Aneurysm

THE LARGEST ARTERY IN THE BODY IS THE
aorta, which takes blood from the heart and runs from
the chest into the abdomen, lying against the spine until
it reaches the pelvis. It divides at that point into iliac
arteries that supply blood to the pelvis, buttocks, and legs
(see Fig. 1). Because the aorta takes the full force of blood
ejected from the heart, it is the most likely artery in the
body to weaken.

The abdominal aorta is commonly affected by atheroma
and the process of atherosclerosis (see chapter Atherosclerosis/
Atherothrombosis). Atherosclerotic disease causes
thickening of the intima. This thickening appears to
reduce the diffusion of oxygen and nutrients from the
aortic lumen to the strong middle wall of aorta. This causes
degeneration of the elastic elements and weakening of the
walls of the aorta. The elastic wall of the aorta may be
stretched causing the vessel to dilate. Tension on the
dilated aortic wall increases, thus, causing further expansion
of the artery with aneurysmal formation. Tension in
the dilated vessel wall rises in accordance with Laplace’s
law, which states that wall tension is proportional to the
product of pressure and radius; as the diameter of the aorta
increases its wall tension rises. The torrential blood flow
imparts considerable hydrodynamic stress on the arterial
wall, especially in the lower abdominal aorta.
Most aneurysms occur in the abdomen just after the
aorta branches to the kidney and before the aorta ends
in its division into iliac arteries to the pelvis (see Fig. 1).
Fortunately, aneurysms that occur before the aorta
branches off to the kidney are rare; at this location repair
of an aneurysm is fraught with danger as kidney failure
may occur. Other sites for aneurysmal formation are in the
thoracic aorta, the iliac arteries in the pelvis, and the
popliteal artery at the back of the knee.
Although hypertension, hyperlipidemia, and smoking
are considered risk factors for the expansion of aneurysms,
only smoking has been identified as a consistent risk factor;
smoking increases the growth rate by 20–25%. Data from
a study by Brady et al. including 1743 patients followed
prospectively indicated that blood pressure and cholesterol
levels did not predict the rate of expansion; aneurysms
expanded significantly faster in current smokers than in
former smokers. In addition, other studies indicated that
the risk of rupture and the risk of death due to rupture
are higher among current smokers than among former
smokers and patients who never smoked by as much as a
factor of 14 for smokers.
Weakening of arteries may occur because of loss of
elasticity of the aortic wall due to aging. Another disease
that affects the aortic wall is cystic medial necrosis, and this
appears histologically as smooth muscle cell necrosis and
degeneration of elastic layers within the media. The cause
of the disease is unknown and mostly affects the thoracic
aorta. Virtually all patients with Marfan syndrome develop
cystic medial necrosis disease and many, at a young age,
develop aneurysms that occur mainly in the ascending
aorta, where the aorta originates from the heart.
Studies indicate that there is a familial, genetic incidence
of abdominal aortic aneurysms. Screening of siblings
older than 50 years of age of patients with aneurysms
revealed an occult aneurysm in approximately 30% of
brothers and less than 10% of sisters. The prevalence of
abdominal aortic aneurysms (3–6 cm) is approximately
3 and 5% in individuals older than 55 and 65, respectively.
The prevalence among men is about five times that
among women. Studies suggest that one-time ultrasound
screening of men at age 65 is sufficient to identify nearly
all those who are at risk. At this age men who have aortic
diameters less than 2.6 cm are all expected to be free from
significant aneurysm (less than 4 cm) 12 years later.

Signs and Symptoms
The occurrence of abdominal aortic aneurysms is common
in men over age 55 and in women after age 70. Aneurysms
may grow to more than 5 cm without causing symptoms
and may go unnoticed by the individual. Abdominal aortic
aneurysms, however, are not always asymptomatic. Back
pain, abdominal pain, and particularly intermittent claudication
in men greater than age 65 may be the clue to
the presence of an abdominal aortic aneurysm. Selective
screening for aneurysms in patients with intermittent
claudication nearly doubles the yield over screening in the
general population.
The asymptomatic mass may be detected by deep
manual palpation of the central abdomen below or above
the umbilicus. The majority of aneurysms are not detected
by palpation and they are particularly obscured by body
habitus. Occasionally mild abdominal pain radiating to
the low back occurs. This mild pain usually has a constant,
gnawing quality and may last for hours or days. Pain of
new onset or progressive increase in the intensity of pain
may indicate expansion of the aneurysm or impending
rupture. The rupture of an abdominal aneurysm is usually
accompanied by increasing severity of pain, lower blood
pressure, hypotension, and a pulsatile mass in the central
abdomen. The patient is usually anxious, sweaty, and in
distress.
A simple ultrasound of the abdomen detects all
abdominal aneurysms and gives a good estimate of their
size. Screening is recommended mainly in patients at
risk. The normal diameter of the aorta is 1.8–2 cm.
Approximately 10% of men have an aortic diameter of
more than 2.9 cm by age 65. An aneurysm is indicated
by an aortic diameter of 3 cm or greater. Aneurysms are
significant when they are greater than 4 cm in diameter
and from this stage must be followed closely every six
months with ultrasonography. A CT is even more accurate
and can determine the size of aneurysms to within a
diameter of 2 mm. Aneurysms more than 4 cm have
less than a 2% risk of rupture, but those larger than 5.5 cm
have a more than a 20% risk of rupture within 2 years;
the risk is considered relatively low with aneurysms less
than 5 cm.

