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Surgery_Schwartz_6602 | Surgery_Schwartz | basement membrane and an elastic lamina. The endothelium produces endothelium-derived relaxing factors such as nitric oxide and prostacy-clin, which help maintain a nonthrombogenic surface through inhibition of platelet aggregation and promotion of platelet disaggregation.1 The capacitance function of veins is facili-tated by circumferential rings of elastic tissue, and smooth muscle located in the media of the vein allows for changes in vein caliber with minimal changes in venous pressure. The adventitia is most prominent in large veins and consists of collagen, elastic fibers, and fibroblasts. When a vein is maxi-mally distended, its diameter may be several times greater than that in the supine position.In the axial veins, unidirectional blood flow is achieved with multiple venous valves. The inferior vena cava (IVC), common iliac veins, portal venous system, and cranial sinuses are valveless. In the axial veins, valves are more numerous distally in the extremities than proximally. | Surgery_Schwartz. basement membrane and an elastic lamina. The endothelium produces endothelium-derived relaxing factors such as nitric oxide and prostacy-clin, which help maintain a nonthrombogenic surface through inhibition of platelet aggregation and promotion of platelet disaggregation.1 The capacitance function of veins is facili-tated by circumferential rings of elastic tissue, and smooth muscle located in the media of the vein allows for changes in vein caliber with minimal changes in venous pressure. The adventitia is most prominent in large veins and consists of collagen, elastic fibers, and fibroblasts. When a vein is maxi-mally distended, its diameter may be several times greater than that in the supine position.In the axial veins, unidirectional blood flow is achieved with multiple venous valves. The inferior vena cava (IVC), common iliac veins, portal venous system, and cranial sinuses are valveless. In the axial veins, valves are more numerous distally in the extremities than proximally. |
Surgery_Schwartz_6603 | Surgery_Schwartz | The inferior vena cava (IVC), common iliac veins, portal venous system, and cranial sinuses are valveless. In the axial veins, valves are more numerous distally in the extremities than proximally. Each valve consists of two thin cusps of a fine connective tissue skeleton covered by endothelium. Venous valves close in response to cephalad-to-caudal blood flow at a velocity of at least 30 cm/s.2Lower Extremity VeinsLower extremity veins are divided into superficial, deep, and perforating veins. The superficial venous system lies above the uppermost fascial layer of the leg and thigh and consists of the great saphenous vein (GSV) and small saphenous vein (SSV) and their tributaries. The GSV originates from the dorsal pedal venous arch and courses cephalad and medially, anterior to the medial malleolus, entering the common femoral vein approxi-mately 4 cm inferior and lateral to the pubic tubercle. The saphe-nous nerve accompanies the GSV medially from the ankle to the level of the knee | Surgery_Schwartz. The inferior vena cava (IVC), common iliac veins, portal venous system, and cranial sinuses are valveless. In the axial veins, valves are more numerous distally in the extremities than proximally. Each valve consists of two thin cusps of a fine connective tissue skeleton covered by endothelium. Venous valves close in response to cephalad-to-caudal blood flow at a velocity of at least 30 cm/s.2Lower Extremity VeinsLower extremity veins are divided into superficial, deep, and perforating veins. The superficial venous system lies above the uppermost fascial layer of the leg and thigh and consists of the great saphenous vein (GSV) and small saphenous vein (SSV) and their tributaries. The GSV originates from the dorsal pedal venous arch and courses cephalad and medially, anterior to the medial malleolus, entering the common femoral vein approxi-mately 4 cm inferior and lateral to the pubic tubercle. The saphe-nous nerve accompanies the GSV medially from the ankle to the level of the knee |
Surgery_Schwartz_6604 | Surgery_Schwartz | malleolus, entering the common femoral vein approxi-mately 4 cm inferior and lateral to the pubic tubercle. The saphe-nous nerve accompanies the GSV medially from the ankle to the level of the knee and supplies cutaneous sensation to the medial leg and ankle. The SSV originates laterally from the dorsal pedal venous arch and courses cephalad in the posterior calf. Most often, it penetrates the popliteal fossa, between the medial and lateral heads of the gastrocnemius muscle, to join the popliteal vein. The termination of the SSV may be quite vari-able, however, with a proximal extension of the SSV (the vein of Giacomini) connecting with the deep femoral vein or GSV. The sural nerve accompanies the SSV laterally along its course and supplies cutaneous sensation to the lateral malleolar region.The deep veins follow the course of major arteries in the extremities. In the lower leg, paired veins parallel the course of the anterior tibial, posterior tibial, and peroneal arteries, to join | Surgery_Schwartz. malleolus, entering the common femoral vein approxi-mately 4 cm inferior and lateral to the pubic tubercle. The saphe-nous nerve accompanies the GSV medially from the ankle to the level of the knee and supplies cutaneous sensation to the medial leg and ankle. The SSV originates laterally from the dorsal pedal venous arch and courses cephalad in the posterior calf. Most often, it penetrates the popliteal fossa, between the medial and lateral heads of the gastrocnemius muscle, to join the popliteal vein. The termination of the SSV may be quite vari-able, however, with a proximal extension of the SSV (the vein of Giacomini) connecting with the deep femoral vein or GSV. The sural nerve accompanies the SSV laterally along its course and supplies cutaneous sensation to the lateral malleolar region.The deep veins follow the course of major arteries in the extremities. In the lower leg, paired veins parallel the course of the anterior tibial, posterior tibial, and peroneal arteries, to join |
Surgery_Schwartz_6605 | Surgery_Schwartz | deep veins follow the course of major arteries in the extremities. In the lower leg, paired veins parallel the course of the anterior tibial, posterior tibial, and peroneal arteries, to join behind the knee forming the popliteal vein. Venous bridges con-nect the paired axial tibial veins in the lower leg. The popliteal vein continues through the adductor hiatus to become the femo-ral vein. In the proximal thigh, the femoral vein joins with the deep femoral vein to form the common femoral vein, becoming the external iliac vein at the inguinal ligament.Multiple perforator veins traverse the deep fascia to connect the superficial and deep venous systems. Potentially clinically important perforator veins are the posterior tibial and paratibial perforators (formerly known as the Cockett and Boyd perforators, respectively). The posterior tibial perforator veins drain the medial lower leg and are relatively constant. They Venous Anatomy981Structure of Veins / 981Lower Extremity Veins / | Surgery_Schwartz. deep veins follow the course of major arteries in the extremities. In the lower leg, paired veins parallel the course of the anterior tibial, posterior tibial, and peroneal arteries, to join behind the knee forming the popliteal vein. Venous bridges con-nect the paired axial tibial veins in the lower leg. The popliteal vein continues through the adductor hiatus to become the femo-ral vein. In the proximal thigh, the femoral vein joins with the deep femoral vein to form the common femoral vein, becoming the external iliac vein at the inguinal ligament.Multiple perforator veins traverse the deep fascia to connect the superficial and deep venous systems. Potentially clinically important perforator veins are the posterior tibial and paratibial perforators (formerly known as the Cockett and Boyd perforators, respectively). The posterior tibial perforator veins drain the medial lower leg and are relatively constant. They Venous Anatomy981Structure of Veins / 981Lower Extremity Veins / |
Surgery_Schwartz_6606 | Surgery_Schwartz | Boyd perforators, respectively). The posterior tibial perforator veins drain the medial lower leg and are relatively constant. They Venous Anatomy981Structure of Veins / 981Lower Extremity Veins / 981Upper Extremity Veins / 982Evaluation of the Venous System982Clinical Evaluation / 982Venous Thromboembolism984Epidemiology / 984Risk Factors / 984Diagnosis / 986Treatment / 987Prophylaxis / 992Other Venous Thrombotic Disorders994Superficial Vein Thrombophlebitis / 994Upper Extremity Vein Thrombosis / 995Mesenteric Vein Thrombosis / 996Varicose Veins996Chronic Venous Insufficiency997Evaluation of Venous Insufficiency / 997Lymphedema1001Pathophysiology / 1001Clinical Diagnosis / 1001Radiologic Diagnosis / 1002Management / 1002Summary1003Brunicardi_Ch24_p0981-p1008.indd 98122/02/19 3:00 PM 982connect the posterior accessory GSV (formerly known as the posterior arch vein, a tributary to the GSV) and the posterior tibial vein. They may become varicose or incompetent in venous | Surgery_Schwartz. Boyd perforators, respectively). The posterior tibial perforator veins drain the medial lower leg and are relatively constant. They Venous Anatomy981Structure of Veins / 981Lower Extremity Veins / 981Upper Extremity Veins / 982Evaluation of the Venous System982Clinical Evaluation / 982Venous Thromboembolism984Epidemiology / 984Risk Factors / 984Diagnosis / 986Treatment / 987Prophylaxis / 992Other Venous Thrombotic Disorders994Superficial Vein Thrombophlebitis / 994Upper Extremity Vein Thrombosis / 995Mesenteric Vein Thrombosis / 996Varicose Veins996Chronic Venous Insufficiency997Evaluation of Venous Insufficiency / 997Lymphedema1001Pathophysiology / 1001Clinical Diagnosis / 1001Radiologic Diagnosis / 1002Management / 1002Summary1003Brunicardi_Ch24_p0981-p1008.indd 98122/02/19 3:00 PM 982connect the posterior accessory GSV (formerly known as the posterior arch vein, a tributary to the GSV) and the posterior tibial vein. They may become varicose or incompetent in venous |
Surgery_Schwartz_6607 | Surgery_Schwartz | 3:00 PM 982connect the posterior accessory GSV (formerly known as the posterior arch vein, a tributary to the GSV) and the posterior tibial vein. They may become varicose or incompetent in venous insufficiency states. The posterior accessory GSV has relevance as it represents a connection of the three ankle perforating veins, which are likely of particular importance in the development of a venous stasis ulcers. The paratibial perforator veins connect the GSV to the deep veins approximately 10 cm below the knee and 1 to 2 cm medial to the tibia. Additional perforators in the thigh are known as the perforators of the femoral canal (also known as Hunter’s and Dodd’s perforators).Venous sinuses are thin-walled, large veins located within the substance of the soleus and gastrocnemius muscles. These sinuses are valveless and are linked by valved, small venous channels that prevent reflux. A large amount of blood can be stored in the venous sinuses before draining into the posterior | Surgery_Schwartz. 3:00 PM 982connect the posterior accessory GSV (formerly known as the posterior arch vein, a tributary to the GSV) and the posterior tibial vein. They may become varicose or incompetent in venous insufficiency states. The posterior accessory GSV has relevance as it represents a connection of the three ankle perforating veins, which are likely of particular importance in the development of a venous stasis ulcers. The paratibial perforator veins connect the GSV to the deep veins approximately 10 cm below the knee and 1 to 2 cm medial to the tibia. Additional perforators in the thigh are known as the perforators of the femoral canal (also known as Hunter’s and Dodd’s perforators).Venous sinuses are thin-walled, large veins located within the substance of the soleus and gastrocnemius muscles. These sinuses are valveless and are linked by valved, small venous channels that prevent reflux. A large amount of blood can be stored in the venous sinuses before draining into the posterior |
Surgery_Schwartz_6608 | Surgery_Schwartz | These sinuses are valveless and are linked by valved, small venous channels that prevent reflux. A large amount of blood can be stored in the venous sinuses before draining into the posterior tibial and peroneal veins. With each contraction of the calf muscle bed, blood is pumped out through the venous channels into the main conduit veins to return to the heart.Upper Extremity VeinsAs in the lower extremity, there are deep and superficial veins in the upper extremity. Deep digital veins form the palmar venous arches of the hand and empty into the paired radial and ulnar veins. These follow the named arteries in the arm and are known as the venae comitantes. They become the brachial veins most often near the antecubital fossa and then combine to contrib-ute to forming the axillary vein. Superficial veins of the upper extremity are the cephalic and basilic veins and their tributaries. The cephalic vein originates at the lateral wrist and courses over the lateral ventral surface of the | Surgery_Schwartz. These sinuses are valveless and are linked by valved, small venous channels that prevent reflux. A large amount of blood can be stored in the venous sinuses before draining into the posterior tibial and peroneal veins. With each contraction of the calf muscle bed, blood is pumped out through the venous channels into the main conduit veins to return to the heart.Upper Extremity VeinsAs in the lower extremity, there are deep and superficial veins in the upper extremity. Deep digital veins form the palmar venous arches of the hand and empty into the paired radial and ulnar veins. These follow the named arteries in the arm and are known as the venae comitantes. They become the brachial veins most often near the antecubital fossa and then combine to contrib-ute to forming the axillary vein. Superficial veins of the upper extremity are the cephalic and basilic veins and their tributaries. The cephalic vein originates at the lateral wrist and courses over the lateral ventral surface of the |
Surgery_Schwartz_6609 | Surgery_Schwartz | veins of the upper extremity are the cephalic and basilic veins and their tributaries. The cephalic vein originates at the lateral wrist and courses over the lateral ventral surface of the forearm. In the upper arm, the cephalic vein terminates in the infraclavicular fossa, piercing the clavipectoral fascia to empty into the axillary vein. The basilic vein runs medially along the forearm and penetrates the deep fascia as it courses past the elbow in the upper arm. It then joins with the deep brachial veins to become the axil-lary vein, a landmark for identification of the axillary vein. The median antecubital vein joins the cephalic and the basilic veins on the ventral surface of the elbow.The axillary vein becomes the subclavian vein at the lat-eral border of the first rib. At the medial border of the scalenus anterior muscle, the subclavian vein joins with the internal jugu-lar vein to become the brachiocephalic vein, with the subclavian vein coursing anterior to the scalenus | Surgery_Schwartz. veins of the upper extremity are the cephalic and basilic veins and their tributaries. The cephalic vein originates at the lateral wrist and courses over the lateral ventral surface of the forearm. In the upper arm, the cephalic vein terminates in the infraclavicular fossa, piercing the clavipectoral fascia to empty into the axillary vein. The basilic vein runs medially along the forearm and penetrates the deep fascia as it courses past the elbow in the upper arm. It then joins with the deep brachial veins to become the axil-lary vein, a landmark for identification of the axillary vein. The median antecubital vein joins the cephalic and the basilic veins on the ventral surface of the elbow.The axillary vein becomes the subclavian vein at the lat-eral border of the first rib. At the medial border of the scalenus anterior muscle, the subclavian vein joins with the internal jugu-lar vein to become the brachiocephalic vein, with the subclavian vein coursing anterior to the scalenus |
Surgery_Schwartz_6610 | Surgery_Schwartz | medial border of the scalenus anterior muscle, the subclavian vein joins with the internal jugu-lar vein to become the brachiocephalic vein, with the subclavian vein coursing anterior to the scalenus anterior muscle. The left and right brachiocephalic veins join to become the superior vena cava, which empties into the right atrium.EVALUATION OF THE VENOUS SYSTEMClinical EvaluationEvaluation of the venous system begins with a detailed history and physical examination. Risk factors for acute and chronic venous disease are identified. They include increased age, his-tory of venous thromboembolism (VTE), malignancy, trauma and spinal cord injury, hospitalization and immobilization, obe-sity, nephrotic syndrome, pregnancy, recent postpartum state, oral contraceptive use or hormone replacement therapy, vari-cose veins, and hypercoagulable states, as well as the postopera-tive state. Venous pathology is often, but not always, associated with visible or palpable signs that can be identified | Surgery_Schwartz. medial border of the scalenus anterior muscle, the subclavian vein joins with the internal jugu-lar vein to become the brachiocephalic vein, with the subclavian vein coursing anterior to the scalenus anterior muscle. The left and right brachiocephalic veins join to become the superior vena cava, which empties into the right atrium.EVALUATION OF THE VENOUS SYSTEMClinical EvaluationEvaluation of the venous system begins with a detailed history and physical examination. Risk factors for acute and chronic venous disease are identified. They include increased age, his-tory of venous thromboembolism (VTE), malignancy, trauma and spinal cord injury, hospitalization and immobilization, obe-sity, nephrotic syndrome, pregnancy, recent postpartum state, oral contraceptive use or hormone replacement therapy, vari-cose veins, and hypercoagulable states, as well as the postopera-tive state. Venous pathology is often, but not always, associated with visible or palpable signs that can be identified |
Surgery_Schwartz_6611 | Surgery_Schwartz | therapy, vari-cose veins, and hypercoagulable states, as well as the postopera-tive state. Venous pathology is often, but not always, associated with visible or palpable signs that can be identified during the physical examination. There is variation among individuals in the prominence of superficial veins when the person is standing (Fig. 24-1). The superficial veins of a lean athletic person, even when normal, will appear large and easily visualized, but these veins will be far less obvious in the obese individual. Signs of superficial venous abnormalities are listed in Table 24-1. Key Points1 Thrombolytic therapy, surgical thrombectomy, and place-ment of inferior vena cava filters are adjunctive treatments that may be indicated in patients with extensive and compli-cated venous thromboembolism.2 Deep vein thrombosis (DVT) and pulmonary embolism are well-recognized complications after major abdominal and orthopedic procedures. The risk is further increased in patients with | Surgery_Schwartz. therapy, vari-cose veins, and hypercoagulable states, as well as the postopera-tive state. Venous pathology is often, but not always, associated with visible or palpable signs that can be identified during the physical examination. There is variation among individuals in the prominence of superficial veins when the person is standing (Fig. 24-1). The superficial veins of a lean athletic person, even when normal, will appear large and easily visualized, but these veins will be far less obvious in the obese individual. Signs of superficial venous abnormalities are listed in Table 24-1. Key Points1 Thrombolytic therapy, surgical thrombectomy, and place-ment of inferior vena cava filters are adjunctive treatments that may be indicated in patients with extensive and compli-cated venous thromboembolism.2 Deep vein thrombosis (DVT) and pulmonary embolism are well-recognized complications after major abdominal and orthopedic procedures. The risk is further increased in patients with |
Surgery_Schwartz_6612 | Surgery_Schwartz | thromboembolism.2 Deep vein thrombosis (DVT) and pulmonary embolism are well-recognized complications after major abdominal and orthopedic procedures. The risk is further increased in patients with malignancy and a history of venous thrombo-embolism. Options for DVT prophylaxis include intermit-tent pneumatic compression, use of graduated compression stockings, and administration of low-dose unfractionated heparin, low molecular weight heparin, fondaparinux, and vitamin K antagonists. Direct thrombin inhibitors and factor Xa inhibitors are approved for prophylactic use only for orthopedic procedures and for recurrent VTE. However, prophylaxis should be stratified based on the patient’s level of risk.3 In patients with established DVT, unfractionated heparin, low molecular weight heparin, fondaparinux, and some factor Xa inhibitors are options for initial antithrombotic therapy. Vitamin-K antagonists, direct thrombin inhibitors, and factor Xa inhibitors are utilized for long-term | Surgery_Schwartz. thromboembolism.2 Deep vein thrombosis (DVT) and pulmonary embolism are well-recognized complications after major abdominal and orthopedic procedures. The risk is further increased in patients with malignancy and a history of venous thrombo-embolism. Options for DVT prophylaxis include intermit-tent pneumatic compression, use of graduated compression stockings, and administration of low-dose unfractionated heparin, low molecular weight heparin, fondaparinux, and vitamin K antagonists. Direct thrombin inhibitors and factor Xa inhibitors are approved for prophylactic use only for orthopedic procedures and for recurrent VTE. However, prophylaxis should be stratified based on the patient’s level of risk.3 In patients with established DVT, unfractionated heparin, low molecular weight heparin, fondaparinux, and some factor Xa inhibitors are options for initial antithrombotic therapy. Vitamin-K antagonists, direct thrombin inhibitors, and factor Xa inhibitors are utilized for long-term |
Surgery_Schwartz_6613 | Surgery_Schwartz | fondaparinux, and some factor Xa inhibitors are options for initial antithrombotic therapy. Vitamin-K antagonists, direct thrombin inhibitors, and factor Xa inhibitors are utilized for long-term anticoagulation. The duration and type of long-term anticoagulation should be stratified based on the provoked or unprovoked nature of the DVT, the location of the DVT, previous occurrence of DVT, and presence of concomitant malignancy.4 High ligation and stripping, endovenous laser, or radiofre-quency ablation and sclerotherapy are effective therapies for patients with saphenous vein valvular insufficiency. Con-comitant varicose veins may be managed with compression therapy, sclerotherapy, and phlebectomy. New nonthermal ablative techniques, including the combination of sclero-therapy with endoluminal mechanical injury as well as injec-tion of cyanoacrylate, show early promising results.5 The mainstay of treatment for chronic venous insufficiency is compression therapy. Sclerotherapy, | Surgery_Schwartz. fondaparinux, and some factor Xa inhibitors are options for initial antithrombotic therapy. Vitamin-K antagonists, direct thrombin inhibitors, and factor Xa inhibitors are utilized for long-term anticoagulation. The duration and type of long-term anticoagulation should be stratified based on the provoked or unprovoked nature of the DVT, the location of the DVT, previous occurrence of DVT, and presence of concomitant malignancy.4 High ligation and stripping, endovenous laser, or radiofre-quency ablation and sclerotherapy are effective therapies for patients with saphenous vein valvular insufficiency. Con-comitant varicose veins may be managed with compression therapy, sclerotherapy, and phlebectomy. New nonthermal ablative techniques, including the combination of sclero-therapy with endoluminal mechanical injury as well as injec-tion of cyanoacrylate, show early promising results.5 The mainstay of treatment for chronic venous insufficiency is compression therapy. Sclerotherapy, |
