Pathological Consequences

The lethal part of the process must begin after the forming thrombus protrudes from the VVP. Prior to this point it is not life-threatening, though layers of blood cells may stiffen the cusp and lead to valve malfunction, impairing venous return and perhaps making varicosity more probable ('post-thrombotic syndrome'); see Section 11.4.5. However, when an incipient thrombus protrudes from its VVP, it places a 'dead' lump of cellular coagulum in the way of the luminal blood flow (Fig. 11.2).

If there is no subsequent interruption of normal pulsatile blood flow and normal oxygenation is maintained, more and more phagocytes and platelets may be recruited to enfold this dead mass in an 'envelope' of living cells. The mass will grow no

Fig. 11.2 Magnetic resonance imaging of a venous thrombus from O'Shaughnessy et al. (2005). This novel technique detects methaemoglobin in thrombi, and thus allows a thrombus/clot to be visualised without need for intravenous contrast (the endovascular methaemoglobin provides sufficient contrast). Femoral and popliteal thrombi are clearly visualised in these images. The conversion of oxyhaemoglobin to methaemoglobin signifies that the blood in thrombi so identified is dead/necrotic, thus confirming the central thesis of this chapter: that venous thrombosis manifests very local 'tissue death' extending to and involving the vascular envelope by massing of deceased leukocytes and platelets. Thrombi are to be thought of as the detritus of dead blood cell masses within the living vascular envelope. We are indebted to Dr. Peter Walton of Dendrite Clinical Systems Ltd., Bell St., Henley on Thames, for permission to reproduce this illustration

Fig. 11.2 Magnetic resonance imaging of a venous thrombus from O'Shaughnessy et al. (2005). This novel technique detects methaemoglobin in thrombi, and thus allows a thrombus/clot to be visualised without need for intravenous contrast (the endovascular methaemoglobin provides sufficient contrast). Femoral and popliteal thrombi are clearly visualised in these images. The conversion of oxyhaemoglobin to methaemoglobin signifies that the blood in thrombi so identified is dead/necrotic, thus confirming the central thesis of this chapter: that venous thrombosis manifests very local 'tissue death' extending to and involving the vascular envelope by massing of deceased leukocytes and platelets. Thrombi are to be thought of as the detritus of dead blood cell masses within the living vascular envelope. We are indebted to Dr. Peter Walton of Dendrite Clinical Systems Ltd., Bell St., Henley on Thames, for permission to reproduce this illustration larger, and indeed small protrusions from a VVP may be successfully removed by circulating phagocytes. However, if this does not happen, then the protuberance of even a tiny piece of thrombus from the mouth of a VVP becomes a potentially fatal development: it may continue to burgeon should successive covering layers of living cells die and become covered in turn by further fresh layers (Fig. 9.1b).

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