id
stringlengths 14
28
| title
stringclasses 18
values | content
stringlengths 2
999
| contents
stringlengths 19
1.02k
|
|---|---|---|---|
Surgery_Schwartz_6702 | Surgery_Schwartz | 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 nonoperatively, but urgent laparotomy is indicated in patients with peritoneal findings. Broad-spectrum antibiotics are admin-istered perioperatively. Operative findings consist of edema and cyanotic discoloration of the mesentery and bowel wall. In more advanced cases, thrombus involves the distal mesenteric veins. The arterial supply to the involved bowel is usually intact. Nonviable bowel is resected, and primary anastomosis can be performed. If the viability of the remaining bowel is in question, a second-look operation is performed within 24 to 48 hours.VARICOSE VEINSVaricose veins are common and are present in at least 10% of the general population.95 The findings of varicose veins may include dilated and tortuous veins, telangiectasias, and fine reticular varicosities. Risk factors for | Surgery_Schwartz. 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 nonoperatively, but urgent laparotomy is indicated in patients with peritoneal findings. Broad-spectrum antibiotics are admin-istered perioperatively. Operative findings consist of edema and cyanotic discoloration of the mesentery and bowel wall. In more advanced cases, thrombus involves the distal mesenteric veins. The arterial supply to the involved bowel is usually intact. Nonviable bowel is resected, and primary anastomosis can be performed. If the viability of the remaining bowel is in question, a second-look operation is performed within 24 to 48 hours.VARICOSE VEINSVaricose veins are common and are present in at least 10% of the general population.95 The findings of varicose veins may include dilated and tortuous veins, telangiectasias, and fine reticular varicosities. Risk factors for |
Surgery_Schwartz_6703 | Surgery_Schwartz | and are present in at least 10% of the general population.95 The findings of varicose veins may include dilated and tortuous veins, telangiectasias, and fine reticular varicosities. Risk factors for varicose veins include obesity, female sex, inactivity, and family history.96 Varicose veins can be classified as primary or secondary. Primary vari-cose veins result from intrinsic abnormalities of the venous wall, whereas secondary varicose veins are associated with deep and/or superficial venous insufficiency.Patients with varicose veins may complain of unsightly appearance, aching, heaviness, pruritus, and early fatigue of the affected leg. These symptoms worsen with prolonged standing and sitting and are relieved by elevation of the leg above the level of the heart. A mild amount of edema is often present. More severe signs include thrombophlebitis, hyperpigmentation, lipodermato-sclerosis, ulceration, and bleeding from attenuated vein clusters.An important component of treatment for | Surgery_Schwartz. and are present in at least 10% of the general population.95 The findings of varicose veins may include dilated and tortuous veins, telangiectasias, and fine reticular varicosities. Risk factors for varicose veins include obesity, female sex, inactivity, and family history.96 Varicose veins can be classified as primary or secondary. Primary vari-cose veins result from intrinsic abnormalities of the venous wall, whereas secondary varicose veins are associated with deep and/or superficial venous insufficiency.Patients with varicose veins may complain of unsightly appearance, aching, heaviness, pruritus, and early fatigue of the affected leg. These symptoms worsen with prolonged standing and sitting and are relieved by elevation of the leg above the level of the heart. A mild amount of edema is often present. More severe signs include thrombophlebitis, hyperpigmentation, lipodermato-sclerosis, ulceration, and bleeding from attenuated vein clusters.An important component of treatment for |
Surgery_Schwartz_6704 | Surgery_Schwartz | is often present. More severe signs include thrombophlebitis, hyperpigmentation, lipodermato-sclerosis, ulceration, and bleeding from attenuated vein clusters.An important component of treatment for patients with vari-cose veins is the use of elastic compression stockings. Patients may be prescribed elastic stockings with compression ranging from 20 to 30, 30 to 40, or even 40 to 50 mmHg. Stockings range in length from knee high to waist high, and they should cover the symptomatic varices. Elastic compression provides sufficient relief of symptoms in many symptomatic patients.Cosmetic concerns may lead to intervention. Addition-ally, interventions are warranted in patients whose symptoms worsen or are unrelieved despite compression therapy or who have lipodermatosclerosis or venous ulcer. Randomized trials of symptomatic patients with varicose veins have demonstrated improved quality of life with interventional treatment. Interven-tional management includes injection sclerotherapy, | Surgery_Schwartz. is often present. More severe signs include thrombophlebitis, hyperpigmentation, lipodermato-sclerosis, ulceration, and bleeding from attenuated vein clusters.An important component of treatment for patients with vari-cose veins is the use of elastic compression stockings. Patients may be prescribed elastic stockings with compression ranging from 20 to 30, 30 to 40, or even 40 to 50 mmHg. Stockings range in length from knee high to waist high, and they should cover the symptomatic varices. Elastic compression provides sufficient relief of symptoms in many symptomatic patients.Cosmetic concerns may lead to intervention. Addition-ally, interventions are warranted in patients whose symptoms worsen or are unrelieved despite compression therapy or who have lipodermatosclerosis or venous ulcer. Randomized trials of symptomatic patients with varicose veins have demonstrated improved quality of life with interventional treatment. Interven-tional management includes injection sclerotherapy, |
Surgery_Schwartz_6705 | Surgery_Schwartz | Randomized trials of symptomatic patients with varicose veins have demonstrated improved quality of life with interventional treatment. Interven-tional management includes injection sclerotherapy, thermal ablation, surgical therapy, or a combination of these techniques. Injection sclerotherapy alone can be successful in varicose veins and in telangiectatic vessels. A recent multicenter, randomized trial compared foam sclerotherapy versus placebo for symp-tomatic varicose veins found significant symptom relief and improved cosmetic appearance with sclerotherapy.97 Sclero-therapy acts by destroying the venous endothelium. Scleros-ing agents include hypertonic saline, sodium tetradecyl sulfate, and polidocanol. Concentrations of 11.7% to 23.4% hypertonic saline, 0.125% to 0.250% sodium tetradecyl sulfate, and 0.5% polidocanol are used for telangiectasias. Larger varicose veins require higher concentrations: 23.4% hypertonic saline, 0.50% to 1% sodium tetradecyl sulfate, and 0.75% to 1.0% | Surgery_Schwartz. Randomized trials of symptomatic patients with varicose veins have demonstrated improved quality of life with interventional treatment. Interven-tional management includes injection sclerotherapy, thermal ablation, surgical therapy, or a combination of these techniques. Injection sclerotherapy alone can be successful in varicose veins and in telangiectatic vessels. A recent multicenter, randomized trial compared foam sclerotherapy versus placebo for symp-tomatic varicose veins found significant symptom relief and improved cosmetic appearance with sclerotherapy.97 Sclero-therapy acts by destroying the venous endothelium. Scleros-ing agents include hypertonic saline, sodium tetradecyl sulfate, and polidocanol. Concentrations of 11.7% to 23.4% hypertonic saline, 0.125% to 0.250% sodium tetradecyl sulfate, and 0.5% polidocanol are used for telangiectasias. Larger varicose veins require higher concentrations: 23.4% hypertonic saline, 0.50% to 1% sodium tetradecyl sulfate, and 0.75% to 1.0% |
Surgery_Schwartz_6706 | Surgery_Schwartz | sulfate, and 0.5% polidocanol are used for telangiectasias. Larger varicose veins require higher concentrations: 23.4% hypertonic saline, 0.50% to 1% sodium tetradecyl sulfate, and 0.75% to 1.0% polidocanol.92 Elastic bandages are wrapped around the leg after injection and worn continuously for 3 to 5 days to produce apposition of the inflamed vein walls and prevent thrombus formation. After the bandages are removed, elastic compression stockings should be worn for a minimum of 2 weeks. Complications from sclero-therapy include allergic reaction, local hyperpigmentation, thrombophlebitis, DVT, and possible skin necrosis.Newer devices combine sclerotherapy with catheter-based mechanical endoluminal injury to achieve nonthermal ablation.98 Additional nonthermal, nonsclerosant ablative techniques using proprietary adhesive formulations with cyanoacrylate are current being evaluated and have demonstrated promising early results.99Patients with symptomatic GSV or SSV reflux may be treated | Surgery_Schwartz. sulfate, and 0.5% polidocanol are used for telangiectasias. Larger varicose veins require higher concentrations: 23.4% hypertonic saline, 0.50% to 1% sodium tetradecyl sulfate, and 0.75% to 1.0% polidocanol.92 Elastic bandages are wrapped around the leg after injection and worn continuously for 3 to 5 days to produce apposition of the inflamed vein walls and prevent thrombus formation. After the bandages are removed, elastic compression stockings should be worn for a minimum of 2 weeks. Complications from sclero-therapy include allergic reaction, local hyperpigmentation, thrombophlebitis, DVT, and possible skin necrosis.Newer devices combine sclerotherapy with catheter-based mechanical endoluminal injury to achieve nonthermal ablation.98 Additional nonthermal, nonsclerosant ablative techniques using proprietary adhesive formulations with cyanoacrylate are current being evaluated and have demonstrated promising early results.99Patients with symptomatic GSV or SSV reflux may be treated |
Surgery_Schwartz_6707 | Surgery_Schwartz | using proprietary adhesive formulations with cyanoacrylate are current being evaluated and have demonstrated promising early results.99Patients with symptomatic GSV or SSV reflux may be treated with endovenous ablation techniques or surgical removal of the affected vein. Endovenous laser and radiofrequency abla-tion (RFA) techniques have gained in popularity in the past several years. Such techniques are generally associ-ated with equally effective but more rapid postprocedure recov-ery than traditional open surgical stripping of the GSV.With either endoluminal technique, the distal thigh or proximal calf GSV is punctured with a 21-gauge needle under ultrasound guidance. A sheath is placed over a guidewire, and the laser fiber or RFA catheter is advanced until it is near to, but not at, the saphenofemoral junction. Tumescent anesthetic is administered around the GSV, and the vein is treated as the catheter is withdrawn. Endovenous laser treatment and RFA result in durable ablation of | Surgery_Schwartz. using proprietary adhesive formulations with cyanoacrylate are current being evaluated and have demonstrated promising early results.99Patients with symptomatic GSV or SSV reflux may be treated with endovenous ablation techniques or surgical removal of the affected vein. Endovenous laser and radiofrequency abla-tion (RFA) techniques have gained in popularity in the past several years. Such techniques are generally associ-ated with equally effective but more rapid postprocedure recov-ery than traditional open surgical stripping of the GSV.With either endoluminal technique, the distal thigh or proximal calf GSV is punctured with a 21-gauge needle under ultrasound guidance. A sheath is placed over a guidewire, and the laser fiber or RFA catheter is advanced until it is near to, but not at, the saphenofemoral junction. Tumescent anesthetic is administered around the GSV, and the vein is treated as the catheter is withdrawn. Endovenous laser treatment and RFA result in durable ablation of |
Surgery_Schwartz_6708 | Surgery_Schwartz | saphenofemoral junction. Tumescent anesthetic is administered around the GSV, and the vein is treated as the catheter is withdrawn. Endovenous laser treatment and RFA result in durable ablation of the GSV, with rates of varicose vein recurrence and clinical severity scores comparable to those seen with open surgery.100,101 Risks of endovenous ablation include DVT, ecchymosis, and saphenous nerve injury.Saphenous vein ligation and stripping may still be the pre-ferred therapy for patients with GSVs of very large diameter (>2 cm). Surgical removal of the GSV usually is performed via small incisions placed medially in the groin and just below the knee. The GSV is removed using a blunt tip catheter or an invagi-nation pin stripper. Complications associated with GSV stripping include ecchymosis, hematoma, lymphocele, DVT, infection, and saphenous nerve injury. GSV stripping is associated with a lower rate of recurrence of varicose veins and a better quality of life than saphenofemoral | Surgery_Schwartz. saphenofemoral junction. Tumescent anesthetic is administered around the GSV, and the vein is treated as the catheter is withdrawn. Endovenous laser treatment and RFA result in durable ablation of the GSV, with rates of varicose vein recurrence and clinical severity scores comparable to those seen with open surgery.100,101 Risks of endovenous ablation include DVT, ecchymosis, and saphenous nerve injury.Saphenous vein ligation and stripping may still be the pre-ferred therapy for patients with GSVs of very large diameter (>2 cm). Surgical removal of the GSV usually is performed via small incisions placed medially in the groin and just below the knee. The GSV is removed using a blunt tip catheter or an invagi-nation pin stripper. Complications associated with GSV stripping include ecchymosis, hematoma, lymphocele, DVT, infection, and saphenous nerve injury. GSV stripping is associated with a lower rate of recurrence of varicose veins and a better quality of life than saphenofemoral |
Surgery_Schwartz_6709 | Surgery_Schwartz | hematoma, lymphocele, DVT, infection, and saphenous nerve injury. GSV stripping is associated with a lower rate of recurrence of varicose veins and a better quality of life than saphenofemoral junction ligation alone.4Brunicardi_Ch24_p0981-p1008.indd 99622/02/19 3:01 PM 997VENOUS AND LYMPHATIC DISEASECHAPTER 24Figure 24-14. Removal of varicose veins via stab avulsions.Larger varicose veins are best treated by surgical exci-sion using the “stab avulsion” technique. Stab avulsions are performed by making 2-mm incisions directly over branch varicosities, and the varicosity is dissected from the surrounding subcutaneous tissue as far proximally and distally as possible through the small incisions (Fig. 24-14). In most cases the vein is simply avulsed with no attempt at ligation. Bleeding is easily controlled with leg elevation, manual compression, and prepro-cedure tumescent anesthesia.CHRONIC VENOUS INSUFFICIENCYChronic venous insufficiency (CVI) affects an estimated 600,000 people | Surgery_Schwartz. hematoma, lymphocele, DVT, infection, and saphenous nerve injury. GSV stripping is associated with a lower rate of recurrence of varicose veins and a better quality of life than saphenofemoral junction ligation alone.4Brunicardi_Ch24_p0981-p1008.indd 99622/02/19 3:01 PM 997VENOUS AND LYMPHATIC DISEASECHAPTER 24Figure 24-14. Removal of varicose veins via stab avulsions.Larger varicose veins are best treated by surgical exci-sion using the “stab avulsion” technique. Stab avulsions are performed by making 2-mm incisions directly over branch varicosities, and the varicosity is dissected from the surrounding subcutaneous tissue as far proximally and distally as possible through the small incisions (Fig. 24-14). In most cases the vein is simply avulsed with no attempt at ligation. Bleeding is easily controlled with leg elevation, manual compression, and prepro-cedure tumescent anesthesia.CHRONIC VENOUS INSUFFICIENCYChronic venous insufficiency (CVI) affects an estimated 600,000 people |
Surgery_Schwartz_6710 | Surgery_Schwartz | is easily controlled with leg elevation, manual compression, and prepro-cedure tumescent anesthesia.CHRONIC VENOUS INSUFFICIENCYChronic venous insufficiency (CVI) affects an estimated 600,000 people in the United States.102 Patients complain of leg fatigue, discomfort, and heaviness. Signs of CVI may include varicose veins, pigmentation, lipodermatosclerosis, and venous ulceration. Importantly, severe CVI is not necessarily associ-ated with varicose veins. Chronic venous ulcers carry significant negative physical, financial, and psychological implications. A quality-of-life study reported that 65% of patients with chronic leg ulcers had severe pain, 81% had decreased mobility, and 100% experienced a negative impact of their disease on their work capacity.103 The socioeconomic impact of chronic venous leg ulcers is staggering, with an estimated 2 million workdays lost per year.102 The annual healthcare cost in the United States to treat CVI is estimated at $1 billion.105CVI can be | Surgery_Schwartz. is easily controlled with leg elevation, manual compression, and prepro-cedure tumescent anesthesia.CHRONIC VENOUS INSUFFICIENCYChronic venous insufficiency (CVI) affects an estimated 600,000 people in the United States.102 Patients complain of leg fatigue, discomfort, and heaviness. Signs of CVI may include varicose veins, pigmentation, lipodermatosclerosis, and venous ulceration. Importantly, severe CVI is not necessarily associ-ated with varicose veins. Chronic venous ulcers carry significant negative physical, financial, and psychological implications. A quality-of-life study reported that 65% of patients with chronic leg ulcers had severe pain, 81% had decreased mobility, and 100% experienced a negative impact of their disease on their work capacity.103 The socioeconomic impact of chronic venous leg ulcers is staggering, with an estimated 2 million workdays lost per year.102 The annual healthcare cost in the United States to treat CVI is estimated at $1 billion.105CVI can be |