Surgery_Schwartz_6614 | Surgery_Schwartz | endoluminal mechanical injury as well as injec-tion of cyanoacrylate, show early promising results.5 The mainstay of treatment for chronic venous insufficiency is compression therapy. Sclerotherapy, perforator vein liga-tion, and venous reconstruction or ablative techniques may be indicated in patients in whom conservative management fails or as a means to decrease ulcer recurrence.6 Lymphedema is categorized as congenital, primary (with early or delayed onset), or secondary. The goals of treatment are to minimize edema and prevent infection. Lymphatic massage, sequential pneumatic compression, use of com-pression garments, and limb elevation are effective forms of therapy.Brunicardi_Ch24_p0981-p1008.indd 98222/02/19 3:00 PM 983VENOUS AND LYMPHATIC DISEASECHAPTER 24Figure 24-1. Varicose vein demonstrating evidence of chronic venous insufficiency.Figure 24-2. Characteristic hyperpigmentation of chronic venous insufficiency.Table 24-1Possible signs of superficial venous | Surgery_Schwartz. endoluminal mechanical injury as well as injec-tion of cyanoacrylate, show early promising results.5 The mainstay of treatment for chronic venous insufficiency is compression therapy. Sclerotherapy, perforator vein liga-tion, and venous reconstruction or ablative techniques may be indicated in patients in whom conservative management fails or as a means to decrease ulcer recurrence.6 Lymphedema is categorized as congenital, primary (with early or delayed onset), or secondary. The goals of treatment are to minimize edema and prevent infection. Lymphatic massage, sequential pneumatic compression, use of com-pression garments, and limb elevation are effective forms of therapy.Brunicardi_Ch24_p0981-p1008.indd 98222/02/19 3:00 PM 983VENOUS AND LYMPHATIC DISEASECHAPTER 24Figure 24-1. Varicose vein demonstrating evidence of chronic venous insufficiency.Figure 24-2. Characteristic hyperpigmentation of chronic venous insufficiency.Table 24-1Possible signs of superficial venous |
Surgery_Schwartz_6615 | Surgery_Schwartz | 24-1. Varicose vein demonstrating evidence of chronic venous insufficiency.Figure 24-2. Characteristic hyperpigmentation of chronic venous insufficiency.Table 24-1Possible signs of superficial venous abnormalitiesTortuosityVaricosityVenous sacculeDistended subdermal venules (corona phlebectatica)Distended intradermal venules (spider angiomata)Warmth, erythema, tenderness (superficial thrombophlebitis)The deep veins cannot be directly assessed clinically, and abnormalities within them can only be inferred indirectly from changes found on clinical examination.Chronic venous insufficiency (CVI) may lead to character-istic changes in the skin and subcutaneous tissues in the affected limb. CVI results from incompetence of venous valves, venous obstruction, or both. Most CVI involves venous reflux, and severe CVI often reflects a combination of reflux and venous obstruction. It is important to remember that although CVI originates with abnormalities of the veins, the target organ of CVI is | Surgery_Schwartz. 24-1. Varicose vein demonstrating evidence of chronic venous insufficiency.Figure 24-2. Characteristic hyperpigmentation of chronic venous insufficiency.Table 24-1Possible signs of superficial venous abnormalitiesTortuosityVaricosityVenous sacculeDistended subdermal venules (corona phlebectatica)Distended intradermal venules (spider angiomata)Warmth, erythema, tenderness (superficial thrombophlebitis)The deep veins cannot be directly assessed clinically, and abnormalities within them can only be inferred indirectly from changes found on clinical examination.Chronic venous insufficiency (CVI) may lead to character-istic changes in the skin and subcutaneous tissues in the affected limb. CVI results from incompetence of venous valves, venous obstruction, or both. Most CVI involves venous reflux, and severe CVI often reflects a combination of reflux and venous obstruction. It is important to remember that although CVI originates with abnormalities of the veins, the target organ of CVI is |
Surgery_Schwartz_6616 | Surgery_Schwartz | and severe CVI often reflects a combination of reflux and venous obstruction. It is important to remember that although CVI originates with abnormalities of the veins, the target organ of CVI is the skin, and the underlying physiologic and biochemical mechanisms leading to the cutaneous abnormalities associated with CVI are poorly understood. A typical leg affected by CVI will be edematous, with edema increasing over the course of the day. The leg may also be indurated and pigmented with eczema and dermatitis. These changes are associated with excessive proteinaceous capillary exudate. Deposition of a pericapil-lary fibrin cuff may limit nutritional exchange. In addition, an increase in white blood cell trapping within the skin microcir-culation in CVI patients may lead to microvascular congestion and thrombosis. Subsequently, white blood cells may migrate into the interstitium and release necrotizing lysosomal enzymes, potentially leading to tissue destruction and eventual | Surgery_Schwartz. and severe CVI often reflects a combination of reflux and venous obstruction. It is important to remember that although CVI originates with abnormalities of the veins, the target organ of CVI is the skin, and the underlying physiologic and biochemical mechanisms leading to the cutaneous abnormalities associated with CVI are poorly understood. A typical leg affected by CVI will be edematous, with edema increasing over the course of the day. The leg may also be indurated and pigmented with eczema and dermatitis. These changes are associated with excessive proteinaceous capillary exudate. Deposition of a pericapil-lary fibrin cuff may limit nutritional exchange. In addition, an increase in white blood cell trapping within the skin microcir-culation in CVI patients may lead to microvascular congestion and thrombosis. Subsequently, white blood cells may migrate into the interstitium and release necrotizing lysosomal enzymes, potentially leading to tissue destruction and eventual |
Surgery_Schwartz_6617 | Surgery_Schwartz | congestion and thrombosis. Subsequently, white blood cells may migrate into the interstitium and release necrotizing lysosomal enzymes, potentially leading to tissue destruction and eventual ulceration.Fibrosis can eventually develop from impaired nutrition, chronic inflammation, and fat necrosis (lipodermatosclerosis). Hemosiderin deposition due to the extravasation of red cells and subsequent lysis in the skin contributes to the characteristic pigmentation of chronic venous disease (Fig. 24-2). Ulceration can develop with longstanding venous hypertension and is associated with alterations in microcirculatory and cutaneous lymphatic anatomy and function. The most common location of venous ulceration is approximately 3 cm proximal to the medial malleolus, frequently referred to the “gaiter” region (Fig. 24-3).Trendelenburg’s test is a clinical test, historically impor-tant but now rarely used, that can help determine whether incompetent valves are present and in which of the three | Surgery_Schwartz. congestion and thrombosis. Subsequently, white blood cells may migrate into the interstitium and release necrotizing lysosomal enzymes, potentially leading to tissue destruction and eventual ulceration.Fibrosis can eventually develop from impaired nutrition, chronic inflammation, and fat necrosis (lipodermatosclerosis). Hemosiderin deposition due to the extravasation of red cells and subsequent lysis in the skin contributes to the characteristic pigmentation of chronic venous disease (Fig. 24-2). Ulceration can develop with longstanding venous hypertension and is associated with alterations in microcirculatory and cutaneous lymphatic anatomy and function. The most common location of venous ulceration is approximately 3 cm proximal to the medial malleolus, frequently referred to the “gaiter” region (Fig. 24-3).Trendelenburg’s test is a clinical test, historically impor-tant but now rarely used, that can help determine whether incompetent valves are present and in which of the three |
Surgery_Schwartz_6618 | Surgery_Schwartz | region (Fig. 24-3).Trendelenburg’s test is a clinical test, historically impor-tant but now rarely used, that can help determine whether incompetent valves are present and in which of the three venous systems (superficial, deep, or perforator) the valves are abnormal. There are two components to this test. First, with the patient supine, the leg is elevated 45° to empty the veins, and the GSV is occluded with the examiner’s hand or with a rub-ber tourniquet. Then, with the GSV still occluded, the patient stands, and the superficial veins are observed for blood filling. The compression on the GSV is released, and the superficial veins are observed for filling with blood. A positive result is the sudden filling of veins with standing while the GSV remains occluded, indicating incompetent perforator and deep veins. Additionally, the GSV valves are incompetent if rapid filling is noted following release of compression. A negative result, indicating no clinically relevant venous reflux, is | Surgery_Schwartz. region (Fig. 24-3).Trendelenburg’s test is a clinical test, historically impor-tant but now rarely used, that can help determine whether incompetent valves are present and in which of the three venous systems (superficial, deep, or perforator) the valves are abnormal. There are two components to this test. First, with the patient supine, the leg is elevated 45° to empty the veins, and the GSV is occluded with the examiner’s hand or with a rub-ber tourniquet. Then, with the GSV still occluded, the patient stands, and the superficial veins are observed for blood filling. The compression on the GSV is released, and the superficial veins are observed for filling with blood. A positive result is the sudden filling of veins with standing while the GSV remains occluded, indicating incompetent perforator and deep veins. Additionally, the GSV valves are incompetent if rapid filling is noted following release of compression. A negative result, indicating no clinically relevant venous reflux, is |
Surgery_Schwartz_6619 | Surgery_Schwartz | and deep veins. Additionally, the GSV valves are incompetent if rapid filling is noted following release of compression. A negative result, indicating no clinically relevant venous reflux, is the gradual filling of the veins from arterial inflow. Interpretation of the findings of Trendelenburg’s test is subjective, and therefore, it has largely been supplanted by the more objective noninvasive vascular laboratory tests to localize sites of venous reflux.Noninvasive Evaluation. Before the development of vascu-lar ultrasound, noninvasive techniques to evaluate the venous system were based on plethysmographic techniques. Although a variety of plethysmographic techniques are used in the Brunicardi_Ch24_p0981-p1008.indd 98322/02/19 3:01 PM 984SPECIFIC CONSIDERATIONSPART IIFigure 24-3. Venous ulceration located proximal to the medial malleolus.evaluation of both acute and chronic venous disease, they are all based on the detection of volume changes in the limb in response to blood | Surgery_Schwartz. and deep veins. Additionally, the GSV valves are incompetent if rapid filling is noted following release of compression. A negative result, indicating no clinically relevant venous reflux, is the gradual filling of the veins from arterial inflow. Interpretation of the findings of Trendelenburg’s test is subjective, and therefore, it has largely been supplanted by the more objective noninvasive vascular laboratory tests to localize sites of venous reflux.Noninvasive Evaluation. Before the development of vascu-lar ultrasound, noninvasive techniques to evaluate the venous system were based on plethysmographic techniques. Although a variety of plethysmographic techniques are used in the Brunicardi_Ch24_p0981-p1008.indd 98322/02/19 3:01 PM 984SPECIFIC CONSIDERATIONSPART IIFigure 24-3. Venous ulceration located proximal to the medial malleolus.evaluation of both acute and chronic venous disease, they are all based on the detection of volume changes in the limb in response to blood |
Surgery_Schwartz_6620 | Surgery_Schwartz | ulceration located proximal to the medial malleolus.evaluation of both acute and chronic venous disease, they are all based on the detection of volume changes in the limb in response to blood flow.Duplex ultrasonography (DUS) augmented by color flow imaging is now the most important noninvasive diagnos-tic method in the evaluation of the venous system. DUS has become standard for the detection of infrainguinal deep vein thrombosis (DVT), with near 100% sensitivity and specificity in symptomatic patients.3 It is also the preferred method of evalu-ation for upper extremity venous thrombosis and is useful in the evaluation of CVI by documenting the presence of valvular reflux and venous obstruction. Overlying bowel gas and large body habitus many times make DUS less applicable to evalu-ation of intra-abdominal veins. Magnetic resonance venogra-phy (MRV) and computed tomography (CT) venography are alternative noninvasive techniques for evaluation of pelvic and intra-abdominal | Surgery_Schwartz. ulceration located proximal to the medial malleolus.evaluation of both acute and chronic venous disease, they are all based on the detection of volume changes in the limb in response to blood flow.Duplex ultrasonography (DUS) augmented by color flow imaging is now the most important noninvasive diagnos-tic method in the evaluation of the venous system. DUS has become standard for the detection of infrainguinal deep vein thrombosis (DVT), with near 100% sensitivity and specificity in symptomatic patients.3 It is also the preferred method of evalu-ation for upper extremity venous thrombosis and is useful in the evaluation of CVI by documenting the presence of valvular reflux and venous obstruction. Overlying bowel gas and large body habitus many times make DUS less applicable to evalu-ation of intra-abdominal veins. Magnetic resonance venogra-phy (MRV) and computed tomography (CT) venography are alternative noninvasive techniques for evaluation of pelvic and intra-abdominal |
Surgery_Schwartz_6621 | Surgery_Schwartz | evalu-ation of intra-abdominal veins. Magnetic resonance venogra-phy (MRV) and computed tomography (CT) venography are alternative noninvasive techniques for evaluation of pelvic and intra-abdominal veins.Invasive Evaluation. Improved accuracy of noninvasive techniques for diagnostic purposes has made the use of invasive procedures more selective. Both venography and intravascular ultrasound (IVUS) are used as adjuncts to percutaneous or open surgical treatment of venous disorders. When planning endo-vascular or open surgical treatment, venography may be used to identify areas of obstruction in infrainguinal, intra-abdominal, and upper extremity veins as well as reflux in intra-abdominal and infrainguinal veins. IVUS, with access generally via the common femoral vein, is used primarily to assess for occlusive lesions of the iliac veins and appears more sensitive than venog-raphy in detecting iliac vein obstruction.4Complications of venography include pain, thrombosis, or hematoma at | Surgery_Schwartz. evalu-ation of intra-abdominal veins. Magnetic resonance venogra-phy (MRV) and computed tomography (CT) venography are alternative noninvasive techniques for evaluation of pelvic and intra-abdominal veins.Invasive Evaluation. Improved accuracy of noninvasive techniques for diagnostic purposes has made the use of invasive procedures more selective. Both venography and intravascular ultrasound (IVUS) are used as adjuncts to percutaneous or open surgical treatment of venous disorders. When planning endo-vascular or open surgical treatment, venography may be used to identify areas of obstruction in infrainguinal, intra-abdominal, and upper extremity veins as well as reflux in intra-abdominal and infrainguinal veins. IVUS, with access generally via the common femoral vein, is used primarily to assess for occlusive lesions of the iliac veins and appears more sensitive than venog-raphy in detecting iliac vein obstruction.4Complications of venography include pain, thrombosis, or hematoma at |
Surgery_Schwartz_6622 | Surgery_Schwartz | assess for occlusive lesions of the iliac veins and appears more sensitive than venog-raphy in detecting iliac vein obstruction.4Complications of venography include pain, thrombosis, or hematoma at the puncture site. Pain is lower with nonionic low-osmolality contrast media than with conventional contrast agents (with 18% vs. 44% of patients experiencing discomfort, respectively).5 Systemic effects of iodinated contrast media include allergic reaction and risk of renal failure. Postvenogra-phy venous thrombosis occurs distal to the venous puncture site in 1% to 9% of patients undergoing venography secondary to intimal damage from the intravenous (IV) contrast agent.5 Com-plications and limitations of IVUS are related to complications at the access site and cost of the catheters.VENOUS THROMBOEMBOLISMEpidemiologyDespite increased awareness and use of prophylactic modalities, DVT or pulmonary embolism (PE), venous thromboembolism (VTE), remain important preventable sources of morbidity | Surgery_Schwartz. assess for occlusive lesions of the iliac veins and appears more sensitive than venog-raphy in detecting iliac vein obstruction.4Complications of venography include pain, thrombosis, or hematoma at the puncture site. Pain is lower with nonionic low-osmolality contrast media than with conventional contrast agents (with 18% vs. 44% of patients experiencing discomfort, respectively).5 Systemic effects of iodinated contrast media include allergic reaction and risk of renal failure. Postvenogra-phy venous thrombosis occurs distal to the venous puncture site in 1% to 9% of patients undergoing venography secondary to intimal damage from the intravenous (IV) contrast agent.5 Com-plications and limitations of IVUS are related to complications at the access site and cost of the catheters.VENOUS THROMBOEMBOLISMEpidemiologyDespite increased awareness and use of prophylactic modalities, DVT or pulmonary embolism (PE), venous thromboembolism (VTE), remain important preventable sources of morbidity |
Surgery_Schwartz_6623 | Surgery_Schwartz | increased awareness and use of prophylactic modalities, DVT or pulmonary embolism (PE), venous thromboembolism (VTE), remain important preventable sources of morbidity and mortality, especially in the surgical patient. The incidence of VTE is approximately 100 per 100,000 people per year in the general population, with 20% of the diagnoses made within 3 months of a surgical procedure. Of the symptomatic patients, one-third will present with PE and two-thirds with DVT.6,7 The estimated number of cases of VTE may well be over 600,000 per year in the United States, making it a major U.S. health problem.8 Furthermore, death occurs in 6% of DVT and 12% of PE cases within 1 month of diagnosis, although not all deaths are directly secondary to VTE, with many related to the under-lying problem leading to the VTE event.6 However, not only does VTE pose a veritable threat to life, it also places patients at higher risk for recurrence and post-VTE sequelae such as pul-monary hypertension and | Surgery_Schwartz. increased awareness and use of prophylactic modalities, DVT or pulmonary embolism (PE), venous thromboembolism (VTE), remain important preventable sources of morbidity and mortality, especially in the surgical patient. The incidence of VTE is approximately 100 per 100,000 people per year in the general population, with 20% of the diagnoses made within 3 months of a surgical procedure. Of the symptomatic patients, one-third will present with PE and two-thirds with DVT.6,7 The estimated number of cases of VTE may well be over 600,000 per year in the United States, making it a major U.S. health problem.8 Furthermore, death occurs in 6% of DVT and 12% of PE cases within 1 month of diagnosis, although not all deaths are directly secondary to VTE, with many related to the under-lying problem leading to the VTE event.6 However, not only does VTE pose a veritable threat to life, it also places patients at higher risk for recurrence and post-VTE sequelae such as pul-monary hypertension and |
Surgery_Schwartz_6624 | Surgery_Schwartz | leading to the VTE event.6 However, not only does VTE pose a veritable threat to life, it also places patients at higher risk for recurrence and post-VTE sequelae such as pul-monary hypertension and postthrombotic syndrome, with 4% and up to 30% incidence, respectively.9-11Risk FactorsThree broadly stated conditions, first described by Rudolf Vir-chow in 1862, contribute to VTE formation: stasis of blood flow, endothelial damage, and hypercoagulability. Of these risk factors, relative hypercoagulability appears most impor-tant in cases of spontaneous VTE, or so-called idiopathic VTE, whereas stasis and endothelial damage likely play a greater role in secondary VTE, or so-called provoked VTE, occurring in association with transient risk factors such as immobiliza-tion, surgical procedures, and trauma. Identifiable risk factors for VTE generally relate to one of the conditions described by Virchow. Often more than one risk factor is present contribut-ing in an exponential, rather than | Surgery_Schwartz. leading to the VTE event.6 However, not only does VTE pose a veritable threat to life, it also places patients at higher risk for recurrence and post-VTE sequelae such as pul-monary hypertension and postthrombotic syndrome, with 4% and up to 30% incidence, respectively.9-11Risk FactorsThree broadly stated conditions, first described by Rudolf Vir-chow in 1862, contribute to VTE formation: stasis of blood flow, endothelial damage, and hypercoagulability. Of these risk factors, relative hypercoagulability appears most impor-tant in cases of spontaneous VTE, or so-called idiopathic VTE, whereas stasis and endothelial damage likely play a greater role in secondary VTE, or so-called provoked VTE, occurring in association with transient risk factors such as immobiliza-tion, surgical procedures, and trauma. Identifiable risk factors for VTE generally relate to one of the conditions described by Virchow. Often more than one risk factor is present contribut-ing in an exponential, rather than |
Surgery_Schwartz_6625 | Surgery_Schwartz | and trauma. Identifiable risk factors for VTE generally relate to one of the conditions described by Virchow. Often more than one risk factor is present contribut-ing in an exponential, rather than additive, manner. Specific risk factors for VTE are listed in Table 24-2.The more common acquired VTE risk factors include older age (>40 years), hospitalization and immobilization, hor-mone replacement and oral contraceptive therapy, pregnancy and the recently postpartum state, prior VTE, malignancy, major surgery, obesity, nephrotic syndrome, trauma and spinal cord injury, long-haul travel (>6 hours), varicose veins, antiphospho-lipid syndrome, myeloproliferative disorders, and polycythemia. Heritable risk factors include male sex, factor V Leiden muta-tion; prothrombin 20210A gene variant; antithrombin, protein C, and protein S deficiencies; and dysfibrinogenemias. In some patients, the cause of the thrombophilia may have both a heri-table and an acquired component. These mixed causes | Surgery_Schwartz. and trauma. Identifiable risk factors for VTE generally relate to one of the conditions described by Virchow. Often more than one risk factor is present contribut-ing in an exponential, rather than additive, manner. Specific risk factors for VTE are listed in Table 24-2.The more common acquired VTE risk factors include older age (>40 years), hospitalization and immobilization, hor-mone replacement and oral contraceptive therapy, pregnancy and the recently postpartum state, prior VTE, malignancy, major surgery, obesity, nephrotic syndrome, trauma and spinal cord injury, long-haul travel (>6 hours), varicose veins, antiphospho-lipid syndrome, myeloproliferative disorders, and polycythemia. Heritable risk factors include male sex, factor V Leiden muta-tion; prothrombin 20210A gene variant; antithrombin, protein C, and protein S deficiencies; and dysfibrinogenemias. In some patients, the cause of the thrombophilia may have both a heri-table and an acquired component. These mixed causes |
Surgery_Schwartz_6626 | Surgery_Schwartz | antithrombin, protein C, and protein S deficiencies; and dysfibrinogenemias. In some patients, the cause of the thrombophilia may have both a heri-table and an acquired component. These mixed causes include homocysteinemia; factors VII, VIII, IX, and XI elevation; hyperfibrinogenemia; and activated protein C resistance in the Brunicardi_Ch24_p0981-p1008.indd 98422/02/19 3:01 PM 985VENOUS AND LYMPHATIC DISEASECHAPTER 24Table 24-2Risk factors for venous thromboembolismAcquiredAdvanced ageHospitalization/immobilizationHormone replacement therapy and oral contraceptive usePregnancy and puerperiumPrior venous thromboembolismMalignancyMajor surgeryObesityNephrotic syndromeTrauma or spinal cord injuryLong-haul travel (>6 hours)Varicose veinsAntiphospholipid antibody syndromeMyeloproliferative diseasePolycythemiaInheritedFactor V LeidenProthrombin 20210AAntithrombin deficiencyProtein C deficiencyProtein S deficiencyFactor XI elevationDysfibrinogenemiaMixed EtiologyHomocysteinemiaFactors | Surgery_Schwartz. antithrombin, protein C, and protein S deficiencies; and dysfibrinogenemias. In some patients, the cause of the thrombophilia may have both a heri-table and an acquired component. These mixed causes include homocysteinemia; factors VII, VIII, IX, and XI elevation; hyperfibrinogenemia; and activated protein C resistance in the Brunicardi_Ch24_p0981-p1008.indd 98422/02/19 3:01 PM 985VENOUS AND LYMPHATIC DISEASECHAPTER 24Table 24-2Risk factors for venous thromboembolismAcquiredAdvanced ageHospitalization/immobilizationHormone replacement therapy and oral contraceptive usePregnancy and puerperiumPrior venous thromboembolismMalignancyMajor surgeryObesityNephrotic syndromeTrauma or spinal cord injuryLong-haul travel (>6 hours)Varicose veinsAntiphospholipid antibody syndromeMyeloproliferative diseasePolycythemiaInheritedFactor V LeidenProthrombin 20210AAntithrombin deficiencyProtein C deficiencyProtein S deficiencyFactor XI elevationDysfibrinogenemiaMixed EtiologyHomocysteinemiaFactors |
