Thrombus: causes, classification, venous, arterial and systemic thrombosis

By Cristiano Antonino On Jul 8, 2022

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A thrombus is a solid mass made up of fibrin containing platelets, red and white blood cells, which is formed by blood clotting within an unruptured cardiovascular system: this distinguishes it from a clot, which forms outside the cardiovascular system when it is unruptured, or within a cardiovascular system after death of the individual

Thrombi can form anywhere in the cardiovascular system and are always anchored to the vessel wall.

The formation of a thrombus essentially has three main predisposing alterations, described by the so-called Virchow triad:

Endothelial injury (including any type of endothelial dysfunction). This is the only factor in the triad capable of completely and independently leading to thrombosis. Damage to the inner surface of a vessel causes endothelial cells to release various substances, including endothelin (potent vasoconstrictors that act in arterioles at the level of the lesion) and von Willebrand factor (vWF), a protein that enables platelet adhesion by mediating the interaction between platelets and the exposed extracellular matrix, which is thrombogenic. In order to induce thrombus formation, however, physical damage to endothelial cells is not exclusively necessary; alterations in their pro- and anti-thrombotic activities, such as increased production of clotting factors or decreased production of anticoagulant factors, are sufficient. The ulceration of atherosclerotic plaques can expose the subendothelial matrix and also cause blood stasis and turbulence
Venous stasis or turbulence of blood flow. Turbulence can cause endothelial damage or dysfunction, countercurrent flows, or areas of stasis; blood stasis in turn is the most important cause of thrombi. Stasis and turbulence promote the activation of the endothelium in a pro-coagulative sense, bring platelets into contact with the endothelium, prevent the removal and dilution of activated coagulation factors as well as the influx of factors that inhibit coagulation.
Hypercoagulability (also called thrombophilia). Hypercoagulability is the alteration of the coagulation pathways, and is the least frequent factor in thrombosis; it can be classified into primary (or genetic), and secondary (or acquired) forms.

Characteristics and classification of thrombus

Arterial or intracardiac thrombi usually arise from endothelial damage; venous thrombi arise from stasis.

Depending on their site and the circumstances of their development, thrombi take on different characteristics; they are classified according to three features: their composition (corpuscular elements and fibrin), their size and their site. In the case of venous thrombi, the distribution of prothrombotic factors takes place slowly and homogeneously along the entire body of the thrombus, allowing it to grow in the direction of the heart. In the case of arterial thrombi, the impetuousness of the flow allows the prothrombotic factors to act only at the top of the thrombus, i.e. in the part that first comes into contact with the flow.

Three types of thrombi are distinguished on the basis of their composition, due to the different possible effects of the speed of blood flow and the rapidity of coagulation:

White thrombi: formed by platelets, fibrin and few red blood cells and few white blood cells; they are peculiar to arteries, where the fast flow does not allow red blood cells to be captured;

Red or ‘stasis’ thrombi: formed by platelets, fibrin and many red blood cells and many white blood cells; they are peculiar to veins, due to the slow flow;
Variegated thrombi: they present alternating clear and red areas (Zahn’s striae), due to a slow process of platelet aggregation that has trapped some red blood cells at times of low blood flow velocity (a condition that occurs, for example, after each contraction at the level of the heart and the first part of the aorta).

Depending on their size, they are divided into thrombi:

obstructive: which occlude the entire lumen of the vessel;
parietal: which do not occlude the entire vessel;
caval: located on the spur of a bifurcation.

Finally, a thrombus can still be subdivided by site:

arterial: these are the ones that cause heart attacks; they form particularly in the coronary arteries, cerebral arteries and those of the lower limbs;
venous: always occlusive, they form at the site of vessel dilatation (varices) or ulcers; 90% of them form in the lower limbs but can also affect the upper limbs, prostate, ovarian and uterine veins;
intracardiac: located particularly in the atria
aneurysmatic: located in the false lumen of arterial aneurysms.

Mural thrombi are also called mural thrombi: those formed in the cardiac cavities or in the aorta.

Classification of thromboses

A) Venous thrombosis

Phlebo-thrombosis
Deep vein thrombosis
Thrombophlebitis
Economy class syndrome
Paget-von Schroetter syndrome

B) Arterial thrombosis

Ascending thrombosis of the abdominal aorta: occurs when an atherosclerotic plaque chronically affects the aortic carrefour or the common iliac arteries. While collateral circulators support the flow to the limb, avoiding major symptoms, upstream of the atherosclerotic stenosis there is turbulent flow and blood stasis causing thrombosis. The latter rises both ‘capillarily’, i.e. climbing up the walls of the aorta, and ‘horizontally’ with overlapping layers. This results in:
Leriche syndrome, characterised by absence of the wrists on both limbs, claudication glutea and impotence in the male.
When the thrombosis reaches the inferior mesenteric artery and blocks it, the collateral circles that the inferior mesenteric artery supplies are compromised.
As it ascends, it also blocks the lumbar arteries resulting in spinal cord ischaemia and paraplegia.
It can reach the renal arteries giving acute renal failure.