.43 3-15

6.0-6.9 0.64 10-20

>=7.0 - 20-50

endovascular repair include a requirement for more frequent ongoing

hospital reviews, and a higher chance of further procedures being

required. According to the latest studies, the EVAR procedure does not

offer any benefit for overall survival or health-related quality of life

compared to open surgery, although aneurysm-related mortality is

lower.[32][33][34][35] In patients unfit for open repair, EVAR plus

conservative management was associated with no benefit, more

complications, subsequent procedures and higher costs compared toconservative management alone.[36] Endovascular treatment for

paraanastomotic aneurysms after aortobiiliac reconstruction is also a

possibility.[37] In 2001 former presidential candidate Bob Dole

underwent surgery for an abdominal aortic aneurysm in which a team of

surgeons led by Doctor Kenneth Ouriel inserted a stent graft:

Ouriel said that the team inserted a Y-shaped tube

through an incision in Dole's leg and placed it inside the

weakened portion of the aorta. The aneurysm will

eventually contract around the stent, which will remain inplace for the rest of Dole's life. --Associated Press[38]

Prognosis

Although the current standard of

determining rupture risk is based

on maximum diameter, it is known

that smaller AAAs that fall below

this threshold (diameter5.5 cm) may remain

stable.[41][42] In one report, it was

shown that 10 - 24% of ruptured

AAAs were less than 5 cm in

diameter.[42] It has also been

reported that of 473 non-repaired AAAs examined from autopsy reports, there were 118 cases of rupture, 13%

which were less than 5 cm in diameter. This study also showed that 60% of the AAAs greater than 5 cm (including

54% of those AAAs between 7.1 and 10 cm) never experienced rupture.[citation needed] Vorp et al. later deduce

from the findings of Darling et al. that if the maximum diameter criterion were followed for the 473 subjects, only7% (34/473) of cases would have succumbed to rupture prior to surgical intervention as the diameter was less tha

5 cm, with 25% (116/473) of cases possibly undergoing unnecessary surgery since these AAAs may never have

ruptured.[43]

Alternative methods of rupture assessment have been recently reported. The majority of these approaches involve

the numerical analysis of AAAs using the common engineering technique of the finite element method (FEM) to

determine the wall stress distributions. Recent reports have shown that these stress distributions have been shown

to correlate to the overall geometry of the AAA rather than solely to the maximum diameter. [44][45][46] It is also

known that wall stress alone does not completely govern failure as an AAA will usually rupture when the wall stres


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exceeds the wall strength. In light of this, rupture assessment may be more accurate if both the patient-specific wal

stress is coupled together with patient-specific wall strength. A non-invasive method of determining patient-

dependent wall strength was recently reported,[47] with more traditional approaches to strength determination via

tensile testing performed by other researchers in the field.[48][49][50] Some of the more recently proposed AAA

rupture-risk assessment methods include: AAA wall stress;[14][51][52] AAA expansion rate;[53] degree of

asymmetry;[46] presence of intraluminal thrombus (ILT);[54] a rupture potential index (RPI);[55][56] a finite element

analysis rupture index (FEARI);[57] biomechanical factors coupled with computer analysis;[58] growth of ILT;[59]

geometrical parameters of the AAA;[60] and also a method of determining AAA growth and rupture based on

mathematical models.[61][62]

The post-operative mortality for an already ruptured AAA has slowly decreased over several decades but remain

higher than 40%.[4] However, if the AAA is surgically repaired before rupture, the post-operative mortality rate is

substantially lower: approximately 1-6%.[63]

Epidemiology

The occurrence of AAA varies markedly by ethnicity. In the United Kingdom the rate of AAA in Caucasian menolder than 65 years is about 4.7%, while in Asian men it is 0.45%. [64] It is also uncommon in individuals of African

and Hispanic heritage.[citation needed]

There are 15,000 deaths yearly in the U.S. secondary to AAA rupture. [65] The frequency varies strongly between

males and females. The peak incidence is among males around 70 years of age, the prevalence among males over

60 years totals 2-6%. The frequency is much higher in smokers than in non-smokers (8:1), and the risk decreases

slowly after smoking cessation.[66] Other risk factors include hypertension and male sex.[8] In the U.S., the

incidence of AAA is 2-4% in the adult population.[6] AAA is 4-6 times more common in male siblings of known

patients, with a risk of 20-30%.[67]

Rupture of the AAA occurs in 1-3% of men aged 65 or more, the mortality is 70-95%.[3]

History

The first historical records about AAA are from Ancient Rome in the 2nd century AD, when Greek surgeon

Antyllus tried to treat the AAA with proximal and distal ligature, central incision and removal of thrombotic materia

from the aneurysm. However, attempts to treat the AAA surgically were unsuccessful until 1923. In that year,

Rudolph Matas (who also proposed the concept of endoaneurysmorrhaphy), performed the first successful aortic

ligation on a human.[68]

Other methods that were successful in treating the AAA included wrapping the aorta withpolyethene cellophane, which induced fibrosis and restricted the growth of the aneurysm. Albert Einstein was

operated on by Rudolf Nissen with use of this technique in 1949, and survived five years after the operation.[69]

Endovascular aneurysm repair was first performed in the late 1980s and has been widely adopted in the subseque

decades. Endovascular repair was first used for treating a ruptured aneurysm in Nottingham in 1994[70]

Former presidential candidate Bob Dole had an abdominal aortic aneurysm in 2001 and was treated surgically by

vascular surgeon Kenneth Ouriel and the operation was successful.[38]

Research


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Risk assessment and experimental models

There have been many calls for alternative approaches to rupture-risk assessment over the past number of years,

with many believing that a biomechanics-based approach may be more suitable than the current diameter approach

Numerical modelling is a valuable tool to researchers allowing approximate wall stresses to be calculated, thus

revealing the rupture potential of a particular aneurysm. Experimental models are required to validate these

numerical results, and provide a further insight into the biomechanical behaviour of the AAA. In vivo, AAAs exhib

a varying range of material strengths[71] from localised weak hypoxic regions[72] to much stronger regions and areaof calcifications.[73] Experimental models can now be manufactured using a novel technique involving the injection-

moulding lost-wax manufacturing process to create patient-specific anatomically-correct AAA replicas.[74] Work

has also focused on developing more realistic material analogues to those in vivo, and recently a novel range of

silicone-rubbers was created allowing the varying material properties of the AAA to be more accurately

represented.[75] These rubber models can also be used in a variety of experimental testing from stress analysis usin

the photoelastic method[76] to deterimining whether the locations of rupture experimentally correlate with those

predicted numerically.[77] New endovascular devices are being developed that are able to treat more complex and

tortuous anatomies.[78]

Prevention and treatment

A recent animal study published in the journalNature Medicine showed that removing a single protein prevents

early damage in blood vessels from triggering a later-stage, frequently lethal complication of atherosclerosis. By

eliminating the gene for a signaling protein called cyclophilin A (CypA) from a strain of mice, researchers were abl

to provide complete protection against abdominal aortic aneurysm (AAA).[79]

Other recent research, published in theAmerican Journal of Pathology, identified Granzyme B (GZMB) (a

protein-degrading enzyme) to be a potential therapeutic target in the treatment of abdominal aortic aneurysms.

Specifically, elimination of this enzyme in mice models - both slowed the progression of aneurysms and improvedsurvival.[80][81]

With the recent advancements in AAA research, coupled with the increasing collaboration between clinicians and

engineers, the future research into AAA rupture-prediction and treatment appears to be in a strong position to

combat what is currently ranked as the 13th leading cause of death in the US and the 10th leading cause of death i

men over the age of 55 years.

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