Thromboembolism pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Pathophysiology

The formation of a thrombus is usually caused by the top three causes, known as (Virchow's triad): (Classically, thrombosis is caused by abnormalities in one or more of the following)

• The composition of the blood (hypercoagulability)
• Quality of the vessel wall (endothelial cell injury)
• Nature of the blood flow (hemostasis)

To elaborate, the pathogenesis includes:

• An injury to the vessel's wall (such as by trauma, infection, or turbulent flow at bifurcations);
• By the slowing or stagnation of blood flow past the point of injury (which may occur after long periods of sedentary behavior (for example, sitting on a long airplane flight);
• By a blood state of hypercoagulability (caused for example, by genetic deficiencies or autoimmune disorders).

High altitude has also been known to induce thrombosis . Occasionally, abnormalities in coagulation are to blame. Intravascular coagulation follows, forming a structureless mass of red blood cells, leukocytes, and fibrin.

Gross Pathology

Images courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology

Thromboembolism

A 67-year-old male was hospitalized because of extensive atherosclerotic cardiovascular disease. Following surgery, during which diseased portions of the femoral arteries were bypassed, he developed massive pulmonary embolism and expired. At autopsy, thrombi were found in the femoral and iliac veins, as well as in the larger pulmonary arteries.

This is a gross photograph of a cut section of lung demonstrating thromboemboli in the pulmonary arteries (arrows).

This is a gross photograph of the heart with the main pulmonary artery opened. Note the thromboembolus filling the pulmonary artery (arrows).

This is a gross photograph of portions of muscle from the legs including sections of leg veins. Note that the leg veins contain thrombus (arrows).

Thromboembolism: Testes

This is a gross photograph of an infarcted testis. Because of the anatomy of the blood supply to the testis, torsion or the blood vessels often leads to venous occlusion (due to compression of the thin walled veins) but not arterial occlusion. Thus, blood still flows into the testis but it can’t get out! This leads to hypoxia and eventually to hemorrhagic necrosis.

Thromboembolism: Bowel Infarction

This is a gross photograph of the fibrous band between the uterus and adjacent tissues. This fibrous scar tissue is probably left over from a previous surgery or an infection. A loop of bowel herniated through the opening produced by this fibrous band and became incarcerated leading to the ischemic necrosis seen in the previous image.

Coronary Thrombosis

Images courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology

This is a gross photograph of thrombosed coronary artery (arrows).

Artificial Heart Valve Thrombosis

Artificial heart valve thrombosis: Gross, aortic valve prosthesis with acute thrombus, ventricular view

Mitral valve prosthesis with thrombosis: Gross, natural color, view from the left atrium, thrombus around rim of caged ball prosthesis.

Microscopic Pathology

Thromboembolism

This is a low-power photomicrograph of lung. A large thrombus is lodged at this branch point in the pulmonary artery. Note the hemorrhage and congestion in the surrounding lung parenchyma.

This is a photomicrograph of the wall of the pulmonary artery (1) containing the thromboembolus. In this case the artery wall looks normal. If this was a thrombus instead of a thromboembolus, you would expect to see some damage in the artery wall that would have initiated the thrombus. Note the lines of Zahn in the thromboembolus (arrows).

This is a low-power photomicrograph of the infarcted lung. The tissue is congested and has a very bland appearance due to coagulation necrosis of the lung parenchyma. You can still see the outlines of the alveoli and the cells that make-up the alveoli but there is almost complete loss of nuclei throughout this section.

Coronary Thrombosis

This is a higher-power photomicrograph of the ruptured fibrous cap (arrows) with hemorrhage (1) into the atherosclerotic plaque.

This is another high-power photomicrograph of the ruptured fibrous cap (arrows) with hemorrhage (1) into the atherosclerotic plaque. Note the presence of cholesterol crystals.

This is a high-power photomicrograph of thrombus attached to the wall of the vessel. There is early organization of the thrombus (arrow).

This is a higher-power photomicrograph of thrombus attached to the wall of the vessel. Note the early organization with in-growth of fibroblasts and small blood vessels from the wall of the artery (arrows).

In this low-power photomicrograph of another coronary artery from this patient, a mural thrombus has undergone re-organization. The mural thrombus has been invaded by the in-growth of fibroblasts and small blood vessels from the wall of the artery. The thrombotic material has been phagocytosed and removed by macrophages and is replaced by fibrous connective tissue and blood vessels. This re-organized thrombus still compromises the lumen of this vessel.

Sources of Systemic Embolism

• Left ventricular thrombus
• Left atrial thrombus
• Pelvic veins or lower extremity thrombus
• Native cardiac valves
• Prosthetic cardiac valves
• Cardiac tumors
• Aortic aneurysm
• Invasive manipulations
• Left ventricular aneurysm

References

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