Download
1 / 26
260 likes | 569 Vues
E N D
2. Venous thromboembolism Venous thromboembolism (VTE) is a composite term for deep vein thrombosis (DVT) and pulmonary embolism (PE).
VTE is a condition that begins with the formation of a blood clot, or thrombus, in one of the veins. This process is called DVT.
The end of the thrombus often breaks free, forming an embolus that circulates in the blood until it becomes lodged in a vessel. If the emboli become lodged in the vessels of the lung the result is a potentially fatal PE.
Even if DVT is asymptomatic, after some years post-thrombotic syndrome may develop as a result of damaged vasculature. This is a chronic condition that may contribute to long-term morbidity. Affected areas of soft tissue are also more susceptible to bacterial infection leading to ulceration.
Pulmonary hypertension may develop from PE and also contribute to the long-term morbidity and even poor survival.
Venous thromboembolism (VTE) is a composite term for deep vein thrombosis (DVT) and pulmonary embolism (PE).
VTE is a condition that begins with the formation of a blood clot, or thrombus, in one of the veins. This process is called DVT.
The end of the thrombus often breaks free, forming an embolus that circulates in the blood until it becomes lodged in a vessel. If the emboli become lodged in the vessels of the lung the result is a potentially fatal PE.
Even if DVT is asymptomatic, after some years post-thrombotic syndrome may develop as a result of damaged vasculature. This is a chronic condition that may contribute to long-term morbidity. Affected areas of soft tissue are also more susceptible to bacterial infection leading to ulceration.
Pulmonary hypertension may develop from PE and also contribute to the long-term morbidity and even poor survival.
3. Deep vein thrombosis Formation of a blood clot or thrombus commonly occurs in the femoral or more distal veins of the legs where a large volume of blood tends to collect at low pressure. Blood stasis can then occur, favouring development of a long thrombus. This process is called deep vein thrombosis (DVT).
Proximal and distal DVT are defined as thrombi located in the deep veins above and below the knee (trifurcation of pes anserinus), respectively.Formation of a blood clot or thrombus commonly occurs in the femoral or more distal veins of the legs where a large volume of blood tends to collect at low pressure. Blood stasis can then occur, favouring development of a long thrombus. This process is called deep vein thrombosis (DVT).
Proximal and distal DVT are defined as thrombi located in the deep veins above and below the knee (trifurcation of pes anserinus), respectively.
4. Pain
Oedema
Discoloration
Varices
Ulceration Post-thrombotic syndrome Post-thrombotic syndrome can be a consequence of deep vein thrombosis (DVT). Even if DVT is asymptomatic, after some years post-thrombotic syndrome may develop as a result of damaged vasculature.
A thrombus can result in vein scarring, valvular damage and muscle pump deterioration, all of which impair blood flow and therefore increase blood pressure. Abnormal capillaries develop in the skin and soft tissues and their permeability to erythrocytes and fibrin leads to haemosiderin (iron) disposition as the red blood cells lyse and release their content (discoloration). Oedema (accumulation of fluid) results from the increase in pressure, and the slowing of blood flow (stasis) leads to tissue hypoxia that can eventually cause skin necrosis and ulceration. Affected areas of soft tissues are also more susceptible to bacterial infection.
The incidence of post-thrombotic syndrome is difficult to establish due to the time between the episode of DVT and the onset of symptoms and the number of undiagnosed cases of DVT. Over the past 20 years the reported prevalence has ranged from 21% to 88% depending on the diagnostic criteria employed, presence of underlying medical conditions and treatment administered (Bernardi & Prandoni 2000; Saarinen et al 2000; Kahn & Ginsberg 2002).
Post-thrombotic syndrome has a major economic impact, as it represents a permanent disability.
References:
Bernardi E, Prandoni P. The post-thrombotic syndrome. Current Opinion in Pulmonary Medicine 2000;6:335-42.
Saarinen J, Kallio T, Lehto M, Hiltunen S, Sisto T. The occurence of the post-thrombotic changes after an acute deep venous thrombosis. A prospective two-year follow-up study. J Cardiovasc Surg 2000;41:441-6.
