Venous thrombi

In general, arterial thrombi are platelet-rich ( white clots ) and form at ruptured atherosclerotic plaques, leading to intraluminal occlusion of arteries that can result in end-organ injury (e.g., myocardial infarction, stroke). In contrast, venous thrombi consist mainly of fibrin and red blood cells ( red clots ), and usually form in low-flow veins of the limbs, producing deep vein thrombosis (DVT) the major threat to life results when lower extremity (and, occasionally, upper extremity) venous thrombi embolize via the right heart chambers into the pulmonary arteries, i.e., pulmonary embolism (PE). 

Hypercoagulable states, in turn, have been traditionally associated with venous thrombosis. Consequently, attention has been paid to alterations of the hemostatic balance. Although this is a systemic variable, focality is favored due to the contribution of decreased blood flow, as confirmed by the preferential development of venous thrombi at the level of valves, an area of stasis where low-velocity flow is moderately turbulent. 

Venous thrombi (red thrombi) are formed mainly from fibrin in simations where vascular stasis exists or in hypercoagulability states. Here the symptoms consist of deep vein thrombosis with the risks of pulmonary embolism and the mainstay of therapy is anti-coagulation with heparin and oral anticoagulants. 

A red thrombus can form around a white thrombus as mentioned above or de novo in low-pressure veins, initially by adherence of platelets (as in arteries) but followed promptly by the process of blood coagulation so that the bulk of the thrombus forms a long tail consisting of a fibrin network in which red cells are enmeshed. These tails become detached easily and travel as emboli to the pulmonary arteries. Such emboli often arise from a deep venous thrombosis (DVT)—a thrombus in the veins of the legs or pelvis. Although all thrombi are mixed, the platelet nidus dominates the arterial thrombus and the fibrin tail the venous thrombus. Arterial thrombi cause serious disease by producing local occlusive ischemia venous thrombi, by giving rise to distant embolization. 

Killewich LA, Bedford GR, Beach KW, et al. Spontaneous lysis of deep venous thrombi rate and outcome. J Vase Surg I 989 9 89-97. 

Autopsy examples have established that paradoxical embolism can occur from venous thrombi through the right to the left side of the heart. Emboli may pass through a patent foramen ovale, which is found in approximately one-quarter of healthy people, an atrial septal defect or a ventriculoseptal defect (Gautier et al. 1991 Jeanrenaud and Kappenberger 1991 Cabanes et al. 1993). There is an increased incidence of patent foramen ovale in... 

Fibrinolytic system the mode of action of drugs that promote fibrinolysis (fibrinolytics) and their uses to lyse arterial and venous thrombi (thrombolysis)... 

Spar, I.L. Goodland, R.L. Schwartz, S.I. Detection of preformed venous thrombi in dogs by means of i-131-labeled antibodies to dog fibrinogen. Circ. Res. 1965, 17, 322-329. 

Embolic detachment of components of venous or mural thrombi can sometimes be involved in the development of thromboembolism or cholesterol embolization. There is a 10% incidence of pulmonary embolism during thrombolysis, lethal in 0-5% (5), pointing to the risk of detachment of white components of venous thrombi, especially if large veins, such as those in the pelvis, are involved (6). However, the risk has not been proven to exceed that reported in patients treated with heparin and/or oral anticoagulants. 

A. P., Graham, P. B. (2002) EP-1873, a gadolinium (Gd) labeled fibrin specific agent that rapidly detects arterial and venous thrombi with MRI, Circulation, 11-120. 

Thromboses in arteries and veins are slightly different. Venous thrombi form in slow moving blood and contain a lot of fibrin. Arterial thrombi usually occur because of damage to artery walls and contain more platelets than fibrin. Formation of emboli is a risk in either case. 

Venous (red) thrombi develop in areas of slow blood flow (e.g., leg veins of a bedridden patient). The clot forms rapidly and lacks the organization of the arterial thrombus. Venous occlusion occurs, but is not the primary damage caused by venous thrombi. More worrisome is the tendency of small pieces (emboli) to detach from venous thrombi and travel to pulmonary arteries. The emboh wedge into pulmonary arteries, prohibiting deoxygenated blood from entering the portion of the limg served by the embolized artery. 