Surgery_Schwartz_6627 | Surgery_Schwartz | diseasePolycythemiaInheritedFactor V LeidenProthrombin 20210AAntithrombin deficiencyProtein C deficiencyProtein S deficiencyFactor XI elevationDysfibrinogenemiaMixed EtiologyHomocysteinemiaFactors VII, VIII, IX, XI elevationHyperfibrinogenemiaActivated protein C resistance without factor V Leidenabsence of factor V Leiden.12 There may be a synergistic effect when particular multiple inherited and acquired risk factors are present in the same patient.Other patient-specific factors associated with venous thrombosis include the traditional cardiovascular risk factors of obesity, hypertension, and diabetes. VTE is more common in whites and African Americans than Asians and Native Americans.13,14 Certain gene variants (single nucleotide polymorphisms) are also associated with a mildly increased risk for VTE, and their presence may interact with other risk factors to increase the overall risk for venous thrombosis.15Anatomic factors may also contribute to development of DVT. At the site | Surgery_Schwartz. diseasePolycythemiaInheritedFactor V LeidenProthrombin 20210AAntithrombin deficiencyProtein C deficiencyProtein S deficiencyFactor XI elevationDysfibrinogenemiaMixed EtiologyHomocysteinemiaFactors VII, VIII, IX, XI elevationHyperfibrinogenemiaActivated protein C resistance without factor V Leidenabsence of factor V Leiden.12 There may be a synergistic effect when particular multiple inherited and acquired risk factors are present in the same patient.Other patient-specific factors associated with venous thrombosis include the traditional cardiovascular risk factors of obesity, hypertension, and diabetes. VTE is more common in whites and African Americans than Asians and Native Americans.13,14 Certain gene variants (single nucleotide polymorphisms) are also associated with a mildly increased risk for VTE, and their presence may interact with other risk factors to increase the overall risk for venous thrombosis.15Anatomic factors may also contribute to development of DVT. At the site |
Surgery_Schwartz_6628 | Surgery_Schwartz | risk for VTE, and their presence may interact with other risk factors to increase the overall risk for venous thrombosis.15Anatomic factors may also contribute to development of DVT. At the site where the right iliac artery crosses over the left iliac vein, the left iliac vein may become chronically compressed predisposing to iliofemoral venous thrombosis, so-called May-Thurner syndrome. External compression of major veins by masses of various types can also lead to venous thrombosis.Many cases of VTE are potentially preventable. Accord-ingly, in current clinical practice, preoperative VTE risk assess-ment is becoming increasingly common to identify patients at moderate and high risk. Scoring systems have been developed that take into account the number of VTE risk factors in an individual patient. These risk stratification scores, such as the Rogers score16 and Caprini score,17 provide individual patient risk stratification and recommendations for prophylactic anti-coagulation. The | Surgery_Schwartz. risk for VTE, and their presence may interact with other risk factors to increase the overall risk for venous thrombosis.15Anatomic factors may also contribute to development of DVT. At the site where the right iliac artery crosses over the left iliac vein, the left iliac vein may become chronically compressed predisposing to iliofemoral venous thrombosis, so-called May-Thurner syndrome. External compression of major veins by masses of various types can also lead to venous thrombosis.Many cases of VTE are potentially preventable. Accord-ingly, in current clinical practice, preoperative VTE risk assess-ment is becoming increasingly common to identify patients at moderate and high risk. Scoring systems have been developed that take into account the number of VTE risk factors in an individual patient. These risk stratification scores, such as the Rogers score16 and Caprini score,17 provide individual patient risk stratification and recommendations for prophylactic anti-coagulation. The |
Surgery_Schwartz_6629 | Surgery_Schwartz | patient. These risk stratification scores, such as the Rogers score16 and Caprini score,17 provide individual patient risk stratification and recommendations for prophylactic anti-coagulation. The ninth edition of the American College of Chest Physicians (ACCP) Guidelines for Prevention of VTE in Non-Orthopedic Surgical Patients acknowledges both the Rogers and Caprini scores and provides recommendations for VTE prophylaxis (Table 24-3). Orthopedic surgical patients are generally excluded from risk assessment scores because of the disproportionately increased risk of VTE in orthopedic surgery compared with the general and abdominopelvic surgery population.Table 24-3Thromboembolism risk and recommended thromboprophylaxis in surgical patientsLEVEL OF RISKAPPROXIMATE DVT RISK WITHOUT THROMBOPROPHYLAXIS (%)SUGGESTED THROMBOPROPHYLAXIS OPTIONSVery low risk General or abdominopelvic surgery<0.5% (Rogers score <7; Caprini score 0)No specific thromboprophylaxisEarly ambulationLow | Surgery_Schwartz. patient. These risk stratification scores, such as the Rogers score16 and Caprini score,17 provide individual patient risk stratification and recommendations for prophylactic anti-coagulation. The ninth edition of the American College of Chest Physicians (ACCP) Guidelines for Prevention of VTE in Non-Orthopedic Surgical Patients acknowledges both the Rogers and Caprini scores and provides recommendations for VTE prophylaxis (Table 24-3). Orthopedic surgical patients are generally excluded from risk assessment scores because of the disproportionately increased risk of VTE in orthopedic surgery compared with the general and abdominopelvic surgery population.Table 24-3Thromboembolism risk and recommended thromboprophylaxis in surgical patientsLEVEL OF RISKAPPROXIMATE DVT RISK WITHOUT THROMBOPROPHYLAXIS (%)SUGGESTED THROMBOPROPHYLAXIS OPTIONSVery low risk General or abdominopelvic surgery<0.5% (Rogers score <7; Caprini score 0)No specific thromboprophylaxisEarly ambulationLow |
Surgery_Schwartz_6630 | Surgery_Schwartz | THROMBOPROPHYLAXIS (%)SUGGESTED THROMBOPROPHYLAXIS OPTIONSVery low risk General or abdominopelvic surgery<0.5% (Rogers score <7; Caprini score 0)No specific thromboprophylaxisEarly ambulationLow risk General or abdominopelvic surgery∼1.5% (Rogers score 7–10; Caprini score 1–2)Mechanical prophylaxisModerate risk General or abdominopelvic surgery∼3.0% (Rogers score >10; Caprini score 3–4)LMWH (at recommended doses), LDUH, or mechanical prophylaxisHigh bleeding risk Mechanical prophylaxisHigh risk General or abdominopelvic surgery∼6% (Caprini score ≥5)LMWH (at recommended doses), fondaparinux and mechanical prophylaxisHigh bleeding risk General or abdominopelvic surgery for cancer Mechanical thromboprophylaxisExtended-duration LMWH (4 weeks)DVT = deep vein thrombosis; INR = international normalized ratio; LDUH = low-dose unfractionated heparin; LMWH = low molecular weight heparin; VTE = venous thromboembolism.Data from Gould MK, Garcia DA, Wren SM, et al: Prevention of VTE in | Surgery_Schwartz. THROMBOPROPHYLAXIS (%)SUGGESTED THROMBOPROPHYLAXIS OPTIONSVery low risk General or abdominopelvic surgery<0.5% (Rogers score <7; Caprini score 0)No specific thromboprophylaxisEarly ambulationLow risk General or abdominopelvic surgery∼1.5% (Rogers score 7–10; Caprini score 1–2)Mechanical prophylaxisModerate risk General or abdominopelvic surgery∼3.0% (Rogers score >10; Caprini score 3–4)LMWH (at recommended doses), LDUH, or mechanical prophylaxisHigh bleeding risk Mechanical prophylaxisHigh risk General or abdominopelvic surgery∼6% (Caprini score ≥5)LMWH (at recommended doses), fondaparinux and mechanical prophylaxisHigh bleeding risk General or abdominopelvic surgery for cancer Mechanical thromboprophylaxisExtended-duration LMWH (4 weeks)DVT = deep vein thrombosis; INR = international normalized ratio; LDUH = low-dose unfractionated heparin; LMWH = low molecular weight heparin; VTE = venous thromboembolism.Data from Gould MK, Garcia DA, Wren SM, et al: Prevention of VTE in |
Surgery_Schwartz_6631 | Surgery_Schwartz | normalized ratio; LDUH = low-dose unfractionated heparin; LMWH = low molecular weight heparin; VTE = venous thromboembolism.Data from Gould MK, Garcia DA, Wren SM, et al: Prevention of VTE in nonorthopedic surgical patients: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines, Chest. 2012 Feb;141(2 Suppl):e227S-e277S.Brunicardi_Ch24_p0981-p1008.indd 98522/02/19 3:01 PM 986SPECIFIC CONSIDERATIONSPART IIFigure 24-4. Phlegmasia cerulea dolens of the left leg. Note the bluish discoloration.Figure 24-5. Duplex ultrasound scan of a normal femoral vein with phasic flow signals.DiagnosisClinical Evaluation. Early in the course of DVT development, venous thrombosis is thought to begin in an area of relative stasis, such as a soleal sinus vein or immediately downstream of the cusps of a venous valve in an axial calf vein. Isolated proxi-mal DVT without tibial vein thrombosis is unusual. Early in the | Surgery_Schwartz. normalized ratio; LDUH = low-dose unfractionated heparin; LMWH = low molecular weight heparin; VTE = venous thromboembolism.Data from Gould MK, Garcia DA, Wren SM, et al: Prevention of VTE in nonorthopedic surgical patients: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines, Chest. 2012 Feb;141(2 Suppl):e227S-e277S.Brunicardi_Ch24_p0981-p1008.indd 98522/02/19 3:01 PM 986SPECIFIC CONSIDERATIONSPART IIFigure 24-4. Phlegmasia cerulea dolens of the left leg. Note the bluish discoloration.Figure 24-5. Duplex ultrasound scan of a normal femoral vein with phasic flow signals.DiagnosisClinical Evaluation. Early in the course of DVT development, venous thrombosis is thought to begin in an area of relative stasis, such as a soleal sinus vein or immediately downstream of the cusps of a venous valve in an axial calf vein. Isolated proxi-mal DVT without tibial vein thrombosis is unusual. Early in the |
Surgery_Schwartz_6632 | Surgery_Schwartz | stasis, such as a soleal sinus vein or immediately downstream of the cusps of a venous valve in an axial calf vein. Isolated proxi-mal DVT without tibial vein thrombosis is unusual. Early in the course of a DVT, there may be no or few clinical findings such as pain or swelling. Even extensive DVT may sometimes be present without signs or symptoms if the patient is nonambula-tory or bedbound. History and physical examination are notori-ously unreliable in the diagnosis of DVT. In addition, symptoms and signs often associated with DVT, such as extremity pain and/or swelling, are nonspecific. In large studies, DVT has been found by venography or DUS in ≤50% of patients in whom it was clinically suspected.18,19 Objective studies are therefore required to confirm a diagnosis of VTE or to exclude the pres-ence of VTE.Clinical symptoms may worsen as DVT propagates and involves the major proximal deep veins. Extensive DVT of the major axial deep venous channels of the lower extremity with | Surgery_Schwartz. stasis, such as a soleal sinus vein or immediately downstream of the cusps of a venous valve in an axial calf vein. Isolated proxi-mal DVT without tibial vein thrombosis is unusual. Early in the course of a DVT, there may be no or few clinical findings such as pain or swelling. Even extensive DVT may sometimes be present without signs or symptoms if the patient is nonambula-tory or bedbound. History and physical examination are notori-ously unreliable in the diagnosis of DVT. In addition, symptoms and signs often associated with DVT, such as extremity pain and/or swelling, are nonspecific. In large studies, DVT has been found by venography or DUS in ≤50% of patients in whom it was clinically suspected.18,19 Objective studies are therefore required to confirm a diagnosis of VTE or to exclude the pres-ence of VTE.Clinical symptoms may worsen as DVT propagates and involves the major proximal deep veins. Extensive DVT of the major axial deep venous channels of the lower extremity with |
Surgery_Schwartz_6633 | Surgery_Schwartz | the pres-ence of VTE.Clinical symptoms may worsen as DVT propagates and involves the major proximal deep veins. Extensive DVT of the major axial deep venous channels of the lower extremity with rel-ative sparing of collateral veins causes a condition called phleg-masia cerulea dolens (Fig. 24-4). This condition is characterized by pain and pitting edema with associated cyanosis. When the thrombosis extends to the collateral veins, massive fluid seques-tration and more significant edema ensue, resulting in a condition known as phlegmasia alba dolens.20 The affected extremity in phlegmasia alba dolens is extremely painful and edematous and pale secondary to arterial insufficiency from dramatically ele-vated below lower knee compartment pressures. Both phlegmasia cerulean dolens and phlegmasia alba dolens can be complicated by venous gangrene and the need for amputation.Vascular Lab and Radiologic Evaluation Duplex Ultrasound DUS is now the most commonly per-formed test for the detection | Surgery_Schwartz. the pres-ence of VTE.Clinical symptoms may worsen as DVT propagates and involves the major proximal deep veins. Extensive DVT of the major axial deep venous channels of the lower extremity with rel-ative sparing of collateral veins causes a condition called phleg-masia cerulea dolens (Fig. 24-4). This condition is characterized by pain and pitting edema with associated cyanosis. When the thrombosis extends to the collateral veins, massive fluid seques-tration and more significant edema ensue, resulting in a condition known as phlegmasia alba dolens.20 The affected extremity in phlegmasia alba dolens is extremely painful and edematous and pale secondary to arterial insufficiency from dramatically ele-vated below lower knee compartment pressures. Both phlegmasia cerulean dolens and phlegmasia alba dolens can be complicated by venous gangrene and the need for amputation.Vascular Lab and Radiologic Evaluation Duplex Ultrasound DUS is now the most commonly per-formed test for the detection |
Surgery_Schwartz_6634 | Surgery_Schwartz | alba dolens can be complicated by venous gangrene and the need for amputation.Vascular Lab and Radiologic Evaluation Duplex Ultrasound DUS is now the most commonly per-formed test for the detection of infrainguinal DVT, both above and below the knee, and has a sensitivity and specificity of >95% in symptomatic patients.3 DUS refers to the combina-tion of real-time B-mode ultrasound with compression and flow augmentation amneuvres combined with pulsed Doppler capa-bility. For VTE detection, color flow imaging is an additional extremely useful adjunct in the evaluation of possible axial calf vein DVT and evaluation of intra-abdominal veins. DUS provides the ability to noninvasively visualize venous anatomy, detect occluded and partially occluded venous segments, and demonstrate physiologic flow characteristics.In the supine patient, normal lower extremity venous flow is phasic (Fig. 24-5), decreasing with inspiration in response to increased intra-abdominal pressure with the descent of | Surgery_Schwartz. alba dolens can be complicated by venous gangrene and the need for amputation.Vascular Lab and Radiologic Evaluation Duplex Ultrasound DUS is now the most commonly per-formed test for the detection of infrainguinal DVT, both above and below the knee, and has a sensitivity and specificity of >95% in symptomatic patients.3 DUS refers to the combina-tion of real-time B-mode ultrasound with compression and flow augmentation amneuvres combined with pulsed Doppler capa-bility. For VTE detection, color flow imaging is an additional extremely useful adjunct in the evaluation of possible axial calf vein DVT and evaluation of intra-abdominal veins. DUS provides the ability to noninvasively visualize venous anatomy, detect occluded and partially occluded venous segments, and demonstrate physiologic flow characteristics.In the supine patient, normal lower extremity venous flow is phasic (Fig. 24-5), decreasing with inspiration in response to increased intra-abdominal pressure with the descent of |
Surgery_Schwartz_6635 | Surgery_Schwartz | flow characteristics.In the supine patient, normal lower extremity venous flow is phasic (Fig. 24-5), decreasing with inspiration in response to increased intra-abdominal pressure with the descent of the diaphragm and then increasing with expiration as the diaphragm rises and intra-abdominal pressure decreases. When the patient is upright, the decrease in intra-abdominal pressure with expira-tion cannot overcome the hydrostatic column of pressure exist-ing between the right atrium and the calf. Muscular contractions of the calf, along with the one-way venous valves, are then required to promote venous return to the heart. Flow also can be increased by leg elevation or compression and decreased by sud-den elevation of intra-abdominal pressure (Valsalva maneuver). In a venous DUS examination performed with the patient supine, spontaneous flow, variation of flow with respiration, and response of flow to Valsalva maneuver are all assessed. From the common femoral through the popliteal | Surgery_Schwartz. flow characteristics.In the supine patient, normal lower extremity venous flow is phasic (Fig. 24-5), decreasing with inspiration in response to increased intra-abdominal pressure with the descent of the diaphragm and then increasing with expiration as the diaphragm rises and intra-abdominal pressure decreases. When the patient is upright, the decrease in intra-abdominal pressure with expira-tion cannot overcome the hydrostatic column of pressure exist-ing between the right atrium and the calf. Muscular contractions of the calf, along with the one-way venous valves, are then required to promote venous return to the heart. Flow also can be increased by leg elevation or compression and decreased by sud-den elevation of intra-abdominal pressure (Valsalva maneuver). In a venous DUS examination performed with the patient supine, spontaneous flow, variation of flow with respiration, and response of flow to Valsalva maneuver are all assessed. From the common femoral through the popliteal |
Surgery_Schwartz_6636 | Surgery_Schwartz | performed with the patient supine, spontaneous flow, variation of flow with respiration, and response of flow to Valsalva maneuver are all assessed. From the common femoral through the popliteal vein, the primary method of detecting DVT with ultrasound is demonstration of the lack of compressibility of the vein with probe pressure on B-mode imaging. Normally, in transverse section, the vein walls should coapt with pressure. Lack of coaptation indicates throm-bus. Axial calf vein thrombi are often best detected by abnor-malities in color flow imaging as compressibility is difficult in the calf.The examination begins at the ankle and continues proxi-mally to the groin. Each vein is visualized, and the flow signal is assessed with distal and proximal compression. Lower extremity DVT can be diagnosed by any of the following DUS findings: lack of spontaneous flow (Fig. 24-6), inability to compress the vein (Fig. 24-7), absence of color filling of the lumen by color flow DUS, loss of | Surgery_Schwartz. performed with the patient supine, spontaneous flow, variation of flow with respiration, and response of flow to Valsalva maneuver are all assessed. From the common femoral through the popliteal vein, the primary method of detecting DVT with ultrasound is demonstration of the lack of compressibility of the vein with probe pressure on B-mode imaging. Normally, in transverse section, the vein walls should coapt with pressure. Lack of coaptation indicates throm-bus. Axial calf vein thrombi are often best detected by abnor-malities in color flow imaging as compressibility is difficult in the calf.The examination begins at the ankle and continues proxi-mally to the groin. Each vein is visualized, and the flow signal is assessed with distal and proximal compression. Lower extremity DVT can be diagnosed by any of the following DUS findings: lack of spontaneous flow (Fig. 24-6), inability to compress the vein (Fig. 24-7), absence of color filling of the lumen by color flow DUS, loss of |
Surgery_Schwartz_6637 | Surgery_Schwartz | be diagnosed by any of the following DUS findings: lack of spontaneous flow (Fig. 24-6), inability to compress the vein (Fig. 24-7), absence of color filling of the lumen by color flow DUS, loss of respiratory flow variation, and venous disten-tion. Again, lack of venous compression on B-mode imaging is the primary diagnostic variable. Several studies comparing B-mode ultrasound to venography for the detection of femo-ropopliteal DVT in patients clinically suspected to have DVT report sensitivities of >91% and specificities of >97%.21,22 The ability of DUS to assess isolated calf vein DVT varies greatly, with sensitivities ranging from 50% to 93% and specificities approaching 100%.23,24Impedance Plethysmography Impedance plethysmography (IPG) was the primary noninvasive method of diagnosing DVT before the widespread use of DUS but is infrequently used today. Changes in electrical resistance resulting from lower extremity blood volume changes are quantified. IPG is less accurate than | Surgery_Schwartz. be diagnosed by any of the following DUS findings: lack of spontaneous flow (Fig. 24-6), inability to compress the vein (Fig. 24-7), absence of color filling of the lumen by color flow DUS, loss of respiratory flow variation, and venous disten-tion. Again, lack of venous compression on B-mode imaging is the primary diagnostic variable. Several studies comparing B-mode ultrasound to venography for the detection of femo-ropopliteal DVT in patients clinically suspected to have DVT report sensitivities of >91% and specificities of >97%.21,22 The ability of DUS to assess isolated calf vein DVT varies greatly, with sensitivities ranging from 50% to 93% and specificities approaching 100%.23,24Impedance Plethysmography Impedance plethysmography (IPG) was the primary noninvasive method of diagnosing DVT before the widespread use of DUS but is infrequently used today. Changes in electrical resistance resulting from lower extremity blood volume changes are quantified. IPG is less accurate than |
Surgery_Schwartz_6638 | Surgery_Schwartz | DVT before the widespread use of DUS but is infrequently used today. Changes in electrical resistance resulting from lower extremity blood volume changes are quantified. IPG is less accurate than DUS for the detection of proximal DVT, with 83% sensitivity in symptomatic patients. It is a poor detector of calf vein DVT.25Brunicardi_Ch24_p0981-p1008.indd 98622/02/19 3:01 PM 987VENOUS AND LYMPHATIC DISEASECHAPTER 24Figure 24-6. Duplex ultrasound of a femoral vein containing thrombus demonstrating no flow within the femoral vein.No compressionCompressionR FVPR FVPFigure 24-7. B-mode ultrasound of the femoral vein in crosssection. The femoral vein does not collapse with external compres-sion (arrows).Figure 24-8. Venogram showing a filling defect in the popliteal vein (arrows).Iodine-125 Fibrinogen Uptake Iodine-125 fibrinogen uptake (FUT) is a seldom-used technique that involves IV administra-tion of radioactive fibrinogen and monitoring for increased uptake in fibrin clots. An | Surgery_Schwartz. DVT before the widespread use of DUS but is infrequently used today. Changes in electrical resistance resulting from lower extremity blood volume changes are quantified. IPG is less accurate than DUS for the detection of proximal DVT, with 83% sensitivity in symptomatic patients. It is a poor detector of calf vein DVT.25Brunicardi_Ch24_p0981-p1008.indd 98622/02/19 3:01 PM 987VENOUS AND LYMPHATIC DISEASECHAPTER 24Figure 24-6. Duplex ultrasound of a femoral vein containing thrombus demonstrating no flow within the femoral vein.No compressionCompressionR FVPR FVPFigure 24-7. B-mode ultrasound of the femoral vein in crosssection. The femoral vein does not collapse with external compres-sion (arrows).Figure 24-8. Venogram showing a filling defect in the popliteal vein (arrows).Iodine-125 Fibrinogen Uptake Iodine-125 fibrinogen uptake (FUT) is a seldom-used technique that involves IV administra-tion of radioactive fibrinogen and monitoring for increased uptake in fibrin clots. An |