Kahn SR, Ginsberg JS. The post-thrombotic syndromme: current knowledge, controversies, and directions for future research. Blood Reviews 2002;16:155-65.Post-thrombotic syndrome can be a consequence of deep vein thrombosis (DVT). Even if DVT is asymptomatic, after some years post-thrombotic syndrome may develop as a result of damaged vasculature.
A thrombus can result in vein scarring, valvular damage and muscle pump deterioration, all of which impair blood flow and therefore increase blood pressure. Abnormal capillaries develop in the skin and soft tissues and their permeability to erythrocytes and fibrin leads to haemosiderin (iron) disposition as the red blood cells lyse and release their content (discoloration). Oedema (accumulation of fluid) results from the increase in pressure, and the slowing of blood flow (stasis) leads to tissue hypoxia that can eventually cause skin necrosis and ulceration. Affected areas of soft tissues are also more susceptible to bacterial infection.
The incidence of post-thrombotic syndrome is difficult to establish due to the time between the episode of DVT and the onset of symptoms and the number of undiagnosed cases of DVT. Over the past 20 years the reported prevalence has ranged from 21% to 88% depending on the diagnostic criteria employed, presence of underlying medical conditions and treatment administered (Bernardi & Prandoni 2000; Saarinen et al 2000; Kahn & Ginsberg 2002).
Post-thrombotic syndrome has a major economic impact, as it represents a permanent disability.
References:
Bernardi E, Prandoni P. The post-thrombotic syndrome. Current Opinion in Pulmonary Medicine 2000;6:335-42.
Saarinen J, Kallio T, Lehto M, Hiltunen S, Sisto T. The occurence of the post-thrombotic changes after an acute deep venous thrombosis. A prospective two-year follow-up study. J Cardiovasc Surg 2000;41:441-6.
Kahn SR, Ginsberg JS. The post-thrombotic syndromme: current knowledge, controversies, and directions for future research. Blood Reviews 2002;16:155-65.
5. Post-thrombotic syndrome Post-thrombotic syndrome can be a consequence of deep vein thrombosis (DVT). Even if DVT is asymptomatic, after some years post-thrombotic syndrome may develop as a result of damaged vasculature.
A thrombus can result in vein scarring, valvular damage and muscle pump deterioration, all of which impair blood flow and therefore increase blood pressure. Abnormal capillaries develop in the skin and soft tissues and their permeability to erythrocytes and fibrin leads to haemosiderin (iron) disposition as the red blood cells lyse and release their content (discoloration). Oedema (accumulation of fluid) results from the increase in pressure, and the slowing of blood flow (stasis) leads to tissue hypoxia that can eventually cause skin necrosis and ulceration. Affected areas of soft tissues are also more susceptible to bacterial infection.
Post-thrombotic syndrome has a major economic impact, as it represents a permanent disability.
Post-thrombotic syndrome can be a consequence of deep vein thrombosis (DVT). Even if DVT is asymptomatic, after some years post-thrombotic syndrome may develop as a result of damaged vasculature.
A thrombus can result in vein scarring, valvular damage and muscle pump deterioration, all of which impair blood flow and therefore increase blood pressure. Abnormal capillaries develop in the skin and soft tissues and their permeability to erythrocytes and fibrin leads to haemosiderin (iron) disposition as the red blood cells lyse and release their content (discoloration). Oedema (accumulation of fluid) results from the increase in pressure, and the slowing of blood flow (stasis) leads to tissue hypoxia that can eventually cause skin necrosis and ulceration. Affected areas of soft tissues are also more susceptible to bacterial infection.
Post-thrombotic syndrome has a major economic impact, as it represents a permanent disability.
6. Ulcus cruris venosum Post-thrombotic syndrome can be a consequence of deep vein thrombosis (DVT). Even if DVT is asymptomatic, after some years post-thrombotic syndrome may develop as a result of damaged vasculature.
A thrombus can result in vein scarring, valvular damage and muscle pump deterioration, all of which impair blood flow and therefore increase blood pressure. Abnormal capillaries develop in the skin and soft tissues and their permeability to erythrocytes and fibrin leads to haemosiderin (iron) disposition as the red blood cells lyse and release their content (discoloration). Oedema (accumulation of fluid) results from the increase in pressure, and the slowing of blood flow (stasis) leads to tissue hypoxia that can eventually cause skin necrosis and ulceration. Affected areas of soft tissues are also more susceptible to bacterial infection.