Surgery_Schwartz_6711 | Surgery_Schwartz | chronic venous leg ulcers is staggering, with an estimated 2 million workdays lost per year.102 The annual healthcare cost in the United States to treat CVI is estimated at $1 billion.105CVI can be primary or secondary. Primary CVI results from intrinsic abnormalities of the vein wall, whereas second-ary CVI, so-called postthrombotic syndrome (PTS), occurs as a result of DVT. The signs and symptoms of CVI can therefore be attributed to venous reflux, venous obstruction, calf muscle pump dysfunction, or a combination of these factors, as well as loss of venous wall elasticity.106 In the majority of patients with CVI, the most important factor appears to be venous reflux, although most severe cases tend to have an obstructive etiology as well. Venous reflux results from abnormalities of the venous valve. Primary valvular reflux or incompetence is diagnosed when there is no known underlying cause of valvular dysfunction. Secondary valvular reflux is diagnosed when an identifiable cause | Surgery_Schwartz. chronic venous leg ulcers is staggering, with an estimated 2 million workdays lost per year.102 The annual healthcare cost in the United States to treat CVI is estimated at $1 billion.105CVI can be primary or secondary. Primary CVI results from intrinsic abnormalities of the vein wall, whereas second-ary CVI, so-called postthrombotic syndrome (PTS), occurs as a result of DVT. The signs and symptoms of CVI can therefore be attributed to venous reflux, venous obstruction, calf muscle pump dysfunction, or a combination of these factors, as well as loss of venous wall elasticity.106 In the majority of patients with CVI, the most important factor appears to be venous reflux, although most severe cases tend to have an obstructive etiology as well. Venous reflux results from abnormalities of the venous valve. Primary valvular reflux or incompetence is diagnosed when there is no known underlying cause of valvular dysfunction. Secondary valvular reflux is diagnosed when an identifiable cause |
Surgery_Schwartz_6712 | Surgery_Schwartz | venous valve. Primary valvular reflux or incompetence is diagnosed when there is no known underlying cause of valvular dysfunction. Secondary valvular reflux is diagnosed when an identifiable cause is present. The most frequent secondary cause is DVT.Evaluation of Venous InsufficiencyEarly diagnostic studies to evaluate CVI required invasive mea-surements of ambulatory venous pressure (AVP) and venous recovery time (VRT). To measure AVP and VRT, a needle is inserted into a dorsal foot vein and connected to a pressure transducer. The patient is asked to perform 10 tiptoe exercises. Initially there is often a slight upward deflection of pressure with the onset of exercise followed by a decline in pressure with each subsequent tiptoe maneuver. After approximately 10 tiptoes, the measured pressure stabilizes and reflects a bal-ance of venous inflow and outflow. The pressure at this point is the AVP, which is measured in millimeters of mercury. The patient is then asked to stop exercising | Surgery_Schwartz. venous valve. Primary valvular reflux or incompetence is diagnosed when there is no known underlying cause of valvular dysfunction. Secondary valvular reflux is diagnosed when an identifiable cause is present. The most frequent secondary cause is DVT.Evaluation of Venous InsufficiencyEarly diagnostic studies to evaluate CVI required invasive mea-surements of ambulatory venous pressure (AVP) and venous recovery time (VRT). To measure AVP and VRT, a needle is inserted into a dorsal foot vein and connected to a pressure transducer. The patient is asked to perform 10 tiptoe exercises. Initially there is often a slight upward deflection of pressure with the onset of exercise followed by a decline in pressure with each subsequent tiptoe maneuver. After approximately 10 tiptoes, the measured pressure stabilizes and reflects a bal-ance of venous inflow and outflow. The pressure at this point is the AVP, which is measured in millimeters of mercury. The patient is then asked to stop exercising |
Surgery_Schwartz_6713 | Surgery_Schwartz | stabilizes and reflects a bal-ance of venous inflow and outflow. The pressure at this point is the AVP, which is measured in millimeters of mercury. The patient is then asked to stop exercising to allow the vein to fill with return of the venous pressure to baseline. The time required for the venous pressure to return from the AVP level to 90% of baseline pressure is referred to as the VRT. A normal VRT typically ranges from 20 to 60 seconds. Values less than 20 seconds indicate significant reflux with increasing severity. To distinguish between superficial and deep venous reflux, a thigh tourniquet can be placed inflated to 50 mmHg to eliminate influence of the superficial venous. A VRT that remains below 20 seconds after tourniquet inflation suggests both superficial and deep venous reflux. Elevations of AVP indicate venous hypertension. The magnitude of AVP reflects the severity of CVI. There is an 80% incidence of venous ulceration in patients with an AVP of >80 | Surgery_Schwartz. stabilizes and reflects a bal-ance of venous inflow and outflow. The pressure at this point is the AVP, which is measured in millimeters of mercury. The patient is then asked to stop exercising to allow the vein to fill with return of the venous pressure to baseline. The time required for the venous pressure to return from the AVP level to 90% of baseline pressure is referred to as the VRT. A normal VRT typically ranges from 20 to 60 seconds. Values less than 20 seconds indicate significant reflux with increasing severity. To distinguish between superficial and deep venous reflux, a thigh tourniquet can be placed inflated to 50 mmHg to eliminate influence of the superficial venous. A VRT that remains below 20 seconds after tourniquet inflation suggests both superficial and deep venous reflux. Elevations of AVP indicate venous hypertension. The magnitude of AVP reflects the severity of CVI. There is an 80% incidence of venous ulceration in patients with an AVP of >80 |
Surgery_Schwartz_6714 | Surgery_Schwartz | deep venous reflux. Elevations of AVP indicate venous hypertension. The magnitude of AVP reflects the severity of CVI. There is an 80% incidence of venous ulceration in patients with an AVP of >80 mmHg.107Plethysmography. Noninvasive plethysmography has been used to evaluate CVI. Venous photoplethysmography indirectly evaluates venous function through the use of infrared light. A light-emitting diode is placed just above the medial malleolus, and the patient then performs a series of tiptoe maneuvers. Pho-toplethysmography provides a measurement of VRT. In limbs with CVI, VRT is shortened compared with that in a normal limb. AVP and VRT are only measures of the overall venous function of a lower extremity venous system. They cannot local-ize the site of reflux or evaluate the function of the calf pump.Air plethysmography is a theoretically attractive but not widely used method to assess calf pump function, venous reflux, and overall lower extremity venous function.108 An air-filled | Surgery_Schwartz. deep venous reflux. Elevations of AVP indicate venous hypertension. The magnitude of AVP reflects the severity of CVI. There is an 80% incidence of venous ulceration in patients with an AVP of >80 mmHg.107Plethysmography. Noninvasive plethysmography has been used to evaluate CVI. Venous photoplethysmography indirectly evaluates venous function through the use of infrared light. A light-emitting diode is placed just above the medial malleolus, and the patient then performs a series of tiptoe maneuvers. Pho-toplethysmography provides a measurement of VRT. In limbs with CVI, VRT is shortened compared with that in a normal limb. AVP and VRT are only measures of the overall venous function of a lower extremity venous system. They cannot local-ize the site of reflux or evaluate the function of the calf pump.Air plethysmography is a theoretically attractive but not widely used method to assess calf pump function, venous reflux, and overall lower extremity venous function.108 An air-filled |
Surgery_Schwartz_6715 | Surgery_Schwartz | the calf pump.Air plethysmography is a theoretically attractive but not widely used method to assess calf pump function, venous reflux, and overall lower extremity venous function.108 An air-filled plastic pressure bladder is placed on the calf to detect volume changes in the leg during a standard set of maneuvers. The patient is first supine, and then the leg is elevated and the minimum volume of venous blood recorded. The patient is then asked to assume an upright position with the examined leg non-weight bearing. The venous volume of the examined leg is determined when the volume curve flattens. The venous fill-ing index (VFI), a measure of reflux, is calculated by dividing the maximum venous volume by the time required to achieve maximum venous volume. Next, the patient performs a single tiptoe maneuver, and the ejection fraction (EF) is determined. The EF is the volume change between the recorded volume before and after the tiptoe maneuver and is a measure of calf pump function. | Surgery_Schwartz. the calf pump.Air plethysmography is a theoretically attractive but not widely used method to assess calf pump function, venous reflux, and overall lower extremity venous function.108 An air-filled plastic pressure bladder is placed on the calf to detect volume changes in the leg during a standard set of maneuvers. The patient is first supine, and then the leg is elevated and the minimum volume of venous blood recorded. The patient is then asked to assume an upright position with the examined leg non-weight bearing. The venous volume of the examined leg is determined when the volume curve flattens. The venous fill-ing index (VFI), a measure of reflux, is calculated by dividing the maximum venous volume by the time required to achieve maximum venous volume. Next, the patient performs a single tiptoe maneuver, and the ejection fraction (EF) is determined. The EF is the volume change between the recorded volume before and after the tiptoe maneuver and is a measure of calf pump function. |
Surgery_Schwartz_6716 | Surgery_Schwartz | tiptoe maneuver, and the ejection fraction (EF) is determined. The EF is the volume change between the recorded volume before and after the tiptoe maneuver and is a measure of calf pump function. At this point, the veins of the leg are allowed to refill. The patient then performs 10 tiptoe maneuvers, and the residual volume fraction is calculated by dividing the venous volume in the leg after 10 tiptoe exercises by the venous volume present before the exercises. The residual volume fraction is a reflection of overall venous function. Theoretically, patients with increased VFIs and normal EFs (indicating the presence of reflux with normal calf pump function) would benefit from anti-reflux surgery, whereas patients with normal VFIs and dimin-ished EFs would not.Venous Duplex Ultrasound. Venous DUS has become the gold standard for evaluation of venous function largely supplanting venographic and plethysmographic techniques. Brunicardi_Ch24_p0981-p1008.indd 99722/02/19 3:01 PM | Surgery_Schwartz. tiptoe maneuver, and the ejection fraction (EF) is determined. The EF is the volume change between the recorded volume before and after the tiptoe maneuver and is a measure of calf pump function. At this point, the veins of the leg are allowed to refill. The patient then performs 10 tiptoe maneuvers, and the residual volume fraction is calculated by dividing the venous volume in the leg after 10 tiptoe exercises by the venous volume present before the exercises. The residual volume fraction is a reflection of overall venous function. Theoretically, patients with increased VFIs and normal EFs (indicating the presence of reflux with normal calf pump function) would benefit from anti-reflux surgery, whereas patients with normal VFIs and dimin-ished EFs would not.Venous Duplex Ultrasound. Venous DUS has become the gold standard for evaluation of venous function largely supplanting venographic and plethysmographic techniques. Brunicardi_Ch24_p0981-p1008.indd 99722/02/19 3:01 PM |
Surgery_Schwartz_6717 | Surgery_Schwartz | DUS has become the gold standard for evaluation of venous function largely supplanting venographic and plethysmographic techniques. Brunicardi_Ch24_p0981-p1008.indd 99722/02/19 3:01 PM 998SPECIFIC CONSIDERATIONSPART IIFigure 24-15. Evaluation of a patient with chronic venous insuf-ficiency with duplex ultrasonography.Figure 24-16. Multilayered dressing for treatment of chronic venous insufficiency.The principle advantage of DUS is that it can be used to evalu-ate reflux in individual venous segments targeting abnormal areas for treatment. The examination has been validated when performed with the patient in the standing position and the examined leg non-weight bearing. Pneumatic pressure cuffs of appropriate size are placed around the thigh, calf, and fore-foot. The ultrasound transducer is positioned over the venous segment to be examined, just proximal to the pneumatic cuff (Fig. 24-15). The cuff is then inflated to a standard pressure for 3 seconds and then rapidly deflated. | Surgery_Schwartz. DUS has become the gold standard for evaluation of venous function largely supplanting venographic and plethysmographic techniques. Brunicardi_Ch24_p0981-p1008.indd 99722/02/19 3:01 PM 998SPECIFIC CONSIDERATIONSPART IIFigure 24-15. Evaluation of a patient with chronic venous insuf-ficiency with duplex ultrasonography.Figure 24-16. Multilayered dressing for treatment of chronic venous insufficiency.The principle advantage of DUS is that it can be used to evalu-ate reflux in individual venous segments targeting abnormal areas for treatment. The examination has been validated when performed with the patient in the standing position and the examined leg non-weight bearing. Pneumatic pressure cuffs of appropriate size are placed around the thigh, calf, and fore-foot. The ultrasound transducer is positioned over the venous segment to be examined, just proximal to the pneumatic cuff (Fig. 24-15). The cuff is then inflated to a standard pressure for 3 seconds and then rapidly deflated. |
Surgery_Schwartz_6718 | Surgery_Schwartz | is positioned over the venous segment to be examined, just proximal to the pneumatic cuff (Fig. 24-15). The cuff is then inflated to a standard pressure for 3 seconds and then rapidly deflated. Ninety-five percent of normal venous valves close within 0.5 second.109 The presence of reflux for >0.5 second is considered abnormal. Typically, the common femoral, femoral, popliteal, and posterior tibial veins, as well as the GSV and SSV, are evaluated in a complete examination.Nonoperative Treatment of Chronic Venous Insufficiency Compression Therapy. Compression therapy is the mainstay of CVI management. Compression can be achieved using a vari-ety of techniques, including elastic compression stockings, paste gauze boots (Unna’s boots), multilayer elastic wraps or dressings (Fig. 24-16), and pneumatic compression devices. Nonelastic compression bandages generally achieve higher and more prolonged degrees of compression than elastic compression bandages. The exact mechanism by which | Surgery_Schwartz. is positioned over the venous segment to be examined, just proximal to the pneumatic cuff (Fig. 24-15). The cuff is then inflated to a standard pressure for 3 seconds and then rapidly deflated. Ninety-five percent of normal venous valves close within 0.5 second.109 The presence of reflux for >0.5 second is considered abnormal. Typically, the common femoral, femoral, popliteal, and posterior tibial veins, as well as the GSV and SSV, are evaluated in a complete examination.Nonoperative Treatment of Chronic Venous Insufficiency Compression Therapy. Compression therapy is the mainstay of CVI management. Compression can be achieved using a vari-ety of techniques, including elastic compression stockings, paste gauze boots (Unna’s boots), multilayer elastic wraps or dressings (Fig. 24-16), and pneumatic compression devices. Nonelastic compression bandages generally achieve higher and more prolonged degrees of compression than elastic compression bandages. The exact mechanism by which |
Surgery_Schwartz_6719 | Surgery_Schwartz | and pneumatic compression devices. Nonelastic compression bandages generally achieve higher and more prolonged degrees of compression than elastic compression bandages. The exact mechanism by which compression therapy can improve CVI remains uncertain. An improvement in skin and 5subcutaneous tissue microcirculatory hemodynamics as well as a direct effect on subcutaneous pressure have been hypothesized as the mechanisms of efficacy of compression therapy.110 Addition-ally, compression therapy has demonstrated quantifiable differ-ences in ulcer healing with decreases in matrix metalloproteins and inflammatory cytokines.111,112 Clinically, routine use of elastic and nonelastic bandages reduces lower extremity edema in patients with CVI. In addition, supine perimalleolar subcutaneous pressure has been demonstrated to increase with elastic compression.111 With edema reduction, cutaneous metabolism may improve due to enhanced diffusion of oxygen and other nutrients to the cellular elements | Surgery_Schwartz. and pneumatic compression devices. Nonelastic compression bandages generally achieve higher and more prolonged degrees of compression than elastic compression bandages. The exact mechanism by which compression therapy can improve CVI remains uncertain. An improvement in skin and 5subcutaneous tissue microcirculatory hemodynamics as well as a direct effect on subcutaneous pressure have been hypothesized as the mechanisms of efficacy of compression therapy.110 Addition-ally, compression therapy has demonstrated quantifiable differ-ences in ulcer healing with decreases in matrix metalloproteins and inflammatory cytokines.111,112 Clinically, routine use of elastic and nonelastic bandages reduces lower extremity edema in patients with CVI. In addition, supine perimalleolar subcutaneous pressure has been demonstrated to increase with elastic compression.111 With edema reduction, cutaneous metabolism may improve due to enhanced diffusion of oxygen and other nutrients to the cellular elements |
