Thrombosis complications

Favorable outcomes (organization and involution)

Even if a vessel is occluded, the body attempts to restore blood flow. The so-called favorable outcomes include the processes of involution and organization of the clot.

• Aseptic autolysis. The clot dissolves under the action of the fibrinolytic system (particularly plasmin), as well as proteolytic enzymes released by macrophages and neutrophils.
• Thrombus canalization. Due to retraction (detachment from the vessel wall), clefts and channels appear within the bulk of the thrombotic masses.
• Vascularization. New small vessels sprout into the interior of the clot. This stage takes about 5 weeks and concludes with recanalization—partial restoration of blood flow. Meanwhile, the thrombus itself is gradually replaced by connective tissue.
• Calcification (petrification). The tissues become impregnated with calcium salts. In the venous bed, such calcified formations are called phleboliths (literally, vein stones).
• Ossification. An extremely rare scenario in which true bone tissue forms inside the clot.

Unfavorable outcomes and systemic consequences

If autolysis does not occur and the attachment of the clot to the wall proves weak, severe complications develop.

The main danger is thromboembolism. A fragment breaks off from the thrombus (most often from its least stable tail). This thromboembolus is carried by the bloodstream to other parts of the vascular bed.

The second formidable complication is septic (purulent) melting. It occurs when pyogenic bacteria penetrate the thrombotic masses.

In general, hypercoagulation and thrombosis cause systemic disruptions of central and microhemodynamics. This leads to primary circulatory hypoxia. Dystrophic processes develop in tissues, organ function declines, and cellular hypotrophy and hypoplasia are observed.

Targets of thromboembolism: arteries and veins

The exact location where the embolus stops determines the clinical picture.

• Arterial bed. The lodging of thromboemboli in the arteries of the systemic or pulmonary circulation causes infarctions (tissue necrosis). The brain (ischemic stroke), myocardium, kidneys, spleen, and retina are most frequently affected. Gangrene can develop in the lower extremities and intestine. In infective endocarditis, emboli frequently fly precisely into vital organs, which becomes one of the causes of death.
• Venous system.Pulmonary embolism (PE) is the most fatal catastrophe in venous thrombosis. Occlusion of the pulmonary trunk leads to acute right ventricular failure, reflex cardiac arrest (due to the pulmonocoronary reflex), and can progress up to sudden death. A less acute but severe late complication of deep vein thrombosis is post-thrombotic syndrome (chronic venous insufficiency).

Obstructive (local) effects

Even if the thrombus does not detach anywhere, it physically blocks the vessel lumen (obstructive thrombosis). If collateral circulation is insufficient, the blood supply zone dies from ischemia.

• Heart. Coronary artery thrombosis is the classic cause of myocardial infarction. However, it is worth remembering: in a third of autopsy cases, there is no thrombus in the vessel, and prolonged vascular spasm turns out to be the cause of acute ischemia.
• Spleen. When the splenic vein is occluded, a venous (red, hemorrhagic) infarction occurs. The necrotic zone becomes impregnated with blood, turns dark red or black, while a clear border (demarcation zone) around it is not pronounced.
• Lower extremities. If venous thrombosis occurs against the background of Buerger's disease (thromboangiitis obliterans), chronic ischemia develops, manifested by intermittent claudication. In severe cases, this ends in gangrene.

For the prophylaxis (in low doses) and treatment (in high doses) of thrombotic complications, such as acute superficial and deep vein thrombosis, PE, myocardial infarction, or ischemic stroke, specific pharmacotherapy is used. The administration of these drugs is performed subcutaneously.

Class and exam questions

What else to study on this topic

• Mechanisms of formation of the mixed thrombus tail
• Pathogenesis of the pulmonocoronary reflex in PE
• Differences between ischemic and hemorrhagic infarctions
• Manifestations of Buerger's disease (thromboangiitis obliterans)
• Infectious and toxic complications of infective endocarditis

Other topics in the "Additional Topics" section

Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.