Post-thrombotic syndrome has a major economic impact, as it represents a permanent disability.Post-thrombotic syndrome can be a consequence of deep vein thrombosis (DVT). Even if DVT is asymptomatic, after some years post-thrombotic syndrome may develop as a result of damaged vasculature.
A thrombus can result in vein scarring, valvular damage and muscle pump deterioration, all of which impair blood flow and therefore increase blood pressure. Abnormal capillaries develop in the skin and soft tissues and their permeability to erythrocytes and fibrin leads to haemosiderin (iron) disposition as the red blood cells lyse and release their content (discoloration). Oedema (accumulation of fluid) results from the increase in pressure, and the slowing of blood flow (stasis) leads to tissue hypoxia that can eventually cause skin necrosis and ulceration. Affected areas of soft tissues are also more susceptible to bacterial infection.
Post-thrombotic syndrome has a major economic impact, as it represents a permanent disability.
7. Severe stasis and ulceration Post-thrombotic syndrome can be a consequence of deep vein thrombosis (DVT). Even if DVT is asymptomatic, after some years post-thrombotic syndrome may develop as a result of damaged vasculature.
A thrombus can result in vein scarring, valvular damage and muscle pump deterioration, all of which impair blood flow and therefore increase blood pressure. Abnormal capillaries develop in the skin and soft tissues and their permeability to erythrocytes and fibrin leads to haemosiderin (iron) disposition as the red blood cells lyse and release their content (discoloration). Oedema (accumulation of fluid) results from the increase in pressure, and the slowing of blood flow (stasis) leads to tissue hypoxia that can eventually cause skin necrosis and ulceration. Affected areas of soft tissues are also more susceptible to bacterial infection.
Post-thrombotic syndrome has a major economic impact, as it represents a permanent disability.Post-thrombotic syndrome can be a consequence of deep vein thrombosis (DVT). Even if DVT is asymptomatic, after some years post-thrombotic syndrome may develop as a result of damaged vasculature.
A thrombus can result in vein scarring, valvular damage and muscle pump deterioration, all of which impair blood flow and therefore increase blood pressure. Abnormal capillaries develop in the skin and soft tissues and their permeability to erythrocytes and fibrin leads to haemosiderin (iron) disposition as the red blood cells lyse and release their content (discoloration). Oedema (accumulation of fluid) results from the increase in pressure, and the slowing of blood flow (stasis) leads to tissue hypoxia that can eventually cause skin necrosis and ulceration. Affected areas of soft tissues are also more susceptible to bacterial infection.
Post-thrombotic syndrome has a major economic impact, as it represents a permanent disability.
8. Embolus The end of a thrombus can break free, forming an embolus that circulates in the blood until it becomes lodged in a vessel.
Emboli from the veins of the legs, e.g. the femoral vein, return to the heart via the venous system and are then ejected from the heart at high pressure into the lung.The end of a thrombus can break free, forming an embolus that circulates in the blood until it becomes lodged in a vessel.
Emboli from the veins of the legs, e.g. the femoral vein, return to the heart via the venous system and are then ejected from the heart at high pressure into the lung.
9. Thrombus formation in a deep vein Thrombus formation in a deep vein (computer graphics superimposed on in-body photograph)
A thrombus forms on the wall of the vein. It is often located in the veins of the calf or thigh. Here, the blood flows slowly towards the heart creating ideal conditions for the thrombus to grow and to extend into the lumen of the vessel. Most of the thrombus floats freely in the blood and is only anchored to the vein at one end.Thrombus formation in a deep vein (computer graphics superimposed on in-body photograph)
A thrombus forms on the wall of the vein. It is often located in the veins of the calf or thigh. Here, the blood flows slowly towards the heart creating ideal conditions for the thrombus to grow and to extend into the lumen of the vessel. Most of the thrombus floats freely in the blood and is only anchored to the vein at one end.