Surgery_Schwartz_6720 | Surgery_Schwartz | has been demonstrated to increase with elastic compression.111 With edema reduction, cutaneous metabolism may improve due to enhanced diffusion of oxygen and other nutrients to the cellular elements of skin and subcutaneous tissues. Increases in subcutaneous tissue pressure with elastic compres-sion bandages may counteract transcapillary Starling forces, which favor leakage of fluid out of the capillary.Before the initiation of therapy for CVI, patients must be educated about their chronic disease and the need to comply with their treatment plan to heal ulcers and prevent recurrence. A definitive diagnosis of venous ulceration must be made before treatment is initiated. A detailed history should be obtained from a patient presenting with lower extremity ulcerations, includ-ing medications used and associated medical conditions that may promote lower extremity ulceration. Arterial insufficiency is assessed by physical examination or noninvasive studies. In addition, systemic conditions | Surgery_Schwartz. has been demonstrated to increase with elastic compression.111 With edema reduction, cutaneous metabolism may improve due to enhanced diffusion of oxygen and other nutrients to the cellular elements of skin and subcutaneous tissues. Increases in subcutaneous tissue pressure with elastic compres-sion bandages may counteract transcapillary Starling forces, which favor leakage of fluid out of the capillary.Before the initiation of therapy for CVI, patients must be educated about their chronic disease and the need to comply with their treatment plan to heal ulcers and prevent recurrence. A definitive diagnosis of venous ulceration must be made before treatment is initiated. A detailed history should be obtained from a patient presenting with lower extremity ulcerations, includ-ing medications used and associated medical conditions that may promote lower extremity ulceration. Arterial insufficiency is assessed by physical examination or noninvasive studies. In addition, systemic conditions |
Surgery_Schwartz_6721 | Surgery_Schwartz | used and associated medical conditions that may promote lower extremity ulceration. Arterial insufficiency is assessed by physical examination or noninvasive studies. In addition, systemic conditions that affect wound healing and leg edema, such as diabetes mellitus, immunosuppression, mal-nutrition, and congestive heart failure, should be improved as much as possible.Compression therapy is most commonly achieved with graduated elastic compression stockings. Elastic compression stockings are available in various compositions, strengths, and lengths, and can be customized for a particular patient. The ben-efits of elastic compression stocking therapy for the treatment of CVI and healing of ulcerations have been well documented.114-117 In a retrospective study involving 113 venous ulcer patients,115 the use of below-knee, 30to 40-mmHg elastic compression stockings, after edema and cellulitis were first resolved if pres-ent, resulted in 93% healing. Complete ulcer healing occurred in 99 | Surgery_Schwartz. used and associated medical conditions that may promote lower extremity ulceration. Arterial insufficiency is assessed by physical examination or noninvasive studies. In addition, systemic conditions that affect wound healing and leg edema, such as diabetes mellitus, immunosuppression, mal-nutrition, and congestive heart failure, should be improved as much as possible.Compression therapy is most commonly achieved with graduated elastic compression stockings. Elastic compression stockings are available in various compositions, strengths, and lengths, and can be customized for a particular patient. The ben-efits of elastic compression stocking therapy for the treatment of CVI and healing of ulcerations have been well documented.114-117 In a retrospective study involving 113 venous ulcer patients,115 the use of below-knee, 30to 40-mmHg elastic compression stockings, after edema and cellulitis were first resolved if pres-ent, resulted in 93% healing. Complete ulcer healing occurred in 99 |
Surgery_Schwartz_6722 | Surgery_Schwartz | the use of below-knee, 30to 40-mmHg elastic compression stockings, after edema and cellulitis were first resolved if pres-ent, resulted in 93% healing. Complete ulcer healing occurred in 99 of 102 patients (97%) who were compliant with stocking use vs. 6 of 11 patients (55%) who were noncompliant (P <.0001). The mean time to ulcer healing was 5 months. The rate of ulcer recurrence was lower in patients who were compliant with their compression therapy. By life table analysis, ulcer recurrence was 29% at 5 years for compliant patients and 100% at 3 years for noncompliant patients.In addition to promoting ulcer healing, elastic compres-sion therapy can also improve quality of life in patients with CVI. In one prospective study,118 112 patients with CVI docu-mented by DUS were administered a questionnaire to quantify the symptoms of swelling, pain, skin discoloration, cosmesis, activity tolerance, depression, and sleep alterations. Patients were treated with 30to 40-mmHg elastic | Surgery_Schwartz. the use of below-knee, 30to 40-mmHg elastic compression stockings, after edema and cellulitis were first resolved if pres-ent, resulted in 93% healing. Complete ulcer healing occurred in 99 of 102 patients (97%) who were compliant with stocking use vs. 6 of 11 patients (55%) who were noncompliant (P <.0001). The mean time to ulcer healing was 5 months. The rate of ulcer recurrence was lower in patients who were compliant with their compression therapy. By life table analysis, ulcer recurrence was 29% at 5 years for compliant patients and 100% at 3 years for noncompliant patients.In addition to promoting ulcer healing, elastic compres-sion therapy can also improve quality of life in patients with CVI. In one prospective study,118 112 patients with CVI docu-mented by DUS were administered a questionnaire to quantify the symptoms of swelling, pain, skin discoloration, cosmesis, activity tolerance, depression, and sleep alterations. Patients were treated with 30to 40-mmHg elastic |
Surgery_Schwartz_6723 | Surgery_Schwartz | a questionnaire to quantify the symptoms of swelling, pain, skin discoloration, cosmesis, activity tolerance, depression, and sleep alterations. Patients were treated with 30to 40-mmHg elastic compression stock-ings. There were overall improvements in symptom severity scores at 1 month after initiation of treatment. Further improve-ments were noted at 16 months after treatment.Patient compliance with compression therapy is crucial in treating CVI and especially venous leg ulcers. Many patients are initially intolerant of compression in areas of hypersensitiv-ity adjacent to an active ulcer or at sites of previously healed ulcers. They may also have difficulty applying elastic stockings. To improve compliance, patients should be instructed to wear their stockings initially only as long as it is easily tolerated and Brunicardi_Ch24_p0981-p1008.indd 99822/02/19 3:01 PM 999VENOUS AND LYMPHATIC DISEASECHAPTER 24Figure 24-17. Elastic compression device with Velcro to facilitate | Surgery_Schwartz. a questionnaire to quantify the symptoms of swelling, pain, skin discoloration, cosmesis, activity tolerance, depression, and sleep alterations. Patients were treated with 30to 40-mmHg elastic compression stock-ings. There were overall improvements in symptom severity scores at 1 month after initiation of treatment. Further improve-ments were noted at 16 months after treatment.Patient compliance with compression therapy is crucial in treating CVI and especially venous leg ulcers. Many patients are initially intolerant of compression in areas of hypersensitiv-ity adjacent to an active ulcer or at sites of previously healed ulcers. They may also have difficulty applying elastic stockings. To improve compliance, patients should be instructed to wear their stockings initially only as long as it is easily tolerated and Brunicardi_Ch24_p0981-p1008.indd 99822/02/19 3:01 PM 999VENOUS AND LYMPHATIC DISEASECHAPTER 24Figure 24-17. Elastic compression device with Velcro to facilitate |
Surgery_Schwartz_6724 | Surgery_Schwartz | long as it is easily tolerated and Brunicardi_Ch24_p0981-p1008.indd 99822/02/19 3:01 PM 999VENOUS AND LYMPHATIC DISEASECHAPTER 24Figure 24-17. Elastic compression device with Velcro to facilitate treatment of chronic venous insufficiency.then gradually to increase the amount of time the stockings are worn. Alternatively, patients can be fitted with lower-strength stockings initially followed by introduction of higher-strength stockings over a period of several weeks. Many commercially available devices, such as silk inner toe liners, adjustable elas-tic compression with Velcro, stockings with zippered sides (Fig. 24-17), and metal fitting aids (Fig. 24-18), are available to assist patients in applying elastic stockings. However, despite all these available adjuncts, many patients remain noncompliant with elastic compression therapy.Another method of compression was developed by the German dermatologist Paul Gerson Unna. Unna’s boot has been used for many years to treat venous | Surgery_Schwartz. long as it is easily tolerated and Brunicardi_Ch24_p0981-p1008.indd 99822/02/19 3:01 PM 999VENOUS AND LYMPHATIC DISEASECHAPTER 24Figure 24-17. Elastic compression device with Velcro to facilitate treatment of chronic venous insufficiency.then gradually to increase the amount of time the stockings are worn. Alternatively, patients can be fitted with lower-strength stockings initially followed by introduction of higher-strength stockings over a period of several weeks. Many commercially available devices, such as silk inner toe liners, adjustable elas-tic compression with Velcro, stockings with zippered sides (Fig. 24-17), and metal fitting aids (Fig. 24-18), are available to assist patients in applying elastic stockings. However, despite all these available adjuncts, many patients remain noncompliant with elastic compression therapy.Another method of compression was developed by the German dermatologist Paul Gerson Unna. Unna’s boot has been used for many years to treat venous |
Surgery_Schwartz_6725 | Surgery_Schwartz | remain noncompliant with elastic compression therapy.Another method of compression was developed by the German dermatologist Paul Gerson Unna. Unna’s boot has been used for many years to treat venous ulcers and is available in many versions. A typical Unna’s boot consists of a three-layer dressing and requires application by trained personnel. A rolled gauze bandage impregnated with calamine, zinc oxide, glyc-erin, sorbitol, gelatin, and magnesium aluminum silicate is first applied with graded compression from the forefoot to just below the knee. The next layer consists of a 10-cm-wide continuous gauze dressing followed by an outer layer of elastic wrap, also applied with graded compression. The bandage becomes stiff after drying, and the rigidity may aid in preventing edema for-mation. Unna’s boot is changed weekly or sooner if the patient experiences significant drainage and soiling of the dressing.Once applied, Unna’s boot requires minimal patient involvement and provides | Surgery_Schwartz. remain noncompliant with elastic compression therapy.Another method of compression was developed by the German dermatologist Paul Gerson Unna. Unna’s boot has been used for many years to treat venous ulcers and is available in many versions. A typical Unna’s boot consists of a three-layer dressing and requires application by trained personnel. A rolled gauze bandage impregnated with calamine, zinc oxide, glyc-erin, sorbitol, gelatin, and magnesium aluminum silicate is first applied with graded compression from the forefoot to just below the knee. The next layer consists of a 10-cm-wide continuous gauze dressing followed by an outer layer of elastic wrap, also applied with graded compression. The bandage becomes stiff after drying, and the rigidity may aid in preventing edema for-mation. Unna’s boot is changed weekly or sooner if the patient experiences significant drainage and soiling of the dressing.Once applied, Unna’s boot requires minimal patient involvement and provides |
Surgery_Schwartz_6726 | Surgery_Schwartz | Unna’s boot is changed weekly or sooner if the patient experiences significant drainage and soiling of the dressing.Once applied, Unna’s boot requires minimal patient involvement and provides continuous compression and topical therapy. However, Unna’s boot has several disadvantages. It Figure 24-18. Metal fitting aid to assist in placement of elastic compression stockings.is bulky and can be uncomfortable, which may affect patient compliance. In addition, the ulcer cannot be monitored after the boot is applied, the technique is labor intensive, and the degree of compression provided is operator dependent. Occasionally, patients may also develop contact dermatitis to the components of Unna’s boot.The efficacy of Unna’s dressing has been studied. A ret-rospective 15-year survey encompassing 998 patients with one or more venous ulcers treated weekly with Unna’s dressing119 reported that 73% of ulcers healed in patients who returned for more than one treatment. The median time to healing | Surgery_Schwartz. Unna’s boot is changed weekly or sooner if the patient experiences significant drainage and soiling of the dressing.Once applied, Unna’s boot requires minimal patient involvement and provides continuous compression and topical therapy. However, Unna’s boot has several disadvantages. It Figure 24-18. Metal fitting aid to assist in placement of elastic compression stockings.is bulky and can be uncomfortable, which may affect patient compliance. In addition, the ulcer cannot be monitored after the boot is applied, the technique is labor intensive, and the degree of compression provided is operator dependent. Occasionally, patients may also develop contact dermatitis to the components of Unna’s boot.The efficacy of Unna’s dressing has been studied. A ret-rospective 15-year survey encompassing 998 patients with one or more venous ulcers treated weekly with Unna’s dressing119 reported that 73% of ulcers healed in patients who returned for more than one treatment. The median time to healing |
Surgery_Schwartz_6727 | Surgery_Schwartz | 998 patients with one or more venous ulcers treated weekly with Unna’s dressing119 reported that 73% of ulcers healed in patients who returned for more than one treatment. The median time to healing for individual ulcers was 9 weeks. Unna’s dressing has been com-pared to other forms of treatment. A randomized, prospective study comparing Unna’s boot to polyurethane foam dressing in 36 patients with venous ulcers demonstrated superior healing over 12 months in patients treated with Unna’s boot (94.7% vs. 41.2%).120 A recent Cochrane Review of 39 randomized controlled trials demonstrated that compression increases ulcer healing rates compared with no compression, multicomponent systems are more effective than single-component systems, and multicomponent systems that include an elastic bandage are more effective than those composed mainly of inelastic constituents.121Other forms of compression dressing available to treat CVI include multilayered dressings and legging orthoses. The | Surgery_Schwartz. 998 patients with one or more venous ulcers treated weekly with Unna’s dressing119 reported that 73% of ulcers healed in patients who returned for more than one treatment. The median time to healing for individual ulcers was 9 weeks. Unna’s dressing has been com-pared to other forms of treatment. A randomized, prospective study comparing Unna’s boot to polyurethane foam dressing in 36 patients with venous ulcers demonstrated superior healing over 12 months in patients treated with Unna’s boot (94.7% vs. 41.2%).120 A recent Cochrane Review of 39 randomized controlled trials demonstrated that compression increases ulcer healing rates compared with no compression, multicomponent systems are more effective than single-component systems, and multicomponent systems that include an elastic bandage are more effective than those composed mainly of inelastic constituents.121Other forms of compression dressing available to treat CVI include multilayered dressings and legging orthoses. The |
Surgery_Schwartz_6728 | Surgery_Schwartz | bandage are more effective than those composed mainly of inelastic constituents.121Other forms of compression dressing available to treat CVI include multilayered dressings and legging orthoses. The purported advantages of multilayered dressings include main-tenance of compression for a longer period of time, more even distribution of compression, and better absorption of wound Brunicardi_Ch24_p0981-p1008.indd 99922/02/19 3:01 PM 1000SPECIFIC CONSIDERATIONSPART IIFigure 24-19. Apligraf skin graft material supplied as a disk on an agarose gel nutrient medium.Figure 24-20. Trocar placement for subfascial endoscopic perfo-rator vein surgery. (Used with permission from Dr. Pankaj Patel.)exudates. However, the efficacy of multilayered dressings depends on the wrapping technique of healthcare personnel. A commercially available legging orthosis consisting of multiple adjustable loop-and-hook closure compression bands provides compression similar to that of Unna’s boot and can be applied | Surgery_Schwartz. bandage are more effective than those composed mainly of inelastic constituents.121Other forms of compression dressing available to treat CVI include multilayered dressings and legging orthoses. The purported advantages of multilayered dressings include main-tenance of compression for a longer period of time, more even distribution of compression, and better absorption of wound Brunicardi_Ch24_p0981-p1008.indd 99922/02/19 3:01 PM 1000SPECIFIC CONSIDERATIONSPART IIFigure 24-19. Apligraf skin graft material supplied as a disk on an agarose gel nutrient medium.Figure 24-20. Trocar placement for subfascial endoscopic perfo-rator vein surgery. (Used with permission from Dr. Pankaj Patel.)exudates. However, the efficacy of multilayered dressings depends on the wrapping technique of healthcare personnel. A commercially available legging orthosis consisting of multiple adjustable loop-and-hook closure compression bands provides compression similar to that of Unna’s boot and can be applied |