Surgery_Schwartz_6639 | Surgery_Schwartz | Fibrinogen Uptake Iodine-125 fibrinogen uptake (FUT) is a seldom-used technique that involves IV administra-tion of radioactive fibrinogen and monitoring for increased uptake in fibrin clots. An increase of 20% or more in one area of a limb indicates an area of thrombus. FUT can detect DVT in the calf, but high background radiation from the pelvis and the urinary tract limits its ability to detect proximal DVT. It also cannot be used in an extremity that has recently undergone surgery or has active inflammation. In a prospective study, FUT had a sensitivity of 73% and specificity of 71% for identification of DVT in a group of symptomatic and asymptomatic patients.26 Currently, FUT is primarily a research tool of historic interest.Venography Venography is the gold standard to which other diagnostic modalities are compared. A small catheter is placed in a dorsal foot vein with injection of a radiopaque contrast agent. Radiographs are obtained in at least two projections. A positive | Surgery_Schwartz. Fibrinogen Uptake Iodine-125 fibrinogen uptake (FUT) is a seldom-used technique that involves IV administra-tion of radioactive fibrinogen and monitoring for increased uptake in fibrin clots. An increase of 20% or more in one area of a limb indicates an area of thrombus. FUT can detect DVT in the calf, but high background radiation from the pelvis and the urinary tract limits its ability to detect proximal DVT. It also cannot be used in an extremity that has recently undergone surgery or has active inflammation. In a prospective study, FUT had a sensitivity of 73% and specificity of 71% for identification of DVT in a group of symptomatic and asymptomatic patients.26 Currently, FUT is primarily a research tool of historic interest.Venography Venography is the gold standard to which other diagnostic modalities are compared. A small catheter is placed in a dorsal foot vein with injection of a radiopaque contrast agent. Radiographs are obtained in at least two projections. A positive |
Surgery_Schwartz_6640 | Surgery_Schwartz | diagnostic modalities are compared. A small catheter is placed in a dorsal foot vein with injection of a radiopaque contrast agent. Radiographs are obtained in at least two projections. A positive study result is failure to fill the deep system with passage of the contrast medium into the superficial system or demonstration of discrete filling defects (Fig. 24-8). A normal study result virtually excludes the presence of DVT. In a study of 160 patients with a normal venogram followed for 3 months, only two patients (1.3%) subsequently developed DVT, and no patients experienced symptoms of PE.27 Venography is not routinely used in clinical practice because of its invasiveness and complication risk. It is still, however, sometimes used in research studies evaluating DVT prophylaxis.TreatmentOnce the diagnosis of VTE has been made, antithrombotic ther-apy should be initiated promptly. If clinical suspicion for VTE is high, it may be prudent to start treatment before the diagnosis is | Surgery_Schwartz. diagnostic modalities are compared. A small catheter is placed in a dorsal foot vein with injection of a radiopaque contrast agent. Radiographs are obtained in at least two projections. A positive study result is failure to fill the deep system with passage of the contrast medium into the superficial system or demonstration of discrete filling defects (Fig. 24-8). A normal study result virtually excludes the presence of DVT. In a study of 160 patients with a normal venogram followed for 3 months, only two patients (1.3%) subsequently developed DVT, and no patients experienced symptoms of PE.27 Venography is not routinely used in clinical practice because of its invasiveness and complication risk. It is still, however, sometimes used in research studies evaluating DVT prophylaxis.TreatmentOnce the diagnosis of VTE has been made, antithrombotic ther-apy should be initiated promptly. If clinical suspicion for VTE is high, it may be prudent to start treatment before the diagnosis is |
Surgery_Schwartz_6641 | Surgery_Schwartz | the diagnosis of VTE has been made, antithrombotic ther-apy should be initiated promptly. If clinical suspicion for VTE is high, it may be prudent to start treatment before the diagnosis is objectively confirmed. The goals of VTE treatment are the pre-vention of mortality and morbidity associated with PE and the prevention of the postthrombotic syndrome (PTS). Treatment regimens may include antithrombotic therapy, temporary or permanent vena cava filter placement, catheter-directed or systemic thrombolytic therapy, and operative thrombectomy.Antithrombotic Therapy. Most often, antithrombotic therapy for VTE is initiated with IV or subcutaneous (SC) unfraction-ated heparin or SC low molecular weight heparin. Fondaparinux, a synthetic pentasaccharide, is sometimes also used as an alter-native to heparin to initiate therapy. An oral vitamin K antago-nist, usually sodium warfarin, is begun shortly after initiation of IV or SC therapy. Either SC or IV therapy is continued until effective | Surgery_Schwartz. the diagnosis of VTE has been made, antithrombotic ther-apy should be initiated promptly. If clinical suspicion for VTE is high, it may be prudent to start treatment before the diagnosis is objectively confirmed. The goals of VTE treatment are the pre-vention of mortality and morbidity associated with PE and the prevention of the postthrombotic syndrome (PTS). Treatment regimens may include antithrombotic therapy, temporary or permanent vena cava filter placement, catheter-directed or systemic thrombolytic therapy, and operative thrombectomy.Antithrombotic Therapy. Most often, antithrombotic therapy for VTE is initiated with IV or subcutaneous (SC) unfraction-ated heparin or SC low molecular weight heparin. Fondaparinux, a synthetic pentasaccharide, is sometimes also used as an alter-native to heparin to initiate therapy. An oral vitamin K antago-nist, usually sodium warfarin, is begun shortly after initiation of IV or SC therapy. Either SC or IV therapy is continued until effective |
Surgery_Schwartz_6642 | Surgery_Schwartz | to heparin to initiate therapy. An oral vitamin K antago-nist, usually sodium warfarin, is begun shortly after initiation of IV or SC therapy. Either SC or IV therapy is continued until effective oral anticoagulation with warfarin is achieved as indi-cated by an international normalized ratio (INR) ≥2 for 24 hours. A minimum of 5 days of heparin or fondaparinux therapy is 1Brunicardi_Ch24_p0981-p1008.indd 98722/02/19 3:01 PM 988SPECIFIC CONSIDERATIONSPART IIrecommended.28 Recently, several oral anticoagulants that function by either directly inhibiting thrombin or inhibit-ing factor Xa have additionally been approved by the United States Food and Drug Administration (FDA) for both treatment and prophylaxis for VTE. A principle advantage is they do not require monitoring of laboratory parameters for use.Unfractionated heparin (UFH) binds to antithrombin via a specific 18-saccharide sequence. This increases antithrombin activity over a thousandfold. The antithrombin-heparin complex | Surgery_Schwartz. to heparin to initiate therapy. An oral vitamin K antago-nist, usually sodium warfarin, is begun shortly after initiation of IV or SC therapy. Either SC or IV therapy is continued until effective oral anticoagulation with warfarin is achieved as indi-cated by an international normalized ratio (INR) ≥2 for 24 hours. A minimum of 5 days of heparin or fondaparinux therapy is 1Brunicardi_Ch24_p0981-p1008.indd 98722/02/19 3:01 PM 988SPECIFIC CONSIDERATIONSPART IIrecommended.28 Recently, several oral anticoagulants that function by either directly inhibiting thrombin or inhibit-ing factor Xa have additionally been approved by the United States Food and Drug Administration (FDA) for both treatment and prophylaxis for VTE. A principle advantage is they do not require monitoring of laboratory parameters for use.Unfractionated heparin (UFH) binds to antithrombin via a specific 18-saccharide sequence. This increases antithrombin activity over a thousandfold. The antithrombin-heparin complex |
Surgery_Schwartz_6643 | Surgery_Schwartz | parameters for use.Unfractionated heparin (UFH) binds to antithrombin via a specific 18-saccharide sequence. This increases antithrombin activity over a thousandfold. The antithrombin-heparin complex primarily inhibits factor IIa (thrombin) and factor Xa and, to a lesser degree, factors IXa, XIa, and XIIa of the coagulation cascade. In addition, UFH also binds to tissue factor pathway inhibitor, which inhibits the conversion of factors X to Xa, and factors IX to IXa. Finally, UFH catalyzes the inhibition of thrombin by heparin cofactor II via a mechanism independent of antithrombin.UFH therapy is most commonly administered with an initial IV bolus of 80 units/kg. Weight-based UFH dosages have been shown to be more effective than standard fixed boluses in rapidly achieving therapeutic levels.29 The initial bolus is followed by a continuous IV drip at 18 units/kg per hour. The half-life of IV UFH ranges from 45 to 90 minutes and is dose dependent. The level of antithrombotic therapy | Surgery_Schwartz. parameters for use.Unfractionated heparin (UFH) binds to antithrombin via a specific 18-saccharide sequence. This increases antithrombin activity over a thousandfold. The antithrombin-heparin complex primarily inhibits factor IIa (thrombin) and factor Xa and, to a lesser degree, factors IXa, XIa, and XIIa of the coagulation cascade. In addition, UFH also binds to tissue factor pathway inhibitor, which inhibits the conversion of factors X to Xa, and factors IX to IXa. Finally, UFH catalyzes the inhibition of thrombin by heparin cofactor II via a mechanism independent of antithrombin.UFH therapy is most commonly administered with an initial IV bolus of 80 units/kg. Weight-based UFH dosages have been shown to be more effective than standard fixed boluses in rapidly achieving therapeutic levels.29 The initial bolus is followed by a continuous IV drip at 18 units/kg per hour. The half-life of IV UFH ranges from 45 to 90 minutes and is dose dependent. The level of antithrombotic therapy |
Surgery_Schwartz_6644 | Surgery_Schwartz | The initial bolus is followed by a continuous IV drip at 18 units/kg per hour. The half-life of IV UFH ranges from 45 to 90 minutes and is dose dependent. The level of antithrombotic therapy should be moni-tored every 6 hours using the activated partial thromboplastin time (aPTT), with the goal range of 1.5 to 2.5 times control values. This should correspond with plasma heparin anti-Xa activity levels of 0.3 to 0.7 IU/mL.Initial anticoagulation with UFH may also be administered SC, although this route is less commonly used. Adjusted-dose therapeutic SC UFH is initiated with 17,500 units, followed by 250 units/kg twice daily, and dosing is adjusted to an aPTT goal range similar to that for IV UFH. Fixed-dose unmonitored SC UFH is started with a bolus of 333 units/kg, followed by 250 units/kg twice daily.30Hemorrhage is the primary complication of UFH therapy. The rate of major hemorrhage (fatal, intracranial, retroperitoneal, or requiring transfusion of >2 units of packed red blood | Surgery_Schwartz. The initial bolus is followed by a continuous IV drip at 18 units/kg per hour. The half-life of IV UFH ranges from 45 to 90 minutes and is dose dependent. The level of antithrombotic therapy should be moni-tored every 6 hours using the activated partial thromboplastin time (aPTT), with the goal range of 1.5 to 2.5 times control values. This should correspond with plasma heparin anti-Xa activity levels of 0.3 to 0.7 IU/mL.Initial anticoagulation with UFH may also be administered SC, although this route is less commonly used. Adjusted-dose therapeutic SC UFH is initiated with 17,500 units, followed by 250 units/kg twice daily, and dosing is adjusted to an aPTT goal range similar to that for IV UFH. Fixed-dose unmonitored SC UFH is started with a bolus of 333 units/kg, followed by 250 units/kg twice daily.30Hemorrhage is the primary complication of UFH therapy. The rate of major hemorrhage (fatal, intracranial, retroperitoneal, or requiring transfusion of >2 units of packed red blood |
Surgery_Schwartz_6645 | Surgery_Schwartz | twice daily.30Hemorrhage is the primary complication of UFH therapy. The rate of major hemorrhage (fatal, intracranial, retroperitoneal, or requiring transfusion of >2 units of packed red blood cells) is approximately 5% in hospitalized patients undergoing UFH therapy (1% in medical patients and 8% in surgical patients).30 For patients with UFH-related bleeding complications, cessation of UFH is required, and anticoagulation may be reversed with protamine sulfate. Protamine sulfate binds to UFH and forms an inactive salt compound. Each milligram of protamine neutral-izes 90 to 115 units of heparin, and the dosage should not exceed 50 mg IV over any 10-minute period. Side effects of protamine sulfate include hypotension, pulmonary edema, and anaphylaxis. Patients with prior exposure to protamine-containing insulin (NPH) and patients with allergy to fish may have an increased risk of hypersensitivity, although no direct relationship has been established. Protamine administration should | Surgery_Schwartz. twice daily.30Hemorrhage is the primary complication of UFH therapy. The rate of major hemorrhage (fatal, intracranial, retroperitoneal, or requiring transfusion of >2 units of packed red blood cells) is approximately 5% in hospitalized patients undergoing UFH therapy (1% in medical patients and 8% in surgical patients).30 For patients with UFH-related bleeding complications, cessation of UFH is required, and anticoagulation may be reversed with protamine sulfate. Protamine sulfate binds to UFH and forms an inactive salt compound. Each milligram of protamine neutral-izes 90 to 115 units of heparin, and the dosage should not exceed 50 mg IV over any 10-minute period. Side effects of protamine sulfate include hypotension, pulmonary edema, and anaphylaxis. Patients with prior exposure to protamine-containing insulin (NPH) and patients with allergy to fish may have an increased risk of hypersensitivity, although no direct relationship has been established. Protamine administration should |
Surgery_Schwartz_6646 | Surgery_Schwartz | insulin (NPH) and patients with allergy to fish may have an increased risk of hypersensitivity, although no direct relationship has been established. Protamine administration should be performed judi-ciously and terminated if any side effects occur.In addition to hemorrhage, heparin also has other, unique, complications. Heparin-induced thrombocytopenia (HIT) results from heparin-associated antiplatelet antibodies (HAAbs) directed against platelet factor 4 complexed with heparin.31 HIT occurs in 1% to 5% of patients treated with heparin.32,33 In patients with repeat heparin exposure (such as vascular surgery patients), the incidence of HAAbs may be as high as 21%.34 HIT occurs most frequently in the second week of therapy and may lead to disastrous venous or arterial thrombotic complications. Therefore, platelet counts should be monitored periodically in patients receiving continuous heparin therapy.HIT is diagnosed based on previous exposure to heparin, platelet count less than | Surgery_Schwartz. insulin (NPH) and patients with allergy to fish may have an increased risk of hypersensitivity, although no direct relationship has been established. Protamine administration should be performed judi-ciously and terminated if any side effects occur.In addition to hemorrhage, heparin also has other, unique, complications. Heparin-induced thrombocytopenia (HIT) results from heparin-associated antiplatelet antibodies (HAAbs) directed against platelet factor 4 complexed with heparin.31 HIT occurs in 1% to 5% of patients treated with heparin.32,33 In patients with repeat heparin exposure (such as vascular surgery patients), the incidence of HAAbs may be as high as 21%.34 HIT occurs most frequently in the second week of therapy and may lead to disastrous venous or arterial thrombotic complications. Therefore, platelet counts should be monitored periodically in patients receiving continuous heparin therapy.HIT is diagnosed based on previous exposure to heparin, platelet count less than |
Surgery_Schwartz_6647 | Surgery_Schwartz | Therefore, platelet counts should be monitored periodically in patients receiving continuous heparin therapy.HIT is diagnosed based on previous exposure to heparin, platelet count less than 100,000, and/or platelet count decline of 50% following exposure. All heparin must be stopped and alter-native anticoagulation initiated immediately to avoid thrombotic complications, which may approach 50% over the subsequent 30 days in affected individuals.35Another complication of prolonged high-dose heparin therapy is osteopenia. Heparin-induced osteopenia results from impairment of bone formation and enhancement of bone resorp-tion by heparin.Low molecular weight heparins (LMWHs) are derived from the depolymerization of porcine UFH. Like UFH, LMWHs bind to antithrombin via a specific pentasaccharide sequence to expose an active site for the neutralization of fac-tor Xa. However, LMWHs have fewer additional saccharide units. This results in less inactivation of thrombin (factor IIa). In | Surgery_Schwartz. Therefore, platelet counts should be monitored periodically in patients receiving continuous heparin therapy.HIT is diagnosed based on previous exposure to heparin, platelet count less than 100,000, and/or platelet count decline of 50% following exposure. All heparin must be stopped and alter-native anticoagulation initiated immediately to avoid thrombotic complications, which may approach 50% over the subsequent 30 days in affected individuals.35Another complication of prolonged high-dose heparin therapy is osteopenia. Heparin-induced osteopenia results from impairment of bone formation and enhancement of bone resorp-tion by heparin.Low molecular weight heparins (LMWHs) are derived from the depolymerization of porcine UFH. Like UFH, LMWHs bind to antithrombin via a specific pentasaccharide sequence to expose an active site for the neutralization of fac-tor Xa. However, LMWHs have fewer additional saccharide units. This results in less inactivation of thrombin (factor IIa). In |
Surgery_Schwartz_6648 | Surgery_Schwartz | sequence to expose an active site for the neutralization of fac-tor Xa. However, LMWHs have fewer additional saccharide units. This results in less inactivation of thrombin (factor IIa). In comparison to UFH, LMWHs have increased bioavailability (>90% after SC injection), longer half-lives (approximately 4 to 6 hours), and more predictable elimination rates.Most patients treated with weight-based onceor twice-daily SC LMWH injections do not require laboratory monitoring for anticoagulant effect, a distinct advantage over continuous IV infusions of UFH. Patients who do require monitoring include those with significant renal insufficiency, pediatric patients, obese patients greater than 120 kg, and pregnant patients. Moni-toring may be performed using anti-Xa activity assays. The ther-apeutic anti-Xa goal range depends on the type of LMWH and the frequency of dosing. There are numerous LMWHs avail-able, and the various preparations differ in their anti-Xa and anti-IIa activities. | Surgery_Schwartz. sequence to expose an active site for the neutralization of fac-tor Xa. However, LMWHs have fewer additional saccharide units. This results in less inactivation of thrombin (factor IIa). In comparison to UFH, LMWHs have increased bioavailability (>90% after SC injection), longer half-lives (approximately 4 to 6 hours), and more predictable elimination rates.Most patients treated with weight-based onceor twice-daily SC LMWH injections do not require laboratory monitoring for anticoagulant effect, a distinct advantage over continuous IV infusions of UFH. Patients who do require monitoring include those with significant renal insufficiency, pediatric patients, obese patients greater than 120 kg, and pregnant patients. Moni-toring may be performed using anti-Xa activity assays. The ther-apeutic anti-Xa goal range depends on the type of LMWH and the frequency of dosing. There are numerous LMWHs avail-able, and the various preparations differ in their anti-Xa and anti-IIa activities. |
Surgery_Schwartz_6649 | Surgery_Schwartz | anti-Xa goal range depends on the type of LMWH and the frequency of dosing. There are numerous LMWHs avail-able, and the various preparations differ in their anti-Xa and anti-IIa activities. Treatment dosing for one LMWH, therefore, cannot be extrapolated for use with another. The anticoagulant effect of LMWHs may be partially reversed (approximately 60%) with protamine sulfate.Numerous well-designed trials comparing SC LMWH with IV and SC UFH for the treatment of DVT have been critically evaluated in several meta-analyses and demonstrate a decrease in thrombotic complications, bleeding, and mortality with LMWHs.36-38 LMWHs also are associated with a decreased rate of HAAb formation and HIT (<2%) compared with UFH (at least in prophylactic doses).30 However, patients with estab-lished HIT also should not receive LMWHs because there is cross-reactivity between the drugs.39A major benefit of LMWHs is that it allows outpatient treatment of VTE.40,41 In a randomized study comparing IV UFH | Surgery_Schwartz. anti-Xa goal range depends on the type of LMWH and the frequency of dosing. There are numerous LMWHs avail-able, and the various preparations differ in their anti-Xa and anti-IIa activities. Treatment dosing for one LMWH, therefore, cannot be extrapolated for use with another. The anticoagulant effect of LMWHs may be partially reversed (approximately 60%) with protamine sulfate.Numerous well-designed trials comparing SC LMWH with IV and SC UFH for the treatment of DVT have been critically evaluated in several meta-analyses and demonstrate a decrease in thrombotic complications, bleeding, and mortality with LMWHs.36-38 LMWHs also are associated with a decreased rate of HAAb formation and HIT (<2%) compared with UFH (at least in prophylactic doses).30 However, patients with estab-lished HIT also should not receive LMWHs because there is cross-reactivity between the drugs.39A major benefit of LMWHs is that it allows outpatient treatment of VTE.40,41 In a randomized study comparing IV UFH |
Surgery_Schwartz_6650 | Surgery_Schwartz | also should not receive LMWHs because there is cross-reactivity between the drugs.39A major benefit of LMWHs is that it allows outpatient treatment of VTE.40,41 In a randomized study comparing IV UFH and the LMWH nadroparin calcium,40 there was no sig-nificant difference in recurrent thromboembolism (8.6% for UFH vs. 6.9% for LMWH) or major bleeding complications (2.0% for UFH vs. 0.5% for LMWH). There was, however, a 67% reduction in mean days in the hospital for the LMWH group.Fondaparinux currently is a synthetic pentasaccharide that has been approved by the FDA for the initial treatment of DVT and PE. Its five-polysaccharide sequence binds and activates antithrombin, causing specific inhibition of factor Xa. In two large noninferiority trials, fondaparinux was compared with the LMWH enoxaparin for the initial treatment of DVT and with IV UFH for the initial treatment of PE.42,43 The rates of recurrent VTE ranged from 3.8% to 5%, with rates of major bleeding of 2% to 2.6%, for all | Surgery_Schwartz. also should not receive LMWHs because there is cross-reactivity between the drugs.39A major benefit of LMWHs is that it allows outpatient treatment of VTE.40,41 In a randomized study comparing IV UFH and the LMWH nadroparin calcium,40 there was no sig-nificant difference in recurrent thromboembolism (8.6% for UFH vs. 6.9% for LMWH) or major bleeding complications (2.0% for UFH vs. 0.5% for LMWH). There was, however, a 67% reduction in mean days in the hospital for the LMWH group.Fondaparinux currently is a synthetic pentasaccharide that has been approved by the FDA for the initial treatment of DVT and PE. Its five-polysaccharide sequence binds and activates antithrombin, causing specific inhibition of factor Xa. In two large noninferiority trials, fondaparinux was compared with the LMWH enoxaparin for the initial treatment of DVT and with IV UFH for the initial treatment of PE.42,43 The rates of recurrent VTE ranged from 3.8% to 5%, with rates of major bleeding of 2% to 2.6%, for all |
Surgery_Schwartz_6651 | Surgery_Schwartz | for the initial treatment of DVT and with IV UFH for the initial treatment of PE.42,43 The rates of recurrent VTE ranged from 3.8% to 5%, with rates of major bleeding of 2% to 2.6%, for all treatment arms. The drug is administered SC once daily with a weight-based dosing protocol: 5 mg, 7.5 mg, or 10 mg for patients weighing <50 kg, 50 to 100 kg, or >100 kg, respectively. The half-life of fondaparinux is approximately 2Brunicardi_Ch24_p0981-p1008.indd 98822/02/19 3:01 PM 989VENOUS AND LYMPHATIC DISEASECHAPTER 2417 hours in patients with normal renal function. There are rare case reports of fondaparinux-induced thrombocytopenia.44Direct thrombin inhibitors (DTIs) include parental forms with recombinant hirudin, argatroban, and bivalirudin, as well as an oral agent, dabigatran. These antithrombotic agents bind to thrombin, inhibiting the conversion of fibrinogen to fibrin as well as thrombin-induced platelet activation. These actions are independent of antithrombin. The parental | Surgery_Schwartz. for the initial treatment of DVT and with IV UFH for the initial treatment of PE.42,43 The rates of recurrent VTE ranged from 3.8% to 5%, with rates of major bleeding of 2% to 2.6%, for all treatment arms. The drug is administered SC once daily with a weight-based dosing protocol: 5 mg, 7.5 mg, or 10 mg for patients weighing <50 kg, 50 to 100 kg, or >100 kg, respectively. The half-life of fondaparinux is approximately 2Brunicardi_Ch24_p0981-p1008.indd 98822/02/19 3:01 PM 989VENOUS AND LYMPHATIC DISEASECHAPTER 2417 hours in patients with normal renal function. There are rare case reports of fondaparinux-induced thrombocytopenia.44Direct thrombin inhibitors (DTIs) include parental forms with recombinant hirudin, argatroban, and bivalirudin, as well as an oral agent, dabigatran. These antithrombotic agents bind to thrombin, inhibiting the conversion of fibrinogen to fibrin as well as thrombin-induced platelet activation. These actions are independent of antithrombin. The parental |