10. A fragment of a thrombus travelling towards the lungs A fragment of a thrombus travelling towards the lungs (computer graphics superimposed on an in-body photograph)
Deep vein thrombosis (DVT) is a serious condition due to the constant threat of a fragment breaking away from the thrombus. The thrombotic material is then carried in the bloodstream, through the heart to the lungs where
it may lodge in the pulmonary circulation.A fragment of a thrombus travelling towards the lungs (computer graphics superimposed on an in-body photograph)
Deep vein thrombosis (DVT) is a serious condition due to the constant threat of a fragment breaking away from the thrombus. The thrombotic material is then carried in the bloodstream, through the heart to the lungs where
it may lodge in the pulmonary circulation.
11. Pulmonary embolism Pulmonary embolism (PE) occurs when part or all of the thrombus breaks free and becomes lodged in a blood vessel in the lung.
If the emboli become lodged in the large vessels of the lung, obstructing a large portion of the vascular tree, the result is a potentially fatal PE.
Dyspnea, syncope, hypotension and cyanosis indicate a massive PE.Pulmonary embolism (PE) occurs when part or all of the thrombus breaks free and becomes lodged in a blood vessel in the lung.
If the emboli become lodged in the large vessels of the lung, obstructing a large portion of the vascular tree, the result is a potentially fatal PE.
Dyspnea, syncope, hypotension and cyanosis indicate a massive PE.
12. Pulmonary embolism kills Pulmonary embolism (PE) occurs when part or all of the thrombus breaks free and becomes lodged in a blood vessel in the lung.
If the emboli become lodged in the big vessels of the lung, obstructing a large portion of the vascular tree, the result is a potentially fatal PE.
Pulmonary embolism (PE) occurs when part or all of the thrombus breaks free and becomes lodged in a blood vessel in the lung.
If the emboli become lodged in the big vessels of the lung, obstructing a large portion of the vascular tree, the result is a potentially fatal PE.
13. Pulmonary embolism Pulmonary embolism (PE) occurs when part or all of the thrombus breaks free and becomes lodged in a blood vessel in the lung.
Pleuritic pain, cough and haemoptysis often suggest a small PE located distally near the pleura.
Symptoms may be vague or absent.Pulmonary embolism (PE) occurs when part or all of the thrombus breaks free and becomes lodged in a blood vessel in the lung.
Pleuritic pain, cough and haemoptysis often suggest a small PE located distally near the pleura.
Symptoms may be vague or absent.
14. Venous thromboembolism (VTE) Autopsy findings: thrombus in the deep veins and embolus in the lungs.Autopsy findings: thrombus in the deep veins and embolus in the lungs.
15. Normal PA chest radiograph PA: posterior-anterior
PA: posterior-anterior
16. Pulmonary hypertension PA chest radiograph Pulmonary hypertension can be a consequence of pulmonary embolism (PE).
Pulmonary hypertension is a term used to describe an increase in pressure in the pulmonary arteries.
Pulmonary hypertension can be caused by the existence of blood clots in the pulmonary arteries, which increase resistence to blood flow and subsequently increased pressure. An increase in pressure in the blood vessels causes the vessel walls to thicken, hindering transfer of oxygen and carbon dioxide between the blood and the inspired air in the lungs. The resulting fall in oxygen levels in the blood then causes greater constriction of the pulmonary arteries and therefore greater increase in pressure.
An additional consequence of pulmonary hypertension is an increased strain on the right side of the heart, which is forced to work harder than usual to overcome the increased resistance and push the blood through from the heart to the lungs. Over time, the right ventricle can become thickened and enlarged, leading to the development of heart failure.
Pulmonary hypertension contributes to the long-time morbidity.
The radiograph demonstrates a convex portion of the left cardiac border just below the aortic knob and a very prominent lower right pulmonary artery segment at the hilum. The pulmonary vessels particularly of the left thorax show an abrupt tapering with much smaller distal vessels particularly visible in the left upper lobe. These findings are observed in the cases of pulmonary hypertension.
PA: posterior-anteriorPulmonary hypertension can be a consequence of pulmonary embolism (PE).
Pulmonary hypertension is a term used to describe an increase in pressure in the pulmonary arteries.