Surgery_Schwartz_6729 | Surgery_Schwartz | personnel. A commercially available legging orthosis consisting of multiple adjustable loop-and-hook closure compression bands provides compression similar to that of Unna’s boot and can be applied daily by the patient.122Skin Substitutes. Several types of skin substitutes are com-mercially available or under clinical study in the United States.105 Bioengineered skin ranges in composition from acellular skin substitutes to partial living skin substitutes. Their mechanism of action in healing venous ulcers is uncertain; however, they may serve as delivery vehicles for various growth factors and cytokines important in wound healing.Apligraf is a commercially available bilayered living skin construct that closely approximates human skin for use in the treatment of venous ulcers. It contains a protective stratum corneum and a keratinocyte-containing epidermis overlying a dermis consisting of dermal fibroblasts in a collagen matrix.122 Apligraf is between 0.5 mm and 1.0 mm thick and is | Surgery_Schwartz. personnel. A commercially available legging orthosis consisting of multiple adjustable loop-and-hook closure compression bands provides compression similar to that of Unna’s boot and can be applied daily by the patient.122Skin Substitutes. Several types of skin substitutes are com-mercially available or under clinical study in the United States.105 Bioengineered skin ranges in composition from acellular skin substitutes to partial living skin substitutes. Their mechanism of action in healing venous ulcers is uncertain; however, they may serve as delivery vehicles for various growth factors and cytokines important in wound healing.Apligraf is a commercially available bilayered living skin construct that closely approximates human skin for use in the treatment of venous ulcers. It contains a protective stratum corneum and a keratinocyte-containing epidermis overlying a dermis consisting of dermal fibroblasts in a collagen matrix.122 Apligraf is between 0.5 mm and 1.0 mm thick and is |
Surgery_Schwartz_6730 | Surgery_Schwartz | a protective stratum corneum and a keratinocyte-containing epidermis overlying a dermis consisting of dermal fibroblasts in a collagen matrix.122 Apligraf is between 0.5 mm and 1.0 mm thick and is supplied as a disk of living tissue on an agarose gel nutrient medium. It must be used within 5 days of release from the manufacturer123 (Fig. 24-19). The disk is easily handled and applied and con-forms to irregularly contoured ulcer beds though it is very costly.A prospective randomized study comparing multilayer compression therapy alone to treatment with Apligraf in addi-tion to multilayered compression therapy has been performed to assess the efficacy of Apligraf in the treatment of venous ulcers.118 More patients treated with Apligraf had ulcer healing at 6 months (63% vs. 49%, P = .02). The median time to com-plete ulcer closure was significantly shorter in patients treated with Apligraf (61 days vs. 181 days, P = .003). The ulcers that showed the greatest benefit with the living skin | Surgery_Schwartz. a protective stratum corneum and a keratinocyte-containing epidermis overlying a dermis consisting of dermal fibroblasts in a collagen matrix.122 Apligraf is between 0.5 mm and 1.0 mm thick and is supplied as a disk of living tissue on an agarose gel nutrient medium. It must be used within 5 days of release from the manufacturer123 (Fig. 24-19). The disk is easily handled and applied and con-forms to irregularly contoured ulcer beds though it is very costly.A prospective randomized study comparing multilayer compression therapy alone to treatment with Apligraf in addi-tion to multilayered compression therapy has been performed to assess the efficacy of Apligraf in the treatment of venous ulcers.118 More patients treated with Apligraf had ulcer healing at 6 months (63% vs. 49%, P = .02). The median time to com-plete ulcer closure was significantly shorter in patients treated with Apligraf (61 days vs. 181 days, P = .003). The ulcers that showed the greatest benefit with the living skin |
Surgery_Schwartz_6731 | Surgery_Schwartz | median time to com-plete ulcer closure was significantly shorter in patients treated with Apligraf (61 days vs. 181 days, P = .003). The ulcers that showed the greatest benefit with the living skin construct were ones that were large and deep (>1000 mm2) or were longstand-ing (>6 months). No evidence of rejection or sensitization has been reported in response to Apligraf application.Surgical/Interventional Treatment of Chronic Venous Insufficiency Perforator Vein Ligation. Incompetence of the perforating veins connecting the superficial and deep venous systems of the lower extremities has been implicated in the development of venous ulcers. The classic open tech-nique described by Linton in 1938 for perforator vein ligation has a high incidence of wound complications and has largely been abandoned.124 A minimally invasive technique termed subfascial endoscopic perforator vein surgery (SEPS) evolved with improvement of endoscopic equipment.DUS is performed preoperatively in patients | Surgery_Schwartz. median time to com-plete ulcer closure was significantly shorter in patients treated with Apligraf (61 days vs. 181 days, P = .003). The ulcers that showed the greatest benefit with the living skin construct were ones that were large and deep (>1000 mm2) or were longstand-ing (>6 months). No evidence of rejection or sensitization has been reported in response to Apligraf application.Surgical/Interventional Treatment of Chronic Venous Insufficiency Perforator Vein Ligation. Incompetence of the perforating veins connecting the superficial and deep venous systems of the lower extremities has been implicated in the development of venous ulcers. The classic open tech-nique described by Linton in 1938 for perforator vein ligation has a high incidence of wound complications and has largely been abandoned.124 A minimally invasive technique termed subfascial endoscopic perforator vein surgery (SEPS) evolved with improvement of endoscopic equipment.DUS is performed preoperatively in patients |
Surgery_Schwartz_6732 | Surgery_Schwartz | abandoned.124 A minimally invasive technique termed subfascial endoscopic perforator vein surgery (SEPS) evolved with improvement of endoscopic equipment.DUS is performed preoperatively in patients undergoing SEPS to document deep venous competence and to identify per-forating veins in the posterior compartment. The patient is posi-tioned on the operating table with the affected leg elevated at 45° to 60°. An Esmarch bandage and a thigh tourniquet are used to exsanguinate the limb. The knee is then flexed, and two small incisions are made in the proximal medial leg away from areas of maximal induration at the ankle. Laparoscopic trocars are then positioned, and the subfascial dissection is performed with a combination of blunt and sharp dissection. Carbon dioxide is then used to insufflate the subfascial space. The thigh tourni-quet is inflated to prevent air embolism. The perforators are then identified and doubly clipped and divided. After completion of the procedure, the leg is | Surgery_Schwartz. abandoned.124 A minimally invasive technique termed subfascial endoscopic perforator vein surgery (SEPS) evolved with improvement of endoscopic equipment.DUS is performed preoperatively in patients undergoing SEPS to document deep venous competence and to identify per-forating veins in the posterior compartment. The patient is posi-tioned on the operating table with the affected leg elevated at 45° to 60°. An Esmarch bandage and a thigh tourniquet are used to exsanguinate the limb. The knee is then flexed, and two small incisions are made in the proximal medial leg away from areas of maximal induration at the ankle. Laparoscopic trocars are then positioned, and the subfascial dissection is performed with a combination of blunt and sharp dissection. Carbon dioxide is then used to insufflate the subfascial space. The thigh tourni-quet is inflated to prevent air embolism. The perforators are then identified and doubly clipped and divided. After completion of the procedure, the leg is |
Surgery_Schwartz_6733 | Surgery_Schwartz | the subfascial space. The thigh tourni-quet is inflated to prevent air embolism. The perforators are then identified and doubly clipped and divided. After completion of the procedure, the leg is wrapped in a compression bandage for 5 days postoperatively.The efficacy of SEPS as a stand-alone procedure in treatment of venous insufficiency is controversial and unproven. In a report from a large North American registry of 146 patients undergoing SEPS125 (Fig. 24-20), healing was achieved in 88% of ulcers (75 of 85) at 1 year. Adjunctive procedures, primarily superficial vein stripping, were performed in 72% of patients. Ulcer recurrence was predicted to be 16% at 1 year and 28% at 2 years by life table analysis. These results are similar to those achieved in some studies with compression therapy alone. A review of several studies from 2003 to 2011 demonstrated, when taken in aggregate, that 2059 limbs with 896 ulcers underwent SEPS and concomitant saphenous vein ablation (70%) with a 0% | Surgery_Schwartz. the subfascial space. The thigh tourni-quet is inflated to prevent air embolism. The perforators are then identified and doubly clipped and divided. After completion of the procedure, the leg is wrapped in a compression bandage for 5 days postoperatively.The efficacy of SEPS as a stand-alone procedure in treatment of venous insufficiency is controversial and unproven. In a report from a large North American registry of 146 patients undergoing SEPS125 (Fig. 24-20), healing was achieved in 88% of ulcers (75 of 85) at 1 year. Adjunctive procedures, primarily superficial vein stripping, were performed in 72% of patients. Ulcer recurrence was predicted to be 16% at 1 year and 28% at 2 years by life table analysis. These results are similar to those achieved in some studies with compression therapy alone. A review of several studies from 2003 to 2011 demonstrated, when taken in aggregate, that 2059 limbs with 896 ulcers underwent SEPS and concomitant saphenous vein ablation (70%) with a 0% |
Surgery_Schwartz_6734 | Surgery_Schwartz | alone. A review of several studies from 2003 to 2011 demonstrated, when taken in aggregate, that 2059 limbs with 896 ulcers underwent SEPS and concomitant saphenous vein ablation (70%) with a 0% to 16% complication rate and achieved ulcer healing in 90% of patients.126 There has been a multicenter, prospective, European trial performed in patients with venous ulcers to evaluate the efficacy of SEPS. Post hoc analysis suggested possible benefit for SEPS in certain categories of patients with venous ulcer. Overall, however, primary analysis of the study’s end points indicated no advantage to SEPS in addition to superficial venous surgery and compression in the healing of venous ulcers.127 The technique appears to have fallen out of favor in most institutions with injection sclerotherapy preferred due to ease of use.Superficial Venous Surgery. Currently it is accepted that superficial venous surgery in addition to compression therapy has a role in the treatment of patients with venous | Surgery_Schwartz. alone. A review of several studies from 2003 to 2011 demonstrated, when taken in aggregate, that 2059 limbs with 896 ulcers underwent SEPS and concomitant saphenous vein ablation (70%) with a 0% to 16% complication rate and achieved ulcer healing in 90% of patients.126 There has been a multicenter, prospective, European trial performed in patients with venous ulcers to evaluate the efficacy of SEPS. Post hoc analysis suggested possible benefit for SEPS in certain categories of patients with venous ulcer. Overall, however, primary analysis of the study’s end points indicated no advantage to SEPS in addition to superficial venous surgery and compression in the healing of venous ulcers.127 The technique appears to have fallen out of favor in most institutions with injection sclerotherapy preferred due to ease of use.Superficial Venous Surgery. Currently it is accepted that superficial venous surgery in addition to compression therapy has a role in the treatment of patients with venous |
Surgery_Schwartz_6735 | Surgery_Schwartz | due to ease of use.Superficial Venous Surgery. Currently it is accepted that superficial venous surgery in addition to compression therapy has a role in the treatment of patients with venous ulcer. The ESCHAR trial was a randomized prospective trial performed in the United Kingdom to evaluate the combination of superficial Brunicardi_Ch24_p0981-p1008.indd 100022/02/19 3:01 PM 1001VENOUS AND LYMPHATIC DISEASECHAPTER 24Figure 24-21. Patient with severe longstanding lymphedema.venous surgery and compression vs. compression alone in the treatment of venous ulcer. Superficial venous surgery had no additive effect to compression alone in the healing of a venous ulcer but significantly reduced venous ulcer recurrence at 4 years. Based on the results of this trial, it is reasonable to offer ablation or removal of the GSV in addition to compression therapy in patients with abnormal saphenous veins and signs and/or symptoms of severe CVI.128Deep Venous Valvular Reconstruction. In the | Surgery_Schwartz. due to ease of use.Superficial Venous Surgery. Currently it is accepted that superficial venous surgery in addition to compression therapy has a role in the treatment of patients with venous ulcer. The ESCHAR trial was a randomized prospective trial performed in the United Kingdom to evaluate the combination of superficial Brunicardi_Ch24_p0981-p1008.indd 100022/02/19 3:01 PM 1001VENOUS AND LYMPHATIC DISEASECHAPTER 24Figure 24-21. Patient with severe longstanding lymphedema.venous surgery and compression vs. compression alone in the treatment of venous ulcer. Superficial venous surgery had no additive effect to compression alone in the healing of a venous ulcer but significantly reduced venous ulcer recurrence at 4 years. Based on the results of this trial, it is reasonable to offer ablation or removal of the GSV in addition to compression therapy in patients with abnormal saphenous veins and signs and/or symptoms of severe CVI.128Deep Venous Valvular Reconstruction. In the |
Surgery_Schwartz_6736 | Surgery_Schwartz | ablation or removal of the GSV in addition to compression therapy in patients with abnormal saphenous veins and signs and/or symptoms of severe CVI.128Deep Venous Valvular Reconstruction. In the absence of sig-nificant deep vein valvular incompetence, saphenous vein stripping and possibly perforator vein ligation can be effective in the treat-ment of CVI. However, in patients with a combination of superfi-cial and deep vein valvular incompetence, the addition of deep vein valvular reconstruction theoretically may improve ulcer healing.130 Numerous techniques of deep vein valve correction have been reported. These techniques consist of repair of existing valves, transplant of venous segments from the arm, transposition of an incompetent vein onto an adjacent competent vein, and implanta-tion of cryopreserved vein segments including competent valves.Successful long-term outcomes of 60% to 80% have been reported for venous valve reconstructions by internal suture repair.129,130 However, | Surgery_Schwartz. ablation or removal of the GSV in addition to compression therapy in patients with abnormal saphenous veins and signs and/or symptoms of severe CVI.128Deep Venous Valvular Reconstruction. In the absence of sig-nificant deep vein valvular incompetence, saphenous vein stripping and possibly perforator vein ligation can be effective in the treat-ment of CVI. However, in patients with a combination of superfi-cial and deep vein valvular incompetence, the addition of deep vein valvular reconstruction theoretically may improve ulcer healing.130 Numerous techniques of deep vein valve correction have been reported. These techniques consist of repair of existing valves, transplant of venous segments from the arm, transposition of an incompetent vein onto an adjacent competent vein, and implanta-tion of cryopreserved vein segments including competent valves.Successful long-term outcomes of 60% to 80% have been reported for venous valve reconstructions by internal suture repair.129,130 However, |
