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Oedema, Haemorrhage and Thrombosis
Published in Jeremy R. Jass, Understanding Pathology, 2020
Thrombi formed in the fast-moving arterial system tend to be small, friable, pale and platelet-rich. Those developing within aneurysms (left ventricular or aortic) show well-developed lines of Zahn. These are pale, platelet-rich lines alternating with fibrin-rich lines that contain admixed red blood cells. Those developing in the relatively sluggish venous system (phlebothrombosis) are composed mainly of fibrin and admixed red blood cells but will still be firmer and drier than a postmortem blood clot. Furthermore, small numbers of platelets will be seen microscopically. Postmortem blood clot is soft, jelly-like and is never firmly adherent to the vessel wall in which it forms. It may be composed largely of yellow coagulated plasma, when it has been likened to ‘chicken fat’. The distinction is important when trying to decide at a postmortem examination if a mass within the pulmonary artery is embolised thrombus (see Chapter 18) or merely postmortem blood clot.
Pulmonary Vascular Lesions
Published in Philip T. Cagle, Timothy C. Allen, Mary Beth Beasley, Diagnostic Pulmonary Pathology, 2008
Barring recent lung/mediastinal trauma (including surgical intervention), thrombi identified within the pulmonary trunk and the lobar and segmental arteries are most commonly due to embolization from deep veins in the leg or pelvis (44). A V- or Y-shaped structure reflects origin within a venous confluence. Grossly, they are firm, rubbery, granular or dry masses that are lighter in color than a postmortem clot. They do not usually conform exactly to the receiving vessel, and if acute, will not adhere strongly to the vessel walls. Distinction of pulmonary thromboemboli from postmortem clots is often problematic. In general, postmortem clots conform more closely to the vessel walls. The classic gross appearance is of a yellow layer consisting of fibrin and platelets (“chicken fat” layer) distinctly partitioned from the deeper burgundy red mass of erythrocytes (“currant jelly” layer). In a true thrombus, the cut surface demonstrates alternating “lines of Zahn.” Microscopically, there is a characteristic pattern of alternating layers of fibrin and platelets with erythrocytes and leukocytes. In the acute stage there is minimal neovascular/fibroblastic organization of the thrombus, although the periphery of an embolus may demonstrate such changes as derived from its relationship with the parent vein in which it was initially formed. Differences in the patient’s coagulation status, microvascular environment, blood flow, and parenchymal disease may result in a variety of appearances of either postmortem clots or recent thrombi/thromboemboli.
Pathogenesis of Thrombosis
Published in Hau C. Kwaan, Meyer M. Samama, Clinical Thrombosis, 2019
Hau C. Kwaan, M. M. Samama, T. Lecompte
As defined by Welch,61 a thrombus is a solid mass or plug formed in the living heart or blood vessel. Since it is formed in vivo with varying degrees of motion of the blood, it possesses structural characteristics different from a blood clot formed in vitro or one formed post-mortem. Such characteristics vary with the condition of blood flow during which the thrombus formation occurs and are also dependent on the presence or absence of injury to the vessel wall. Arterial thrombi are generally the result of some injury or disease of the vessel wall and are associated with active blood flow. Platelets form the early nidus of such a thrombus and, as the thrombus grows, more platelets are brought to it from circulating blood until complete occlusion of the vessel occurs. Thus, the thrombus is not only rich in platelets, but it also shows the characteristic “lines of Zahn”,62 which are layers of altered platelets deposited on fibrin and red cells. Leukocytes tend to infiltrate and gather at the margin of these platelet masses. In contrast, stasis plays an important role in the formation of venous thrombi. Therefore, they are richer in fibrin and red cells with the main body of the thrombus appearing more akin to a blood clot. Such differences are not always apparent, since mixed thrombi are frequently encountered in both arterial and venous thrombosis. Where there is a more active flow upstream in a thrombus, more platelet deposition may occur, while the main body of the thrombus downstream tends to be formed from stagnation of flow and is richer in fibrin and red cells, giving the overall appearance of having “a white head and a red tail”. Thrombi should be viewed as constantly in a dynamic process of resolution by lysis, organization, or embolization, while continuous deposition of platelets and of fibrin is taking place. Consequently, during the course of thrombosis, the nature and constituents of a thrombus may alter. The consideration of multiple factors affecting the rate of resolution, the degree of vascular occlusion by the thrombus, degree of vascular injury, and condition of the blood flow may determine the constituents of a thrombus at any given moment of its natural history. Such considerations are important in the choice of a thrombolytic, antiplatelet, or anticoagulant modality as the appropriate therapeutic approach.
Immunothrombosis and thromboinflammation in host defense and disease
Published in Platelets, 2021
Kimberly Martinod, Carsten Deppermann
Alternating erythrocyte-rich and platelet-rich zones termed lines of Zahn are considered hallmarks of early venous thrombi. Histological analysis of thrombus samples obtained from human VTE patients analyzed for leukocytes and NETs also showed platelet/VWF-rich islands surrounded by NETting neutrophils [136]. Neither these structures nor platelets are present in more organized deep vein thrombi, indicating that they are not essential to the maintenance of thrombus stability long-term and that any potential platelet or NET-mediated therapies would need to be initiated early. These organized structures also do not support the hypothesis that platelets are merely bystanders trapped in a surrounding venous thrombus. Furthermore, the active role of platelets in pulmonary embolism is certainly not to be overlooked [137]. In contrast to more organized pulmonary emboli which resemble DVT thrombi, autopsy samples from patients who died of sudden-onset pulmonary embolism show a paucity of red blood cells and mainly consist of fibrin and FVIII, lined with platelet aggregates [138].