Treatment
Patients with aneurysms less than 4 cm are managed
conservatively and should be given a beta-blocking drug
that reduces blood pressure and more important, decreases
cardiac ejection velocity and hydrodynamic stress on the
arterial wall. The systolic blood pressure should be kept
lower than 140 mmHg, and diastolic less than 85 mmHg
with the use of a beta-blocker and other antihypertensive
agents. Propranolol should not be used in smokers because
the drug is rendered ineffective.
Aneurysmal repair is usually indicated when aneurysms
are greater than 5.5 cm because of the high risk of rupture
and an overall mortality rate of more than 80%. Only
10–15% of patients survive the rupture. Patients who
manage to reach a hospital have a 50% mortality rate. All
vascular surgeons would recommend repair of aneurysms
6 cm or larger.
1. Surgical Treatment
Repair consists of opening of the aneurysm and inserting
a synthetic prosthetic tube graft, usually fabricated
of Dacron or expanded polytetrafluoroethylene
(Gore-Tex). Operative mortality is approximately 5%
overall for effective repair, but it is less in low-risk patients.
Operative mortality reaches 50% for repair of a ruptured
aneurysm.
2. Endovascular Stent Grafts
During the past decade a noninvasive but costly technique,
endovascular abdominal aortic aneurysm repair, has gained
some acceptance following the first Russian description
of the experimental procedure in 1986. In 1991, Parodi
introduced this minimally invasive percutaneous approach
used to exclude blood flow through abdominal aortic
aneurysms. The bypass excludes blood flow through the
aneurysm which shrinks over time, and the risk of rupture
is lessened. This technique involves minor surgery. A
modular, bifurcated endovascular graft is introduced
through an artery in the leg and is advanced to occlude
and bypass the aneurysm. Since Parodi’s description,
several types of endovascular grafts have been tested in
Europe and the United States with the Food and Drug
Administration’s (FDA) approval. The number of failures
indicates the preponderance of newer types of grafts.
Endovascular graft deployment requires radiological and
surgical skills. A stent graft system is introduced through
the femoral artery and either self- or balloon-expanding
stents are used to trap a Dacron prosthesis with the
proximal end precisely below the renal artery. Some devices
use hooks and barbs to secure better fixation and prevent
device migration; stents in the wall facilitate fixation to
the iliac artery.
This repair succeeds in excluding the aneurysm from
circulation while allowing blood to flow through the
prosthetic stent graft lumen to the distal aorta and iliac
vessels to the legs. This represents a major breakthrough
because many patients with aneurysms are elderly and have
other diseases, particularly prior heart attacks and heart
failure, which carry an increased risk for major surgical
intervention.
Unfortunately, less than 50% of patients have aneurysm
anatomy that is suitable for endovascular grafts. More than
90% of females are rejected because of anatomical criteria
that include a smaller iliac artery diameter and aortic
pathology, but the more common criteria is encroachment
of the aneurysm on the renal arteries. In addition, there
are several problems encountered that include a high
incidence of endovascular leaks and approximately 5%
of patients have aneurysms that continue to grow; 1%
of patients may go on to rupture their aneurysm.
Many devices have been introduced and have become
obsolete within a couple of years because no engineer or
manufacturer has been able to resolve the issue of
endoleaks. Also biomaterial failure because of poor graft
design leading to stent fractures, graft limb thrombosis,
and iliac limb dislodgment may occur in modular grafts.
The FDA issued a public health warning because of serious
adverse events that occurred with approved products
in 2002; a similar warning was given in the UK.
At present there is no evidence from clinical trials that
the risk of rupture of an aneurysm is reduced following
endovascular stent grafting. The risk of rupture is 1% per
year, similar to the risk in patients who have not undergone
surgery and are followed by ultrasonography. No large
randomized clinical trial has convincingly documented
that this repair technique confers a mortality benefit either
preoperatively or long term compared to surgical repair.
Most reports stem from single center, nonrandomized
studies, but randomized trials comparing endovascular
repair with surgery are now in progress. This technology
requires further refinement to be generally acceptable.
When the refinements are made, it will be useful in the
elderly and in patients with comorbid conditions who are
at high risk for surgery.