Surgery_Schwartz_6737 | Surgery_Schwartz | of cryopreserved vein segments including competent valves.Successful long-term outcomes of 60% to 80% have been reported for venous valve reconstructions by internal suture repair.129,130 However, among patients who initially had ulcer-ation, 40% to 50% still had persistence or recurrence of ulcers in the long term.127,129Valve transplantation involves replacement of a segment of incompetent femoral vein or popliteal vein with a segment of axillary or brachial vein with competent valves. Early results are similar to those for venous valve reconstruction.129,130 How-ever, in the long term, the transplanted venous segments tend to develop incompetence, intimal hyperplasia, and cusp sinus thrombosis with long-term outcomes that are poorer than those for venous valve reconstructions. The outcomes for venous transposition are similar to those for valve transplantation.Currently, reconstruction techniques for deep venous insufficiency and associated CVI are rarely performed.Venous | Surgery_Schwartz. of cryopreserved vein segments including competent valves.Successful long-term outcomes of 60% to 80% have been reported for venous valve reconstructions by internal suture repair.129,130 However, among patients who initially had ulcer-ation, 40% to 50% still had persistence or recurrence of ulcers in the long term.127,129Valve transplantation involves replacement of a segment of incompetent femoral vein or popliteal vein with a segment of axillary or brachial vein with competent valves. Early results are similar to those for venous valve reconstruction.129,130 How-ever, in the long term, the transplanted venous segments tend to develop incompetence, intimal hyperplasia, and cusp sinus thrombosis with long-term outcomes that are poorer than those for venous valve reconstructions. The outcomes for venous transposition are similar to those for valve transplantation.Currently, reconstruction techniques for deep venous insufficiency and associated CVI are rarely performed.Venous |
Surgery_Schwartz_6738 | Surgery_Schwartz | The outcomes for venous transposition are similar to those for valve transplantation.Currently, reconstruction techniques for deep venous insufficiency and associated CVI are rarely performed.Venous Stenting. Currently there is great interest in the role of venous stents in the treatment of CVI. Stenotic lesions of the iliac veins, primarily documented with IVUS, are being reported in a very high percentage of patients with edema, lipo-dermatosclerosis, or ulceration secondary to venous disease. It appears possible to percutaneously place stents in the iliac veins with near 100% technical success and excellent patency of the stent out to 4 years. Retrospective case series suggest favorable effects on ulcer healing, symptoms of CVI, and quality of life in patients with CVI. The role of venous stenting as an indepen-dent procedure in the treatment of patients with CVI remains an area of active investigation.131LYMPHEDEMAPathophysiologyLymphedema is extremity swelling that results from a | Surgery_Schwartz. The outcomes for venous transposition are similar to those for valve transplantation.Currently, reconstruction techniques for deep venous insufficiency and associated CVI are rarely performed.Venous Stenting. Currently there is great interest in the role of venous stents in the treatment of CVI. Stenotic lesions of the iliac veins, primarily documented with IVUS, are being reported in a very high percentage of patients with edema, lipo-dermatosclerosis, or ulceration secondary to venous disease. It appears possible to percutaneously place stents in the iliac veins with near 100% technical success and excellent patency of the stent out to 4 years. Retrospective case series suggest favorable effects on ulcer healing, symptoms of CVI, and quality of life in patients with CVI. The role of venous stenting as an indepen-dent procedure in the treatment of patients with CVI remains an area of active investigation.131LYMPHEDEMAPathophysiologyLymphedema is extremity swelling that results from a |
Surgery_Schwartz_6739 | Surgery_Schwartz | stenting as an indepen-dent procedure in the treatment of patients with CVI remains an area of active investigation.131LYMPHEDEMAPathophysiologyLymphedema is extremity swelling that results from a reduction in lymphatic transport and accumulation of lymph within the interstitial space. It is caused by anatomic and or physiologic abnormalities such as lymphatic hypoplasia, functional insuf-ficiency, or absence of lymphatic valves.The original classification system, described by Allen, is based on the cause of the lymphedema. Primary lymphedema is further subdivided into congenital lymphedema, lymph-edema praecox, and lymphedema tarda. Congenital lymph-edema may involve a single lower extremity, multiple limbs, the genitalia, or the face. The edema typically develops before 2 years 6of age and may be associated with specific hereditary syndromes (Turner syndrome, Milroy syndrome, Klippel-Trénaunay-Weber syndrome). Lymphedema praecox is the most common form of primary lymphedema, | Surgery_Schwartz. stenting as an indepen-dent procedure in the treatment of patients with CVI remains an area of active investigation.131LYMPHEDEMAPathophysiologyLymphedema is extremity swelling that results from a reduction in lymphatic transport and accumulation of lymph within the interstitial space. It is caused by anatomic and or physiologic abnormalities such as lymphatic hypoplasia, functional insuf-ficiency, or absence of lymphatic valves.The original classification system, described by Allen, is based on the cause of the lymphedema. Primary lymphedema is further subdivided into congenital lymphedema, lymph-edema praecox, and lymphedema tarda. Congenital lymph-edema may involve a single lower extremity, multiple limbs, the genitalia, or the face. The edema typically develops before 2 years 6of age and may be associated with specific hereditary syndromes (Turner syndrome, Milroy syndrome, Klippel-Trénaunay-Weber syndrome). Lymphedema praecox is the most common form of primary lymphedema, |
Surgery_Schwartz_6740 | Surgery_Schwartz | age and may be associated with specific hereditary syndromes (Turner syndrome, Milroy syndrome, Klippel-Trénaunay-Weber syndrome). Lymphedema praecox is the most common form of primary lymphedema, accounting for 94% of cases. Lymphedema praecox is far more common in women, with the gender ratio favoring women 10:1. The onset is during childhood or the teen-age years, and the swelling involves the foot and calf. Lymph-edema tarda is uncommon, accounting for <10% of cases of primary lymphedema. The onset of edema is after 35 years of age.Secondary lymphedema is far more common than primary lymphedema. Secondary lymphedema develops as a result of lymphatic obstruction or disruption. Axillary node dissection leading to lymphedema of the arm is the most common cause of secondary lymphedema in the United States. Other causes of secondary lymphedema include radiation therapy, trauma, infection, and malignancy. Globally, filariasis (an infection caused by Wuchereria bancrofti, Brugia malayi, | Surgery_Schwartz. age and may be associated with specific hereditary syndromes (Turner syndrome, Milroy syndrome, Klippel-Trénaunay-Weber syndrome). Lymphedema praecox is the most common form of primary lymphedema, accounting for 94% of cases. Lymphedema praecox is far more common in women, with the gender ratio favoring women 10:1. The onset is during childhood or the teen-age years, and the swelling involves the foot and calf. Lymph-edema tarda is uncommon, accounting for <10% of cases of primary lymphedema. The onset of edema is after 35 years of age.Secondary lymphedema is far more common than primary lymphedema. Secondary lymphedema develops as a result of lymphatic obstruction or disruption. Axillary node dissection leading to lymphedema of the arm is the most common cause of secondary lymphedema in the United States. Other causes of secondary lymphedema include radiation therapy, trauma, infection, and malignancy. Globally, filariasis (an infection caused by Wuchereria bancrofti, Brugia malayi, |
Surgery_Schwartz_6741 | Surgery_Schwartz | the United States. Other causes of secondary lymphedema include radiation therapy, trauma, infection, and malignancy. Globally, filariasis (an infection caused by Wuchereria bancrofti, Brugia malayi, and Brugia timori) and environmental exposure to minerals in volcanic soil resulting in podoconiosis in barefoot populations are the most common causes of secondary lymphedema.Clinical DiagnosisIn most patients, the diagnosis of lymphedema can be made based on the history and physical examination alone. Patients commonly complain of heaviness and fatigue in the affected extremity. The limb size increases throughout the day and decreases to some extent, usually minimally, over the course of the night when the patient is recumbent. The limb, however, never completely nor-malizes. In the lower extremity, the swelling classically involves the dorsum of the foot, and the toes have a squared-off appear-ance. In advanced cases, hyperkeratosis of the skin develops, and fluid weeps from | Surgery_Schwartz. the United States. Other causes of secondary lymphedema include radiation therapy, trauma, infection, and malignancy. Globally, filariasis (an infection caused by Wuchereria bancrofti, Brugia malayi, and Brugia timori) and environmental exposure to minerals in volcanic soil resulting in podoconiosis in barefoot populations are the most common causes of secondary lymphedema.Clinical DiagnosisIn most patients, the diagnosis of lymphedema can be made based on the history and physical examination alone. Patients commonly complain of heaviness and fatigue in the affected extremity. The limb size increases throughout the day and decreases to some extent, usually minimally, over the course of the night when the patient is recumbent. The limb, however, never completely nor-malizes. In the lower extremity, the swelling classically involves the dorsum of the foot, and the toes have a squared-off appear-ance. In advanced cases, hyperkeratosis of the skin develops, and fluid weeps from |
Surgery_Schwartz_6742 | Surgery_Schwartz | lower extremity, the swelling classically involves the dorsum of the foot, and the toes have a squared-off appear-ance. In advanced cases, hyperkeratosis of the skin develops, and fluid weeps from lymph-filled vesicles (Fig. 24-21).Brunicardi_Ch24_p0981-p1008.indd 100122/02/19 3:01 PM 1002SPECIFIC CONSIDERATIONSPART IIFigure 24-22. Lymphoscintigraphy of the lower extremity.Figure 24-23. Normal lymphangiogram of the pelvis.Recurrent cellulitis is a common complication of lymph-edema. Repeated infection results in further lymphatic damage, worsening existing disease. The clinical presentation of cellu-litis ranges from subtle erythema and worsening of edema to a rapidly progressive soft tissue infection with systemic toxicity.Many medical conditions can cause edema. If the symp-toms are mild, distinguishing lymphedema from other causes of leg swelling can be difficult. Venous insufficiency is often confused with lymphedema. However, patients with advanced venous insufficiency | Surgery_Schwartz. lower extremity, the swelling classically involves the dorsum of the foot, and the toes have a squared-off appear-ance. In advanced cases, hyperkeratosis of the skin develops, and fluid weeps from lymph-filled vesicles (Fig. 24-21).Brunicardi_Ch24_p0981-p1008.indd 100122/02/19 3:01 PM 1002SPECIFIC CONSIDERATIONSPART IIFigure 24-22. Lymphoscintigraphy of the lower extremity.Figure 24-23. Normal lymphangiogram of the pelvis.Recurrent cellulitis is a common complication of lymph-edema. Repeated infection results in further lymphatic damage, worsening existing disease. The clinical presentation of cellu-litis ranges from subtle erythema and worsening of edema to a rapidly progressive soft tissue infection with systemic toxicity.Many medical conditions can cause edema. If the symp-toms are mild, distinguishing lymphedema from other causes of leg swelling can be difficult. Venous insufficiency is often confused with lymphedema. However, patients with advanced venous insufficiency |
Surgery_Schwartz_6743 | Surgery_Schwartz | are mild, distinguishing lymphedema from other causes of leg swelling can be difficult. Venous insufficiency is often confused with lymphedema. However, patients with advanced venous insufficiency typically have lipodermatosclerosis in the gaiter region, skin ulceration, and/or varicose veins. Bilateral pitting edema is typically associated with congestive heart fail-ure, renal failure, or a hypoproteinemic state.Radiologic DiagnosisDuplex Ultrasound. When a patient is evaluated for edema, it is often difficult to distinguish the early stages of lymphedema from venous insufficiency. DUS of the venous system can determine if there is concomitant venous thrombosis or venous reflux, perhaps contributing to extremity edema. The diagnostic modalities discussed in the following sections have limited use in clinical practice. They are invasive and tedious and rarely change the management of a patient with lymphedema. Most physicians rely on the patient’s history and physical examina-tion | Surgery_Schwartz. are mild, distinguishing lymphedema from other causes of leg swelling can be difficult. Venous insufficiency is often confused with lymphedema. However, patients with advanced venous insufficiency typically have lipodermatosclerosis in the gaiter region, skin ulceration, and/or varicose veins. Bilateral pitting edema is typically associated with congestive heart fail-ure, renal failure, or a hypoproteinemic state.Radiologic DiagnosisDuplex Ultrasound. When a patient is evaluated for edema, it is often difficult to distinguish the early stages of lymphedema from venous insufficiency. DUS of the venous system can determine if there is concomitant venous thrombosis or venous reflux, perhaps contributing to extremity edema. The diagnostic modalities discussed in the following sections have limited use in clinical practice. They are invasive and tedious and rarely change the management of a patient with lymphedema. Most physicians rely on the patient’s history and physical examina-tion |
Surgery_Schwartz_6744 | Surgery_Schwartz | limited use in clinical practice. They are invasive and tedious and rarely change the management of a patient with lymphedema. Most physicians rely on the patient’s history and physical examina-tion alone to make the diagnosis of lymphedema.Lymphoscintigraphy. Lymphoscintigraphy has become the most commonly, but still overall uncommonly, used diagnostic test to identify lymphatic abnormalities. It has largely replaced lymphangiography. A radiolabeled sulfur colloid (technetium 99 m sulfur colloid) is injected into the subdermal, interdigital region of the affected limb. The lymphatic transport is moni-tored with a whole-body gamma camera, and major lymphatics and nodes can be visualized (Fig. 24-22). In normal individu-als, tracer activity may be detected in the inguinal region within 15 to 60 minutes. Within 3 hours, uptake should be present in the pelvic and abdominal lymph nodes. In patients with lymph-edema, various patterns may be seen on lymphoscintigraphy. There may be delayed | Surgery_Schwartz. limited use in clinical practice. They are invasive and tedious and rarely change the management of a patient with lymphedema. Most physicians rely on the patient’s history and physical examina-tion alone to make the diagnosis of lymphedema.Lymphoscintigraphy. Lymphoscintigraphy has become the most commonly, but still overall uncommonly, used diagnostic test to identify lymphatic abnormalities. It has largely replaced lymphangiography. A radiolabeled sulfur colloid (technetium 99 m sulfur colloid) is injected into the subdermal, interdigital region of the affected limb. The lymphatic transport is moni-tored with a whole-body gamma camera, and major lymphatics and nodes can be visualized (Fig. 24-22). In normal individu-als, tracer activity may be detected in the inguinal region within 15 to 60 minutes. Within 3 hours, uptake should be present in the pelvic and abdominal lymph nodes. In patients with lymph-edema, various patterns may be seen on lymphoscintigraphy. There may be delayed |
Surgery_Schwartz_6745 | Surgery_Schwartz | to 60 minutes. Within 3 hours, uptake should be present in the pelvic and abdominal lymph nodes. In patients with lymph-edema, various patterns may be seen on lymphoscintigraphy. There may be delayed or absent transport to the inguinal nodes. Increased cutaneous collaterals may be seen with obstruction of the primary axial channels. There may also be localized regions of reduced uptake in patients with prior node dissection or radia-tion therapy.Lymphangiography. Radiologic lymphangiography is per-formed by first visualizing the lymphatics by injecting colored dye into the hand or foot. The visualized lymphatic segment is exposed through a small incision and cannulated with a 27to 30-gauge needle. An oil-based dye is then injected slowly into the lymphatics over several hours. The lym-phatic channels and nodes are then visualized with traditional radiographs (Figs. 24-23 and 24-24). Lymphangiography is reserved for patients with lymphangiectasia or lymphatic fis-tulas, and patients | Surgery_Schwartz. to 60 minutes. Within 3 hours, uptake should be present in the pelvic and abdominal lymph nodes. In patients with lymph-edema, various patterns may be seen on lymphoscintigraphy. There may be delayed or absent transport to the inguinal nodes. Increased cutaneous collaterals may be seen with obstruction of the primary axial channels. There may also be localized regions of reduced uptake in patients with prior node dissection or radia-tion therapy.Lymphangiography. Radiologic lymphangiography is per-formed by first visualizing the lymphatics by injecting colored dye into the hand or foot. The visualized lymphatic segment is exposed through a small incision and cannulated with a 27to 30-gauge needle. An oil-based dye is then injected slowly into the lymphatics over several hours. The lym-phatic channels and nodes are then visualized with traditional radiographs (Figs. 24-23 and 24-24). Lymphangiography is reserved for patients with lymphangiectasia or lymphatic fis-tulas, and patients |
