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Thrombosis in the Venous System

Pathogenesis:At one time, venous thrombosis was widely referred to as thrombophlebitis, implying that an inflammatory or infectious process had injured the vein, thereby causing thrombosis. However, with the rec­ognition that in most cases there is no evidence of inflam­mation, the term phlebothrombosis is more accurate. Nevertheless, both terms have been replaced for the most part by the expression “deep venous thrombosis”. This term is particularly appropriate for the most common manifestation of the disorder, namely, thrombosis of the deep venous system of the legs.

Deep venous thrombosis is caused in general by the same factors that dispose toward arterial and cardiac thrombosis, namely endothelial injury, stasis, and a hypercoagulable state. Conditions that favour the develop­ment of deep venous thrombosis include the following:

Stasis (heart failure, chronic venous insufficiency, postoperative immobilization, prolonged bed rest)

Injury (trauma, surgery, childbirth)

Hypercoagulability (oral contraceptives, late preg­nancy, cancer)

Advanced age

Sickle-cell disease

Pathology:The large majority (more than 90%) of venous thromboses occur in the deep veins of the legs, with the remainder usually involving veins in the pelvis. Most venous thrombi begin in the calf veins, usually in the sinuses above the venous valves. In this location, ve­nous thrombi have several potential fates:

Lysis: Venous thrombi generally remain small and are eventually lysed, posing no further threat to health.

Organization: Many thrombi undergo organization similar to thrombi of arterial origin. Small organized venous thrombi may be incorporated into the wall of the vessel, whereas larger ones may undergo canali­zation, with partial restoration of venous drainage.

Propagation: It is not uncommon for venous thrombi to serve as a nidus for further thrombosis and thereby propagate proximally to involve the larger iliofemoral veins.

Embolization: Large venous thrombi or those that have propagated proximally represent a significant hazard to life, since they may dislodge and be carried to the lungs as pulmonary emboli.

Clinical Features: Small thrombi in the calf veins are ordinarily asymptomatic, and even larger thrombi in the iliofemoral system may cause no symptoms. Some pa­tients have tenderness in the calf, often associated with forced dorsiflexion of the foot (Homans' sign). Occlusive thrombosis of the femoral or iliac veins leads to severe congestion, edema, and cyanosis of the lower extremity. Symptomatic deep venous thrombosis is treated with systemic anticoagulants, and there is now interest in new thrombolytic therapy.

The function of the venous valves is always impaired in a vein subjected to thrombosis, organization, and canalization. As a result, chronic deep venous insufficiency (i.e., a failure of venous drainage) is virtually inevitable If the lesion is restricted to a small segment of the deep venous system, the condition may remain asymptomatic However, more extensive involvement results in pigmentation, edema, and induration of the skin of the leg. Ulceration above the medial malleolus is often troublesome and difficult to treat.

EMBOLISM. Embolism is the passage through the venous or arterial circulations of any material capable of lodging in a blood vessel and thereby obstructing the lumen. The usual embolus is a thromboembolus - that is, a blood clot formed in one location that detaches from the vessel wall an travels to a distant site.

Pulmonary Emboli. For the clinician, pulmonary embolism remains an important diagnostic and therapeutic challenge. In fact, pulmonary thromboemboli are reported in more than half of cases. The large majority of pulmonary emboli rises from the deep veins of the lower extremities; the fatal ones arise from the iliofemoral veins. Depending on the size of the embolus and the health of the patient and his or her circulatory status, the clinical types of acute pulmonary embolism vary, but they can be divided into the following syndromes:

asymptomatic small pulmonary emboli;

transient dyspnea and tachypnea without other symptoms;

pulmonary infarction, with pleuritic chest pain, hemoptysis, and pleural effusion;

cardiovascular collapse with sudden death.


Lesson ¹ 8

Methodical instruction for students



Aim: to study etiology, pathogenesis and morphogenesis of the inflammation and also morphology and consequences for the organism of exudative inflammation.

Objectives of the lesson:

1. To study morphology and pathogenesis of inflammation.

2. To describe the activities of inflammation mediators.

3. To study the main causes and phases of inflammation.

3. To study the classification of inflammations.

4. To study morphological characteristic of different kinds of exudative inflammations.

5. To study the consequences and significance of exudative inflammation for the organism.

Date: 2016-03-03; view: 201

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