Surgery_Schwartz_6652 | Surgery_Schwartz | antithrombotic agents bind to thrombin, inhibiting the conversion of fibrinogen to fibrin as well as thrombin-induced platelet activation. These actions are independent of antithrombin. The parental DTIs should be reserved for (a) patients in whom there is a high clinical suspi-cion or confirmation of HIT, and (b) patients who have a his-tory of HIT or test positive for heparin-associated antibodies whereas dabigatran can be used as an alternative to Warfarin when INR monitoring is difficult or impractical. In patients with established HIT, DTIs should be administered for at least 7 days, or until the platelet count normalizes. Warfarin may then be introduced slowly, overlapping therapy with a DTI for at least 5 days, or dabigatran may be continued instead of Warfarin.45Bivalirudin is approved primarily for patients with or without HIT who undergo percutaneous coronary intervention and is rarely used outside of that setting.Argatroban is indicated for the prophylaxis and treatment of | Surgery_Schwartz. antithrombotic agents bind to thrombin, inhibiting the conversion of fibrinogen to fibrin as well as thrombin-induced platelet activation. These actions are independent of antithrombin. The parental DTIs should be reserved for (a) patients in whom there is a high clinical suspi-cion or confirmation of HIT, and (b) patients who have a his-tory of HIT or test positive for heparin-associated antibodies whereas dabigatran can be used as an alternative to Warfarin when INR monitoring is difficult or impractical. In patients with established HIT, DTIs should be administered for at least 7 days, or until the platelet count normalizes. Warfarin may then be introduced slowly, overlapping therapy with a DTI for at least 5 days, or dabigatran may be continued instead of Warfarin.45Bivalirudin is approved primarily for patients with or without HIT who undergo percutaneous coronary intervention and is rarely used outside of that setting.Argatroban is indicated for the prophylaxis and treatment of |
Surgery_Schwartz_6653 | Surgery_Schwartz | primarily for patients with or without HIT who undergo percutaneous coronary intervention and is rarely used outside of that setting.Argatroban is indicated for the prophylaxis and treatment of thrombosis in HIT. It also is approved for patients with, or at risk for, HIT undergoing percutaneous coronary intervention. Antithrombotic prophylaxis and therapy are initiated with a con-tinuous IV infusion of 2 µg/kg per minute, without the need for a bolus. The half-life ranges from 39 to 51 minutes, and the dosage is adjusted to maintain an aPTT of 1.5 to 3 times normal. Large ini-tial boluses and higher rates of continuous infusion are reserved for patients with coronary artery thrombosis and myocardial infarc-tion. In these patients, therapy is monitored using the activated clotting time. Argatroban is metabolized and excreted by the liver; therefore, dosage adjustments are needed in patients with hepatic impairment. There is no reversal agent for argatroban.The oral agent, dabigatran, | Surgery_Schwartz. primarily for patients with or without HIT who undergo percutaneous coronary intervention and is rarely used outside of that setting.Argatroban is indicated for the prophylaxis and treatment of thrombosis in HIT. It also is approved for patients with, or at risk for, HIT undergoing percutaneous coronary intervention. Antithrombotic prophylaxis and therapy are initiated with a con-tinuous IV infusion of 2 µg/kg per minute, without the need for a bolus. The half-life ranges from 39 to 51 minutes, and the dosage is adjusted to maintain an aPTT of 1.5 to 3 times normal. Large ini-tial boluses and higher rates of continuous infusion are reserved for patients with coronary artery thrombosis and myocardial infarc-tion. In these patients, therapy is monitored using the activated clotting time. Argatroban is metabolized and excreted by the liver; therefore, dosage adjustments are needed in patients with hepatic impairment. There is no reversal agent for argatroban.The oral agent, dabigatran, |
Surgery_Schwartz_6654 | Surgery_Schwartz | is metabolized and excreted by the liver; therefore, dosage adjustments are needed in patients with hepatic impairment. There is no reversal agent for argatroban.The oral agent, dabigatran, is US FDA-approved since 2014 for the treatment of VTE and prophylaxis for recurrent VTE. Additionally, limited approval was obtained in 2015 for prophylaxis of VTE after hip replacement surgery. It is admin-istered as a prodrug, dabigatran etexilate, that is converted to the active form, dabigatran, in the liver. The half-life ranges from 12 to 17 hours; it is therefore administered once daily for prophylaxis and twice daily for VTE therapy. Absorption is not dietary dependent, and no drug level monitoring is required. Dabigatran is metabolized in the kidney, and dose adjustment is required for renal insufficiency. Data on use in obese patients is limited; therefore, use is not recommended for patients with a body mass index ≥40 kg/m2 or ≥120 kg.46 Dyspepsia is a com-mon side effect that may limit | Surgery_Schwartz. is metabolized and excreted by the liver; therefore, dosage adjustments are needed in patients with hepatic impairment. There is no reversal agent for argatroban.The oral agent, dabigatran, is US FDA-approved since 2014 for the treatment of VTE and prophylaxis for recurrent VTE. Additionally, limited approval was obtained in 2015 for prophylaxis of VTE after hip replacement surgery. It is admin-istered as a prodrug, dabigatran etexilate, that is converted to the active form, dabigatran, in the liver. The half-life ranges from 12 to 17 hours; it is therefore administered once daily for prophylaxis and twice daily for VTE therapy. Absorption is not dietary dependent, and no drug level monitoring is required. Dabigatran is metabolized in the kidney, and dose adjustment is required for renal insufficiency. Data on use in obese patients is limited; therefore, use is not recommended for patients with a body mass index ≥40 kg/m2 or ≥120 kg.46 Dyspepsia is a com-mon side effect that may limit |
Surgery_Schwartz_6655 | Surgery_Schwartz | Data on use in obese patients is limited; therefore, use is not recommended for patients with a body mass index ≥40 kg/m2 or ≥120 kg.46 Dyspepsia is a com-mon side effect that may limit use in some patients.47 Dabigatran may be reversed with idarucizumab in emergent situations.48 It is contraindicated in patients with mechanical heart valves.Direct factor Xa inhibitors, which are comprised of the oral agents rivaroxaban, apixiban, and edoxaban, are FDA approved for treatment in VTE and prophylaxis for recurrent VTE. Additionally, rivaroxoban and apixiban are approved by the FDA for VTE prophylaxis following knee and hip replace-ment surgery. These medications function by inactivating cir-culating and thrombus-bound factor Xa. They are metabolized in the kidney (25–35%) and in the liver; therefore, use is not rec-ommended in patients with renal insufficiency (creatinine clear-ance <30 mL/min for rivaroxaban, or <15 mL/min for apixiban and edoxaban) or severe hepatic insufficiency. As | Surgery_Schwartz. Data on use in obese patients is limited; therefore, use is not recommended for patients with a body mass index ≥40 kg/m2 or ≥120 kg.46 Dyspepsia is a com-mon side effect that may limit use in some patients.47 Dabigatran may be reversed with idarucizumab in emergent situations.48 It is contraindicated in patients with mechanical heart valves.Direct factor Xa inhibitors, which are comprised of the oral agents rivaroxaban, apixiban, and edoxaban, are FDA approved for treatment in VTE and prophylaxis for recurrent VTE. Additionally, rivaroxoban and apixiban are approved by the FDA for VTE prophylaxis following knee and hip replace-ment surgery. These medications function by inactivating cir-culating and thrombus-bound factor Xa. They are metabolized in the kidney (25–35%) and in the liver; therefore, use is not rec-ommended in patients with renal insufficiency (creatinine clear-ance <30 mL/min for rivaroxaban, or <15 mL/min for apixiban and edoxaban) or severe hepatic insufficiency. As |
Surgery_Schwartz_6656 | Surgery_Schwartz | therefore, use is not rec-ommended in patients with renal insufficiency (creatinine clear-ance <30 mL/min for rivaroxaban, or <15 mL/min for apixiban and edoxaban) or severe hepatic insufficiency. As with the oral DTI, dabigatran, data on use in obese patients is limited; there-fore, use is not recommended in these patients. Additionally, these agents are contraindicated in pregnancy. There are no specific reversal agents available for direct factor Xa inhibi-tors. For severe cases of hemorrhage, indirect partial reversal may be achieved with use of prothrombin complex concentrate administration.49Rixaroxaban has a half-life of 7 to 17 hours. Therapy does not require monitoring. Prophylactic dosing is 10 mg once daily, and therapeutic dosing is 15 mg twice daily for 21 days, fol-lowed by 20 mg once daily thereafter.Apixiban has a half-life of 5 to 9 hours. Therapy does not require monitoring, and there are no dietary restrictions. If monitoring is desired in situations of bleeding or | Surgery_Schwartz. therefore, use is not rec-ommended in patients with renal insufficiency (creatinine clear-ance <30 mL/min for rivaroxaban, or <15 mL/min for apixiban and edoxaban) or severe hepatic insufficiency. As with the oral DTI, dabigatran, data on use in obese patients is limited; there-fore, use is not recommended in these patients. Additionally, these agents are contraindicated in pregnancy. There are no specific reversal agents available for direct factor Xa inhibi-tors. For severe cases of hemorrhage, indirect partial reversal may be achieved with use of prothrombin complex concentrate administration.49Rixaroxaban has a half-life of 7 to 17 hours. Therapy does not require monitoring. Prophylactic dosing is 10 mg once daily, and therapeutic dosing is 15 mg twice daily for 21 days, fol-lowed by 20 mg once daily thereafter.Apixiban has a half-life of 5 to 9 hours. Therapy does not require monitoring, and there are no dietary restrictions. If monitoring is desired in situations of bleeding or |
Surgery_Schwartz_6657 | Surgery_Schwartz | 20 mg once daily thereafter.Apixiban has a half-life of 5 to 9 hours. Therapy does not require monitoring, and there are no dietary restrictions. If monitoring is desired in situations of bleeding or concern for subor supratherapeutic dosing, serum anti-Xa levels can be obtained. Prophylactic dosing is 2.5 mg twice daily, and thera-peutic dosing is 10 mg daily for 7 days, followed by 5 mg twice daily thereafter.Edoxaban has a half-life of 10 to 14 hours. Therapy does not require monitoring. Typical dosing is 60 mg once daily, and 30 mg once daily if creatinine clearance ranges from 15 to 50 mL/min, or body weight ≤60 kg.Vitamin K antagonists, which include warfarin and other coumarin derivatives, are the traditional mainstay of long-term antithrombotic therapy in patients with VTE. Warfarin inhib-its the γ-carboxylation of vitamin K–dependent procoagulants (factors II, VII, IX, and X) and anticoagulants (proteins C and S), resulting in formation of less functional proteins. | Surgery_Schwartz. 20 mg once daily thereafter.Apixiban has a half-life of 5 to 9 hours. Therapy does not require monitoring, and there are no dietary restrictions. If monitoring is desired in situations of bleeding or concern for subor supratherapeutic dosing, serum anti-Xa levels can be obtained. Prophylactic dosing is 2.5 mg twice daily, and thera-peutic dosing is 10 mg daily for 7 days, followed by 5 mg twice daily thereafter.Edoxaban has a half-life of 10 to 14 hours. Therapy does not require monitoring. Typical dosing is 60 mg once daily, and 30 mg once daily if creatinine clearance ranges from 15 to 50 mL/min, or body weight ≤60 kg.Vitamin K antagonists, which include warfarin and other coumarin derivatives, are the traditional mainstay of long-term antithrombotic therapy in patients with VTE. Warfarin inhib-its the γ-carboxylation of vitamin K–dependent procoagulants (factors II, VII, IX, and X) and anticoagulants (proteins C and S), resulting in formation of less functional proteins. |
Surgery_Schwartz_6658 | Surgery_Schwartz | Warfarin inhib-its the γ-carboxylation of vitamin K–dependent procoagulants (factors II, VII, IX, and X) and anticoagulants (proteins C and S), resulting in formation of less functional proteins. Warfarin usu-ally requires several days to achieve full effect because normal circulating coagulation proteins must first undergo their normal degradation. Factors X and II have the longest half-lives, in the range of 36 and 72 hours, respectively. A steady-state concen-tration of warfarin is usually not reached for 4 to 5 days.Warfarin therapy is monitored by measuring the INR, calculated using the following equation:INR = (patient prothrombin time/laboratorynormal prothrombin time)ISIwhere ISI is the international sensitivity index. The ISI describes the strength of the thromboplastin that is added to activate the extrinsic coagulation pathway. The therapeutic target INR range is usually 2.0 to 3.0, but the response to warfarin is variable and depends on liver function, diet, age, and | Surgery_Schwartz. Warfarin inhib-its the γ-carboxylation of vitamin K–dependent procoagulants (factors II, VII, IX, and X) and anticoagulants (proteins C and S), resulting in formation of less functional proteins. Warfarin usu-ally requires several days to achieve full effect because normal circulating coagulation proteins must first undergo their normal degradation. Factors X and II have the longest half-lives, in the range of 36 and 72 hours, respectively. A steady-state concen-tration of warfarin is usually not reached for 4 to 5 days.Warfarin therapy is monitored by measuring the INR, calculated using the following equation:INR = (patient prothrombin time/laboratorynormal prothrombin time)ISIwhere ISI is the international sensitivity index. The ISI describes the strength of the thromboplastin that is added to activate the extrinsic coagulation pathway. The therapeutic target INR range is usually 2.0 to 3.0, but the response to warfarin is variable and depends on liver function, diet, age, and |
Surgery_Schwartz_6659 | Surgery_Schwartz | is added to activate the extrinsic coagulation pathway. The therapeutic target INR range is usually 2.0 to 3.0, but the response to warfarin is variable and depends on liver function, diet, age, and concomitant medica-tions. In patients receiving anticoagulation therapy without con-comitant thrombolysis or venous thrombectomy, the vitamin K antagonist may be started on the same day as the initial paren-teral anticoagulant, usually at doses ranging from 5 to 10 mg. Smaller initial doses may be needed in older and malnourished patients, in those with liver disease or congestive heart failure, and in those who have recently undergone major surgery.49The recommended duration of warfarin antithrombotic therapy is stratified based on whether the DVT was provoked or unprovoked, whether it was the first or a recurrent episode, where the DVT is located, and whether malignancy or thrombophilia is present. Current ACCP recommendations for duration of warfarin therapy are summarized in Table | Surgery_Schwartz. is added to activate the extrinsic coagulation pathway. The therapeutic target INR range is usually 2.0 to 3.0, but the response to warfarin is variable and depends on liver function, diet, age, and concomitant medica-tions. In patients receiving anticoagulation therapy without con-comitant thrombolysis or venous thrombectomy, the vitamin K antagonist may be started on the same day as the initial paren-teral anticoagulant, usually at doses ranging from 5 to 10 mg. Smaller initial doses may be needed in older and malnourished patients, in those with liver disease or congestive heart failure, and in those who have recently undergone major surgery.49The recommended duration of warfarin antithrombotic therapy is stratified based on whether the DVT was provoked or unprovoked, whether it was the first or a recurrent episode, where the DVT is located, and whether malignancy or thrombophilia is present. Current ACCP recommendations for duration of warfarin therapy are summarized in Table |
Surgery_Schwartz_6660 | Surgery_Schwartz | the first or a recurrent episode, where the DVT is located, and whether malignancy or thrombophilia is present. Current ACCP recommendations for duration of warfarin therapy are summarized in Table 24-4.In patients with proximal DVT, several randomized clini-cal trials have demonstrated that shorter-term antithrombotic therapy (4 to 6 weeks) is associated with a higher rate of VTE recurrence than 3 to 6 months of anticoagulation.50-52 In these trials, most of the patients with transient risk factors had a low rate of recurrent VTE, and most recurrences were in patients with continuing risk factors. The ACCP recommendation, there-fore, is that 3 months of anticoagulation are sufficient to prevent 3Brunicardi_Ch24_p0981-p1008.indd 98922/02/19 3:01 PM 990SPECIFIC CONSIDERATIONSPART IITable 24-4Summary of American College of Chest Physicians recommendations regarding duration of long-term antithrombotic therapy for deep vein thrombosis (DVT)CLINICAL SUBGROUPANTITHROMBOTIC TREATMENT | Surgery_Schwartz. the first or a recurrent episode, where the DVT is located, and whether malignancy or thrombophilia is present. Current ACCP recommendations for duration of warfarin therapy are summarized in Table 24-4.In patients with proximal DVT, several randomized clini-cal trials have demonstrated that shorter-term antithrombotic therapy (4 to 6 weeks) is associated with a higher rate of VTE recurrence than 3 to 6 months of anticoagulation.50-52 In these trials, most of the patients with transient risk factors had a low rate of recurrent VTE, and most recurrences were in patients with continuing risk factors. The ACCP recommendation, there-fore, is that 3 months of anticoagulation are sufficient to prevent 3Brunicardi_Ch24_p0981-p1008.indd 98922/02/19 3:01 PM 990SPECIFIC CONSIDERATIONSPART IITable 24-4Summary of American College of Chest Physicians recommendations regarding duration of long-term antithrombotic therapy for deep vein thrombosis (DVT)CLINICAL SUBGROUPANTITHROMBOTIC TREATMENT |
Surgery_Schwartz_6661 | Surgery_Schwartz | 24-4Summary of American College of Chest Physicians recommendations regarding duration of long-term antithrombotic therapy for deep vein thrombosis (DVT)CLINICAL SUBGROUPANTITHROMBOTIC TREATMENT DURATIONFirst episode DVT/transient risk/surgeryVKA or LMWH for 3 monthsFirst episode DVT/unprovokedVKA or LMWH for 3 monthsConsider for long-term therapy if:• Proximal DVT• Minimal bleeding risk• Stable coagulation monitoringDistal DVT/unprovoked• Symptomatic• Asymptomatic and no risk factors for progressionVKA for 3 monthsSerial imaging in 2 weeks, if progression VKA for 3 monthsSecond episode DVT/unprovokedDVT and cancerVKA for extended therapyLMWH for extended therapy over VKALMWH = low molecular weight heparin; VKA = vitamin K antagonist.Data from Kearon C, Akl EA, Comerota AJ, et al: Antithrombotic therapy for VTE disease: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines, Chest. 2012 Feb;141(2 | Surgery_Schwartz. 24-4Summary of American College of Chest Physicians recommendations regarding duration of long-term antithrombotic therapy for deep vein thrombosis (DVT)CLINICAL SUBGROUPANTITHROMBOTIC TREATMENT DURATIONFirst episode DVT/transient risk/surgeryVKA or LMWH for 3 monthsFirst episode DVT/unprovokedVKA or LMWH for 3 monthsConsider for long-term therapy if:• Proximal DVT• Minimal bleeding risk• Stable coagulation monitoringDistal DVT/unprovoked• Symptomatic• Asymptomatic and no risk factors for progressionVKA for 3 monthsSerial imaging in 2 weeks, if progression VKA for 3 monthsSecond episode DVT/unprovokedDVT and cancerVKA for extended therapyLMWH for extended therapy over VKALMWH = low molecular weight heparin; VKA = vitamin K antagonist.Data from Kearon C, Akl EA, Comerota AJ, et al: Antithrombotic therapy for VTE disease: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines, Chest. 2012 Feb;141(2 |
Surgery_Schwartz_6662 | Surgery_Schwartz | therapy for VTE disease: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines, Chest. 2012 Feb;141(2 Suppl): e419S-e496S.recurrent VTE in patients with DVT occurring around the time of a transient risk factor (e.g., hospitalization or orthopedic or major general surgery).In contrast to patients with thrombosis related to transient risk factors, patients with unprovoked VTE are much more likely to develop recurrence (rates as high as 40% at 10 years). In this latter group of patients, numerous clinical trials have compared 3 to 6 months of anticoagulation therapy with extended-duration warfarin therapy, both at low intensity (INR of 1.5 to 2.0) and at conventional intensity (INR of 2.0 to 3.0).53-55 In patients with idiopathic DVT, extended-duration antithrombotic therapy is associated with a relative reduction in the rate of recurrent VTE by 75% to >90%. In addition, conventional-intensity | Surgery_Schwartz. therapy for VTE disease: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines, Chest. 2012 Feb;141(2 Suppl): e419S-e496S.recurrent VTE in patients with DVT occurring around the time of a transient risk factor (e.g., hospitalization or orthopedic or major general surgery).In contrast to patients with thrombosis related to transient risk factors, patients with unprovoked VTE are much more likely to develop recurrence (rates as high as 40% at 10 years). In this latter group of patients, numerous clinical trials have compared 3 to 6 months of anticoagulation therapy with extended-duration warfarin therapy, both at low intensity (INR of 1.5 to 2.0) and at conventional intensity (INR of 2.0 to 3.0).53-55 In patients with idiopathic DVT, extended-duration antithrombotic therapy is associated with a relative reduction in the rate of recurrent VTE by 75% to >90%. In addition, conventional-intensity |
Surgery_Schwartz_6663 | Surgery_Schwartz | In patients with idiopathic DVT, extended-duration antithrombotic therapy is associated with a relative reduction in the rate of recurrent VTE by 75% to >90%. In addition, conventional-intensity warfarin reduces the risk even further compared with low-intensity war-farin (0.7 events per 100 person-years vs. 1.9 events per 100 person-years) without an increase in bleeding complications.56In patients with VTE in association with a hypercoagulable condition, the optimal duration of anticoagulation therapy is influ-enced more by the clinical circumstances at the time of the VTE (idiopathic vs. secondary) than by the actual presence or absence of the more common thrombophilic conditions. In patients with VTE related to malignancy, increasing evidence suggests that longer-term therapy with LMWH (up to 6 months) is associated with a lower VTE recurrence than treatment using conventional vitamin K antagonists.57,58 The primary complication of warfarin therapy is hemorrhage, and the risk is | Surgery_Schwartz. In patients with idiopathic DVT, extended-duration antithrombotic therapy is associated with a relative reduction in the rate of recurrent VTE by 75% to >90%. In addition, conventional-intensity warfarin reduces the risk even further compared with low-intensity war-farin (0.7 events per 100 person-years vs. 1.9 events per 100 person-years) without an increase in bleeding complications.56In patients with VTE in association with a hypercoagulable condition, the optimal duration of anticoagulation therapy is influ-enced more by the clinical circumstances at the time of the VTE (idiopathic vs. secondary) than by the actual presence or absence of the more common thrombophilic conditions. In patients with VTE related to malignancy, increasing evidence suggests that longer-term therapy with LMWH (up to 6 months) is associated with a lower VTE recurrence than treatment using conventional vitamin K antagonists.57,58 The primary complication of warfarin therapy is hemorrhage, and the risk is |
Surgery_Schwartz_6664 | Surgery_Schwartz | (up to 6 months) is associated with a lower VTE recurrence than treatment using conventional vitamin K antagonists.57,58 The primary complication of warfarin therapy is hemorrhage, and the risk is related to the magnitude of INR prolongation. Depending on the INR and the presence of bleeding, warfarin anticoagulation may be reversed by (a) omit-ting or decreasing subsequent dosages, (b) administering oral or parenteral vitamin K, or (c) administering fresh frozen plasma, prothrombin complex concentrate, or recombinant factor VIIa.49Warfarin therapy rarely may be associated with the devel-opment of skin necrosis and limb gangrene. These conditions occur more commonly in women (4:1), and the most commonly affected areas are the breast, buttocks, and thighs. This com-plication, which usually occurs in the first days of therapy, is occasionally, but not exclusively, associated with protein C or S deficiency and malignancy. Patients who require continued anticoagulation may restart | Surgery_Schwartz. (up to 6 months) is associated with a lower VTE recurrence than treatment using conventional vitamin K antagonists.57,58 The primary complication of warfarin therapy is hemorrhage, and the risk is related to the magnitude of INR prolongation. Depending on the INR and the presence of bleeding, warfarin anticoagulation may be reversed by (a) omit-ting or decreasing subsequent dosages, (b) administering oral or parenteral vitamin K, or (c) administering fresh frozen plasma, prothrombin complex concentrate, or recombinant factor VIIa.49Warfarin therapy rarely may be associated with the devel-opment of skin necrosis and limb gangrene. These conditions occur more commonly in women (4:1), and the most commonly affected areas are the breast, buttocks, and thighs. This com-plication, which usually occurs in the first days of therapy, is occasionally, but not exclusively, associated with protein C or S deficiency and malignancy. Patients who require continued anticoagulation may restart |
