An 75-Year-Old With Sudden-Onset Severe Abdominal Pain

Background

An 75-year-old man is presented to the emergency department (ED) by ambulance with

severe abdominal pain that began suddenly 2 hours before presentation. The pain is mainly in his
back and radiates toward his left inguinal region. The patient felt light-headed at the onset of the
pain to the extent that he had to grip the sink to steady himself. He also reports significant
nausea, although he has not vomited.

He has no urinary symptoms. His medical history includes type 2 diabetes, hypertension,
hyperlipidemia, ischemic heart disease, and intermittent claudication of his lower extremities.
His medications include metformin, ramipril, simvastatin, aspirin, and a glyceryl trinitrate pump
spray. He smoked 10-20 cigarettes a day for over 60 years but stopped 5 years ago.

Physical Examination and Workup

The physical examination reveals tenderness in the left iliac fossa and left costovertebral angle.
His vital signs are remarkable for a heart rate of 105 beats/min and a blood pressure of 110/90
mm Hg. The patient is prescribed further analgesia and 1 L of crystalloid is administered. He is
then referred to the surgical assessment unit (SAU) as a case of possible ureteric colic, with an
abdominal radiograph taken during transit (Figure 1).

Figure 1.

On arrival to the SAU, the patient and his abdominal film are reviewed by the on-call surgical
doctor. After assessment of his airway, breathing, circulation, level of consciousness, and
exposure for examination of his abdomen, oxygen is given via a face mask, intravenous access is
obtained at 2 sites, and a urinary catheter is inserted. Blood is drawn for laboratory analysis,
including blood urea nitrogen, electrolytes, a complete blood cell count, coagulation panel, and
cross matching. The patient's electrolytes, complete blood cell count, and coagulation panel
results are unremarkable. Arterial blood gas analysis is obtained and reveals a metabolic
acidosis.
Intravenous fluids are continued and the patient is sent for an urgent CT scan of the abdomen.
Once completed, he is transferred by ambulance to a regional center for immediate intervention.
Discussion
The CT scan revealed the presence of an abdominal aortic aneurysm (AAA) with a calcified wall
and mural thrombus, with extraluminal blood indicating a rupture of the aneurysm (Figure 2).

Figure 2.

An aneurysm is defined as a focal increase in the diameter of a vessel to greater than 50% of
normal; anything less is considered arteriomegaly. The abdominal aorta is approximately 2 cm in
diameter, and an AAA is usually said to be present when a segment of aorta has a diameter of
greater than 3 cm.
AAA has a prevalence of 1.3%-8.9% in men and 1%-2.2% in women older than 55 years. It is
responsible for 1%-3% of all deaths among men aged 65-85 years in developed countries. The
incidence is higher in select groups; 5% of patients with coronary artery disease and as many as
50% of those with popliteal or femoral artery aneurysms have concomitant AAA. Data from a 7-
year prospective study of a cohort of 4345 patients, which identified 119 cases of AAA,
identified male gender and increasing age as strong risk factors for the development of AAA.
Another study demonstrated an association between short leukocyte telomere length and AAA,
further supporting the notion that vascular biological aging is indeed an etiology of AAA.
Smoking, hypertension, and hypercholesterolemia are also associated with a significantly
increased risk for AAA. Interestingly, diabetes is usually protective against aneurysm formation.
AAA may cause various symptoms, including abdominal, back, and/or groin pain; however, the
vast majority of AAAs are asymptomatic. Symptoms are usually a result of rapid aneurysm sac
expansion or rupture. Pain may be mild to severe. A patient may present reporting a mass or
swelling in the abdomen, or an awareness of the pulsation of the AAA. Complications of AAA
include internal thrombosis, distal embolization, and aortoenteric fistula. AAA rupture is the
most significant, immediate cause of mortality. Complaints of feeling light-headed or syncope, in
association with back or abdominal pain, should alert the clinician to the possibility of AAA
rupture. Approximately 50% of patients die soon after rupture, and of those surviving to surgery,
the mortality is approximately 54%. Most early deaths result from free intraperitoneal rupture
and exsanguination. Extraperitoneal rupture is associated with a more favorable course, as the
bleeding may be temporarily tamponaded by peri-aortic tissue.
Given the asymptomatic nature of most AAAs, as well as the dismal outcome after rupture,
significant attention has been paid to screening for AAA. The first study to examine AAA
screening across a large population was the MASS study. This study involved a population
sample of 67,800 men aged 65-74 years. Patients were randomly assigned to receive either
screening ultrasonography or no intervention. Over 10 years, 155 deaths related to AAA
occurred in the screening group vs 296 in the group that did not receive screening. This equates
to a relative risk reduction of 48% (95% confidence interval, 37%-57%). This study also reported
that the cost-effectiveness of such a screening program was favorable. A Cochrane review found
evidence of a significant reduction in mortality from AAA rupture in men aged 65-79 years who
undergo screening.
These findings have prompted the initiation of screening programs in several nations. For
example, in the United Kingdom, the National Health Service (NHS) AAA screening program
invites all men for a screening ultrasound at 65 years. Men older than 65 years who have not
been screened or treated for AAA can personally make a request for screening. In the United
States, the SAAAVE Act allows for AAA screening ultrasound in patients with a family history
of AAA or a history of smoking more than 100 cigarettes, as long as they participate in their
"Welcome to Medicare" physical examination within 6 months of turning 65.
Multiple imaging modalities, including CT and ultrasonography, have been used to both screen
and detail AAA. Three dimensional (3D) reconstruction CT (orthogonal CT) provides a truly
accurate model of aneurysm architecture. Angulation of the aneurysm can make traditional axial
CT images misleading. When ultrasound and CT are compared with orthogonal CT, ultrasound
produces the most accurate estimation of size overall.[8] Traditional CT can be used if the aorta
cannot be visualized with ultrasound after repeated efforts.