Pulmonary hypertension can be caused by the existence of blood clots in the pulmonary arteries, which increase resistence to blood flow and subsequently increased pressure. An increase in pressure in the blood vessels causes the vessel walls to thicken, hindering transfer of oxygen and carbon dioxide between the blood and the inspired air in the lungs. The resulting fall in oxygen levels in the blood then causes greater constriction of the pulmonary arteries and therefore greater increase in pressure.
An additional consequence of pulmonary hypertension is an increased strain on the right side of the heart, which is forced to work harder than usual to overcome the increased resistance and push the blood through from the heart to the lungs. Over time, the right ventricle can become thickened and enlarged, leading to the development of heart failure.
Pulmonary hypertension contributes to the long-time morbidity.
The radiograph demonstrates a convex portion of the left cardiac border just below the aortic knob and a very prominent lower right pulmonary artery segment at the hilum. The pulmonary vessels particularly of the left thorax show an abrupt tapering with much smaller distal vessels particularly visible in the left upper lobe. These findings are observed in the cases of pulmonary hypertension.
PA: posterior-anterior
17. Venous thromboembolism is a major problem Venous thromboembolism (VTE) is the third commonest cardiovascular disorder after ischaemic heart disease and stroke, accounting for 10% of deaths in the hospitals. The annual incidence for DVT and PE in the general population of the Western world has been estimated at 1.0 and 0.5 per 1000, respectively (Van Beek & Ten Cate 1996).
Each year in the USA alone, DVT is estimated to affect 2 million patients and to be the cause of 600.000 hospital admissions and 60,000 deaths (the majority from PE) (Hirsch & Hoak 1996).
The combined annual incidence of VTE in France, Germany, Italy and the UK has been reported to be approximately 620.000 (Oger 2000). These numbers do not of course include the clinically silent, non-fatal cases, the number of which cannot be determined (Geerts et al 2004).
More than 90% of all clinically significant PEs are a consequence of DVT (Carey et al 1998).
The mortality of PE in untreated patients is around 30% but can be reduced to 2-8% with adequate anticoagulant therapy (Torbicki et al 2000).
The incidence of VTE has actualy decreased in recent years, most likely due to the success of prophylactic treatment in addition to advances in surgical and postoperative care. The incidence of this preventable condition is still too high, however. In addition, most studies have indicated that the elderly are particularly susceptible to PE. With the average age of the population increasing, VTE is set to be an escalating health problem. The silent clinical nature of VTE also disguises its high prevalence.
References:
Van Beek EJR, Ten Cate JW. The diagnosis of venous thromboembolism: an overview. In: Hull RD, Raskob JE, Pineo GF, editors. Venous thromboembolism: an evidence-based atlas. Futura Publishing Co 1996; pp 93-9
Hirsch J, Hoak J. Management of deep vein thrombosis and pulmonary embolism: a statement for healthcare professionals. Council on Thrombosis (in consultation with the Council on Cardiovascular Radiology) American Heart Association. Circulation 1996;93:2212-45.
Oger E. Incidence of venous thromboembolism: a community-based study in Western France. EPI-GETBP Study Group. Thromb Haemost 2000;83:657-60.
Geerts WH, Pineo GF, Heit JA, Bergqvist D, Lassen MR, Colwell CW, Ray JG. Prevention of venous thromboembolism. The Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy. Chest 2004;126:338S-400S.
Carey CF, Lee HH, Woelje KF. The Washington Manual of Medical Therapeutics. Philadelphia: Lippincott Williams and Wilkins 1998
Torbicki A, Van Beek EJR, Charbonnier B, Meyer G, Morpugo M, Palla A et al. Guidelines on diagnosis and management of acute pulmonary embolism. European Heart Journal 2000;21:1301-36.Venous thromboembolism (VTE) is the third commonest cardiovascular disorder after ischaemic heart disease and stroke, accounting for 10% of deaths in the hospitals. The annual incidence for DVT and PE in the general population of the Western world has been estimated at 1.0 and 0.5 per 1000, respectively (Van Beek & Ten Cate 1996).