Surgery_Schwartz_6665 | Surgery_Schwartz | usually occurs in the first days of therapy, is occasionally, but not exclusively, associated with protein C or S deficiency and malignancy. Patients who require continued anticoagulation may restart low-dose warfarin (2 mg) while receiving concomitant therapeutic heparin. The warfarin dosage is then gradually increased over a 1to 2-week period.49Systemic and Catheter-Directed Thrombolysis. Patients with extensive proximal, iliofemoral DVT may benefit from systemic thrombolysis or catheter-directed thrombolysis (CDT). CDT appears to be more effective (see later in chapter) and potentially reduces acute congestive lower extremity symp-toms more rapidly than anticoagulation alone and decreases the development of PTS.Several thrombolytic agents are available, including strep-tokinase, urokinase, alteplase (recombinant tissue plasminogen activator), reteplase, and tenecteplase. All share the ability to con-vert plasminogen to plasmin, which leads to the degradation of fibrin. They differ | Surgery_Schwartz. usually occurs in the first days of therapy, is occasionally, but not exclusively, associated with protein C or S deficiency and malignancy. Patients who require continued anticoagulation may restart low-dose warfarin (2 mg) while receiving concomitant therapeutic heparin. The warfarin dosage is then gradually increased over a 1to 2-week period.49Systemic and Catheter-Directed Thrombolysis. Patients with extensive proximal, iliofemoral DVT may benefit from systemic thrombolysis or catheter-directed thrombolysis (CDT). CDT appears to be more effective (see later in chapter) and potentially reduces acute congestive lower extremity symp-toms more rapidly than anticoagulation alone and decreases the development of PTS.Several thrombolytic agents are available, including strep-tokinase, urokinase, alteplase (recombinant tissue plasminogen activator), reteplase, and tenecteplase. All share the ability to con-vert plasminogen to plasmin, which leads to the degradation of fibrin. They differ |
Surgery_Schwartz_6666 | Surgery_Schwartz | alteplase (recombinant tissue plasminogen activator), reteplase, and tenecteplase. All share the ability to con-vert plasminogen to plasmin, which leads to the degradation of fibrin. They differ with regard to their half-lives, their potential for inducing fibrinogenolysis (generalized lytic state), their poten-tial for antigenicity, and their FDA-approved indications for use.Streptokinase is purified from β-hemolytic Streptococcus and is approved for the treatment of acute myocardial infarction, PE, DVT, arterial thromboembolism, and occluded central lines and arteriovenous shunts. It is not specific for fibrin-bound plas-minogen, however, and its use is limited by its significant rates of antigenicity. Fevers and shivering occur in 1% to 4% of patients.Urokinase is derived from human neonatal kidney cells grown in tissue culture. Currently, it is only approved for lysis of massive PE or PE associated with unstable hemodynamics.Alteplase, reteplase, and tenecteplase all are | Surgery_Schwartz. alteplase (recombinant tissue plasminogen activator), reteplase, and tenecteplase. All share the ability to con-vert plasminogen to plasmin, which leads to the degradation of fibrin. They differ with regard to their half-lives, their potential for inducing fibrinogenolysis (generalized lytic state), their poten-tial for antigenicity, and their FDA-approved indications for use.Streptokinase is purified from β-hemolytic Streptococcus and is approved for the treatment of acute myocardial infarction, PE, DVT, arterial thromboembolism, and occluded central lines and arteriovenous shunts. It is not specific for fibrin-bound plas-minogen, however, and its use is limited by its significant rates of antigenicity. Fevers and shivering occur in 1% to 4% of patients.Urokinase is derived from human neonatal kidney cells grown in tissue culture. Currently, it is only approved for lysis of massive PE or PE associated with unstable hemodynamics.Alteplase, reteplase, and tenecteplase all are |
Surgery_Schwartz_6667 | Surgery_Schwartz | human neonatal kidney cells grown in tissue culture. Currently, it is only approved for lysis of massive PE or PE associated with unstable hemodynamics.Alteplase, reteplase, and tenecteplase all are recombinant variants of tissue plasminogen activator. Alteplase is indicated for the treatment of acute myocardial infarction, acute ischemic stroke, and acute massive PE. However, it often is used for CDT of DVT. Reteplase and tenecteplase are indicated only for the treatment of acute myocardial infarction.Systemic thrombolysis was evaluated in numerous older prospective and randomized clinical trials, and its efficacy was summarized in a recent Cochrane Review.59 In 12 studies involving over 700 patients, systemic thrombolysis was associ-ated with significantly more clot lysis (relative risk [RR] 0.24 to 0.37) and significantly less PTS (RR 0.66). However, venous function was not significantly improved. In addition, more bleeding complications occurred (RR 1.73).In an effort to minimize | Surgery_Schwartz. human neonatal kidney cells grown in tissue culture. Currently, it is only approved for lysis of massive PE or PE associated with unstable hemodynamics.Alteplase, reteplase, and tenecteplase all are recombinant variants of tissue plasminogen activator. Alteplase is indicated for the treatment of acute myocardial infarction, acute ischemic stroke, and acute massive PE. However, it often is used for CDT of DVT. Reteplase and tenecteplase are indicated only for the treatment of acute myocardial infarction.Systemic thrombolysis was evaluated in numerous older prospective and randomized clinical trials, and its efficacy was summarized in a recent Cochrane Review.59 In 12 studies involving over 700 patients, systemic thrombolysis was associ-ated with significantly more clot lysis (relative risk [RR] 0.24 to 0.37) and significantly less PTS (RR 0.66). However, venous function was not significantly improved. In addition, more bleeding complications occurred (RR 1.73).In an effort to minimize |
Surgery_Schwartz_6668 | Surgery_Schwartz | [RR] 0.24 to 0.37) and significantly less PTS (RR 0.66). However, venous function was not significantly improved. In addition, more bleeding complications occurred (RR 1.73).In an effort to minimize bleeding complications and increase efficacy, CDT techniques were developed for the treat-ment of symptomatic primarily iliofemoral DVT. With catheterdirected therapy, venous access may be achieved through percutaneous catheterization of the ipsilateral popliteal vein, retrograde catheterization through the contralateral femoral vein, or retrograde cannulation from the internal jugular vein. Multi–side-hole infusion catheters, with or without infusion wires, are used to deliver the lytic agent directly into the throm-bus. Lytic agents may be administered alone or, now more commonly, in combination with catheter-based methods to Brunicardi_Ch24_p0981-p1008.indd 99022/02/19 3:01 PM 991VENOUS AND LYMPHATIC DISEASECHAPTER 24ABFigure 24-9. Preoperative computed tomography imaging and | Surgery_Schwartz. [RR] 0.24 to 0.37) and significantly less PTS (RR 0.66). However, venous function was not significantly improved. In addition, more bleeding complications occurred (RR 1.73).In an effort to minimize bleeding complications and increase efficacy, CDT techniques were developed for the treat-ment of symptomatic primarily iliofemoral DVT. With catheterdirected therapy, venous access may be achieved through percutaneous catheterization of the ipsilateral popliteal vein, retrograde catheterization through the contralateral femoral vein, or retrograde cannulation from the internal jugular vein. Multi–side-hole infusion catheters, with or without infusion wires, are used to deliver the lytic agent directly into the throm-bus. Lytic agents may be administered alone or, now more commonly, in combination with catheter-based methods to Brunicardi_Ch24_p0981-p1008.indd 99022/02/19 3:01 PM 991VENOUS AND LYMPHATIC DISEASECHAPTER 24ABFigure 24-9. Preoperative computed tomography imaging and |
Surgery_Schwartz_6669 | Surgery_Schwartz | with catheter-based methods to Brunicardi_Ch24_p0981-p1008.indd 99022/02/19 3:01 PM 991VENOUS AND LYMPHATIC DISEASECHAPTER 24ABFigure 24-9. Preoperative computed tomography imaging and intraoperative photo demonstrating erosion of IVC filter through the IVC wall.physically break up the clot—so-called pharmacomechanical thrombolysis. One commonly used device to perform phar-macomechanical thrombolysis is the AngioJet, which utilizes pulsed injection of thrombolytic via a percutaneously inserted catheter followed by active aspiration to remove the thrombus.The efficacy of CDT for the treatment of symptomatic iliofemoral DVT has been reported previously in a large, multi-center, randomized control trial. Two-hundred and nine patients with proximal DVT identified within 21 days of onset of symp-toms were assigned to conventional anticoagulant therapy vs. conventional anticoagulant therapy plus CDT. In the CDT group, placement of a venous stent was permitted for any identified iliac | Surgery_Schwartz. with catheter-based methods to Brunicardi_Ch24_p0981-p1008.indd 99022/02/19 3:01 PM 991VENOUS AND LYMPHATIC DISEASECHAPTER 24ABFigure 24-9. Preoperative computed tomography imaging and intraoperative photo demonstrating erosion of IVC filter through the IVC wall.physically break up the clot—so-called pharmacomechanical thrombolysis. One commonly used device to perform phar-macomechanical thrombolysis is the AngioJet, which utilizes pulsed injection of thrombolytic via a percutaneously inserted catheter followed by active aspiration to remove the thrombus.The efficacy of CDT for the treatment of symptomatic iliofemoral DVT has been reported previously in a large, multi-center, randomized control trial. Two-hundred and nine patients with proximal DVT identified within 21 days of onset of symp-toms were assigned to conventional anticoagulant therapy vs. conventional anticoagulant therapy plus CDT. In the CDT group, placement of a venous stent was permitted for any identified iliac |
Surgery_Schwartz_6670 | Surgery_Schwartz | of symp-toms were assigned to conventional anticoagulant therapy vs. conventional anticoagulant therapy plus CDT. In the CDT group, placement of a venous stent was permitted for any identified iliac vein stenotic lesion. At 6 months, iliac vein patency was signifi-cantly improved in the thrombolysis group (65.9% vs. 47.4%). At 2 years, in the CDT group, there was an absolute risk reduc-tion of nearly 15% for development of PTS, translating to a num-ber needed to treat of seven patients to prevent one case of PTS.60 However, these results were, in part, contradictory to the results reported the more recent Acute Venous Thrombosis: Throm-bus Removal with Adjunctive Catheter-Directed Thrombolysis (ATTRACT) trial, a prospective, randomized, multicenter trial evaluating nearly 700 patients comparing anticoagulant use with CDT in patients with acute femoropopliteal, and/or iliac vein DVT.61 However, the purpose of this trial was to see if indica-tions for CDT should be extended for isolated | Surgery_Schwartz. of symp-toms were assigned to conventional anticoagulant therapy vs. conventional anticoagulant therapy plus CDT. In the CDT group, placement of a venous stent was permitted for any identified iliac vein stenotic lesion. At 6 months, iliac vein patency was signifi-cantly improved in the thrombolysis group (65.9% vs. 47.4%). At 2 years, in the CDT group, there was an absolute risk reduc-tion of nearly 15% for development of PTS, translating to a num-ber needed to treat of seven patients to prevent one case of PTS.60 However, these results were, in part, contradictory to the results reported the more recent Acute Venous Thrombosis: Throm-bus Removal with Adjunctive Catheter-Directed Thrombolysis (ATTRACT) trial, a prospective, randomized, multicenter trial evaluating nearly 700 patients comparing anticoagulant use with CDT in patients with acute femoropopliteal, and/or iliac vein DVT.61 However, the purpose of this trial was to see if indica-tions for CDT should be extended for isolated |
Surgery_Schwartz_6671 | Surgery_Schwartz | anticoagulant use with CDT in patients with acute femoropopliteal, and/or iliac vein DVT.61 However, the purpose of this trial was to see if indica-tions for CDT should be extended for isolated femoropopliteal DVT (43% of the patients in this study) and therefore, was under-powered to compare treatment efficacy for iliofemoral DVT, which known to have a higher risk of PTS. The study found that PTS occurred with equal frequency in the two groups (47% vs. 48%, P = NS), but patients who were treated with pharmacom-echanical CDT plus anticoagulation were less likely to develop moderate-to-severe PTS than those treated with anticoagulation alone (18% vs. 24%, P = .003). There was no difference between the two groups in quality of life. There was an increase in both overall hemorrhage (4.5% vs. 1.7%) and major hemorrhage (1.7% vs 0.3%) with CDT but no fatal or intracranial hemor-rhage in either cohort. Taken in combination, the findings from these trials support selective use of CDT with | Surgery_Schwartz. anticoagulant use with CDT in patients with acute femoropopliteal, and/or iliac vein DVT.61 However, the purpose of this trial was to see if indica-tions for CDT should be extended for isolated femoropopliteal DVT (43% of the patients in this study) and therefore, was under-powered to compare treatment efficacy for iliofemoral DVT, which known to have a higher risk of PTS. The study found that PTS occurred with equal frequency in the two groups (47% vs. 48%, P = NS), but patients who were treated with pharmacom-echanical CDT plus anticoagulation were less likely to develop moderate-to-severe PTS than those treated with anticoagulation alone (18% vs. 24%, P = .003). There was no difference between the two groups in quality of life. There was an increase in both overall hemorrhage (4.5% vs. 1.7%) and major hemorrhage (1.7% vs 0.3%) with CDT but no fatal or intracranial hemor-rhage in either cohort. Taken in combination, the findings from these trials support selective use of CDT with |
Surgery_Schwartz_6672 | Surgery_Schwartz | 1.7%) and major hemorrhage (1.7% vs 0.3%) with CDT but no fatal or intracranial hemor-rhage in either cohort. Taken in combination, the findings from these trials support selective use of CDT with anticoagulation in young patients with acute iliofemoral DVT and anticoagulation alone in the remaining patient with DVT.There are contraindications to thrombolytic therapy. Absolute contraindications include prior history of ischemic or hemorrhagic stroke within 3 months, head trauma within 3 months, neurologic surgery within 6 months, known intra-cranial neoplasm, internal bleeding within 6 weeks, active or known bleeding disorder, traumatic cardiopulmonary resuscita-tion within 3 weeks or suspected aortic dissection. Fortunately, serious remote bleeding is uncommon, and intracranial hem-orrhage rarely occurs. The majority of bleeding complications are limited to the venous access site. Symptomatic pulmonary embolism occurs uncommonly and is very rarely fatal.Inferior Vena Caval | Surgery_Schwartz. 1.7%) and major hemorrhage (1.7% vs 0.3%) with CDT but no fatal or intracranial hemor-rhage in either cohort. Taken in combination, the findings from these trials support selective use of CDT with anticoagulation in young patients with acute iliofemoral DVT and anticoagulation alone in the remaining patient with DVT.There are contraindications to thrombolytic therapy. Absolute contraindications include prior history of ischemic or hemorrhagic stroke within 3 months, head trauma within 3 months, neurologic surgery within 6 months, known intra-cranial neoplasm, internal bleeding within 6 weeks, active or known bleeding disorder, traumatic cardiopulmonary resuscita-tion within 3 weeks or suspected aortic dissection. Fortunately, serious remote bleeding is uncommon, and intracranial hem-orrhage rarely occurs. The majority of bleeding complications are limited to the venous access site. Symptomatic pulmonary embolism occurs uncommonly and is very rarely fatal.Inferior Vena Caval |
Surgery_Schwartz_6673 | Surgery_Schwartz | hem-orrhage rarely occurs. The majority of bleeding complications are limited to the venous access site. Symptomatic pulmonary embolism occurs uncommonly and is very rarely fatal.Inferior Vena Caval Filters. Since the introduction of the Kimray-Greenfield filter in the United States in 1973, numerous vena caval filters have been developed. Although the designs are variable, they all are designed to prevent pulmonary emboli, while allowing continuation of venous blood flow through the IVC. Early filters were placed surgically through the femoral vein. Currently, less invasive techniques allow percutaneous filter placement through a femoral vein, internal jugular vein, or a peripheral vein under fluoroscopic or ultrasound guidance.Placement of an IVC filter is indicated for patients who have manifestations of lower extremity VTE and absolute contraindications to anticoagulation, those that have a bleeding complication from anticoagulation therapy of acute VTE, or those who develop | Surgery_Schwartz. hem-orrhage rarely occurs. The majority of bleeding complications are limited to the venous access site. Symptomatic pulmonary embolism occurs uncommonly and is very rarely fatal.Inferior Vena Caval Filters. Since the introduction of the Kimray-Greenfield filter in the United States in 1973, numerous vena caval filters have been developed. Although the designs are variable, they all are designed to prevent pulmonary emboli, while allowing continuation of venous blood flow through the IVC. Early filters were placed surgically through the femoral vein. Currently, less invasive techniques allow percutaneous filter placement through a femoral vein, internal jugular vein, or a peripheral vein under fluoroscopic or ultrasound guidance.Placement of an IVC filter is indicated for patients who have manifestations of lower extremity VTE and absolute contraindications to anticoagulation, those that have a bleeding complication from anticoagulation therapy of acute VTE, or those who develop |
Surgery_Schwartz_6674 | Surgery_Schwartz | have manifestations of lower extremity VTE and absolute contraindications to anticoagulation, those that have a bleeding complication from anticoagulation therapy of acute VTE, or those who develop recurrent DVT or PE despite adequate anticoagula-tion therapy and for patients with severe pulmonary hypertension.When possible, anticoagulation therapy should be contin-ued in patients with vena cava filters. The duration of antico-agulation is determined by the underlying VTE and not by the presence of the IVC filter itself. Practically speaking, however, many patients who require an IVC filter for recurrent VTE are the same ones who would benefit most from indefinite antico-agulation. In patients who are not able to receive anticoagulants due to recent surgery or trauma, the clinician should continually reassess if anticoagulation may be started safely at a later date.Placement of permanent IVC filters has been evaluated as an adjunct to routine anticoagulation in patients with proximal | Surgery_Schwartz. have manifestations of lower extremity VTE and absolute contraindications to anticoagulation, those that have a bleeding complication from anticoagulation therapy of acute VTE, or those who develop recurrent DVT or PE despite adequate anticoagula-tion therapy and for patients with severe pulmonary hypertension.When possible, anticoagulation therapy should be contin-ued in patients with vena cava filters. The duration of antico-agulation is determined by the underlying VTE and not by the presence of the IVC filter itself. Practically speaking, however, many patients who require an IVC filter for recurrent VTE are the same ones who would benefit most from indefinite antico-agulation. In patients who are not able to receive anticoagulants due to recent surgery or trauma, the clinician should continually reassess if anticoagulation may be started safely at a later date.Placement of permanent IVC filters has been evaluated as an adjunct to routine anticoagulation in patients with proximal |
Surgery_Schwartz_6675 | Surgery_Schwartz | continually reassess if anticoagulation may be started safely at a later date.Placement of permanent IVC filters has been evaluated as an adjunct to routine anticoagulation in patients with proximal DVT.62 Routine IVC filter placement has not been shown to prolong early or late survival in patients with proximal DVT but did decrease the rate of PE (HR, 0.22; 95% CI, 0.05–0.90); however, there is an increased rate of recurrent DVT in patients with IVC filters (HR, 1.87; 95% CI, 1.10–3.20).IVC filters are associated with acute and late complica-tions. Acute complications include thrombosis or bleeding at the insertion site and misplacement of the filter. Late complications include thrombosis of the IVC, DVT, breaking, migration, or ero-sion of the filter through the IVC (Fig. 24-9). The rate of fatal complications is <0.12%.63 As a result of the increasing number Brunicardi_Ch24_p0981-p1008.indd 99122/02/19 3:01 PM 992SPECIFIC CONSIDERATIONSPART IIFigure 24-10. Autopsy specimen | Surgery_Schwartz. continually reassess if anticoagulation may be started safely at a later date.Placement of permanent IVC filters has been evaluated as an adjunct to routine anticoagulation in patients with proximal DVT.62 Routine IVC filter placement has not been shown to prolong early or late survival in patients with proximal DVT but did decrease the rate of PE (HR, 0.22; 95% CI, 0.05–0.90); however, there is an increased rate of recurrent DVT in patients with IVC filters (HR, 1.87; 95% CI, 1.10–3.20).IVC filters are associated with acute and late complica-tions. Acute complications include thrombosis or bleeding at the insertion site and misplacement of the filter. Late complications include thrombosis of the IVC, DVT, breaking, migration, or ero-sion of the filter through the IVC (Fig. 24-9). The rate of fatal complications is <0.12%.63 As a result of the increasing number Brunicardi_Ch24_p0981-p1008.indd 99122/02/19 3:01 PM 992SPECIFIC CONSIDERATIONSPART IIFigure 24-10. Autopsy specimen |
Surgery_Schwartz_6676 | Surgery_Schwartz | rate of fatal complications is <0.12%.63 As a result of the increasing number Brunicardi_Ch24_p0981-p1008.indd 99122/02/19 3:01 PM 992SPECIFIC CONSIDERATIONSPART IIFigure 24-10. Autopsy specimen showing a massive pulmonary embolism.of reported complications with IVC filters, the FDA issued a warning in 2010 recommending removal of IVC filters as soon as they are no longer needed.64 This was followed by an update in 2014 where the recommendation was made to remove IVC filters within 29 and 54 days after implantation based upon a mathemati-cal model that suggested an increased risk-to-benefit ratio at this time point.65In some patients, the need for an IVC filter may be self-limited. Such patients can be treated with so-called removable IVC filters. Depending on the device, removable IVC filters are potentially removable by percutaneous endovascular tech-niques for up to several months after their initial implantation, assuming the filter is no longer required and does not have | Surgery_Schwartz. rate of fatal complications is <0.12%.63 As a result of the increasing number Brunicardi_Ch24_p0981-p1008.indd 99122/02/19 3:01 PM 992SPECIFIC CONSIDERATIONSPART IIFigure 24-10. Autopsy specimen showing a massive pulmonary embolism.of reported complications with IVC filters, the FDA issued a warning in 2010 recommending removal of IVC filters as soon as they are no longer needed.64 This was followed by an update in 2014 where the recommendation was made to remove IVC filters within 29 and 54 days after implantation based upon a mathemati-cal model that suggested an increased risk-to-benefit ratio at this time point.65In some patients, the need for an IVC filter may be self-limited. Such patients can be treated with so-called removable IVC filters. Depending on the device, removable IVC filters are potentially removable by percutaneous endovascular tech-niques for up to several months after their initial implantation, assuming the filter is no longer required and does not have |