A potential AAA screening test is measurement of baseline insulin-like growth factor I (IGF-I).
In a prospective, long-term study, Lindholt et al demonstrated that IGF-I is a novel biomarker for
AAA.[9] Baseline levels of serum IGF-I not only had a positive correlation with the size and
growth rate of the aneurysms, but they also predicted the need for future surgery.[9] Decision-
making regarding operative management vs observation for AAA is informed mainly by the
results of the UKSAT trial[10] and the ADAM trial.[2] The UKSAT randomized 1090 small
aneurysms (4-5.5 cm) to operation or surveillance. No significant difference in overall mortality
was demonstrated for those offered early surgery. Similar findings were found in the ADAM
trial, and these 2 studies led to the recommendation that surgical repair should be considered in
all aneurysms over 5.5 cm; those patients with AAAs less than 5.5 cm should be enrolled on an
ultrasonographic surveillance program. Surgical AAA repair should also be considered when the
aneurysm expands by more than 0.6-0.8 cm in a single 12-month period.[11] The threshold for
surgical repair in women is typically 5 cm, given a relatively smaller normal aortic size
compared with men.

These recommendations are rooted in the physics of transmural pressure and the higher rupture
rates associated with larger aneurysms. The law of LaPlace states that the tension in the wall of a
sphere is proportional to the product of the transmural pressure across the wall and the radius of
the sphere, and inversely proportional to the thickness of its wall; it can also be interpreted as
stating that in a long pliable tube the site of largest diameter requires the least pressure to distend.
This explains why an aneurysm tends to enlarge and why larger aneurysms rupture more
frequently (it is because of the higher wall tension). As a result of the tendency of larger
aneurysms to expand at a faster rate, AAAs of 4.5-5.4 cm in diameter will need 6-month
ultrasound follow-up, and AAAs of 3-4.5 cm in diameter need yearly ultrasound follow-up; these
intervals are practiced in the NHS (United Kingdom).

