The occluded popliteal vein is enlarged to a diameter of the 11.6 mm
The compression is performed so strong that even the popliteal artery is narrowed (arrow).
(left: without compression, right: with compression). The compression is performed so strong that even the popliteal artery is narrowed (arrow).
(SFV) using compression sonography.
(left: without compression, right: with compression).
Exclusion of an acute thrombosis of the left superficial femoral vein(SFV) using compression sonography.
Acute thrombosis of the left superficial femoral vein using color coded duplex sonography . The diameter of the occluded vein is 8.5 mm
Swelling associated with cutaneous cyanosis and indicating an acute deep vein thrombosis affecting the right leg
Visible subcutaneous collateral veins indicating an acute deep vein thrombosis affecting the left leg
Untreated, spontaneous lysis of such a thrombosis would be unlikely. Complications include pulmonary embolism (≈ 50% of cases), postphlebitic syndrome and recurrent VTE. Anticoagulant therapy for at least 3 months is indicated.
This venogram shows a serpentine thrombus in the superficial femoral vein above the knee.
Chronic venous insufficiency is characterized by trophic changes in the skin (smooth and shiny skin), hyperpigmentation and edema.
The advanced state of venous insufficiency is characterized by trophic changes (shiny smooth skin), hyperpigmentation and an active venous ulcer.
In more advanced venous insufficiency, there is stasis dermatitis with hyperpigmentation and ulceration. In this photo, two stasis ulcers with fibrotic healing are shown.
Early disease with dilated lateral malleolar veins and ‘corona phlebectatica’, a myriad of tiny superficial venules. The condition is associated with underlying disease in the large veins of the lower extremity.
Vein with thrombus in lumen.
Venous thrombi tend to form in the cusps of veins.
This longitudinal view reveals that more than half of the venous lumen is occluded by thrombus (black area). Areas of blood flow within the vein appear red. This imaging technique renders a thrombus as black, while areas of blood flow are colorised.
Thrombus (dark area) occluding more than half the diameter of the common femoral artery (as seen in this longitudinal view). This imaging technique renders the thrombus as black, while areas of blood flow are colorised.
Cross-sectional view of the politeal vein showing partial obstruction of the vessel lumen. This imaging technique renders the thrombus (no flow) as black, while areas of blood flow are colorised.
Thrombi partially obstruct venous return, which can lead to symptoms such as venous distension and lower extremity oedema.
Cross-sectional view of the common femoral vein showing a significant degree of thrombotic occlusion of the vessel lumen. This imaging technique renders the thrombus as black, while areas of blood flow are colorised.
The most common type of VTE is deep vein thrombosis (DVT), which occurs in veins deep within the muscles of the leg and pelvis.
This post-mortem exam shows a fresh pulmonary embolus in a major pulmonary artery. The lethality of a pulmonary embolus is not dependent on size alone but rather the underlying cardiovascular condition of the patient.
Section of pulmonary parenchyma with middle right (round) blood vessel containing embolus. The surrounding lung parenchyma has undergone haemorrhagic infarction.
The pathway of a pulmonary embolism (PE) from the lower half of the body: inferior vena cava, to right atrium, to right ventricle, to the pulmonary artery. This might eventually obstructs blood flow to the lung. Patients with deep vein thrombosis (DVT) are at risk of PE, a life-threatening event.
Whole lung in which pulmonary arteries are obstructed by fresh (red) thrombus (circles).
Fragments of thrombi can break free to form potentially life-threatening pulmonary emboli.
This electron microscopic image shows activated platelets. Platelets can be activated by a number of substances including collagen, thromboxanes, adenosine diphosphate and thrombin. One striking feature of activation is the change in platelet morphology from an ovoid disk to an amorphous form with projecting fingers.
A thrombus can block the flow of blood through a vein or artery and can detach from the vessel wall to become a life-threatening embolus when it lodges in the lungs or other vital organs.
The right side of the heart delivers deoxygenated blood to the lungs; the left side pumps oxygenated blood to the systemic circulation.
The pathologist Rudolph Virchow was the first to describe the three main factors that predispose to thrombosis.