Surgery_Schwartz_6677 | Surgery_Schwartz | IVC filters are potentially removable by percutaneous endovascular tech-niques for up to several months after their initial implantation, assuming the filter is no longer required and does not have large amounts of trapped thrombi. IVC filters that have been in place for an extended period of time may require adjunctive techniques, including laser-assisted removal or open surgical removal when they are embedded within the vena cava. All tem-porary IVC filters are approved for permanent implantation, and many so-called temporary filters end up as permanent devices with all the potential complications of permanent IVC filters.Operative Venous Thrombectomy. In patients with acute iliofemoral DVT, surgical therapy is generally reserved for patients who worsen with anticoagulation therapy and those with phlegmasia cerulea dolens and impending venous gan-grene. If the patient has phlegmasia cerulea dolens, a fasciotomy of the calf compartments is first performed. In iliofemoral DVT, a | Surgery_Schwartz. IVC filters are potentially removable by percutaneous endovascular tech-niques for up to several months after their initial implantation, assuming the filter is no longer required and does not have large amounts of trapped thrombi. IVC filters that have been in place for an extended period of time may require adjunctive techniques, including laser-assisted removal or open surgical removal when they are embedded within the vena cava. All tem-porary IVC filters are approved for permanent implantation, and many so-called temporary filters end up as permanent devices with all the potential complications of permanent IVC filters.Operative Venous Thrombectomy. In patients with acute iliofemoral DVT, surgical therapy is generally reserved for patients who worsen with anticoagulation therapy and those with phlegmasia cerulea dolens and impending venous gan-grene. If the patient has phlegmasia cerulea dolens, a fasciotomy of the calf compartments is first performed. In iliofemoral DVT, a |
Surgery_Schwartz_6678 | Surgery_Schwartz | and those with phlegmasia cerulea dolens and impending venous gan-grene. If the patient has phlegmasia cerulea dolens, a fasciotomy of the calf compartments is first performed. In iliofemoral DVT, a longitudinal venotomy is made in the common femoral vein, and a venous balloon embolectomy catheter is passed through the thrombus into the IVC and pulled back several times until no further thrombus can be extracted. The distal thrombus in the leg is removed by manual pressure beginning in the foot. This is accomplished by application of a tight rubber elastic wrap beginning at the foot and extending to the thigh. If the thrombus in the femoral vein is old and cannot be extracted, the vein may be ligated. For a thrombus that extends into the IVC, the IVC is exposed transperitoneally and controlled below the renal veins. The IVC is opened, and the thrombus is removed by gentle mas-sage. An intraoperative completion venogram determines if any residual thrombus or stenosis is present. If a | Surgery_Schwartz. and those with phlegmasia cerulea dolens and impending venous gan-grene. If the patient has phlegmasia cerulea dolens, a fasciotomy of the calf compartments is first performed. In iliofemoral DVT, a longitudinal venotomy is made in the common femoral vein, and a venous balloon embolectomy catheter is passed through the thrombus into the IVC and pulled back several times until no further thrombus can be extracted. The distal thrombus in the leg is removed by manual pressure beginning in the foot. This is accomplished by application of a tight rubber elastic wrap beginning at the foot and extending to the thigh. If the thrombus in the femoral vein is old and cannot be extracted, the vein may be ligated. For a thrombus that extends into the IVC, the IVC is exposed transperitoneally and controlled below the renal veins. The IVC is opened, and the thrombus is removed by gentle mas-sage. An intraoperative completion venogram determines if any residual thrombus or stenosis is present. If a |
Surgery_Schwartz_6679 | Surgery_Schwartz | below the renal veins. The IVC is opened, and the thrombus is removed by gentle mas-sage. An intraoperative completion venogram determines if any residual thrombus or stenosis is present. If a residual iliac vein stenosis is present, intraoperative angioplasty and stenting can be performed. In most cases, an arteriovenous fistula is then created by anastomosing the great saphenous vein (GSV) end to side with the superficial femoral artery in an effort to main-tain patency of the thrombectomized iliofemoral venous seg-ment. Heparin is administered postoperatively for several days. Warfarin anticoagulation is maintained for at least 6 months after thrombectomy. Complications of iliofemoral thrombec-tomy include PE in up to 20% of patients67 and death in <1% of patients.68One study followed 77 limbs for a mean of 8.5 years after thrombectomy for acute iliofemoral DVT. In limbs with suc-cessful thrombectomy, valvular competence in the thrombecto-mized venous segment was 80% at 5 years and | Surgery_Schwartz. below the renal veins. The IVC is opened, and the thrombus is removed by gentle mas-sage. An intraoperative completion venogram determines if any residual thrombus or stenosis is present. If a residual iliac vein stenosis is present, intraoperative angioplasty and stenting can be performed. In most cases, an arteriovenous fistula is then created by anastomosing the great saphenous vein (GSV) end to side with the superficial femoral artery in an effort to main-tain patency of the thrombectomized iliofemoral venous seg-ment. Heparin is administered postoperatively for several days. Warfarin anticoagulation is maintained for at least 6 months after thrombectomy. Complications of iliofemoral thrombec-tomy include PE in up to 20% of patients67 and death in <1% of patients.68One study followed 77 limbs for a mean of 8.5 years after thrombectomy for acute iliofemoral DVT. In limbs with suc-cessful thrombectomy, valvular competence in the thrombecto-mized venous segment was 80% at 5 years and |
Surgery_Schwartz_6680 | Surgery_Schwartz | limbs for a mean of 8.5 years after thrombectomy for acute iliofemoral DVT. In limbs with suc-cessful thrombectomy, valvular competence in the thrombecto-mized venous segment was 80% at 5 years and 56% at 10 years. More than 90% of patients had minimal or no symptoms of PTS. There were 12 (16%) early thrombectomy failures. Patients were required to wear compression stockings for at least 1 year after thrombectomy.69Survival rates for surgical pulmonary embolectomy have improved over the past 20 years with the addition of cardio-pulmonary bypass. Emergency pulmonary embolectomy for acute PE is rarely indicated. Patients with preterminal massive PE (Fig. 24-10) for whom thrombolysis has failed or who have contraindications to thrombolytics may be candidates for this procedure. Open pulmonary artery embolectomy is performed through a posterolateral thoracotomy with direct visualization of the pulmonary arteries. Mortality rates range between 20% and 40%.70-72Percutaneous catheter-based | Surgery_Schwartz. limbs for a mean of 8.5 years after thrombectomy for acute iliofemoral DVT. In limbs with suc-cessful thrombectomy, valvular competence in the thrombecto-mized venous segment was 80% at 5 years and 56% at 10 years. More than 90% of patients had minimal or no symptoms of PTS. There were 12 (16%) early thrombectomy failures. Patients were required to wear compression stockings for at least 1 year after thrombectomy.69Survival rates for surgical pulmonary embolectomy have improved over the past 20 years with the addition of cardio-pulmonary bypass. Emergency pulmonary embolectomy for acute PE is rarely indicated. Patients with preterminal massive PE (Fig. 24-10) for whom thrombolysis has failed or who have contraindications to thrombolytics may be candidates for this procedure. Open pulmonary artery embolectomy is performed through a posterolateral thoracotomy with direct visualization of the pulmonary arteries. Mortality rates range between 20% and 40%.70-72Percutaneous catheter-based |
Surgery_Schwartz_6681 | Surgery_Schwartz | artery embolectomy is performed through a posterolateral thoracotomy with direct visualization of the pulmonary arteries. Mortality rates range between 20% and 40%.70-72Percutaneous catheter-based techniques for removal of a PE involve mechanical thrombus fragmentation or embolec-tomy using suction devices. Mechanical clot fragmentation is followed by CDT. Results of catheter-based fragmentation are based on small case series. In a study in which a fragmentation device was used in 10 patients with acute massive PE, frag-mentation was successful in 7 patients with a mortality rate of 20%.73 Transvenous catheter pulmonary suction embolectomy has also been performed for acute massive PE with a reported 76% successful extraction rate and a 30-day survival of 70%.74ProphylaxisPatients who undergo major general surgical, gynecologic, urologic, and neurosurgical procedures without thrombopro-phylaxis have a significant incidence of perioperative DVT. An estimated one-third of the 150,000 to | Surgery_Schwartz. artery embolectomy is performed through a posterolateral thoracotomy with direct visualization of the pulmonary arteries. Mortality rates range between 20% and 40%.70-72Percutaneous catheter-based techniques for removal of a PE involve mechanical thrombus fragmentation or embolec-tomy using suction devices. Mechanical clot fragmentation is followed by CDT. Results of catheter-based fragmentation are based on small case series. In a study in which a fragmentation device was used in 10 patients with acute massive PE, frag-mentation was successful in 7 patients with a mortality rate of 20%.73 Transvenous catheter pulmonary suction embolectomy has also been performed for acute massive PE with a reported 76% successful extraction rate and a 30-day survival of 70%.74ProphylaxisPatients who undergo major general surgical, gynecologic, urologic, and neurosurgical procedures without thrombopro-phylaxis have a significant incidence of perioperative DVT. An estimated one-third of the 150,000 to |
Surgery_Schwartz_6682 | Surgery_Schwartz | major general surgical, gynecologic, urologic, and neurosurgical procedures without thrombopro-phylaxis have a significant incidence of perioperative DVT. An estimated one-third of the 150,000 to 200,000 VTE-related deaths per year in the United States occur following surgery.75 The goal of prophylaxis is to reduce the mortality and morbidity associated with VTE. The first manifestation of VTE may be a life-threatening PE (Fig. 24-11), and as indicated earlier, clinical evaluation to detect DVT before PE is unreliable.Effective methods of VTE prophylaxis involve the use of one or more pharmacologic or mechanical modalities. Cur-rently available pharmacologic agents include low-dose UFH, LMWH, synthetic pentasaccharides, and vitamin K antago-nists. Mechanical methods include intermittent pneumatic com-pression (IPC) and graduated compression stockings. There is insufficient evidence to consider aspirin alone as adequate DVT prophylaxis. Methods of prophylaxis vary with regard to | Surgery_Schwartz. major general surgical, gynecologic, urologic, and neurosurgical procedures without thrombopro-phylaxis have a significant incidence of perioperative DVT. An estimated one-third of the 150,000 to 200,000 VTE-related deaths per year in the United States occur following surgery.75 The goal of prophylaxis is to reduce the mortality and morbidity associated with VTE. The first manifestation of VTE may be a life-threatening PE (Fig. 24-11), and as indicated earlier, clinical evaluation to detect DVT before PE is unreliable.Effective methods of VTE prophylaxis involve the use of one or more pharmacologic or mechanical modalities. Cur-rently available pharmacologic agents include low-dose UFH, LMWH, synthetic pentasaccharides, and vitamin K antago-nists. Mechanical methods include intermittent pneumatic com-pression (IPC) and graduated compression stockings. There is insufficient evidence to consider aspirin alone as adequate DVT prophylaxis. Methods of prophylaxis vary with regard to |
Surgery_Schwartz_6683 | Surgery_Schwartz | pneumatic com-pression (IPC) and graduated compression stockings. There is insufficient evidence to consider aspirin alone as adequate DVT prophylaxis. Methods of prophylaxis vary with regard to efficacy, and the 2012 ACCP Clinical Practice Guidelines strat-ify their uses according to the patient’s level of VTE risk, bleed-ing risk, and the values and preferences of individual patients (see Table 24-3).Venous Thromboembolism Prophylaxis in Nonorthopedic Surgery. The risk for VTE associated with a surgical procedure depends on the type of operation, type of anesthesia, duration of surgery, and other risk factors, such as patient age, presence of cancer, prior VTE, obesity, presence of infection, and known thrombophilic disorders. VTE risk can be stratified according to Brunicardi_Ch24_p0981-p1008.indd 99222/02/19 3:01 PM 993VENOUS AND LYMPHATIC DISEASECHAPTER 24Figure 24-11. Computed tomography angiogram showing mul-tiple pulmonary embolisms (arrows). (Used with permission from Dr. | Surgery_Schwartz. pneumatic com-pression (IPC) and graduated compression stockings. There is insufficient evidence to consider aspirin alone as adequate DVT prophylaxis. Methods of prophylaxis vary with regard to efficacy, and the 2012 ACCP Clinical Practice Guidelines strat-ify their uses according to the patient’s level of VTE risk, bleed-ing risk, and the values and preferences of individual patients (see Table 24-3).Venous Thromboembolism Prophylaxis in Nonorthopedic Surgery. The risk for VTE associated with a surgical procedure depends on the type of operation, type of anesthesia, duration of surgery, and other risk factors, such as patient age, presence of cancer, prior VTE, obesity, presence of infection, and known thrombophilic disorders. VTE risk can be stratified according to Brunicardi_Ch24_p0981-p1008.indd 99222/02/19 3:01 PM 993VENOUS AND LYMPHATIC DISEASECHAPTER 24Figure 24-11. Computed tomography angiogram showing mul-tiple pulmonary embolisms (arrows). (Used with permission from Dr. |
Surgery_Schwartz_6684 | Surgery_Schwartz | 99222/02/19 3:01 PM 993VENOUS AND LYMPHATIC DISEASECHAPTER 24Figure 24-11. Computed tomography angiogram showing mul-tiple pulmonary embolisms (arrows). (Used with permission from Dr. Scott Ambruster.)Table 24-5Risk assessment model from the Patient Safety in Surgery StudyRISK FACTORRISK SCORE POINTSOperation type other than endocrine Respiratory and hernia Thoracoabdominal aneurysm, embolectomy/thrombectomy, venous reconstruction, and endovascular repair Aneurysm Mouth, palate Stomach, intestines Integument Hernia9744432ASA, physical status classification 3,4, or 5 2 Female sex211Work RVU >17 10–1732Two points for each of these conditions Disseminated cancer Chemotherapy for malignancy within 30 days of operation Preoperative serum sodium >145 mmol/L Transfusion >4 units packed RBCs in 72 hours before operation Ventilator dependent2One point for each of these conditions Wound class (clean/contaminated) Preoperative hematocrit ≤38% Preoperative bilirubin >1 mg/dL Dyspnea Albumin | Surgery_Schwartz. 99222/02/19 3:01 PM 993VENOUS AND LYMPHATIC DISEASECHAPTER 24Figure 24-11. Computed tomography angiogram showing mul-tiple pulmonary embolisms (arrows). (Used with permission from Dr. Scott Ambruster.)Table 24-5Risk assessment model from the Patient Safety in Surgery StudyRISK FACTORRISK SCORE POINTSOperation type other than endocrine Respiratory and hernia Thoracoabdominal aneurysm, embolectomy/thrombectomy, venous reconstruction, and endovascular repair Aneurysm Mouth, palate Stomach, intestines Integument Hernia9744432ASA, physical status classification 3,4, or 5 2 Female sex211Work RVU >17 10–1732Two points for each of these conditions Disseminated cancer Chemotherapy for malignancy within 30 days of operation Preoperative serum sodium >145 mmol/L Transfusion >4 units packed RBCs in 72 hours before operation Ventilator dependent2One point for each of these conditions Wound class (clean/contaminated) Preoperative hematocrit ≤38% Preoperative bilirubin >1 mg/dL Dyspnea Albumin |
Surgery_Schwartz_6685 | Surgery_Schwartz | in 72 hours before operation Ventilator dependent2One point for each of these conditions Wound class (clean/contaminated) Preoperative hematocrit ≤38% Preoperative bilirubin >1 mg/dL Dyspnea Albumin ≤3.5 mg/dL Emergency1Zero points for each of these conditions ASA physical class of 1 Work RVU <10 Male sex0ASA = American Society of Anesthesiologists; RBCs = red blood cells; RVU = relative value unit.Reproduced with permission from Rogers SO Jr, Kilaru RK, Hosokawa P, et al: Multivariable predictors of postoperative venous thromboembolic events after general and vascular surgery: results from the patient safety in surgery study, J Am Coll Surg. 2007 Jun;204(6):1211-1221.the previously mentioned risk assessment models, the Caprini score and Rogers score. These risk assessment models are included in the prophylaxis guidelines for nonorthopedic sur-gery (Tables 24-5 and 24-6). A composite score is created using assigned values for each risk factor. The cumulative score for each patient is | Surgery_Schwartz. in 72 hours before operation Ventilator dependent2One point for each of these conditions Wound class (clean/contaminated) Preoperative hematocrit ≤38% Preoperative bilirubin >1 mg/dL Dyspnea Albumin ≤3.5 mg/dL Emergency1Zero points for each of these conditions ASA physical class of 1 Work RVU <10 Male sex0ASA = American Society of Anesthesiologists; RBCs = red blood cells; RVU = relative value unit.Reproduced with permission from Rogers SO Jr, Kilaru RK, Hosokawa P, et al: Multivariable predictors of postoperative venous thromboembolic events after general and vascular surgery: results from the patient safety in surgery study, J Am Coll Surg. 2007 Jun;204(6):1211-1221.the previously mentioned risk assessment models, the Caprini score and Rogers score. These risk assessment models are included in the prophylaxis guidelines for nonorthopedic sur-gery (Tables 24-5 and 24-6). A composite score is created using assigned values for each risk factor. The cumulative score for each patient is |
Surgery_Schwartz_6686 | Surgery_Schwartz | in the prophylaxis guidelines for nonorthopedic sur-gery (Tables 24-5 and 24-6). A composite score is created using assigned values for each risk factor. The cumulative score for each patient is then used to predict thrombosis risk and provide recommendations regarding VTE prophylaxis.Patients at very low risk (<0.5%; Rogers score <7; Caprini score 0) who undergo general or abdominopelvic procedures do not require pharmacologic or mechanical pro-phylaxis; however, early ambulation is required. Patients at low risk (<1.5%; Rogers score 7–10; Caprini score 1–2) should receive mechanical prophylaxis. Patients at moderate risk (3%; Rogers score >10; Caprini score 3–4) should receive LMWH at recommended doses, low-dose UFH, or mechanical pro-phylaxis. Patients at high risk (6%; Caprini score ≥5) should receive LMWH at recommended doses or low-dose UFH and mechanical prophylaxis. Thromboprophylaxis should con-tinue until discharge, except in select high-risk patients with malignancy in whom | Surgery_Schwartz. in the prophylaxis guidelines for nonorthopedic sur-gery (Tables 24-5 and 24-6). A composite score is created using assigned values for each risk factor. The cumulative score for each patient is then used to predict thrombosis risk and provide recommendations regarding VTE prophylaxis.Patients at very low risk (<0.5%; Rogers score <7; Caprini score 0) who undergo general or abdominopelvic procedures do not require pharmacologic or mechanical pro-phylaxis; however, early ambulation is required. Patients at low risk (<1.5%; Rogers score 7–10; Caprini score 1–2) should receive mechanical prophylaxis. Patients at moderate risk (3%; Rogers score >10; Caprini score 3–4) should receive LMWH at recommended doses, low-dose UFH, or mechanical pro-phylaxis. Patients at high risk (6%; Caprini score ≥5) should receive LMWH at recommended doses or low-dose UFH and mechanical prophylaxis. Thromboprophylaxis should con-tinue until discharge, except in select high-risk patients with malignancy in whom |
Surgery_Schwartz_6687 | Surgery_Schwartz | should receive LMWH at recommended doses or low-dose UFH and mechanical prophylaxis. Thromboprophylaxis should con-tinue until discharge, except in select high-risk patients with malignancy in whom extended-duration prophylaxis (up to 4–6 weeks) may be beneficial. Patients with significant risk for bleeding should receive mechanical prophylaxis until this risk subsides.75Overall, low-dose UFH and LMWH reduce the risk for symptomatic and asymptomatic VTE by 60% to 70%. The risks for bleeding differ, depending on the dosage. Lower dosages of LMWH appear to be associated with less bleeding risk than low-dose UFH, but the latter produces less bleeding risk than higher prophylactic dosages of LMWH.76 Other advantages of LMWH include once-daily dosing protocols and a lower rate of heparin-associated antibody formation.Fondaparinux has been compared with the LMWH dalte-parin in patients who undergo high-risk major abdominal sur-gery. It also has been compared with IPC alone in patients | Surgery_Schwartz. should receive LMWH at recommended doses or low-dose UFH and mechanical prophylaxis. Thromboprophylaxis should con-tinue until discharge, except in select high-risk patients with malignancy in whom extended-duration prophylaxis (up to 4–6 weeks) may be beneficial. Patients with significant risk for bleeding should receive mechanical prophylaxis until this risk subsides.75Overall, low-dose UFH and LMWH reduce the risk for symptomatic and asymptomatic VTE by 60% to 70%. The risks for bleeding differ, depending on the dosage. Lower dosages of LMWH appear to be associated with less bleeding risk than low-dose UFH, but the latter produces less bleeding risk than higher prophylactic dosages of LMWH.76 Other advantages of LMWH include once-daily dosing protocols and a lower rate of heparin-associated antibody formation.Fondaparinux has been compared with the LMWH dalte-parin in patients who undergo high-risk major abdominal sur-gery. It also has been compared with IPC alone in patients |
Surgery_Schwartz_6688 | Surgery_Schwartz | antibody formation.Fondaparinux has been compared with the LMWH dalte-parin in patients who undergo high-risk major abdominal sur-gery. It also has been compared with IPC alone in patients undergoing non–high-risk abdominal surgery.77,78 Fondaparinux demonstrated rates of VTE prevention, bleeding complications, and mortality similar to those of LMWH. It was more beneficial than IPC alone in reducing VTE but with a higher rate of bleed-ing (1.6% vs. 0.2%).Prophylactic insertion of IVC filters has been suggested for VTE prophylaxis in high-risk trauma patients, bariatric surgical patients, and some patients with malignancy who have contraindications for LMWH therapy.79 A 5-year study of prophylactic IVC filter placement in 132 trauma patients at high risk of PE (head injury, spinal cord injury, pelvic or Brunicardi_Ch24_p0981-p1008.indd 99322/02/19 3:01 PM 994SPECIFIC CONSIDERATIONSPART IITable 24-6Caprini risk assessment model1 POINT2 POINTS3 POINTS5 POINTSAge 41–60Age 61–74Age | Surgery_Schwartz. antibody formation.Fondaparinux has been compared with the LMWH dalte-parin in patients who undergo high-risk major abdominal sur-gery. It also has been compared with IPC alone in patients undergoing non–high-risk abdominal surgery.77,78 Fondaparinux demonstrated rates of VTE prevention, bleeding complications, and mortality similar to those of LMWH. It was more beneficial than IPC alone in reducing VTE but with a higher rate of bleed-ing (1.6% vs. 0.2%).Prophylactic insertion of IVC filters has been suggested for VTE prophylaxis in high-risk trauma patients, bariatric surgical patients, and some patients with malignancy who have contraindications for LMWH therapy.79 A 5-year study of prophylactic IVC filter placement in 132 trauma patients at high risk of PE (head injury, spinal cord injury, pelvic or Brunicardi_Ch24_p0981-p1008.indd 99322/02/19 3:01 PM 994SPECIFIC CONSIDERATIONSPART IITable 24-6Caprini risk assessment model1 POINT2 POINTS3 POINTS5 POINTSAge 41–60Age 61–74Age |
Surgery_Schwartz_6689 | Surgery_Schwartz | injury, pelvic or Brunicardi_Ch24_p0981-p1008.indd 99322/02/19 3:01 PM 994SPECIFIC CONSIDERATIONSPART IITable 24-6Caprini risk assessment model1 POINT2 POINTS3 POINTS5 POINTSAge 41–60Age 61–74Age ≥75Stroke (<1 month)Minor surgeryArthroscopic surgeryHistory of VTEElective arthroplastyBMI >25 kg/m2Major open surgery (> 45 minutes)Family history of VTEHip, pelvis, or leg fractureSwollen legsLaparoscopic surgery (> 45 minutes)Factor V LeidenAcute spinal cord injury (<1 month)Varicose veinsMalignancyProthrombin 20210A Pregnancy or postpartumConfined to bed (>72 hours)Lupus anticoagulant History of unexplained or recurrent spontaneous abortionImmobilizing plaster castAnticardiolipin antibody Oral contraceptives of hormone replacementCentral venous accessElevated serum homocysteine Sepsis (<1 month) Heparin-induced thrombocytopenia Serious lung disease, including pneumonia (<1 month) Other congenital or acquired thrombophilia Abnormal pulmonary function test Acute myocardial | Surgery_Schwartz. injury, pelvic or Brunicardi_Ch24_p0981-p1008.indd 99322/02/19 3:01 PM 994SPECIFIC CONSIDERATIONSPART IITable 24-6Caprini risk assessment model1 POINT2 POINTS3 POINTS5 POINTSAge 41–60Age 61–74Age ≥75Stroke (<1 month)Minor surgeryArthroscopic surgeryHistory of VTEElective arthroplastyBMI >25 kg/m2Major open surgery (> 45 minutes)Family history of VTEHip, pelvis, or leg fractureSwollen legsLaparoscopic surgery (> 45 minutes)Factor V LeidenAcute spinal cord injury (<1 month)Varicose veinsMalignancyProthrombin 20210A Pregnancy or postpartumConfined to bed (>72 hours)Lupus anticoagulant History of unexplained or recurrent spontaneous abortionImmobilizing plaster castAnticardiolipin antibody Oral contraceptives of hormone replacementCentral venous accessElevated serum homocysteine Sepsis (<1 month) Heparin-induced thrombocytopenia Serious lung disease, including pneumonia (<1 month) Other congenital or acquired thrombophilia Abnormal pulmonary function test Acute myocardial |