Each year in the USA alone, DVT is estimated to affect 2 million patients and to be the cause of 600.000 hospital admissions and 60,000 deaths (the majority from PE) (Hirsch & Hoak 1996).
The combined annual incidence of VTE in France, Germany, Italy and the UK has been reported to be approximately 620.000 (Oger 2000). These numbers do not of course include the clinically silent, non-fatal cases, the number of which cannot be determined (Geerts et al 2004).
More than 90% of all clinically significant PEs are a consequence of DVT (Carey et al 1998).
The mortality of PE in untreated patients is around 30% but can be reduced to 2-8% with adequate anticoagulant therapy (Torbicki et al 2000).
The incidence of VTE has actualy decreased in recent years, most likely due to the success of prophylactic treatment in addition to advances in surgical and postoperative care. The incidence of this preventable condition is still too high, however. In addition, most studies have indicated that the elderly are particularly susceptible to PE. With the average age of the population increasing, VTE is set to be an escalating health problem. The silent clinical nature of VTE also disguises its high prevalence.
References:
Van Beek EJR, Ten Cate JW. The diagnosis of venous thromboembolism: an overview. In: Hull RD, Raskob JE, Pineo GF, editors. Venous thromboembolism: an evidence-based atlas. Futura Publishing Co 1996; pp 93-9
Hirsch J, Hoak J. Management of deep vein thrombosis and pulmonary embolism: a statement for healthcare professionals. Council on Thrombosis (in consultation with the Council on Cardiovascular Radiology) American Heart Association. Circulation 1996;93:2212-45.
Oger E. Incidence of venous thromboembolism: a community-based study in Western France. EPI-GETBP Study Group. Thromb Haemost 2000;83:657-60.
Geerts WH, Pineo GF, Heit JA, Bergqvist D, Lassen MR, Colwell CW, Ray JG. Prevention of venous thromboembolism. The Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy. Chest 2004;126:338S-400S.
Carey CF, Lee HH, Woelje KF. The Washington Manual of Medical Therapeutics. Philadelphia: Lippincott Williams and Wilkins 1998
Torbicki A, Van Beek EJR, Charbonnier B, Meyer G, Morpugo M, Palla A et al. Guidelines on diagnosis and management of acute pulmonary embolism. European Heart Journal 2000;21:1301-36.
18. Classification of level of VTE risk According to the ACCP guidelines on the prevention of VTE, effective prophylaxis requires assessment for each patient´s specific clinical risk factors. Four categories for the level of risk for VTE have been defined based on the expected rates of DVT and PE in the absence of prophylaxis.
Patients are considered to have a low risk if they are undergoing minor surgery and are aged under 40 years with no other risk factors.
Patients aged 40-60 years with no additional risk factors undergoing surgery, and patients with additional risk factors undergoing minor surgery are classified as having a moderate risk of VTE.
The high-risk category is reserved for patients undergoing surgery who are aged 40-60 years with additional risk factors.
Patients are described as having the highest risk if they are undergoing surgery with multiple risk factors (age above 40 years, history of VTE, malignancy and/or surgical procedures, e.g. hip or knee arthroplasty, hip fracture surgery, major trauma, spinal cord injury).
Reference:
Geerts WH, Pineo GF, Heit JA, Bergqvist D, Lassen MR, Colwell CW, Ray JG. Prevention of venous thromboembolism. The Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy. Chest 2004;126:338S-400S.According to the ACCP guidelines on the prevention of VTE, effective prophylaxis requires assessment for each patient´s specific clinical risk factors. Four categories for the level of risk for VTE have been defined based on the expected rates of DVT and PE in the absence of prophylaxis.
Patients are considered to have a low risk if they are undergoing minor surgery and are aged under 40 years with no other risk factors.
Patients aged 40-60 years with no additional risk factors undergoing surgery, and patients with additional risk factors undergoing minor surgery are classified as having a moderate risk of VTE.
The high-risk category is reserved for patients undergoing surgery who are aged 40-60 years with additional risk factors.
Patients are described as having the highest risk if they are undergoing surgery with multiple risk factors (age above 40 years, history of VTE, malignancy and/or surgical procedures, e.g. hip or knee arthroplasty, hip fracture surgery, major trauma, spinal cord injury).