A variety of clinical states are associated with thrombosis. The present discussion is limited to a few of the more prominent thromboembolic diseases further Information on this subject may be found in several reviews.3,7-9 The most common clinical states which Involve clot-like, venous thrombi are deep vein thrombosis, particularly as a postsurgical complication, and pulmonary embolism. Anticoagulants such as heparin and the coumarins have been known for years to be effective in the prevention of these types of thrombi and more recent experience has demonstrated the efficacy of fibrinolytic agents such as streptokinase for their dissolution.3,9 Platelet aggregation Inhibitors have only recently been evaluated clinically in the prevention of venous thrombosis. These studies are crucial to the resolution of the controversy as to whether platelets play a vital role in the initiation of venous thrombi.10 There is persistent histological evidence that indicates venous thrombi begin as platelet aggregates.H Myocardial infarction and stroke are... 

Thrombosis is the formation of a clot. A thrombus may form in any vessel, artery, or vein when blood flow is impeded. For example, a venous thrombus can... 

Venous and arterial thrombus formation is common and is potentially a life-threatening event. A venous thrombus is an intravascular deposit predomi-... 

The general drawback of the Wessler model is the static nature of the venous thrombus development. To overcome this problem some investigators have developed more dynamic models with reperfusion of the occluded vessel segments after clot development. Depending on the time of test compound administration (pre- or post-thrombus initiation), the effect on thrombus growth and fibrinolysis can be evaluated. Levi et al. (1992) have used this model to assess the effects of a murine monoclonal anti-human PAI-1 antibody and Biemond et al. (1996) compared the effect of thrombin and factor Xa inhibitors with a low molecular weight heparin. 

Normal development, fertility, and survival serum is completely deficient in serum spreading factor and plasminogen activator inhibitor 1 binding activities delayed arterial and venous thrombus formation (Eitzman et al. 2000 Zheng et al. 1995). 

Although a thrombus can form in any part of the venous circulation, the majority begin in the lower extremities. Once formed, a venous thrombus may either (1) remain asymptomatic, (2) lyse spontaneously, (3) obstruct the venous circulation, (4) propagate into... 

Clinical effects produced by thrombi and emboli are (1) no serious effects, the silent thrombus or embolus (2) oedema of a limb, venous thrombus and perivenous lymphangitis (3) post-thrombotic ulceration (4) gangrene of a limb (thrombosis of main artery or embolus from heart or aorta) (5) gangrene of bowel (thrombosis of mesenteric artery or vein, arterial embolism) ... 

Fig. 6.22 Venous thrombus and venous infarct. 2D TOP MRV (a) and MIP image of the MR venogram (b) show absent flow in the left transverse sinus corresponding to thrombus arrow).

Leach, J.L.,W.M. Strub, andM.F. Gaskhl-Shipley, Cerebral venous thrombus signal intensity and susceptibility effects on gradient recalled-echo MR imaging. AJNR Am J Neuroradiol, 2007. 28(5) p. 940-5. 

Complications tend to occur when pacing catheters are left in place for longer then 72h (35). Infections can track down the catheter and care should be taken whenever the catheter or vascular sheath is manipulated. The catheter should be left within a sterile sleeve that allows for subsequent advancement and withdrawal. Acute thrombosis of the vein can occur, leading to extremity engorgment and to thromboembolic events. Routine anticoagulation, however, is not considered to be necessary unless there is a septal defect that could allow a venous thrombus to cause a stroke (paradoxical embolism). 

Thrombosis is the development of a thrombus , consisting of platelets, fibrin, red and white blood cells in the arterial or venous circulation. Platelet-rich white thrombi are found in the arterial system and can be prevented by antiplatelet drugs. 

Venous thromboembolism (VTE) is one of the most common cardiovascular disorders in the United States. VTE is manifested as deep vein thrombosis (DVT) and pulmonary embolism (PE) resulting from thrombus formation in the venous circulation (Fig. 7-1).1 It is often provoked by prolonged immobility and vascular injury and is most frequently seen in patients who have been hospitalized for a serious medical illness, trauma, or major surgery. VTE can also occur with little or no provocation in patients who have an underlying hypercoagulable disorder. 