Surgery_Schwartz_6746 | Surgery_Schwartz | channels and nodes are then visualized with traditional radiographs (Figs. 24-23 and 24-24). Lymphangiography is reserved for patients with lymphangiectasia or lymphatic fis-tulas, and patients who are being considered for microvascular reconstruction.ManagementAn important aspect of the management of lymphedema is patient understanding that there is no cure for lymphedema. The primary goals of treatment are to minimize swelling and to prevent recurrent infections. Controlling the chronic limb swelling can improve discomfort, heaviness, and tightness, and potentially reduce the progression of disease.132Brunicardi_Ch24_p0981-p1008.indd 100222/02/19 3:01 PM 1003VENOUS AND LYMPHATIC DISEASECHAPTER 24Figure 24-24. Normal lymphangiogram of the thigh and lower leg.Compression Garments. Graded compression stockings are widely used in the treatment of lymphedema. The stockings reduce the amount of swelling in the involved extremity by decreasing edema accumulation while the extremity is | Surgery_Schwartz. channels and nodes are then visualized with traditional radiographs (Figs. 24-23 and 24-24). Lymphangiography is reserved for patients with lymphangiectasia or lymphatic fis-tulas, and patients who are being considered for microvascular reconstruction.ManagementAn important aspect of the management of lymphedema is patient understanding that there is no cure for lymphedema. The primary goals of treatment are to minimize swelling and to prevent recurrent infections. Controlling the chronic limb swelling can improve discomfort, heaviness, and tightness, and potentially reduce the progression of disease.132Brunicardi_Ch24_p0981-p1008.indd 100222/02/19 3:01 PM 1003VENOUS AND LYMPHATIC DISEASECHAPTER 24Figure 24-24. Normal lymphangiogram of the thigh and lower leg.Compression Garments. Graded compression stockings are widely used in the treatment of lymphedema. The stockings reduce the amount of swelling in the involved extremity by decreasing edema accumulation while the extremity is |
Surgery_Schwartz_6747 | Surgery_Schwartz | compression stockings are widely used in the treatment of lymphedema. The stockings reduce the amount of swelling in the involved extremity by decreasing edema accumulation while the extremity is dependent. When worn daily, compression stockings have been associated with long-term maintenance of reduced limb circumference.134 They may also protect the tissues against chronically elevated intrinsic pressures, which lead to thickening of the skin and sub-cutaneous tissue.135 Compression stockings also offer a degree of protection against external trauma that may lead to cellulitis.The amount of compression required for controlling lymphedema ranges from 20 to 60 mmHg and varies among patients. The stockings can be custom made or prefabricated and are available in aboveand below-knee lengths. The stock-ings should be worn during waking hours. The garments should be replaced approximately every 6 months when they lose elasticity.Bedrest and Leg Elevation. Elevation is an important aspect | Surgery_Schwartz. compression stockings are widely used in the treatment of lymphedema. The stockings reduce the amount of swelling in the involved extremity by decreasing edema accumulation while the extremity is dependent. When worn daily, compression stockings have been associated with long-term maintenance of reduced limb circumference.134 They may also protect the tissues against chronically elevated intrinsic pressures, which lead to thickening of the skin and sub-cutaneous tissue.135 Compression stockings also offer a degree of protection against external trauma that may lead to cellulitis.The amount of compression required for controlling lymphedema ranges from 20 to 60 mmHg and varies among patients. The stockings can be custom made or prefabricated and are available in aboveand below-knee lengths. The stock-ings should be worn during waking hours. The garments should be replaced approximately every 6 months when they lose elasticity.Bedrest and Leg Elevation. Elevation is an important aspect |
Surgery_Schwartz_6748 | Surgery_Schwartz | The stock-ings should be worn during waking hours. The garments should be replaced approximately every 6 months when they lose elasticity.Bedrest and Leg Elevation. Elevation is an important aspect of controlling lower extremity swelling and is often the first recommended intervention. However, continuous elevation throughout the day can interfere with quality of life more than lymphedema itself. Elevation is an adjunct to lymphedema ther-apy but is not the mainstay of treatment.Intermittent Pneumatic Compression Therapy. The use of IPC with a single-chamber or multichamber pump temporar-ily reduces edema and provides another adjunct to the use of compression stockings. These devices have been shown to be effective in reducing limb volume; however, use of compres-sion stockings is necessary to maintain the volume reduction when the patient is no longer supine because fluid transport is not associated with the transport of macromolecules (proteins) from the tissue. Typically, IPC is | Surgery_Schwartz. The stock-ings should be worn during waking hours. The garments should be replaced approximately every 6 months when they lose elasticity.Bedrest and Leg Elevation. Elevation is an important aspect of controlling lower extremity swelling and is often the first recommended intervention. However, continuous elevation throughout the day can interfere with quality of life more than lymphedema itself. Elevation is an adjunct to lymphedema ther-apy but is not the mainstay of treatment.Intermittent Pneumatic Compression Therapy. The use of IPC with a single-chamber or multichamber pump temporar-ily reduces edema and provides another adjunct to the use of compression stockings. These devices have been shown to be effective in reducing limb volume; however, use of compres-sion stockings is necessary to maintain the volume reduction when the patient is no longer supine because fluid transport is not associated with the transport of macromolecules (proteins) from the tissue. Typically, IPC is |
Surgery_Schwartz_6749 | Surgery_Schwartz | to maintain the volume reduction when the patient is no longer supine because fluid transport is not associated with the transport of macromolecules (proteins) from the tissue. Typically, IPC is used for 4 to 6 hours per day at home when the patient is supine, with pressure ranges between 30 and 60 mmHg demonstrated to be most effective.135Lymphatic Massage. Manual lymphatic drainage is a form of massage developed by Vodder136 that is directed at reduc-ing edema. In combination with the use of compression stock-ings, manual lymphatic drainage is associated with a long-term reduction in edema and fewer infections per patient per year.137Antibiotic Therapy. Patients with lymphedema are at increased risk of developing cellulitis in the affected extremity due to microscopic breakdown in the skin barrier either second-ary to swelling or unrecognized and untreated tinea pedis. Recur-rent infection can damage the lymphatics, aggravating the edema and increasing the risk for subsequent | Surgery_Schwartz. to maintain the volume reduction when the patient is no longer supine because fluid transport is not associated with the transport of macromolecules (proteins) from the tissue. Typically, IPC is used for 4 to 6 hours per day at home when the patient is supine, with pressure ranges between 30 and 60 mmHg demonstrated to be most effective.135Lymphatic Massage. Manual lymphatic drainage is a form of massage developed by Vodder136 that is directed at reduc-ing edema. In combination with the use of compression stock-ings, manual lymphatic drainage is associated with a long-term reduction in edema and fewer infections per patient per year.137Antibiotic Therapy. Patients with lymphedema are at increased risk of developing cellulitis in the affected extremity due to microscopic breakdown in the skin barrier either second-ary to swelling or unrecognized and untreated tinea pedis. Recur-rent infection can damage the lymphatics, aggravating the edema and increasing the risk for subsequent |
Surgery_Schwartz_6750 | Surgery_Schwartz | the skin barrier either second-ary to swelling or unrecognized and untreated tinea pedis. Recur-rent infection can damage the lymphatics, aggravating the edema and increasing the risk for subsequent infection. Staphylococcus and β-hemolytic Streptococcus are the most common organisms causing soft tissue infection. Aggressive antibiotic therapy and elevation with compression are recommended at the earliest signs or symptoms of cellulitis. The drug of choice is penicil-lin or a cephalosporin active against Streptococcus for 5 days. In patients with recurrent cellulitis despite methods to reduced edema, treatment with monthly intramuscular injections of ben-zathine penicillin 1.2 MU, twice-daily erythromycin 250 mg, or penicillin V 1 g daily has proven effective at suppression.138Surgery. A variety of surgical procedures have been devised for the treatment of lymphedema. Surgical treatment involves either excision of extra tissue139 or anastomosis of a lymphatic vessel to another | Surgery_Schwartz. the skin barrier either second-ary to swelling or unrecognized and untreated tinea pedis. Recur-rent infection can damage the lymphatics, aggravating the edema and increasing the risk for subsequent infection. Staphylococcus and β-hemolytic Streptococcus are the most common organisms causing soft tissue infection. Aggressive antibiotic therapy and elevation with compression are recommended at the earliest signs or symptoms of cellulitis. The drug of choice is penicil-lin or a cephalosporin active against Streptococcus for 5 days. In patients with recurrent cellulitis despite methods to reduced edema, treatment with monthly intramuscular injections of ben-zathine penicillin 1.2 MU, twice-daily erythromycin 250 mg, or penicillin V 1 g daily has proven effective at suppression.138Surgery. A variety of surgical procedures have been devised for the treatment of lymphedema. Surgical treatment involves either excision of extra tissue139 or anastomosis of a lymphatic vessel to another |
Surgery_Schwartz_6751 | Surgery_Schwartz | variety of surgical procedures have been devised for the treatment of lymphedema. Surgical treatment involves either excision of extra tissue139 or anastomosis of a lymphatic vessel to another lymphatic or vein.140 In excisional procedures, part or all of the edematous tissue is removed. This does not improve lymphatic drainage but debulks redundant tissue. The microsurgical procedures involve the creation of a lymphati-colymphatic or lymphaticovenous anastomosis, which theo-retically improves lymphatic drainage. No long-term follow-up data are available for these interventions, and therefore opera-tive therapy for lymphedema is not well accepted worldwide. Furthermore, operative intervention has the potential to further obliterate lymphatic channels, worsening the edema.141SUMMARYLymphedema is a chronic condition caused by ineffective lymphatic transport, which results in edema and skin damage. Lymphedema is not curable, but the symptoms and long-term effects can be controlled with a | Surgery_Schwartz. variety of surgical procedures have been devised for the treatment of lymphedema. Surgical treatment involves either excision of extra tissue139 or anastomosis of a lymphatic vessel to another lymphatic or vein.140 In excisional procedures, part or all of the edematous tissue is removed. This does not improve lymphatic drainage but debulks redundant tissue. The microsurgical procedures involve the creation of a lymphati-colymphatic or lymphaticovenous anastomosis, which theo-retically improves lymphatic drainage. No long-term follow-up data are available for these interventions, and therefore opera-tive therapy for lymphedema is not well accepted worldwide. Furthermore, operative intervention has the potential to further obliterate lymphatic channels, worsening the edema.141SUMMARYLymphedema is a chronic condition caused by ineffective lymphatic transport, which results in edema and skin damage. Lymphedema is not curable, but the symptoms and long-term effects can be controlled with a |
Surgery_Schwartz_6752 | Surgery_Schwartz | is a chronic condition caused by ineffective lymphatic transport, which results in edema and skin damage. Lymphedema is not curable, but the symptoms and long-term effects can be controlled with a combination of elastic com-pression stockings, limb elevation, pneumatic compression, and massage. Controlling the edema protects the skin and potentially prevents cellulitis.REFERENCESEntries highlighted in bright blue are key references. 1. Moncada S, Radomski MW, Palmer RM. Endothelium-derived relaxing factor. Identification as nitric oxide and role in the control of vascular tone and platelet function. Biochem Pharmacol. 1988;37:2495-2501. 2. van Bemmelen PS, Beach K, Bedford G, et al. The mecha-nism of venous valve closure. Its relationship to the velocity of reverse flow. Arch Surg. 1990;125:617-619. 3. Moneta GL, Strandness DE, Jr. Basic data concerning nonin-vasive vascular testing. Ann Vasc Surg. 1989;3:190-193. 4. Neglen P, Berry MA, Raju S. Endovascular surgery in the treatment of | Surgery_Schwartz. is a chronic condition caused by ineffective lymphatic transport, which results in edema and skin damage. Lymphedema is not curable, but the symptoms and long-term effects can be controlled with a combination of elastic com-pression stockings, limb elevation, pneumatic compression, and massage. Controlling the edema protects the skin and potentially prevents cellulitis.REFERENCESEntries highlighted in bright blue are key references. 1. Moncada S, Radomski MW, Palmer RM. Endothelium-derived relaxing factor. Identification as nitric oxide and role in the control of vascular tone and platelet function. Biochem Pharmacol. 1988;37:2495-2501. 2. van Bemmelen PS, Beach K, Bedford G, et al. The mecha-nism of venous valve closure. Its relationship to the velocity of reverse flow. Arch Surg. 1990;125:617-619. 3. Moneta GL, Strandness DE, Jr. Basic data concerning nonin-vasive vascular testing. Ann Vasc Surg. 1989;3:190-193. 4. Neglen P, Berry MA, Raju S. Endovascular surgery in the treatment of |
Surgery_Schwartz_6753 | Surgery_Schwartz | GL, Strandness DE, Jr. Basic data concerning nonin-vasive vascular testing. Ann Vasc Surg. 1989;3:190-193. 4. Neglen P, Berry MA, Raju S. Endovascular surgery in the treatment of chronic primary and post-thrombotic iliac vein obstruction. Eur J Vasc Endovasc Surg. 2000;20(6):560-571. 5. Bettman MA, Robbins A, Braun SD, et al. Contrast venogra-phy of the leg: diagnostic efficacy, tolerance, and complica-tion rates with ionic and nonionic contrast media. Radiology. 1987;165:113-116.Brunicardi_Ch24_p0981-p1008.indd 100322/02/19 3:01 PM 1004SPECIFIC CONSIDERATIONSPART II 6. White R. The epidemiology of venous thromboembolism. Circulation. 2003;107:I4-I8. 7. Spyropoulos AC, Hussein M, Lin J, et al. Rates of symptom-atic venous thromboembolism in US surgical patients: a ret-rospective administrative database. J Thromb Thrombolysis. 2009;28:458-464. 8. Heit JA, Cohen AT, Anderson FA. Estimated annual number of incident and recurrent, non-fatal and fatal venous thromboem-bolism (VTE) | Surgery_Schwartz. GL, Strandness DE, Jr. Basic data concerning nonin-vasive vascular testing. Ann Vasc Surg. 1989;3:190-193. 4. Neglen P, Berry MA, Raju S. Endovascular surgery in the treatment of chronic primary and post-thrombotic iliac vein obstruction. Eur J Vasc Endovasc Surg. 2000;20(6):560-571. 5. Bettman MA, Robbins A, Braun SD, et al. Contrast venogra-phy of the leg: diagnostic efficacy, tolerance, and complica-tion rates with ionic and nonionic contrast media. Radiology. 1987;165:113-116.Brunicardi_Ch24_p0981-p1008.indd 100322/02/19 3:01 PM 1004SPECIFIC CONSIDERATIONSPART II 6. White R. The epidemiology of venous thromboembolism. Circulation. 2003;107:I4-I8. 7. Spyropoulos AC, Hussein M, Lin J, et al. Rates of symptom-atic venous thromboembolism in US surgical patients: a ret-rospective administrative database. J Thromb Thrombolysis. 2009;28:458-464. 8. Heit JA, Cohen AT, Anderson FA. Estimated annual number of incident and recurrent, non-fatal and fatal venous thromboem-bolism (VTE) |
Surgery_Schwartz_6754 | Surgery_Schwartz | database. J Thromb Thrombolysis. 2009;28:458-464. 8. Heit JA, Cohen AT, Anderson FA. Estimated annual number of incident and recurrent, non-fatal and fatal venous thromboem-bolism (VTE) events in the US. Blood. 2005;106:910. 9. Pengo V, Lensing AWA, Prins MH, et al. Incidence of chronic thromboembolic pulmonary hypertension after pulmonary embolism. N Engl J Med. 2004;350:2257-2264. 10. Kahn SR, Ginsberg JS. The post-thrombotic syndrome: current knowledge, controversies and directions for future research. Blood Rev. 2002;16:155-165. 11. Mohr DN, Silverstein MD, Heit JA, et al. The venous sta-sis syndrome after deep venous thrombosis or pulmonary embolism: a population-based study. Mayo Clin Proc. 2000;75:1249-1256. 12. Rosendaal FR. Risk factors for venous thrombotic disease. Thromb Haemost. 1999;82:610. 13. Ageno W, Becattini C, Brighton T, et al. Cardiovascular risk factors and venous thromboembolism: a meta-analysis. Circulation. 2008;117:93-102. 14. White R, Zhou H, Romano P. | Surgery_Schwartz. database. J Thromb Thrombolysis. 2009;28:458-464. 8. Heit JA, Cohen AT, Anderson FA. Estimated annual number of incident and recurrent, non-fatal and fatal venous thromboem-bolism (VTE) events in the US. Blood. 2005;106:910. 9. Pengo V, Lensing AWA, Prins MH, et al. Incidence of chronic thromboembolic pulmonary hypertension after pulmonary embolism. N Engl J Med. 2004;350:2257-2264. 10. Kahn SR, Ginsberg JS. The post-thrombotic syndrome: current knowledge, controversies and directions for future research. Blood Rev. 2002;16:155-165. 11. Mohr DN, Silverstein MD, Heit JA, et al. The venous sta-sis syndrome after deep venous thrombosis or pulmonary embolism: a population-based study. Mayo Clin Proc. 2000;75:1249-1256. 12. Rosendaal FR. Risk factors for venous thrombotic disease. Thromb Haemost. 1999;82:610. 13. Ageno W, Becattini C, Brighton T, et al. Cardiovascular risk factors and venous thromboembolism: a meta-analysis. Circulation. 2008;117:93-102. 14. White R, Zhou H, Romano P. |