Reference:
Geerts WH, Pineo GF, Heit JA, Bergqvist D, Lassen MR, Colwell CW, Ray JG. Prevention of venous thromboembolism. The Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy. Chest 2004;126:338S-400S.
19. Thromboembolic risk categories According to the ACCP guidelines on the prevention of VTE, effective prophylaxis requires assessment for each patient´s specific clinical risk factors. Four categories for the level of risk for VTE have been defined based on the expected rates of DVT and PE in the absence of prophylaxis.
Patients are considered to have a low risk if they are undergoing minor surgery and are aged under 40 years with no other risk factors. In this category the frequences of calf DVT, proximal DVT and fatal PE are 2%, 0.4% and below 0.01%, respectively.
Patients aged 40-60 years with no additional risk factors undergoing surgery, and patients with additional risk factors undergoing minor surgery are classified as having a moderate risk of VTE. In this group the frequency of calf DVT is 10-20%, proximal DVT 2-4% and fatal PE 0.1-0.4%
The high-risk category is reserved for patients undergoing surgery who are aged 40-60 years with additional risk factors. The frequency of calf DVT, proximal DVT and fatal PE are 20-40%, 4-8% and 0.4-1.0%, respectively in this patient group.
Patients are described as having the highest risk if they are undergoing surgery with multiple risk factors (age above 40 years, history of VTE, malignancy and/or surgical procedures, e.g. hip or knee arthroplasty, hip fracture surgery, major trauma, spinal cord injury). In such patients, the frequency of calf DVT is 40-80%, proximal DVT 10-20% and fatal PE 0.2-5%, respectively.
Reference:
Geerts WH, Pineo GF, Heit JA, Bergqvist D, Lassen MR, Colwell CW, Ray JG. Prevention of venous thromboembolism. The Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy. Chest 2004;126:338S-400S.
According to the ACCP guidelines on the prevention of VTE, effective prophylaxis requires assessment for each patient´s specific clinical risk factors. Four categories for the level of risk for VTE have been defined based on the expected rates of DVT and PE in the absence of prophylaxis.
Patients are considered to have a low risk if they are undergoing minor surgery and are aged under 40 years with no other risk factors. In this category the frequences of calf DVT, proximal DVT and fatal PE are 2%, 0.4% and below 0.01%, respectively.
Patients aged 40-60 years with no additional risk factors undergoing surgery, and patients with additional risk factors undergoing minor surgery are classified as having a moderate risk of VTE. In this group the frequency of calf DVT is 10-20%, proximal DVT 2-4% and fatal PE 0.1-0.4%
The high-risk category is reserved for patients undergoing surgery who are aged 40-60 years with additional risk factors. The frequency of calf DVT, proximal DVT and fatal PE are 20-40%, 4-8% and 0.4-1.0%, respectively in this patient group.
Patients are described as having the highest risk if they are undergoing surgery with multiple risk factors (age above 40 years, history of VTE, malignancy and/or surgical procedures, e.g. hip or knee arthroplasty, hip fracture surgery, major trauma, spinal cord injury). In such patients, the frequency of calf DVT is 40-80%, proximal DVT 10-20% and fatal PE 0.2-5%, respectively.
Reference:
Geerts WH, Pineo GF, Heit JA, Bergqvist D, Lassen MR, Colwell CW, Ray JG. Prevention of venous thromboembolism. The Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy. Chest 2004;126:338S-400S.
20. Pregnancy
Oral contraceptives
Hormone replacement therapy
Immobilisation
Surgery Acquired
Age
History of VTE
Malignancy
Antiphospholipid antibody syndrome
Genetic
Thrombophilia VTE – risk factors The aetiology of VTE is characteristically multifactorial. Persistent (acquired and genetic) and transient risk factors combine to increase the risk of reaching a threshold for thrombus formation.The aetiology of VTE is characteristically multifactorial. Persistent (acquired and genetic) and transient risk factors combine to increase the risk of reaching a threshold for thrombus formation.