Blood flow in the major veins of the lower extremity depends, in part, on the pumping action produced by leg muscle contractions. Retrograde flow is prevented by venous valves.
A burst of thrombin formation (represented by blue spheres) triggered by activated Factor X is a pivotal step in the coagulation cascade.
Platelets are the main cellular components of white thrombi, which tend to form in the arterial system. In contrast, red blood cells predominate in red thrombi, which form in veins.
Red blood cells predominate in red thrombi, which form in veins. In contrast, platelets are the main cellular components of white thrombi, which tend to form in the arterial system.
The process of coagulation depends on a complex interplay of enzymatic and cellular activity, culminating in the formation of a stable vascular “plug”. The subsequent process of clot dissolution that occurs during the healing phase is known as “fibrinolysis”.
Plasminogen activators from injured endothelium convert plasminogen to plasmin which in turn breaks up the fibrin strands into smaller fragments, including d-dimer.
The natural inhibitors of coagulation include tissue factor pathway inhibitor (TFPI), activated protein C (APC), and antithrombin (AT).
Vitamin K antagonists lower levels of factors II, VII, IX and X. The heparins and fondaparinux work indirectly through antithrombin. Rivaroxaban and apixaban (both under development) directly inhibit Factor Xa and several anticoagulants directly inhibit thrombin.
Thrombin converts fibrinogen to fibrin monomers which polymerize to form fibrin strands, Factor XIII, activated by fibrin, cross-links the fibrin strands to create a fibrin scaffold for a stable clot.
Activated Factor X, functioning as part of the prothrombinase complex on the surface of activated platelets, converts large amounts of prothrombin to thrombin, in the “thrombin burst.”
Clotting is initiated by the activation of Factor VII by membrane-bound tissue factor. This leads to activation of Factor X, which then produces small amounts of thrombin.
An overview of the coagulation cascade, showing the initiation, propagation, and clot formation phases.
Intraluminal view of a coronary artery with atherosclerotic plaques and a thrombus originating at the site of an ulcerated plaque.
In STEMI patients the ST segment is elevated; in NSTEMI patients the ST segment is not elevated, and instead other patterns are seen. The most common characteristics of NSTEMI ECGs are ST depression and T inversion.
An area of cardiac muscle damage due to acute occlusion in a coronary artery that delivers blood to that area
In acute coronary syndrome, a coronary artery plaque erodes or ruptures, leading to the formation of a blood clot, which blocks the blood flow.
An area of ischemic damage in the brain causing a stroke due to embolic obstruction of the cerebral artery to this area
An embolus originating from a left atrial thrombus formed in atrial fibrillation lodges at a bifurcation of cerebral arteries and obstructs blood flow, leading to stroke
An embolus originating from a left atrial thrombus formed in atrial fibrillation travels along the carotid artery to the brain
A thrombus formed in the left atrium in atrial fibrillation embolises and subsequently travels through the left ventricle and out to the systemic circulation
Coronary artery with thin muscular media and prominent intimal hyperplasia with calcification. Lumen obstructed by thrombus (arrow)
Coronary bypass graft completely occluded by acute thrombosis (arrow).
Cardiac ventricle from patient who suffered an acute fatal myocardial infarction. Cross-sectional view of coronary artery reveals dark red thrombi (circles).
Dilated left atrium with mitral stenosis and calcified plaques on the atrial wall (circle), possibly caused by chronic hypertension
Section of atrium with adherent mural thrombus (circle)
Key findings: ST-segment elevation in the inferior leads (II, III, aVF) and V6, consistent with transmural ischemia.
Extremely large thrombus protruding into the left atrium.
Key findings: Marked ST-segment depression in the lateral precordial leads (V5, V6) consistent with subendocardial injury.
Patient right coronary lumen and restoration of normal coronary blood flow.
Inflation of an angioplasty balloon.
Passage of a guide wire through the area of acute obstruction.
Obstruction caused by acute atherothrombosis within the right coronary artery, as seen with radio-opaque dye injection during coronary catheterisation.
Key findings: absence of P waves, irregularly irregular R-R intervals, and irregular fluctuations in the baseline (most noticeable in leads III and V1).