Page 133 - Textbook of Pathology, 6th Edition

thrombi is facilitated by turbulence in the blood flow, while iv) Shock 117
stasis initiates the venous thrombi even without evidence of v) Tissue damage e.g. trauma, fractures, burns, surgery
endothelial injury. vi) Late pregnancy and puerperium
5. HYPERCOAGULABILITY OF BLOOD. The occurrence vii) Certain drugs (e.g. anaesthetic agents, oral contra-
of thrombosis in some conditions such as in nephrotic ceptives).
syndrome, advanced cancers, extensive trauma, burns and CHAPTER 5
during puerperium is explained on the basis of hypercoagul- Morphologic Features
ability of blood. The effect of hypercoagulability on Thrombosis may occur in the heart, arteries, veins and the
thrombosis is favoured by advancing age, smoking, use of
oral contraceptives and obesity. Hypercoagulability may capillaries. Beside the differences in mechanisms of thrombus
occur by the following changes in the composition of blood: formation at these sites, the clinical effects of these are even
i) Increase in coagulation factors e.g. fibrinogen, prothrombin, more different. Arterial thrombi produce ischaemia and
factor VIIa, VIIIa and Xa. infarction, whereas cardiac and venous thrombi cause
ii) Increase in platelet count and their adhesiveness. embolism.
iii) Decreased levels of coagulation inhibitors e.g. antithrombin The general morphologic features of thrombi are as
III, fibrin split products. under:
Predisposing Factors Grossly, thrombi may be of various shapes, sizes and
A number of primary (genetic) and secondary (acquired) composition depending upon the site of origin. Arterial
factors favour thrombosis. thrombi tend to be white and mural while the venous
Primary (Genetic) factors: thrombi are red and occlusive. Mixed or laminated
i) Deficiency of antithrombin thrombi are also common and consist of alternate white
ii) Deficiency of protein C or S and red layers called lines of Zahn. Red thrombi are soft,
iii) Defects in fibrinolysis red and gelatinous whereas white thrombi are firm and Derangements of Homeostasis and Haemodynamics
iv) Mutation in factor V pale.
Microscopically, the composition of thrombus is deter-
Secondary (acquired) factors: mined by the rate of flow of blood i.e. whether it is formed
a) Risk factors: in the rapid arterial and cardiac circulation, or in the slow
i) Advanced age
ii) Prolonged bed-rest moving flow in veins. The lines of Zahn are formed by
iii) Immobilisation alternate layers of light-staining aggregated platelets
iv) Cigarette smoking admixed with fibrin meshwork and dark-staining layer
of red cells. Red (venous) thrombi have more abundant
b) Clinical conditions predisposing to thrombosis: red cells, leucocytes and platelets entrapped in fibrin
i) Heart diseases (e.g. myocardial infarction, CHF,
rheumatic mitral stenosis, cardiomyopathy) meshwork. Thus, red thrombi closely resemble blood clots
ii) Vascular diseases (e.g. atherosclerosis, aneurysms of the in vitro (Fig. 5.22).
aorta and other vessels, varicosities of leg veins) Red thrombi (antemortem) have to be distinguished from
iii) Hypercoagulable conditions (e.g. polycythaemia, postmortem clots (Table 5.5).
dehydration, nephrotic syndrome , disseminated cancers)

Figure 5.22 Thrombus in an artery. The thrombus is adherent to the arterial wall and is seen occluding most of the lumen. It shows lines of
Zahn composed of granular-looking platelets and fibrin meshwork with entangled red cells and leucocytes.