Surgery_Schwartz_6755 | Surgery_Schwartz | 1999;82:610. 13. Ageno W, Becattini C, Brighton T, et al. Cardiovascular risk factors and venous thromboembolism: a meta-analysis. Circulation. 2008;117:93-102. 14. White R, Zhou H, Romano P. Incidence of idiopathic deep venous thrombosis and secondary thromboembo-lism among ethnic groups in California. Ann Intern Med. 1998;128:737-740. 15. Bezemer ID, Bare LA, Doggen CJM, et al. Gene variants asso-ciated with deep vein thrombosis. JAMA. 2008;299:1306-1314. 16. 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;204:1211-1221. 17. Bahl V, Hu HM, Henke PK, Wakefield TW, Campbell DA, Jr, Caprini JA. A validation study of retrospective venous thromboembolism risk scoring method. Ann Surg. 2010;251:344-350. 18. Markel A, Manzo RA, Bergelin RO, et al. Pattern and dis-tribution of thrombi in acute venous thrombosis. Arch | Surgery_Schwartz. 1999;82:610. 13. Ageno W, Becattini C, Brighton T, et al. Cardiovascular risk factors and venous thromboembolism: a meta-analysis. Circulation. 2008;117:93-102. 14. White R, Zhou H, Romano P. Incidence of idiopathic deep venous thrombosis and secondary thromboembo-lism among ethnic groups in California. Ann Intern Med. 1998;128:737-740. 15. Bezemer ID, Bare LA, Doggen CJM, et al. Gene variants asso-ciated with deep vein thrombosis. JAMA. 2008;299:1306-1314. 16. 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;204:1211-1221. 17. Bahl V, Hu HM, Henke PK, Wakefield TW, Campbell DA, Jr, Caprini JA. A validation study of retrospective venous thromboembolism risk scoring method. Ann Surg. 2010;251:344-350. 18. Markel A, Manzo RA, Bergelin RO, et al. Pattern and dis-tribution of thrombi in acute venous thrombosis. Arch |
Surgery_Schwartz_6756 | Surgery_Schwartz | retrospective venous thromboembolism risk scoring method. Ann Surg. 2010;251:344-350. 18. Markel A, Manzo RA, Bergelin RO, et al. Pattern and dis-tribution of thrombi in acute venous thrombosis. Arch Surg. 1992;127:305-309. 19. Nicolaides AN, Kakkar VV, Field ES, et al. The origin of deep vein thrombosis: a venographic study. Br J Radiol. 1971;44:653-663. 20. Brockman SK, Vasko JS. The pathologic physiology of phleg-masia cerulea dolens. Surgery. 1966;59:997-1007. 21. Lensing AW, Prandoni P, Brandjes D, et al. Detection of deep-vein thrombosis by real-time B-mode ultrasonography. N Engl J Med. 1989;320:342-345. 22. O’Leary DH, Kane RA, Chase BM. A prospective study of the efficacy of B-scan sonography in the detection of deep venous thrombosis in the lower extremities. J Clin Ultrasound. 1988;16:1-8. 23. Mussurakis S, Papaioannou S, Voros D, et al. Compression ultrasonography as a reliable imaging monitor in deep venous thrombosis. Surg Gynecol Obstet. 1990;171:233-239. 24. Habscheid | Surgery_Schwartz. retrospective venous thromboembolism risk scoring method. Ann Surg. 2010;251:344-350. 18. Markel A, Manzo RA, Bergelin RO, et al. Pattern and dis-tribution of thrombi in acute venous thrombosis. Arch Surg. 1992;127:305-309. 19. Nicolaides AN, Kakkar VV, Field ES, et al. The origin of deep vein thrombosis: a venographic study. Br J Radiol. 1971;44:653-663. 20. Brockman SK, Vasko JS. The pathologic physiology of phleg-masia cerulea dolens. Surgery. 1966;59:997-1007. 21. Lensing AW, Prandoni P, Brandjes D, et al. Detection of deep-vein thrombosis by real-time B-mode ultrasonography. N Engl J Med. 1989;320:342-345. 22. O’Leary DH, Kane RA, Chase BM. A prospective study of the efficacy of B-scan sonography in the detection of deep venous thrombosis in the lower extremities. J Clin Ultrasound. 1988;16:1-8. 23. Mussurakis S, Papaioannou S, Voros D, et al. Compression ultrasonography as a reliable imaging monitor in deep venous thrombosis. Surg Gynecol Obstet. 1990;171:233-239. 24. Habscheid |
Surgery_Schwartz_6757 | Surgery_Schwartz | 1988;16:1-8. 23. Mussurakis S, Papaioannou S, Voros D, et al. Compression ultrasonography as a reliable imaging monitor in deep venous thrombosis. Surg Gynecol Obstet. 1990;171:233-239. 24. Habscheid W, Hohmann M, Wilhelm T, et al. Real-time ultra-sound in the diagnosis of acute deep venous thrombosis of the lower extremity. Angiology. 1990;41:599-608. 25. Comerota AJ, Katz ML, Grossi RJ, et al. The comparative value of noninvasive testing for diagnosis and surveillance of deep vein thrombosis. J Vasc Surg. 1988;7:40-49. 26. Gomes AS, Webber MM, Buffkin D. Contrast venography vs. radionuclide venography: a study of discrepancies and their possible significance. Radiology. 1982;142:719-728. 27. Hull R, Hirsh J, Sackett DL, et al. Clinical validity of a nega-tive venogram in patients with clinically suspected venous thrombosis. Circulation. 1981;64:622-625. 28. Kearon C, Akl E, Comerota A, et al. Antithrombotic ther-apy for venous thromboembolic disease: antithrombotic therapy and | Surgery_Schwartz. 1988;16:1-8. 23. Mussurakis S, Papaioannou S, Voros D, et al. Compression ultrasonography as a reliable imaging monitor in deep venous thrombosis. Surg Gynecol Obstet. 1990;171:233-239. 24. Habscheid W, Hohmann M, Wilhelm T, et al. Real-time ultra-sound in the diagnosis of acute deep venous thrombosis of the lower extremity. Angiology. 1990;41:599-608. 25. Comerota AJ, Katz ML, Grossi RJ, et al. The comparative value of noninvasive testing for diagnosis and surveillance of deep vein thrombosis. J Vasc Surg. 1988;7:40-49. 26. Gomes AS, Webber MM, Buffkin D. Contrast venography vs. radionuclide venography: a study of discrepancies and their possible significance. Radiology. 1982;142:719-728. 27. Hull R, Hirsh J, Sackett DL, et al. Clinical validity of a nega-tive venogram in patients with clinically suspected venous thrombosis. Circulation. 1981;64:622-625. 28. Kearon C, Akl E, Comerota A, et al. Antithrombotic ther-apy for venous thromboembolic disease: antithrombotic therapy and |
Surgery_Schwartz_6758 | Surgery_Schwartz | clinically suspected venous thrombosis. Circulation. 1981;64:622-625. 28. Kearon C, Akl E, Comerota A, et al. Antithrombotic ther-apy for venous thromboembolic disease: antithrombotic therapy and prevention of thrombosis. American College of Chest Physicians evidence-based clinical practice guidelines (9th edition). Chest. 2012;141(2 suppl):e419S-e496S. The most recent American College of Chest Physicians clinical practice guidelines on antithrombotic therapy for venous thromboembolic disease. These recommendations cover multimodality therapies and are based upon an exhaustive review of the literature, including randomized clinical trials. 29. Raschke RA, Reilly BM, Guidry JR, et al. The weight-based heparin dosing nomogram compared with a standard care nomogram. A randomized controlled trial. Ann Intern Med. 1993;119:874-881. 30. Hylek EM, Regan S, Henault LE, et al. Challenges to the effective use of unfractionated heparin in the hospital-ized management of acute thrombosis. Arch | Surgery_Schwartz. clinically suspected venous thrombosis. Circulation. 1981;64:622-625. 28. Kearon C, Akl E, Comerota A, et al. Antithrombotic ther-apy for venous thromboembolic disease: antithrombotic therapy and prevention of thrombosis. American College of Chest Physicians evidence-based clinical practice guidelines (9th edition). Chest. 2012;141(2 suppl):e419S-e496S. The most recent American College of Chest Physicians clinical practice guidelines on antithrombotic therapy for venous thromboembolic disease. These recommendations cover multimodality therapies and are based upon an exhaustive review of the literature, including randomized clinical trials. 29. Raschke RA, Reilly BM, Guidry JR, et al. The weight-based heparin dosing nomogram compared with a standard care nomogram. A randomized controlled trial. Ann Intern Med. 1993;119:874-881. 30. Hylek EM, Regan S, Henault LE, et al. Challenges to the effective use of unfractionated heparin in the hospital-ized management of acute thrombosis. Arch |
Surgery_Schwartz_6759 | Surgery_Schwartz | trial. Ann Intern Med. 1993;119:874-881. 30. Hylek EM, Regan S, Henault LE, et al. Challenges to the effective use of unfractionated heparin in the hospital-ized management of acute thrombosis. Arch Intern Med. 2003;163:621-627. 31. Amiral J, Bridey F, Dreyfus M, et al. Platelet factor 4 com-plexed to heparin is the target for antibodies generated in heparin-induced thrombocytopenia. Thromb Haemost. 1992;68:95-96. 32. Warkentin TE, Levine MN, Hirsh J, et al. Heparin-induced thrombocytopenia in patients treated with low-molecular-weight heparin or unfractionated heparin. N Engl J Med. 1995;332:1330-1335. 33. Warkentin TE, Kelton JG. Heparin and platelets. Hematol Oncol Clin North Am. 1990;4:243-264. 34. Calaitges JG, Liem TK, Spadone D, et al. The role of heparin-associated antiplatelet antibodies in the outcome of arterial reconstruction. J Vasc Surg. 1999;29:779-786. 35. Warkentin TE, Kelton JG. A 14-year study of heparin-induced thrombocytopenia. Am J Med. | Surgery_Schwartz. trial. Ann Intern Med. 1993;119:874-881. 30. Hylek EM, Regan S, Henault LE, et al. Challenges to the effective use of unfractionated heparin in the hospital-ized management of acute thrombosis. Arch Intern Med. 2003;163:621-627. 31. Amiral J, Bridey F, Dreyfus M, et al. Platelet factor 4 com-plexed to heparin is the target for antibodies generated in heparin-induced thrombocytopenia. Thromb Haemost. 1992;68:95-96. 32. Warkentin TE, Levine MN, Hirsh J, et al. Heparin-induced thrombocytopenia in patients treated with low-molecular-weight heparin or unfractionated heparin. N Engl J Med. 1995;332:1330-1335. 33. Warkentin TE, Kelton JG. Heparin and platelets. Hematol Oncol Clin North Am. 1990;4:243-264. 34. Calaitges JG, Liem TK, Spadone D, et al. The role of heparin-associated antiplatelet antibodies in the outcome of arterial reconstruction. J Vasc Surg. 1999;29:779-786. 35. Warkentin TE, Kelton JG. A 14-year study of heparin-induced thrombocytopenia. Am J Med. |
Surgery_Schwartz_6760 | Surgery_Schwartz | antiplatelet antibodies in the outcome of arterial reconstruction. J Vasc Surg. 1999;29:779-786. 35. Warkentin TE, Kelton JG. A 14-year study of heparin-induced thrombocytopenia. Am J Med. 1996;101:502-507. 36. Gould MK, Dembitzer AD, Doyle RL, et al. Low-molecular-weight heparins compared with unfractionated heparin for treatment of acute deep venous thrombosis: a meta-anal-ysis of randomized, controlled trials. Ann Intern Med. 1999;130:800-809. 37. Dolovich LR, Ginsberg JS, Douketis JD, et al. A meta-analysis comparing low-molecular-weight heparins with unfraction-ated heparin in the treatment of venous thromboembolism: examining some unanswered questions regarding location of treatment, product type, and dosing frequency. Arch Intern Med. 2000;160:181-188. 38. Van Dongen CJJ, van der Belt AGM, Prins MH, et al. Fixed dose subcutaneous low molecular weight heparins versus adjusted dose unfractionated heparin for venous thromboem-bolism. Cochrane Database Syst Rev. | Surgery_Schwartz. antiplatelet antibodies in the outcome of arterial reconstruction. J Vasc Surg. 1999;29:779-786. 35. Warkentin TE, Kelton JG. A 14-year study of heparin-induced thrombocytopenia. Am J Med. 1996;101:502-507. 36. Gould MK, Dembitzer AD, Doyle RL, et al. Low-molecular-weight heparins compared with unfractionated heparin for treatment of acute deep venous thrombosis: a meta-anal-ysis of randomized, controlled trials. Ann Intern Med. 1999;130:800-809. 37. Dolovich LR, Ginsberg JS, Douketis JD, et al. A meta-analysis comparing low-molecular-weight heparins with unfraction-ated heparin in the treatment of venous thromboembolism: examining some unanswered questions regarding location of treatment, product type, and dosing frequency. Arch Intern Med. 2000;160:181-188. 38. Van Dongen CJJ, van der Belt AGM, Prins MH, et al. Fixed dose subcutaneous low molecular weight heparins versus adjusted dose unfractionated heparin for venous thromboem-bolism. Cochrane Database Syst Rev. |
Surgery_Schwartz_6761 | Surgery_Schwartz | CJJ, van der Belt AGM, Prins MH, et al. Fixed dose subcutaneous low molecular weight heparins versus adjusted dose unfractionated heparin for venous thromboem-bolism. Cochrane Database Syst Rev. 2004;4:CD001100. 39. Kikta MJ, Keller MP, Humphrey PW, et al. Can low molecular weight heparins and heparinoids be safely given to patients with heparin-induced thrombocytopenia syndrome? Surgery. 1993;114:705-710. 40. Koopman MM, Prandoni P, Piovella F, et al. Treatment of venous thrombosis with intravenous unfractionated heparin administered in the hospital as compared with subcutaneous low-molecular-weight heparin administered at home. The Tas-man Study Group. N Engl J Med. 1996;334:682-687. 41. Levine M, Gent M, Hirsh J, et al. A comparison of low-molecularweight heparin administered primarily at home with unfraction-ated heparin administered in the hospital for proximal deep-vein thrombosis. N Engl J Med. 1996;334:677-681. 42. Büller HR, Davidson BL, Decousus H, et al. Fondaparinux or | Surgery_Schwartz. CJJ, van der Belt AGM, Prins MH, et al. Fixed dose subcutaneous low molecular weight heparins versus adjusted dose unfractionated heparin for venous thromboem-bolism. Cochrane Database Syst Rev. 2004;4:CD001100. 39. Kikta MJ, Keller MP, Humphrey PW, et al. Can low molecular weight heparins and heparinoids be safely given to patients with heparin-induced thrombocytopenia syndrome? Surgery. 1993;114:705-710. 40. Koopman MM, Prandoni P, Piovella F, et al. Treatment of venous thrombosis with intravenous unfractionated heparin administered in the hospital as compared with subcutaneous low-molecular-weight heparin administered at home. The Tas-man Study Group. N Engl J Med. 1996;334:682-687. 41. Levine M, Gent M, Hirsh J, et al. A comparison of low-molecularweight heparin administered primarily at home with unfraction-ated heparin administered in the hospital for proximal deep-vein thrombosis. N Engl J Med. 1996;334:677-681. 42. Büller HR, Davidson BL, Decousus H, et al. Fondaparinux or |
Surgery_Schwartz_6762 | Surgery_Schwartz | at home with unfraction-ated heparin administered in the hospital for proximal deep-vein thrombosis. N Engl J Med. 1996;334:677-681. 42. Büller HR, Davidson BL, Decousus H, et al. Fondaparinux or enoxaparin for the initial treatment of symptomatic deep venous thrombosis: a randomized trial. Ann Intern Med. 2004;140:867-873. 43. The Matisse Investigators. Subcutaneous fondaparinux versus intravenous unfractionated heparin in the initial treatment of pulmonary embolism. N Engl J Med. 2003;349:1695-1702.Brunicardi_Ch24_p0981-p1008.indd 100422/02/19 3:01 PM 1005VENOUS AND LYMPHATIC DISEASECHAPTER 24 44. Warkentin TE, Maurer BT, Aster RH. Heparin-induced throm-bocytopenia associated with fondaparinux. N Engl J Med. 2007;356:2653-2655. 45. Kelton JG. The pathophysiology of heparin-induced thrombocytopenia: biological basis for treatment. Chest. 2005;127:9S-20S. 46. Martin K, Beyer-Westendorf J, Davidson BL, Huisman MV, Sandset PM, Moll S. Use of the direct oral anticoagulants in obese | Surgery_Schwartz. at home with unfraction-ated heparin administered in the hospital for proximal deep-vein thrombosis. N Engl J Med. 1996;334:677-681. 42. Büller HR, Davidson BL, Decousus H, et al. Fondaparinux or enoxaparin for the initial treatment of symptomatic deep venous thrombosis: a randomized trial. Ann Intern Med. 2004;140:867-873. 43. The Matisse Investigators. Subcutaneous fondaparinux versus intravenous unfractionated heparin in the initial treatment of pulmonary embolism. N Engl J Med. 2003;349:1695-1702.Brunicardi_Ch24_p0981-p1008.indd 100422/02/19 3:01 PM 1005VENOUS AND LYMPHATIC DISEASECHAPTER 24 44. Warkentin TE, Maurer BT, Aster RH. Heparin-induced throm-bocytopenia associated with fondaparinux. N Engl J Med. 2007;356:2653-2655. 45. Kelton JG. The pathophysiology of heparin-induced thrombocytopenia: biological basis for treatment. Chest. 2005;127:9S-20S. 46. Martin K, Beyer-Westendorf J, Davidson BL, Huisman MV, Sandset PM, Moll S. Use of the direct oral anticoagulants in obese |
Surgery_Schwartz_6763 | Surgery_Schwartz | thrombocytopenia: biological basis for treatment. Chest. 2005;127:9S-20S. 46. Martin K, Beyer-Westendorf J, Davidson BL, Huisman MV, Sandset PM, Moll S. Use of the direct oral anticoagulants in obese patients: guidance from the SSC of the ISTH. J Thromb Haemost. 2016;14(6):1308-1313. 47. Schulman S, Shortt B, Robinson M, Eikelboom JW. Adher-ence to anticoagulant treatment with dabigatran in a real-world setting. J Thromb Haemost. 2013;11(7):1295-1299. 48. Pollack CV, Jr, Reilly PA, Eikelboom J, et al. Idarucizumab for Dabigatran Reversal. N Engl J Med. 2015;373(6):511-520. 49. Eerenberg ES, Kamphuisen PW, Sijpkens MK, Meijers JC, Buller HR, Levi M. Reversal of rivaroxaban and dabigatran by prothrombin complex concentrate: a randomized, placebo-controlled, crossover study in healthy subjects. Circulation. 2011;124(14):1573-1579. 50. Holbrook A, Schulman S, Witt DM, et al. Evidence based management of anticoagulant therapy. American College of Chest Physicians Evidence-Based Clinical | Surgery_Schwartz. thrombocytopenia: biological basis for treatment. Chest. 2005;127:9S-20S. 46. Martin K, Beyer-Westendorf J, Davidson BL, Huisman MV, Sandset PM, Moll S. Use of the direct oral anticoagulants in obese patients: guidance from the SSC of the ISTH. J Thromb Haemost. 2016;14(6):1308-1313. 47. Schulman S, Shortt B, Robinson M, Eikelboom JW. Adher-ence to anticoagulant treatment with dabigatran in a real-world setting. J Thromb Haemost. 2013;11(7):1295-1299. 48. Pollack CV, Jr, Reilly PA, Eikelboom J, et al. Idarucizumab for Dabigatran Reversal. N Engl J Med. 2015;373(6):511-520. 49. Eerenberg ES, Kamphuisen PW, Sijpkens MK, Meijers JC, Buller HR, Levi M. Reversal of rivaroxaban and dabigatran by prothrombin complex concentrate: a randomized, placebo-controlled, crossover study in healthy subjects. Circulation. 2011;124(14):1573-1579. 50. Holbrook A, Schulman S, Witt DM, et al. Evidence based management of anticoagulant therapy. American College of Chest Physicians Evidence-Based Clinical |
