ABDOMINAL AORTIC ANEURYSM

PRESENTOR – DR.R.RAGUL PRADEEP

MODERATOR – DR.SATHYASEELAN
INTRODUCTION

•Ruptured AAA is the 15th leading killer overall and the

10th leading killer for men older than 55 years in the United
States.
•More than 5000 people die from ruptured AAA every year,
and 4% to 5% of sudden deaths are caused by ruptured
AAA.
•Roughly half of patients with ruptured AAA die before they
reach the hospital, whereas half of those who do arrive do
not survive despite treatment.
• Under all circumstances, ruptured AAAs result in an
overall mortality of 80% to 90%
DEFINITION AND LOCATION

•An aneurysm is defined as a permanent, localized (ie, focal) dilation

of an artery having at least a 50% increase in diameter compared with
the expected normal diameter of the artery .

•More than 80% of AAAs are located in the Infrarenal portion of the
aorta.

• Thus, because the normal diameter of this portion in patients older

than 50 years is estimated to be 10 to 20 mm, an infrarenal
abdominal aorta larger than 30 mm is considered to be an AAA.
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 .

ETIOLOGY

• Atherosclerosis

• Family History and First degree Relatives

• Ehler-Danlos Syndrome(Collagen Defect)

• Syphilis

• Marfan syndrome
DEGENERATION
•A degenerative process in the Aortic wall is the most common
cause, and more than 90% of AAAs are degenerative.

• Moreover, there is usually some degree of calcification and

atherosclerotic disease present in such AAAs i.e Atherosclerosis
is also associated with degeneration of the Aortic wall.

•Metalloproteinases, a family of Elastases are abundant in AAA

walls to degrade the extracellular matrix proteins such as Elastin
and Collagen, making the Aortic wall fragile and prone to
forming Aneurysm

•Smoking is strongly related to this process.

INFLAMMATION
• AAA sometimes occur with a marked inflammatory change
consisting of a thick, fibrotic process in the retroperitoneum.

•These inflammatory AAAs account for 5% to 10% of all AAAs.

• Special attention should be paid, especially when performing open

aneurysm repair, because inflammation often involves surrounding
organs such as the Duodenum and Ureter.

• Some specific diseases such as Takayasu arteritis and Behchet

disease can cause aortic inflammation.

•Steroids are useful for remission of the inflammatory change.

INFECTION

•Infectious or mycotic AAAs are a rare condition, but the

mortality is high.

•Rapid destruction of the arterial wall resulting in rupture and

persistent infection after the aneurysm repair accounts for the
poor outcomes of infectious AAAs.
CONNECTIVE TISSUE ABNORMALITIES

•AAAs in patients with Marfan syndrome or Ehlers-Danlos

syndrome often extend up to the thoracic region and persist as a
chronic state after aortic dissection.

• Patients with such connective tissue abnormalities tend to

develop larger AAAs at a younger age than patients with
ordinary degenerative AAAs
RISK FACTORS
ASYMPTOMATIC AAAs

•Screening with Ultrasonography (US) on specific high-risk

patients is established as the most effective way to filter
asymptomatic AAAs, which are usually found accidentally by
various imaging modalities performed for other purposes in
clinical settings.

•US screening for men between 65 and 75 years of age who

have a smoking history.
HISTORY TAKING
The important information that should be taken from AAA
patients are:

(1) when and how the AAA was diagnosed

(2) the underlying medical conditions, especially
hypertension, dyslipidemia, diabetes mellitus, renal dysfunction,
cerebrovascular diseases, heart disease, pulmonary disease,
peripheral vascular disease, and previous surgical history
(3) allergic history and current medications
(4) smoking history
(5) family history of any aortic aneurysms or dissections.
EXAMINATION

•An AAA can be palpable as a pulsatile mass at or above the

umbilicus, but the accuracy of manipulation highly depends on the
patient’s physique and the size of the AAA.

•Examination of peripheral arteries are also important. From 1% to

10% of AAAs complicate other peripheral arterial aneurysms,
synchronously or metachronously, particularly in the Femoral arteries
and Popliteal arteries

•Presence of a bruit indicates possible stenotic lesions or

arteriovenous fistula
IMAGING MODALITIES AND DIAGNOSIS

•Diagnosis of an AAA is confirmed by several imaging modalities,

including abdominal US, computed tomography (CT), magnetic
resonance imaging (MRI), or angiography.

•A combination of each finding provides accurate location, shape, and

size of an AAA
ULTRASONOGRAPHY
ADVANTAGES:
• noninvasiveness
• low cost
•The sensitivity and specificity are more than 90% when it is
performed by well-trained doctors.
• US is most useful for periodic follow-up to measure AAA size after
the initial diagnosis

DISADVANTAGES:
•The patient’s physique and the location of the aneurysm also affects
the quality
•The findings around the suprarenal or pelvic regions are often poor
because of intestinal gas.
CT

•Contrast-enhanced CT is the most reliable, indispensable

modality, not only for diagnosis but also for decision making for
AAAs.

•It is the current gold standard.

• CT can accurately and objectively detect AAA formation

regardless of location or the patient’s physique.
In addition, three-dimensional CT angiography composed of thin slice
( <3mm)images obtained by multidetector row CT scanners clearly
describes the details of the lesion, such as the

• Location

• Length of the aneurysmal neck

• The anatomic relationship to the visceral branches

• The patency of the lumbar arteries

• The existence of concomitant iliac arterial aneurysms

All important observations decide how to treat the AAA, either by open
repair or endovascular aneurysm repair (EVAR).
Disadvantages of CT

• Radiation Exposure

•Requirement for a contrast medium

• Higher cost compared with USG.