Around 90% of detected aneurysms are below the threshold of 5.5 cm required for intervention
and require surveillance to monitor expansion into the interventional range. Numerous
approaches designed to limit expansion have been suggested. Large studies have indicated that
propranolol does not inhibit aneurysm expansion. Numerous studies agree that tobacco use is
associated with an increased rate of aneurysm expansion. Level B and C evidence is available to
suggest that 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) may inhibit
aneurysm expansion. Some animal data, but no human data, suggest that angiotensin-converting
enzyme inhibitors or losartan, an angiotensin receptor blocker, decrease the rate of AAA
expansion, when used to treat concomitant hypertension. Optimizing glycemic control is also
associated with a reduction in the rate of expansion of AAA in patients with diabetes. Weight
loss, regular exercise if possible, and a healthy diet should also be encouraged.
Open surgical repair or endovascular aneurysm repair (EVAR) are the current operative options
available. EVAR is a less-invasive approach to addressing AAA. EVAR involves transluminal
placement of a modular stent-graft system into the AAA via remote arterial access (usually, the
femoral artery) under local, regional, or, most commonly, general anesthetic. Concerns about the
proximity of the renal arteries and other vessels to the aneurysm have been overcome by the use
of fenestrated grafts. However, the proximal neck of the aneurysm is considered unfavorable
anatomically for EVAR if 1 or more of the following situations exist: angulation >60°, diameter
>30 mm, short length <15 mm, conical shape, and extensive thrombus or calcification. In
addition, surgical access through the femoral vessels in the groin can be difficult in the setting of
extensive iliac artery occlusive disease or vessel tortuosity, thereby limiting the applicability of
this procedure in some patients or requiring the use of adjunctive, open surgical, or endovascular
techniques to gain access to the aorta.
The EVAR 1 trial randomly assigned 1082 elective patients (patients from multiple centers that
were also fit for open repair) to either open repair or EVAR. The 30-day operative mortality was
1.6% in the EVAR group and 4.6% in the open-repair group. However, those in the EVAR group
were at a significantly higher risk for graft complication (hazard ratio [HR], 4.39) and graft-
related intervention (HR, 2.86) during follow-up; no difference in all-cause or aneurysm-related
mortality was noted after 8 years of follow-up between the groups, with the initial benefit from
EVAR erased in long-term follow-up. Since the study, a steady increase has been observed in the
proportion of EVAR compared with open repair performed in the United Kingdom and
elsewhere.
The EVAR 2 trial randomly assigned 338 patients (from 1999 to 2003) older than 60 years with
at least 5.5-cm aneurysms who were unfit for open repair to no intervention or EVAR. This study
demonstrated a considerable 30-day mortality (9%) in those treated with EVAR compared with
no intervention, and showed no significant difference between the EVAR group and the no
intervention group for all-cause mortality (HR, 1.21). These findings are in contrast with other
studies that claim appreciable long-term benefits are associated with EVAR in patients unfit for
surgery, at a cost of a small 30-day mortality rate of between 1.6% and 2.9%. Some of the longer
benefit may be due to a statistically higher rate of antiplatelet and statin prescription in the newer
studies, as well as the increased expertise available in higher-volume centers, and newer-
generation grafts. The Cronenwett model suggests that patients with AAAs >5.5 cm with low
operative risk and poor anatomic suitability for EVAR who are younger than 70 years should
have open repair, and those at high risk operatively with excellent anatomy for EVAR and who
are older than 70 years should have EVAR. These two extreme examples seem obvious, and
many patients fall between the two; informed patient preference and local expertise influence the
final treatment in such cases.
The Society for Vascular Surgery practice guidelines for the Care of Patients with AAA include
specific recommendations for surveillance following repair, as follows:
Surveillance during the first year post surgery should include CT angiography at 1 month and 12
months.
If no endoleak or AAA enlargement is documented after the first year, color duplex ultrasound is
suggested as an alternative to CT imaging for annual postoperative surveillance of EVAR.
Color duplex ultrasonography and a noncontrast CT scan are recommended as a substitute for
CT angiography for post-EVAR surveillance of patients with renal insufficiency.
Noncontrast CT scanning of the entire aorta is recommended at 5-year intervals after open
surgical repair or EVAR.
Open repair of AAA is of proven durability with a 36-year population-based study confirming
that the vast majority of patients (91.6%) remain free of any significant graft-related
complication during their remaining lifetime.[26] The noted complications included anastomotic
pseudoaneurysm, graft thrombosis, graft enteric erosion/fistula, graft infection, anastomotic
hemorrhage, colonic ischemia, and atheroembolism; 2.6% of patient complications were
recognized within 30 days of the procedure, and the later complications were noted at a median
of 6.1 years.

Clinical and radiologic follow-up should be geared to recognize these complications and should
follow the recommendations detailed by such bodies as the Society for Vascular Surgery. As
noted above, persons with AAA are at risk for synchronous and metachronous aneurysm
elsewhere, and follow-up should take this into account. EVAR does not have the risks of
anastomotic pseudoaneurysm, anastomotic hemorrhage, but it does have those of graft migration
and endoleak in addition to the other risks. Endoleak describes the situation of incomplete
isolation of the aneurysm sack by the graft, leading to continued flow and pressurization of the
sac. Again, follow-up should be planned according to the recommendations for detecting these
complications.
Emergency repair of ruptured or leaking aneurysms can be performed with EVAR if anatomic
conditions are optimal and the patients hemodynamic status allows; if not, open repair should be
used as proximal aortic control can be obtained swiftly. If these conditions are met, data suggest
benefits for such patients undergoing EVAR, such as a reduction in the mortality, prolonged
intensive care requirement and total hospital stay compared with open repair. Highly
symptomatic but unruptured aneurysms can be managed with EVAR and open repair in the same
manner as asymptomatic aneurysms (but on a more urgent basis), the threshold is often less than
5.5 cm for repair in these cases.
The UKSAT and the ADAM trials led to the practice that aneurysms less than 5.5 cm are
surveyed with ultrasound and those larger than 5.5 cm are repaired. The NHS screening program
surveys AAAs of 3-4.4 cm yearly and those between 4.5 cm and 5.5 cm biannually. The normal
aorta is around 2 cm in diameter, and it is considered aneurysmal when more than 3 cm.
The term endoleak describes when a graft fails to isolate the aneurysm sac, leading to continued
pressurization and aneurysm sac expansion. Type I endoleak occurs at the proximal or distal
edge of the endograft, if the proximal or distal seal zones between the stent-graft and blood
vessel wall are not adequate. Type II endoleak results from a blood vessel that is filling the
original aneurysm sac in a retrograde fashion. Type III endoleak results from a leak between
overlapping, modular components of a stent-graft system. Type IV endoleak is very similar to
type III endoleak, in that it results from blood flowing from within the endograft through the
stent, but this time it results from a flaw in the graft material itself. Type V endoleaks have been
described as being due to "endotension" with an enlarging aneurysm sac without a visible
endoleak, which can be dealt with by reinforcing the indwelling stent graft or re-lining the graft.