21. Thrombophilia and risk of recurrence Antithrombin deficiency
Homozygous factor VLeiden
Combined defects
Antiphospholipid antibodies (LA/ACA)
Protein C deficiency
Protein S deficiency
Heterozygous factor VLeiden
Heterozygous prothrombin gene mutation The most common genetic risk factor for VTE is a defect in factor V (Factor V Leiden).
A mutation of the prothrombin gene is the second most common genetic risk factor for VTE.
The most common genetic risk factor for VTE is a defect in factor V (Factor V Leiden).
A mutation of the prothrombin gene is the second most common genetic risk factor for VTE.
22. Pathogenesis of VTE Virchow´s triad The pathogenesis of VTE is multifactorial as demonstrated by the German pathologist, Rudolf Virchow, who over a century ago proposed a triad of essential factors for VTE: 1. Stasis
2. Injury to the vessel wall
3. Hypercoagulability
Virchow postulated that all three of these conditions are required for the development of deep vein thrombosis (DVT). Typically, a vein is over-streched producing micro-tears of the inner surface of the vessel. Platelets aggregate in the region of the vessel injury providing primary haemostasis. If the injury is small, this platelet plug may be sufficient to stem blood loss, with subsequent activation of the coagulation cascade normally only occuring in response to a large injury. In the presence of stasis and hypercoagulability, however, even if the injury in the vessel is small, the coagulation cascade may become activated. The three components of Virchow´s triad combine to promote thrombus formation.The pathogenesis of VTE is multifactorial as demonstrated by the German pathologist, Rudolf Virchow, who over a century ago proposed a triad of essential factors for VTE:1. Stasis
2. Injury to the vessel wall
3. Hypercoagulability
Virchow postulated that all three of these conditions are required for the development of deep vein thrombosis (DVT). Typically, a vein is over-streched producing micro-tears of the inner surface of the vessel. Platelets aggregate in the region of the vessel injury providing primary haemostasis. If the injury is small, this platelet plug may be sufficient to stem blood loss, with subsequent activation of the coagulation cascade normally only occuring in response to a large injury. In the presence of stasis and hypercoagulability, however, even if the injury in the vessel is small, the coagulation cascade may become activated. The three components of Virchow´s triad combine to promote thrombus formation.
23. Pathogenesis of VTE Virchow´s triad The pathogenesis of VTE is multifactorial as demonstrated by the German pathologist, Rudolf Virchow, who over a century ago proposed a triad of essential factors for VTE: 1. Stasis
2. Injury to the vessel wall
3. Hypercoagulability
The pathogenesis of VTE is multifactorial as demonstrated by the German pathologist, Rudolf Virchow, who over a century ago proposed a triad of essential factors for VTE:1. Stasis
2. Injury to the vessel wall
3. Hypercoagulability
24. Pathogenesis of VTE Virchow´s triad The pathogenesis of VTE is multifactorial as demonstrated by the German pathologist, Rudolf Virchow, who over a century ago proposed a triad of essential factors for VTE: 1. Stasis
2. Injury to the vessel wall
3. Hypercoagulability
The pathogenesis of VTE is multifactorial as demonstrated by the German pathologist, Rudolf Virchow, who over a century ago proposed a triad of essential factors for VTE:1. Stasis
2. Injury to the vessel wall
3. Hypercoagulability
25. Pathogenesis of VTE Virchow´s triad The pathogenesis of VTE is multifactorial as demonstrated by the German pathologist, Rudolf Virchow, who over a century ago proposed a triad of essential factors for VTE: 1. Stasis
2. Injury to the vessel wall
3. Hypercoagulability
The pathogenesis of VTE is multifactorial as demonstrated by the German pathologist, Rudolf Virchow, who over a century ago proposed a triad of essential factors for VTE:1. Stasis
2. Injury to the vessel wall
3. Hypercoagulability
26. Vessel wall with activated endothelium (colour-enhanced scanning electron micrograph).
This scanning electron micrograph shows how the entothelium has reacted to compression and damage during surgery. The endothelial cells are activated and the clotting cascade has started.Vessel wall with activated endothelium (colour-enhanced scanning electron micrograph).
This scanning electron micrograph shows how the entothelium has reacted to compression and damage during surgery. The endothelial cells are activated and the clotting cascade has started.
