Keywords
abdominal aortic aneurysm - thrombosis - ischemia
Introduction
Sudden thrombosis of an abdominal aortic aneurysm (AAA) is an uncommon condition.
Its incidence is reported to be 0.6 to 2.8% of all surgically managed AAA cases.[1]
[2]
[3] Shumacker reported the first case of thrombosis of AAA in 1959,[4] and Jannetta and Roberts performed the first successful revascularization of thrombosed
AAA in 1961.[5] For the most part, patients with thrombosed AAAs present with symptoms of acute
limb ischemia, including pain, coolness, paresthesia, absent pulses, and mottling
of the skin.[6]
Several factors appear to be associated with acute AAA thrombosis: obstructive iliac
disease with propagation of thrombus from occluded distal arteries, cardioaortic embolization,
and accumulation of intrasaccular mural thrombus ultimately obstructing aortic flow.[2]
[7]
The aim of this report is to describe an unusual case of acute thrombosis of AAA without
signs of acute limb ischemia.
Case Presentation
A 70-year-old woman presented in our vascular clinic due to an asymptomatic juxtarenal
10 cm AAA identified as an incidental finding in a recent computed tomography (CT)
scan ([Fig. 1]). Her medical history included mild hypertension under drug medication. At physical
examination of the abdomen, a large pulsating mass was present with normal pulsation
of femoral and tibial vessels. There were no complaints of previous intermittent claudication.
Fig. 1 An asymptomatic juxtarenal 10 cm abdominal aortic aneurysm identified as incidental
finding.
The woman was planned for open repair. She was very anxious about the result and the
possible complications of the surgical procedure. The woman had intense stress, phobia
for surgery, and was consulted by a psychiatrist.
To better define the aneurysm anatomy (with 1mm imaging slices), we performed a new
CT angiography (CTA) 48 hours after admission, which surprisingly revealed complete
thrombosis of the AAA just below both renal arteries without any signs of acute renal
insufficiency, mesenteric ischemia, or limb ischemia ([Fig. 2]). The most impressive element of the CTA was the rich collateralization between
the thoracic aorta and the common femoral arteries through the superficial epigastric
and other arteries of thoracic and abdominal wall. This collateralization was not
evident in the first CT 2 days earlier.
Fig. 2 A computed tomography (CT) angiography 10 days after the first CT revealed an acute
thrombosis of abdominal aortic aneurysm just below both the renal arteries with rich
collateralization between the thoracic aorta and the common femoral arteries through
the superficial epigastric arteries and other arteries of thoracic and abdominal wall.
The following physical examination revealed the absence of the previous pulsating
mass and absence of femoral and distal leg pulses. Both legs were warm with normal
skin color. The surgical procedure was postponed and the woman was discharged from
the hospital with double antiplatelet therapy and weekly follow-up for the possible
signs of limb ischemia.
After a month, the patient presented with severe intermittent claudication in the
left lower limb. The following digital subtraction angiogram revealed a thrombosed
abdominal aorta with collateral vessels between the aorta and both common femoral
arteries ([Fig. 2]). The woman underwent a left axillary–femoral bypass with polytetrafluoroethylene
No. 8 graft. The patient's postoperative course was uneventful and the symptom of
intermittent claudication disappeared. She was discharged on fourth postoperative
day with antiplatelet (salicylic acid 100 mg, once daily) and statin (atorvastatin
20 mg, once daily) medication.
Discussion
Acute thrombosis of AAA is a rare and often devastating complication of aortic aneurysms.
Symptoms of acute lower limb ischemia (45.7%) associated with absent femoral pulses
(68.6%) are the most common clinical signs.[2]
[3] Acute neurological deficits with lower limb paresis on both sides and paralysis
have also been described.[8]
[9] In all reported cases, an emergent surgical intervention was performed to avoid
an otherwise catastrophic outcome (death or limb loss). All patients were treated
either with aortobiilliac/aortobifemoral bypass or with extra-anatomic revascularization
of the lower extremities. Late rupture of thrombosed AAA has been reported in 15%
of cases treated with axillobifemoral bypass.[10]
[11]
[12]
[13] Kumar reported successful endovascular treatment of a thrombosed aneurysm in a high-risk
patient.[14]
In our report, we present a case of acute thrombosis of AAA during hospitalization,
which was not manifested with symptoms of acute limb ischemia. In a previously described
“silent” presentation of an occluded AAA, a reconstruction with a tubular graft was
performed.[15] In our case, impressive development of the rich collateralization through the superficial
arteries of thoracic and abdominal wall in the time period of 10 days between the
first CT and the CTA was noted. The lower limbs were viable without the need of an
emergent surgical revascularization procedure.
There is no relationship between aneurysmal size and the likelihood of thrombosis.
The transverse diameter of reported thrombosed AAA ranges from 3.5 to 10.5 cm.[6] According to the literature, several mechanisms that may explain an acute thrombosis
of an AAA have been described:
-
Acute low-flow state due to occlusive iliac artery disease
-
A hypercoagulation disorder or hypercoagulability due to a neoplasm[3]
[16]
-
A cardioaortic embolization due to cardiac arrhythmias causing an occlusion of the
inflow or the outflow of the aneurysm
-
A dislocation of a fragment of the mural thrombus within the aneurysm sac causing
an occlusion of the outflow of the aneurysm
-
A hypotension and low flow state due to hemorrhage, fever, dehydration, or other cardiac
causes
Interestingly, in our case the patient was very anxious about the dangers of aortic
reconstruction. We speculate that acute stress caused by the recognition of a large
AAA and the possible complications of the planned surgical procedure may have predisposed
to an acute thrombosis of the AAA. It is known that stress-related hormones (adrenocorticotropic
hormone and cortisol) influence platelet-mediated thrombosis.[17] These hormones may fulfill an important role in acute arterial thrombosis by increasing
the platelet aggregation. Moreover, according to a recent report, a poststress situation
may increase D-dimers and clotting factors such as FVII:C, FVIII:C, FXII:C, and von
Willebrand factor antigen.[18]
In conclusion, acute thrombosis of AAA, although a complication with high morbidity
and mortality, in some cases may be associated with a silent course without signs
of acute limb ischemia. Preoperative anxiety, stress, and phobia for surgery may be
factors predisposing to acute thrombosis of an AAA.
