A thrombus is a blood clot that forms within a blood vessel. While this process is a natural part of hemostasis, pathological clots can impede blood flow. The term “intraluminal” specifies the location of this clot, meaning it is situated within the lumen, or the open channel, of the vessel. An intraluminal thrombus (ILT) is a finding that indicates an underlying vascular abnormality.
Defining the Intraluminal Thrombus
The ILT is most frequently associated with the dilated sac of an Abdominal Aortic Aneurysm (AAA), a localized enlargement of the lower aorta. An ILT is present in approximately 70% to 80% of AAA cases. Unlike acute clots, the ILT in an AAA is typically non-occlusive, lining the vessel wall while still allowing blood to flow through the central channel. The thrombus is a highly organized, layered structure that adheres firmly to the aneurysm wall.
The ILT exhibits a laminar appearance, consisting of multiple layers that reflect its chronic, slow formation over time. The inner layer directly faces the flowing blood, while the outermost layer, known as the abluminal layer, is in contact with the thinned aortic wall. This composition shows varying degrees of fibrin density and cellular components. The most active biological processes occur near the vessel wall.
Pathophysiology of Thrombus Formation
The development of an ILT within an aneurysm sac is a direct consequence of the physical and biological changes caused by the vessel’s abnormal dilation. According to Virchow’s Triad, thrombus formation is promoted by altered blood flow, damage to the vessel lining, and changes in blood coagulability. The dilated aneurysm causes significant alterations in hemodynamics, creating areas of slow, turbulent blood flow (stasis) near the wall. This stagnant environment allows clotting factors and platelets to accumulate and activate, initiating chronic clot growth.
The aneurysm itself contributes to the process through constant inflammation and degradation of the aortic wall. The damaged endothelial lining releases pro-coagulant factors that promote platelet aggregation and fibrin mesh formation. As the ILT matures, it sequesters inflammatory cells, including neutrophils and macrophages. These cells release proteolytic enzymes, notably Matrix Metalloproteinases (MMPs), which facilitate the degradation of the thrombus and the underlying aortic wall. This combination of disturbed flow and chronic inflammation drives the continuous deposition of new clot material, causing the ILT to grow thicker.
The Dual Threat: Rupture and Embolism
The presence of an ILT poses two distinct threats: promoting aneurysm rupture and risking distal embolization. While the thrombus was once theorized to be protective by reducing mechanical wall tension, its biochemical effects on the aortic wall are now understood to be detrimental. The thick, acellular nature of the ILT acts as a metabolic barrier, severely limiting the diffusion of oxygen and nutrients to the underlying aortic tissue. This deprivation leads to localized hypoxia in the aortic wall beneath the thrombus.
The resulting oxygen stress triggers the release of destructive enzymes, accelerating the breakdown of structural proteins like elastin and collagen. This proteolytic activity and induced cell death weaken the aortic wall, increasing the likelihood of rupture, especially in regions with a thick ILT burden. The second threat arises from the inner layer of the ILT that faces the bloodstream. This luminal surface is soft and unstable, making it susceptible to fragmentation and thromboembolism. These emboli travel downstream, potentially blocking smaller arteries in the legs or feet, leading to “blue toe syndrome” or localized tissue death.
Monitoring and Clinical Intervention
The management of an aneurysm containing an ILT begins with careful monitoring, primarily using non-invasive imaging techniques like computed tomography (CT) scans and ultrasound. These imaging modalities not only measure the overall size of the aneurysm but also allow physicians to visualize the ILT, assessing its volume, thickness, and adherence to the wall. Because aneurysm size is the most validated predictor of rupture, intervention is typically recommended when the maximum diameter reaches a threshold, such as 5.5 centimeters in men or 5.0 centimeters in women. However, the presence and characteristics of the ILT are also factored into risk assessment, as a rapidly expanding aneurysm or one with a high ILT volume fraction may prompt earlier intervention.
For patients who do not meet the size criteria for immediate repair, watchful surveillance is adopted, involving regular imaging to track growth. When intervention becomes necessary, the goal is to permanently isolate the aneurysm sac and the ILT from the high-pressure arterial blood flow. Two primary surgical methods are utilized: Open Surgical Repair (OSR) and Endovascular Aneurysm Repair (EVAR). OSR involves a major abdominal incision to replace the diseased aortic segment with a synthetic graft, physically removing the aneurysm and the contained thrombus. EVAR is a less invasive procedure involving the insertion of a stent-graft through the femoral arteries, which relines the aorta from the inside, creating a sealed channel for blood flow.