However, non-Enhanced CT images still provide much valuable

information. Therefore, all asymptomatic patients with AAA
should be evaluated by CT with or without contrast medium .
MRI

•Contrast-enhanced Magnetic Resonance (MR) Angiography describes

the detailed structure of an AAA as well as does contrast-enhanced CT
angiography.

•Nonenhanced MR Angiography alone can describe the whole shape

of an AAA, it is useful when planning an EVAR for patients with renal
dysfunction
ADVANTAGE:

•No Radiation Exposure

DISADVANTAGES

•Time consuming process.

•Contraindication for patients with claustrophobia

• Magnetic material implantation

• Higher cost compared with CT

ANGIOGRAPHY

•Diagnostic Angiography has been almost

completely replaced by other modalities because of
its invasiveness and the administration of contrast
medium.
CRITERIA FOR INTERVENTION
•Patients with small AAAs are managed conservatively.

•The purpose of such treatments is to reduce the expansion rate of

AAAs and to optimize each patient’s underlying medical condition in
preparation for future aneurysm repair.

1.Smoking cessation

2.b-blockers and Statins

3. NSAIDS- inhibits Elastase

4.Doxycylline( Matrix Metalloprotease Inhibitor)

AAA SURGICAL TECHNIQUES:

• Open Repair

• Endo Vascular Aneurysmal Repair(EVAR)

• Laparoscopic Repair
OPEN REPAIR

•Since the first graft replacement was reported by Dubost in

1951,open repair was the only option for preventing AAA ruptures
until the first EVAR was reported by Parodi in 1991.

•Open repair, which consists of directly opening the aneurysmal sac

and implanting a synthetic graft with physical suture stitches, is still
the only curative treatment of AAAs.

•Once an AAA is resected and replaced with a synthetic graft, the

aneurysm has certainly disappeared, and the patient essentially
needs no further follow-up radiologic studies.
Transperitoneal Approach

Advantages :
• Most rapid
• Greatest versatility
• Provides widest access
• Enables evaluation and treatment of concomitant intra-
abdominal disease

Disadvantages:
• Longer postoperative ileus
• Potential for greater fluid losses
• Difficulty with exposure and control for suprarenal aneurysms
• Higher incidence of incisional hernia
Retroperitoneal Approach
Advantages:
• Avoids hostile abdomen
• Facilitates suprarenal exposure and control
• Potential reduction of postoperative ileus
• Obesity
• Inflammatory AAA
• Horseshoe kidney

Disadvantages:
• Poor access to right renal and iliac arteries
• Cannot evaluate intra-abdominal disease
• Flank bulge
ENDOVASCULAR ANEURYSMAL REPAIR

•Based on the concept that pressure reduction inside the aneurysm

can prevent its future rupture, the initial purpose of EVAR is not to
delete the aneurysm but to decompress it.

•Although some successful EVARs can eliminate AAAs by complete

decompression leading to aneurysmal wall remodeling and shrinkage
after several months.

• AAAs still remain after EVAR in most cases.

• Therefore, the only way to judge whether an EVAR has been

successful is to continue observing the aneurysm size after each
procedure
•Patients treated with EVAR are routinely examined for AAA size by CT
or US at 1, 6, and 12 months after the procedure, and annually
thereafter.

1.If the size is decreasing- it means the EVAR has been successful.

2.If the size remains the same- it means the intrasac pressure is still
not high enough to expand.

3.If the size is increasing- it calls for action in response to endoleaks

ENDOLEAKS AFTER EVAR:
•Endoleaks are a complication unique to endovascular repair for
aortic aneurysms.
• Defined as the remaining blood flow inside the aneurysmal sac after
the endograft insertion.

Endoleaks are classified into 4 types:

1.Type I (perigraft blood flow caused by an inadequate seal at the
proximal or distal end of the endograft).
2.TYPE II(retrograde blood flow into the AAA from visceral vessels
[such as the lumbar artery, inferior mesenteric artery, accessory renal
artery, or hypogastric artery) without attachment site connection). ;
3.Type III (perigraft blood flow from module disconnection or fabric
disruption).
4. Type IV (perigraft blood flow from porous fabric).
•Type I and type III Endoleaks are usually detected at the time of EVAR
by completion of an angiogram and are then treated properly.

•However, they sometimes appear at a later stage to cause chronic

AAA size expansion.

•Type II Endoleaks, especially from patent lumbar arteries or the

inferior mesenteric artery, cause chronic expansion in many cases.

• Type IV Endoleaks often disappear spontaneously within several

weeks.
SYMPTOMATIC OR RUPTURED AAA
Clinical Presentation and Management:

The classic triad of symptoms for ruptured AAA is:

(1) Hypotension.
(2) Abdominal or Back pain.
(3) A Pulsatile abdominal mass.

•When a patient with known Infrarenal AAA that is larger than 55 mm

presents with this triad and the general status is unstable, the patient
should be brought to the operating room immediately to open the
abdomen and clamp the AAA neck as quickly as possible.
•If the patient is clinically stable, an urgent CT with or without
contrast medium and duplex US are useful for ruling out rupture.

•But the patient should at least be hospitalized for close observation

even if rupture is ruled out, and a quick repair of the AAA is desirable.

• Also, a quick repair is necessary for some rapidly expanding AAAs

even if they are asymptomatic, because they are considered to be at
risk of rupture if the expansion rate is more than 5 mm per 6 months.
 REFERENCES

• SABISTON’S TEXTBOOK OF SURGERY ; 21ST EDITION

• MAINGOT’S ABDOMINAL OPERATIONS ; 13TH EDITION

• SCHWARTZ PRINCIPLES OF SURGERY; 10TH EDITION