Surgery_Schwartz_6690 | Surgery_Schwartz | (<1 month) Heparin-induced thrombocytopenia Serious lung disease, including pneumonia (<1 month) Other congenital or acquired thrombophilia Abnormal pulmonary function test Acute myocardial infarction Congestive heart failure History of inflammatory bowel disease Medical patient at bed rest BMI = body mass index; VTE = venous thromboembolism.Data from Bahl V, Hu HM, Henke PK, et al: A validation study of retrospective venous thromboembolism risk scoring method, Ann Surg. 2010 Feb; 251(2):344-350.long bone fractures) reported a 0% incidence of symptom-atic PE in patients with a correctly positioned IVC filter.80 In 47 patients with a malpositioned IVC filter (strut malposition or filter tilt), there was a 6.3% incidence of symptomatic PE with three deaths. DVT occurred at the insertion site in 3.1% of the patients. IVC patency was 97.1% at 3 years.Fatal and nonfatal PE can still occur in patients with vena cava interruption. As noted earlier, long-term complications | Surgery_Schwartz. (<1 month) Heparin-induced thrombocytopenia Serious lung disease, including pneumonia (<1 month) Other congenital or acquired thrombophilia Abnormal pulmonary function test Acute myocardial infarction Congestive heart failure History of inflammatory bowel disease Medical patient at bed rest BMI = body mass index; VTE = venous thromboembolism.Data from Bahl V, Hu HM, Henke PK, et al: A validation study of retrospective venous thromboembolism risk scoring method, Ann Surg. 2010 Feb; 251(2):344-350.long bone fractures) reported a 0% incidence of symptom-atic PE in patients with a correctly positioned IVC filter.80 In 47 patients with a malpositioned IVC filter (strut malposition or filter tilt), there was a 6.3% incidence of symptomatic PE with three deaths. DVT occurred at the insertion site in 3.1% of the patients. IVC patency was 97.1% at 3 years.Fatal and nonfatal PE can still occur in patients with vena cava interruption. As noted earlier, long-term complications |
Surgery_Schwartz_6691 | Surgery_Schwartz | the insertion site in 3.1% of the patients. IVC patency was 97.1% at 3 years.Fatal and nonfatal PE can still occur in patients with vena cava interruption. As noted earlier, long-term complications associated with permanent IVC filters include IVC thrombo-sis and DVT. Currently, the ACCP recommends IVC filters be placed only if a proximal DVT is present and anticoagula-tion therapy is contraindicated. Placement of an IVC filter in the setting of severe pulmonary embolism development while anticoagulated remains controversial. IVC filter insertion is not recommended for primary prophylaxis.75Removable IVC filters may be placed in patients with a temporarily increased risk of PE.81 The best patient groups for retrievable filter placement may include young trauma patients with transient immobility, patients undergoing surgi-cal procedures associated with a high risk of PE, and patients with hypercoagulable states who cannot receive anticoagula-tion therapy for a short period of time. | Surgery_Schwartz. the insertion site in 3.1% of the patients. IVC patency was 97.1% at 3 years.Fatal and nonfatal PE can still occur in patients with vena cava interruption. As noted earlier, long-term complications associated with permanent IVC filters include IVC thrombo-sis and DVT. Currently, the ACCP recommends IVC filters be placed only if a proximal DVT is present and anticoagula-tion therapy is contraindicated. Placement of an IVC filter in the setting of severe pulmonary embolism development while anticoagulated remains controversial. IVC filter insertion is not recommended for primary prophylaxis.75Removable IVC filters may be placed in patients with a temporarily increased risk of PE.81 The best patient groups for retrievable filter placement may include young trauma patients with transient immobility, patients undergoing surgi-cal procedures associated with a high risk of PE, and patients with hypercoagulable states who cannot receive anticoagula-tion therapy for a short period of time. |
Surgery_Schwartz_6692 | Surgery_Schwartz | patients undergoing surgi-cal procedures associated with a high risk of PE, and patients with hypercoagulable states who cannot receive anticoagula-tion therapy for a short period of time. Careful follow-up is required to assure all potentially removable filters are in fact removed.OTHER VENOUS THROMBOTIC DISORDERSSuperficial Vein ThrombophlebitisSuperficial vein thrombophlebitis (SVT) most commonly occurs in varicose veins but can occur in normal veins. When SVT recurs at variable sites in normal superficial veins, thrombophlebitis migrans, it may signify a hidden visceral malignancy or a systemic disorder such as a blood dyscrasia and/or a collagen vascular disease. SVT also frequently occurs as a complication of indwelling catheters, with or without asso-ciated extravasation of injected material. Upper extremity vein thrombosis has been reported to occur in 38% of patients with peripherally inserted central catheters; 57% of these developed in the cephalic vein (Fig. 24-12).82 | Surgery_Schwartz. patients undergoing surgi-cal procedures associated with a high risk of PE, and patients with hypercoagulable states who cannot receive anticoagula-tion therapy for a short period of time. Careful follow-up is required to assure all potentially removable filters are in fact removed.OTHER VENOUS THROMBOTIC DISORDERSSuperficial Vein ThrombophlebitisSuperficial vein thrombophlebitis (SVT) most commonly occurs in varicose veins but can occur in normal veins. When SVT recurs at variable sites in normal superficial veins, thrombophlebitis migrans, it may signify a hidden visceral malignancy or a systemic disorder such as a blood dyscrasia and/or a collagen vascular disease. SVT also frequently occurs as a complication of indwelling catheters, with or without asso-ciated extravasation of injected material. Upper extremity vein thrombosis has been reported to occur in 38% of patients with peripherally inserted central catheters; 57% of these developed in the cephalic vein (Fig. 24-12).82 |
Surgery_Schwartz_6693 | Surgery_Schwartz | material. Upper extremity vein thrombosis has been reported to occur in 38% of patients with peripherally inserted central catheters; 57% of these developed in the cephalic vein (Fig. 24-12).82 Suppurative SVT may occur in veins with indwelling catheters and may be associated with generalized sepsis.Clinical signs of SVT include redness, warmth, and ten-derness along the distribution of the affected veins, often asso-ciated with a palpable cord. Patients with suppurative SVT may have fever and leukocytosis. DUS should be performed in patients with signs and symptoms of acute SVT to confirm the diagnosis and to determine if any associated DVT is present. Concomitant lower extremity DVT may be present in 5% to 40% of patients with SVT; most occur in patients with greater Brunicardi_Ch24_p0981-p1008.indd 99422/02/19 3:01 PM 995VENOUS AND LYMPHATIC DISEASECHAPTER 24Figure 24-12. Duplex ultrasound of a brachial vein containing thrombus and percutaneously inserted central catheter | Surgery_Schwartz. material. Upper extremity vein thrombosis has been reported to occur in 38% of patients with peripherally inserted central catheters; 57% of these developed in the cephalic vein (Fig. 24-12).82 Suppurative SVT may occur in veins with indwelling catheters and may be associated with generalized sepsis.Clinical signs of SVT include redness, warmth, and ten-derness along the distribution of the affected veins, often asso-ciated with a palpable cord. Patients with suppurative SVT may have fever and leukocytosis. DUS should be performed in patients with signs and symptoms of acute SVT to confirm the diagnosis and to determine if any associated DVT is present. Concomitant lower extremity DVT may be present in 5% to 40% of patients with SVT; most occur in patients with greater Brunicardi_Ch24_p0981-p1008.indd 99422/02/19 3:01 PM 995VENOUS AND LYMPHATIC DISEASECHAPTER 24Figure 24-12. Duplex ultrasound of a brachial vein containing thrombus and percutaneously inserted central catheter |
Surgery_Schwartz_6694 | Surgery_Schwartz | 99422/02/19 3:01 PM 995VENOUS AND LYMPHATIC DISEASECHAPTER 24Figure 24-12. Duplex ultrasound of a brachial vein containing thrombus and percutaneously inserted central catheter (PICC).Figure 24-13. Upper extremity venogram showing stenosis of the right subclavian vein at the first rib (arrow).saphenous vein SVT within 1 cm of the saphenofemoral junction. A follow-up DUS should be performed in 5 to 7 days in patients with SVT in the proximal GSV but without deep vein involvement. Approximately 10% to 20% of patients with SVT involving the proximal GSV experience progression to deep venous involvement within 1 week.83,84Treatment of SVT is quite variable. A Cochrane Review reported that LMWHs and nonsteroidal anti-inflammatory drugs both reduce the rate of SVT extension or recurrence.85 Addi-tionally, a multicenter, randomized, blinded trial comparing use of fondaparinux to placebo in lower extremity SVT found use of fondaparinux reduced the rate of VTE formation by 85%, though the | Surgery_Schwartz. 99422/02/19 3:01 PM 995VENOUS AND LYMPHATIC DISEASECHAPTER 24Figure 24-12. Duplex ultrasound of a brachial vein containing thrombus and percutaneously inserted central catheter (PICC).Figure 24-13. Upper extremity venogram showing stenosis of the right subclavian vein at the first rib (arrow).saphenous vein SVT within 1 cm of the saphenofemoral junction. A follow-up DUS should be performed in 5 to 7 days in patients with SVT in the proximal GSV but without deep vein involvement. Approximately 10% to 20% of patients with SVT involving the proximal GSV experience progression to deep venous involvement within 1 week.83,84Treatment of SVT is quite variable. A Cochrane Review reported that LMWHs and nonsteroidal anti-inflammatory drugs both reduce the rate of SVT extension or recurrence.85 Addi-tionally, a multicenter, randomized, blinded trial comparing use of fondaparinux to placebo in lower extremity SVT found use of fondaparinux reduced the rate of VTE formation by 85%, though the |
Surgery_Schwartz_6695 | Surgery_Schwartz | Addi-tionally, a multicenter, randomized, blinded trial comparing use of fondaparinux to placebo in lower extremity SVT found use of fondaparinux reduced the rate of VTE formation by 85%, though the incidence of VTE formation was low in both groups (0.2% vs. 1.3%, P <.001). The number needed to treat to prevent one episode of VTE was 88 patients. There was no difference in mortality between the two arms of the trial.85Topical medications appear to improve local symptoms. Surgical treatment, combined with the use of graduated com-pression stockings, is associated with a lower rate of VTE and SVT progression.86 The treatment is individualized and depends on the location of the thrombus and the severity of symptoms. In patients with SVT not within 1 cm of the saphenofemoral junction, treatment consists of compression and administra-tion of an anti-inflammatory medication such as indomethacin. In patients with suppurative SVT, antibiotics and removal of any existing indwelling catheters | Surgery_Schwartz. Addi-tionally, a multicenter, randomized, blinded trial comparing use of fondaparinux to placebo in lower extremity SVT found use of fondaparinux reduced the rate of VTE formation by 85%, though the incidence of VTE formation was low in both groups (0.2% vs. 1.3%, P <.001). The number needed to treat to prevent one episode of VTE was 88 patients. There was no difference in mortality between the two arms of the trial.85Topical medications appear to improve local symptoms. Surgical treatment, combined with the use of graduated com-pression stockings, is associated with a lower rate of VTE and SVT progression.86 The treatment is individualized and depends on the location of the thrombus and the severity of symptoms. In patients with SVT not within 1 cm of the saphenofemoral junction, treatment consists of compression and administra-tion of an anti-inflammatory medication such as indomethacin. In patients with suppurative SVT, antibiotics and removal of any existing indwelling catheters |
Surgery_Schwartz_6696 | Surgery_Schwartz | consists of compression and administra-tion of an anti-inflammatory medication such as indomethacin. In patients with suppurative SVT, antibiotics and removal of any existing indwelling catheters are mandatory. Excision of the vein may be necessary but is usually reserved for patients with systemic symptoms or when excision of the involved vein is straightforward. If the SVT extends proximally to within 1 cm of the saphenofemoral junction, extension into the com-mon femoral vein is more likely to occur. In these patients, anticoagulation therapy for 6 weeks and GSV ligation appear equally effective in preventing thrombus extension into the deep venous system.87,88Upper Extremity Vein ThrombosisAxillary-subclavian venous thrombosis (ASVT) is classified into two forms. Primary ASVT occurs in only a small minority of all patients with ASVT. In the primary form, no clear cause for the thrombosis is readily identifiable at initial evaluation. Patients with primary ASVT often give a | Surgery_Schwartz. consists of compression and administra-tion of an anti-inflammatory medication such as indomethacin. In patients with suppurative SVT, antibiotics and removal of any existing indwelling catheters are mandatory. Excision of the vein may be necessary but is usually reserved for patients with systemic symptoms or when excision of the involved vein is straightforward. If the SVT extends proximally to within 1 cm of the saphenofemoral junction, extension into the com-mon femoral vein is more likely to occur. In these patients, anticoagulation therapy for 6 weeks and GSV ligation appear equally effective in preventing thrombus extension into the deep venous system.87,88Upper Extremity Vein ThrombosisAxillary-subclavian venous thrombosis (ASVT) is classified into two forms. Primary ASVT occurs in only a small minority of all patients with ASVT. In the primary form, no clear cause for the thrombosis is readily identifiable at initial evaluation. Patients with primary ASVT often give a |
Surgery_Schwartz_6697 | Surgery_Schwartz | in only a small minority of all patients with ASVT. In the primary form, no clear cause for the thrombosis is readily identifiable at initial evaluation. Patients with primary ASVT often give a history of performing prolonged, repetitive motion activities, which results in damage to the subclavian vein, usually where it passes between the head of the clavicle and the first rib in association with the subclavius muscle. This condition is also known as venous thoracic outlet syndrome, effort thrombosis, and Paget-Schroetter syndrome. Secondary ASVT is more common and is associated with an easily identified cause such as an indwelling catheter or a hyper-coagulable state. Over 30% of patients with tunneled subclavian vein access devices develop ASVT.89A patient with ASVT may be asymptomatic or may pres-ent with varying degrees of upper extremity edema, tenderness, and conspicuous superficial venous enlargement. DUS can be performed initially to confirm the diagnosis, but limitations to | Surgery_Schwartz. in only a small minority of all patients with ASVT. In the primary form, no clear cause for the thrombosis is readily identifiable at initial evaluation. Patients with primary ASVT often give a history of performing prolonged, repetitive motion activities, which results in damage to the subclavian vein, usually where it passes between the head of the clavicle and the first rib in association with the subclavius muscle. This condition is also known as venous thoracic outlet syndrome, effort thrombosis, and Paget-Schroetter syndrome. Secondary ASVT is more common and is associated with an easily identified cause such as an indwelling catheter or a hyper-coagulable state. Over 30% of patients with tunneled subclavian vein access devices develop ASVT.89A patient with ASVT may be asymptomatic or may pres-ent with varying degrees of upper extremity edema, tenderness, and conspicuous superficial venous enlargement. DUS can be performed initially to confirm the diagnosis, but limitations to |
Surgery_Schwartz_6698 | Surgery_Schwartz | or may pres-ent with varying degrees of upper extremity edema, tenderness, and conspicuous superficial venous enlargement. DUS can be performed initially to confirm the diagnosis, but limitations to the exam by the clavicle and collateralization can lead to a false-negative study. Venography is recommended when there is nonconcordance between the duplex study and clinical suspi-cion. Anticoagulation therapy should be initiated once ASVT is diagnosed to prevent PE and decrease symptoms.Treatment of patients with primary upper extremity venous thrombosis is controversial because the natural history of the disease may vary from minimal to no symptoms to significant symptoms with vigorous upper extremity activities. In recent years, patients presenting with acute symptomatic primary ASVT are often considered candidates for CDT therapy with the goal of minimizing long-term symptoms of venous congestion. Venography is performed through a catheter placed using an ultrasound-guided | Surgery_Schwartz. or may pres-ent with varying degrees of upper extremity edema, tenderness, and conspicuous superficial venous enlargement. DUS can be performed initially to confirm the diagnosis, but limitations to the exam by the clavicle and collateralization can lead to a false-negative study. Venography is recommended when there is nonconcordance between the duplex study and clinical suspi-cion. Anticoagulation therapy should be initiated once ASVT is diagnosed to prevent PE and decrease symptoms.Treatment of patients with primary upper extremity venous thrombosis is controversial because the natural history of the disease may vary from minimal to no symptoms to significant symptoms with vigorous upper extremity activities. In recent years, patients presenting with acute symptomatic primary ASVT are often considered candidates for CDT therapy with the goal of minimizing long-term symptoms of venous congestion. Venography is performed through a catheter placed using an ultrasound-guided |
Surgery_Schwartz_6699 | Surgery_Schwartz | ASVT are often considered candidates for CDT therapy with the goal of minimizing long-term symptoms of venous congestion. Venography is performed through a catheter placed using an ultrasound-guided percutaneous basilic vein approach to docu-ment the extent of the thrombus (Fig. 24-13). A guidewire is traversed through the thrombus, and a catheter is placed within the thrombus. Typically, tissue plasminogen activator is admin-istered through a multi–side-hole infusion catheter. Various catheter-based mechanical techniques may also be employed to speed thrombus removal. Heparin is administered concurrently with the thrombolytic infusion. After completion of thrombo-lytic therapy, a follow-up venogram is obtained. Correctable anatomic abnormalities may then be considered for treatment. Adjuvant procedures after thrombolytic therapy may include Brunicardi_Ch24_p0981-p1008.indd 99522/02/19 3:01 PM 996SPECIFIC CONSIDERATIONSPART IIcervical or first rib resection for thoracic outlet | Surgery_Schwartz. ASVT are often considered candidates for CDT therapy with the goal of minimizing long-term symptoms of venous congestion. Venography is performed through a catheter placed using an ultrasound-guided percutaneous basilic vein approach to docu-ment the extent of the thrombus (Fig. 24-13). A guidewire is traversed through the thrombus, and a catheter is placed within the thrombus. Typically, tissue plasminogen activator is admin-istered through a multi–side-hole infusion catheter. Various catheter-based mechanical techniques may also be employed to speed thrombus removal. Heparin is administered concurrently with the thrombolytic infusion. After completion of thrombo-lytic therapy, a follow-up venogram is obtained. Correctable anatomic abnormalities may then be considered for treatment. Adjuvant procedures after thrombolytic therapy may include Brunicardi_Ch24_p0981-p1008.indd 99522/02/19 3:01 PM 996SPECIFIC CONSIDERATIONSPART IIcervical or first rib resection for thoracic outlet |
Surgery_Schwartz_6700 | Surgery_Schwartz | procedures after thrombolytic therapy may include Brunicardi_Ch24_p0981-p1008.indd 99522/02/19 3:01 PM 996SPECIFIC CONSIDERATIONSPART IIcervical or first rib resection for thoracic outlet abnormalities, scalenectomy, surgical venous reconstruction, and balloon angioplasty of residual venous stenosis.90 The ACCP guidelines recommend the same intensity and duration of anticoagulant therapy in patients who undergo thrombolysis as in patients who are treated with anticoagulation alone.Mesenteric Vein ThrombosisFive percent to 15% of cases of acute mesenteric ischemia occur as a result of mesenteric vein thrombosis (MVT). Mortality rates in patients with MVT may approach 50%.91 The usual present-ing symptom is nonspecific abdominal pain and distention, often accompanied by nausea, vomiting, and diarrhea.92 Perito-neal signs, suggesting intestinal infarction, are present in fewer than half of MVT patients. MVT is more common in patients with a hypercoagulable states, malignancy, and | Surgery_Schwartz. procedures after thrombolytic therapy may include Brunicardi_Ch24_p0981-p1008.indd 99522/02/19 3:01 PM 996SPECIFIC CONSIDERATIONSPART IIcervical or first rib resection for thoracic outlet abnormalities, scalenectomy, surgical venous reconstruction, and balloon angioplasty of residual venous stenosis.90 The ACCP guidelines recommend the same intensity and duration of anticoagulant therapy in patients who undergo thrombolysis as in patients who are treated with anticoagulation alone.Mesenteric Vein ThrombosisFive percent to 15% of cases of acute mesenteric ischemia occur as a result of mesenteric vein thrombosis (MVT). Mortality rates in patients with MVT may approach 50%.91 The usual present-ing symptom is nonspecific abdominal pain and distention, often accompanied by nausea, vomiting, and diarrhea.92 Perito-neal signs, suggesting intestinal infarction, are present in fewer than half of MVT patients. MVT is more common in patients with a hypercoagulable states, malignancy, and |
Surgery_Schwartz_6701 | Surgery_Schwartz | and diarrhea.92 Perito-neal signs, suggesting intestinal infarction, are present in fewer than half of MVT patients. MVT is more common in patients with a hypercoagulable states, malignancy, and cirrhosis. MVT also occurs as a rare complication of laparoscopic surgery.92,93Most cases of MVT are diagnosed with contrast-enhanced CT scanning or magnetic resonance imaging (MRI) in the course of an evaluation for abdominal pain. The sensitivity and speci-ficity for CT and MRI approach 100% and 98%, respectively.94 Ultrasound can also be used and has reported sensitivity and specificity of 93% and 99%, respectively.Patients with MVT are treated with fluid resuscitation, heparin anticoagulation, and bowel rest. Once the patient’s clinical status improves, oral intake can be carefully started. The patient is transitioned to oral anticoagulation over 3 to 4 days and, depending on the etiology of the MVT, continued for 3 to 6 months or indefinitely. Most patients with MVT can be treated | Surgery_Schwartz. and diarrhea.92 Perito-neal signs, suggesting intestinal infarction, are present in fewer than half of MVT patients. MVT is more common in patients with a hypercoagulable states, malignancy, and cirrhosis. MVT also occurs as a rare complication of laparoscopic surgery.92,93Most cases of MVT are diagnosed with contrast-enhanced CT scanning or magnetic resonance imaging (MRI) in the course of an evaluation for abdominal pain. The sensitivity and speci-ficity for CT and MRI approach 100% and 98%, respectively.94 Ultrasound can also be used and has reported sensitivity and specificity of 93% and 99%, respectively.Patients with MVT are treated with fluid resuscitation, heparin anticoagulation, and bowel rest. Once the patient’s clinical status improves, oral intake can be carefully started. The patient is transitioned to oral anticoagulation over 3 to 4 days and, depending on the etiology of the MVT, continued for 3 to 6 months or indefinitely. Most patients with MVT can be treated |
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