Complications of MI include cardiogenic shock, heart failure, valvular dysfunction, various arrhythmias, pericarditis, stroke secondary to left ventricular (LV) thrombus embolization, venous thromboembolism, and LV free-wall rupture. 

Venous thromboembolism (VTE) results from clot formation in the venous circulation and is manifested as deep vein thrombosis (DVT) and pulmonary embolism (PE). A DVT is a thrombus composed of cellular material (red and white blood cells, platelets) bound together with fibrin strands. A PE is a thrombus that arises from the systemic circulation and lodges in the pulmonary artery or one of its branches, causing complete or partial obstruction of pulmonary blood flow. 

Venous thrombectomy may be performed to remove a massive obstructive thrombus in a patient with significant iliofemoral venous thrombosis, particularly if the patient is either not a candidate for or has not responded to thrombolysis. Full-dose anticoagulation therapy is essential during the entire operative and postoperative period. These patients need indefinite oral anticoagulation therapy targeted to an INR of 2.5 (range 2.0 to 3.0). 

CVD is a generic denomination mainly integrated by coronary heart disease (CHD) and stroke. Although not considered as a form of CVD in some instances, venous thromboembolic disease (VTED) shares with the other forms of CVD the territorial assignment, the vascular tree, although clear differences exist in the main pathophysiological mechanisms. In most CVD forms, however, thrombus formation plays a crucial role. 

The vascular tree is divided into two main, well-demarcated areas composed of the arterial and the venous trees. They both define different microenvironments that create the conditions for the development of focal episodes determining the occurrence of obstructive phenomena that are at the base of CVD. Arterial episodes (CHD and stroke) occur at sites of inflamed arteries, while VTED or venous stroke episodes develop as a result of thrombus formation at discrete locations in the venous tree. 

Thrombosis is the other phenomenon that crucially contributes to both the arterial and the venous forms of CVD, although the type of thrombus,... 

Use of heparin and heparinoids is aimed at inhibiting thrombus propagation into large and small vessels and prevent arterial (and venous) re-embolisation. Very few clinicians use this approach, at least for the time being. 

Pathophysiologically, thrombosis is the same sequence of events but now occurring in abnormal anatomical sites with intravascular obstruction that results in distal tissue ischaemia. These are often systemic disorders affecting the whole circulation and are described as hypercoagulable syndromes. Defects may lie at the level of the endothelium, inappropriate activation of the coagulation cascade or impaired activity of the fibrinolytic system. Segments of thrombus can become detached and travel peripherally in arterial tree, giving rise to acute insufficiency. Conversely, on the venous side, these are... 

Venous stasis resulting from prolonged bed rest, cardiac failure, or pelvic, abdominal, or hip surgery may precipitate thrombus formation in the deep veins of the leg or calf and may lead to fatal pulmonary embolism. Heparin may also be used prophylactically following surgery. 

Treatment for established venous thrombosis is initiated with unfractionated or low-molecular-weight heparin for the first 5-7 days, with an overlap with warfarin. Once therapeutic effects of warfarin have been established, therapy with warfarin is continued for a minimum of 3-6 months. Patients with recurrent disease or identifiable, nonreversible risk factors may be treated indefinitely. Small thrombi confined to the calf veins may be managed without anticoagulants if there is documentation over time that the thrombus is not extending. 

I11 the therapy of deep venous thrombosis, heparin is commonly administered. This drug takes effect immediately to prevent further thrombus formation. However, heparin is regarded as a hazardous drug and possibly may be tlie leading cause of drug-related deaths 111 hospitalized patients who are relatively well. Usually administered intravenously, preferably by pump-dnven infusion at a constant rate rather than by intermittent injections, it sometimes may cause major bleeding, which is particularly hazardous if it is intracranial. The action of heparin can be terminated almost immediately by intravenous injection of protamine sulfate, but where there may be less urgency, vitamin Ki may be used. The vitamin preparation may be administered intravenously, intramuscularly, or subcutaneously. 

Finally, thrombolytic drugs are gaining acceptance in treating other types of arterial and venous occlusion. For example, thrombolytic therapy can help dissolve clots in peripheral arteries (femoral, popliteal, and so forth)56 these drugs can help resolve thrombus formation in the large veins (DVT).68 This treatment... 

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