Surgery_Schwartz_6764 | Surgery_Schwartz | Circulation. 2011;124(14):1573-1579. 50. Holbrook A, Schulman S, Witt DM, et al. Evidence based management of anticoagulant therapy. American College of Chest Physicians Evidence-Based Clinical Practice Guide-lines, 9th ed. Chest. 2012;114:e152S-e184S. 51. Schulman S, Rhedin A-S, Lindmarker P, et al. A comparison of six weeks with six months of oral anticoagulant therapy after a first episode of venous thromboembolism. N Engl J Med. 1995;332:1661-1665. 52. Research Committee of the British Thoracic Society. Optimal duration of anticoagulation for deep vein thrombosis and pul-monary embolism. Lancet. 1992;340:873-876. 53. Levine MN, Hirsh J, Gent M, et al. Optimal duration of oral anticoagulant therapy: a randomized trial comparing four weeks with three months of warfarin in patients with proximal deep vein thrombosis. Thromb Haemost. 1995;74:606-611. 54. Kearon C, Gent M, Hirsh J, et al. A comparison of three months of anticoagulation with extended anticoagulation for a first episode | Surgery_Schwartz. Circulation. 2011;124(14):1573-1579. 50. Holbrook A, Schulman S, Witt DM, et al. Evidence based management of anticoagulant therapy. American College of Chest Physicians Evidence-Based Clinical Practice Guide-lines, 9th ed. Chest. 2012;114:e152S-e184S. 51. Schulman S, Rhedin A-S, Lindmarker P, et al. A comparison of six weeks with six months of oral anticoagulant therapy after a first episode of venous thromboembolism. N Engl J Med. 1995;332:1661-1665. 52. Research Committee of the British Thoracic Society. Optimal duration of anticoagulation for deep vein thrombosis and pul-monary embolism. Lancet. 1992;340:873-876. 53. Levine MN, Hirsh J, Gent M, et al. Optimal duration of oral anticoagulant therapy: a randomized trial comparing four weeks with three months of warfarin in patients with proximal deep vein thrombosis. Thromb Haemost. 1995;74:606-611. 54. Kearon C, Gent M, Hirsh J, et al. A comparison of three months of anticoagulation with extended anticoagulation for a first episode |
Surgery_Schwartz_6765 | Surgery_Schwartz | proximal deep vein thrombosis. Thromb Haemost. 1995;74:606-611. 54. Kearon C, Gent M, Hirsh J, et al. A comparison of three months of anticoagulation with extended anticoagulation for a first episode of idiopathic venous thromboembolism. N Engl J Med. 1999;340:901-907. 55. Agnelli G, Prandoni P, Santamaria MG, et al. Three months versus one year of oral anticoagulant therapy for idiopathic deep venous thrombosis. N Engl J Med. 2001;345:165-169. 56. Ridker PM, Goldhaber SZ, Danielson E, et al. Long-term, low-intensity warfarin therapy for the prevention of recurrent venous thromboembolism. N Engl J Med. 2003;348:1425. 57. Kearon C, Ginsber JS, Kovacs MJ, et al. Comparison of low-intensity warfarin therapy with conventional-intensity warfarin therapy for long-term prevention of recurrent venous thrombo-embolism. N Engl J Med. 2003;349:631-639. 58. Lee AYY, Levine MN, Baker RI, et al. Low-molecular-weight heparin versus a coumarin for the prevention of recurrent venous thromboembolism in | Surgery_Schwartz. proximal deep vein thrombosis. Thromb Haemost. 1995;74:606-611. 54. Kearon C, Gent M, Hirsh J, et al. A comparison of three months of anticoagulation with extended anticoagulation for a first episode of idiopathic venous thromboembolism. N Engl J Med. 1999;340:901-907. 55. Agnelli G, Prandoni P, Santamaria MG, et al. Three months versus one year of oral anticoagulant therapy for idiopathic deep venous thrombosis. N Engl J Med. 2001;345:165-169. 56. Ridker PM, Goldhaber SZ, Danielson E, et al. Long-term, low-intensity warfarin therapy for the prevention of recurrent venous thromboembolism. N Engl J Med. 2003;348:1425. 57. Kearon C, Ginsber JS, Kovacs MJ, et al. Comparison of low-intensity warfarin therapy with conventional-intensity warfarin therapy for long-term prevention of recurrent venous thrombo-embolism. N Engl J Med. 2003;349:631-639. 58. Lee AYY, Levine MN, Baker RI, et al. Low-molecular-weight heparin versus a coumarin for the prevention of recurrent venous thromboembolism in |
Surgery_Schwartz_6766 | Surgery_Schwartz | thrombo-embolism. N Engl J Med. 2003;349:631-639. 58. Lee AYY, Levine MN, Baker RI, et al. Low-molecular-weight heparin versus a coumarin for the prevention of recurrent venous thromboembolism in patients with cancer. N Engl J Med. 2003;349:146-153. 59. Akl EA, Barba M, Rohilla S, et al. Anticoagulation for the long term treatment of venous thromboembolism in patients with cancer. Cochrane Database Syst Rev. 2008;2:CD006650. 60. Watson LI, Armon MP. Thrombolysis for treatment of acute deep vein thrombosis. Cochrane Database Syst Rev. 2004;4:CD002783. 61. Vedantham S, Goldhaber S, Julian J, et al. Pharmacomechanical Catheter-Directed Thrombolysis for Deep-Vein Thrombosis. N Engl J Med. 2017;377:2240-2252. 62. Vedantham S, Goldhaber S, Julian, J, et al. Interventional ther-apy for prevention of the post-thrombotic syndrome: results of the NHLBI-sponsored ATTRACT trial. 2017. Unpublished manuscript. 63. Decousus H, Leizorovicz A, Parent F, et al. A clinical trial of vena caval filters in | Surgery_Schwartz. thrombo-embolism. N Engl J Med. 2003;349:631-639. 58. Lee AYY, Levine MN, Baker RI, et al. Low-molecular-weight heparin versus a coumarin for the prevention of recurrent venous thromboembolism in patients with cancer. N Engl J Med. 2003;349:146-153. 59. Akl EA, Barba M, Rohilla S, et al. Anticoagulation for the long term treatment of venous thromboembolism in patients with cancer. Cochrane Database Syst Rev. 2008;2:CD006650. 60. Watson LI, Armon MP. Thrombolysis for treatment of acute deep vein thrombosis. Cochrane Database Syst Rev. 2004;4:CD002783. 61. Vedantham S, Goldhaber S, Julian J, et al. Pharmacomechanical Catheter-Directed Thrombolysis for Deep-Vein Thrombosis. N Engl J Med. 2017;377:2240-2252. 62. Vedantham S, Goldhaber S, Julian, J, et al. Interventional ther-apy for prevention of the post-thrombotic syndrome: results of the NHLBI-sponsored ATTRACT trial. 2017. Unpublished manuscript. 63. Decousus H, Leizorovicz A, Parent F, et al. A clinical trial of vena caval filters in |
Surgery_Schwartz_6767 | Surgery_Schwartz | of the post-thrombotic syndrome: results of the NHLBI-sponsored ATTRACT trial. 2017. Unpublished manuscript. 63. Decousus H, Leizorovicz A, Parent F, et al. A clinical trial of vena caval filters in the prevention of pulmonary embolism in patients with proximal deep-vein thrombosis. Prévention du Risque d’Embolie Pulmonaire par Interruption Cave Study Group. N Engl J Med. 1998;338:409-415. 64. Becker DM, Philbrick JT, Selby JB. Inferior vena cava filters. Indications, safety, effectiveness. Arch Intern Med. 1992;152:1985-1994. 65. Morales JP, Li X, Irony TZ, Ibrahim NG, Moynahan M, Cavanaugh KJ Jr. Decision analysis of retrievable inferior vena cava filters in patients without pulmonary embolism. J Vasc Surg Venous Lymphat Disord. 2013;1(4):376-384. 66. Morales JP, Li X, Irony TZ, Ibrahim NG, Moynahan M, Cava-naugh KJ, Jr. Decision analysis of retrievable inferior vena cava filters in patients without pulmonary embolism. J Vasc Surg Venous Lymphat Disord. 2013;1(4):376-384. 67. Plate | Surgery_Schwartz. of the post-thrombotic syndrome: results of the NHLBI-sponsored ATTRACT trial. 2017. Unpublished manuscript. 63. Decousus H, Leizorovicz A, Parent F, et al. A clinical trial of vena caval filters in the prevention of pulmonary embolism in patients with proximal deep-vein thrombosis. Prévention du Risque d’Embolie Pulmonaire par Interruption Cave Study Group. N Engl J Med. 1998;338:409-415. 64. Becker DM, Philbrick JT, Selby JB. Inferior vena cava filters. Indications, safety, effectiveness. Arch Intern Med. 1992;152:1985-1994. 65. Morales JP, Li X, Irony TZ, Ibrahim NG, Moynahan M, Cavanaugh KJ Jr. Decision analysis of retrievable inferior vena cava filters in patients without pulmonary embolism. J Vasc Surg Venous Lymphat Disord. 2013;1(4):376-384. 66. Morales JP, Li X, Irony TZ, Ibrahim NG, Moynahan M, Cava-naugh KJ, Jr. Decision analysis of retrievable inferior vena cava filters in patients without pulmonary embolism. J Vasc Surg Venous Lymphat Disord. 2013;1(4):376-384. 67. Plate |
Surgery_Schwartz_6768 | Surgery_Schwartz | NG, Moynahan M, Cava-naugh KJ, Jr. Decision analysis of retrievable inferior vena cava filters in patients without pulmonary embolism. J Vasc Surg Venous Lymphat Disord. 2013;1(4):376-384. 67. Plate G, Ohlin P, Eklof B. Pulmonary embolism in acute ilio-femoral venous thrombosis. Br J Surg. 1985;72:912-915. 68. Eklof B, Kistner RL, Masuda EM. Surgical treatment of acute iliofemoral deep venous thrombosis. In: Gloviczki P, Yao JST, eds. Handbook of Venous Disorders. New York: Arnold; 2001:202. This chapter reviews outcomes following surgical treatment for acute iliofemoral deep venous thrombo-sis in addition to an illustrative review of surgical technique. 69. Juhan CM, Alimi YS, Barthelemy PJ, et al. Late results of ilio-femoral venous thrombectomy. J Vasc Surg. 1997;25:417-422. 70. Schmid C, Zietlow S, Wagner TO, et al. Fulminant pulmonary embolism: symptoms, diagnostics, operative technique, and results. Ann Thorac Surg. 1991;52:1102-1105. 71. Kieny R, Charpentier A, Kieny MT. What | Surgery_Schwartz. NG, Moynahan M, Cava-naugh KJ, Jr. Decision analysis of retrievable inferior vena cava filters in patients without pulmonary embolism. J Vasc Surg Venous Lymphat Disord. 2013;1(4):376-384. 67. Plate G, Ohlin P, Eklof B. Pulmonary embolism in acute ilio-femoral venous thrombosis. Br J Surg. 1985;72:912-915. 68. Eklof B, Kistner RL, Masuda EM. Surgical treatment of acute iliofemoral deep venous thrombosis. In: Gloviczki P, Yao JST, eds. Handbook of Venous Disorders. New York: Arnold; 2001:202. This chapter reviews outcomes following surgical treatment for acute iliofemoral deep venous thrombo-sis in addition to an illustrative review of surgical technique. 69. Juhan CM, Alimi YS, Barthelemy PJ, et al. Late results of ilio-femoral venous thrombectomy. J Vasc Surg. 1997;25:417-422. 70. Schmid C, Zietlow S, Wagner TO, et al. Fulminant pulmonary embolism: symptoms, diagnostics, operative technique, and results. Ann Thorac Surg. 1991;52:1102-1105. 71. Kieny R, Charpentier A, Kieny MT. What |
Surgery_Schwartz_6769 | Surgery_Schwartz | C, Zietlow S, Wagner TO, et al. Fulminant pulmonary embolism: symptoms, diagnostics, operative technique, and results. Ann Thorac Surg. 1991;52:1102-1105. 71. Kieny R, Charpentier A, Kieny MT. What is the place of pulmonary embolectomy today? J Cardiovasc Surg. 1991;32:549-554. 72. Gulba DC, Schmid C, Borst HG, et al. Medical compared with surgical treatment for massive pulmonary embolism. Lancet. 1994;343:576-577. 73. Schmitz-Rode T, Janssens U, Schild HH, et al. Fragmentation of massive pulmonary embolism using a pigtail rotation cath-eter. Chest. 1998;114:1427-1436. 74. Greenfield LJ, Proctor MC, Williams DM, et al. Long-term experience with transvenous catheter pulmonary embolec-tomy. J Vasc Surg. 1993;18:450-457. 75. 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;141(2 suppl): | Surgery_Schwartz. C, Zietlow S, Wagner TO, et al. Fulminant pulmonary embolism: symptoms, diagnostics, operative technique, and results. Ann Thorac Surg. 1991;52:1102-1105. 71. Kieny R, Charpentier A, Kieny MT. What is the place of pulmonary embolectomy today? J Cardiovasc Surg. 1991;32:549-554. 72. Gulba DC, Schmid C, Borst HG, et al. Medical compared with surgical treatment for massive pulmonary embolism. Lancet. 1994;343:576-577. 73. Schmitz-Rode T, Janssens U, Schild HH, et al. Fragmentation of massive pulmonary embolism using a pigtail rotation cath-eter. Chest. 1998;114:1427-1436. 74. Greenfield LJ, Proctor MC, Williams DM, et al. Long-term experience with transvenous catheter pulmonary embolec-tomy. J Vasc Surg. 1993;18:450-457. 75. 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;141(2 suppl): |
Surgery_Schwartz_6770 | Surgery_Schwartz | surgical patients: antithrombotic therapy and prevention of thrombosis, 9th ed: American College of Chest Physicians evidence-based clinical practice guidelines. Chest. 2012;141(2 suppl): e227S-e277S. The most recent American College of Chest Physicians clinical practice guidelines on prevention of venous thromboembolism in nonorthopedic surgical patients. These recommendations review evidence-based literature regarding perioperative venous thromboembolism prophylaxis. 76. Mismetti P, Laporte S, Darmon JY, et al. Meta-analysis of low molecular weight heparin in the prevention of venous throm-boembolism in general surgery. Br J Surg. 2001;88:913-930. 77. Agnelli G, Bergqvist D, Cohen AT, et al. Randomized clinical trial of postoperative fondaparinux versus perioperative dalte-parin for prevention of venous thromboembolism in high-risk abdominal surgery. Br J Surg. 2005;92:1212-1220. 78. Turpie AG, Bauer KA, Caprini JA, et al. Fondaparinux combined with intermittent pneumatic | Surgery_Schwartz. surgical patients: antithrombotic therapy and prevention of thrombosis, 9th ed: American College of Chest Physicians evidence-based clinical practice guidelines. Chest. 2012;141(2 suppl): e227S-e277S. The most recent American College of Chest Physicians clinical practice guidelines on prevention of venous thromboembolism in nonorthopedic surgical patients. These recommendations review evidence-based literature regarding perioperative venous thromboembolism prophylaxis. 76. Mismetti P, Laporte S, Darmon JY, et al. Meta-analysis of low molecular weight heparin in the prevention of venous throm-boembolism in general surgery. Br J Surg. 2001;88:913-930. 77. Agnelli G, Bergqvist D, Cohen AT, et al. Randomized clinical trial of postoperative fondaparinux versus perioperative dalte-parin for prevention of venous thromboembolism in high-risk abdominal surgery. Br J Surg. 2005;92:1212-1220. 78. Turpie AG, Bauer KA, Caprini JA, et al. Fondaparinux combined with intermittent pneumatic |
Surgery_Schwartz_6771 | Surgery_Schwartz | for prevention of venous thromboembolism in high-risk abdominal surgery. Br J Surg. 2005;92:1212-1220. 78. Turpie AG, Bauer KA, Caprini JA, et al. Fondaparinux combined with intermittent pneumatic compression versus intermittent pneumatic compression alone for prevention of venous thrombo-embolism after abdominal surgery: a randomized, double-blind comparison. J Thromb Haemost. 2007;5:1854-1861. 79. Rogers FB, Shackford SR, Ricci MA, et al. Routine prophy-lactic vena cava filter insertion in severely injured trauma patients decreases the incidence of pulmonary embolism. J Am Coll Surg. 1995;180:641-647. 80. Rogers FB, Strindberg G, Shackford SR, et al. Five-year follow-up of prophylactic vena cava filters in high-risk trauma patients. Arch Surg. 1998;133:406-411.Brunicardi_Ch24_p0981-p1008.indd 100522/02/19 3:01 PM 1006SPECIFIC CONSIDERATIONSPART II 81. Millward SF, Oliva VL, Bell SD, et al. Gunther tulip retriev-able vena cava filter: results from the Registry of the Canadian | Surgery_Schwartz. for prevention of venous thromboembolism in high-risk abdominal surgery. Br J Surg. 2005;92:1212-1220. 78. Turpie AG, Bauer KA, Caprini JA, et al. Fondaparinux combined with intermittent pneumatic compression versus intermittent pneumatic compression alone for prevention of venous thrombo-embolism after abdominal surgery: a randomized, double-blind comparison. J Thromb Haemost. 2007;5:1854-1861. 79. Rogers FB, Shackford SR, Ricci MA, et al. Routine prophy-lactic vena cava filter insertion in severely injured trauma patients decreases the incidence of pulmonary embolism. J Am Coll Surg. 1995;180:641-647. 80. Rogers FB, Strindberg G, Shackford SR, et al. Five-year follow-up of prophylactic vena cava filters in high-risk trauma patients. Arch Surg. 1998;133:406-411.Brunicardi_Ch24_p0981-p1008.indd 100522/02/19 3:01 PM 1006SPECIFIC CONSIDERATIONSPART II 81. Millward SF, Oliva VL, Bell SD, et al. Gunther tulip retriev-able vena cava filter: results from the Registry of the Canadian |
Surgery_Schwartz_6772 | Surgery_Schwartz | 100522/02/19 3:01 PM 1006SPECIFIC CONSIDERATIONSPART II 81. Millward SF, Oliva VL, Bell SD, et al. Gunther tulip retriev-able vena cava filter: results from the Registry of the Canadian Interventional Radiology Association. J Vasc Intervent Radiol. 2001;12:1053-1058. 82. Allen AW, Megargell JL, Brown DB, et al. Venous thrombosis associated with the placement of peripherally inserted central catheters. J Vasc Intervent Radiol. 2000;11:1309-1314. 83. Chengelis DL, Bendick PJ, Glover JL, et al. Progression of superficial venous thrombosis to deep vein thrombosis. J Vasc Surg. 1996;24:745-749. 84. Lutter KS, Kerr TM, Roedersheimer LR, et al. Superficial thrombophlebitis diagnosed by duplex scanning. Surgery. 1991;110:42-46. 85. Di Nisio M, Wichers IM, Middeldorp S. Treatment for superfi-cial thrombophlebitis of the leg. Cochrane Database Syst Rev. 2013(4):CD004982. 86. Decousus H, Prandoni P, Mismetti P, et al. Fondaparinux for the treatment of superficial-vein thrombosis in the legs. | Surgery_Schwartz. 100522/02/19 3:01 PM 1006SPECIFIC CONSIDERATIONSPART II 81. Millward SF, Oliva VL, Bell SD, et al. Gunther tulip retriev-able vena cava filter: results from the Registry of the Canadian Interventional Radiology Association. J Vasc Intervent Radiol. 2001;12:1053-1058. 82. Allen AW, Megargell JL, Brown DB, et al. Venous thrombosis associated with the placement of peripherally inserted central catheters. J Vasc Intervent Radiol. 2000;11:1309-1314. 83. Chengelis DL, Bendick PJ, Glover JL, et al. Progression of superficial venous thrombosis to deep vein thrombosis. J Vasc Surg. 1996;24:745-749. 84. Lutter KS, Kerr TM, Roedersheimer LR, et al. Superficial thrombophlebitis diagnosed by duplex scanning. Surgery. 1991;110:42-46. 85. Di Nisio M, Wichers IM, Middeldorp S. Treatment for superfi-cial thrombophlebitis of the leg. Cochrane Database Syst Rev. 2013(4):CD004982. 86. Decousus H, Prandoni P, Mismetti P, et al. Fondaparinux for the treatment of superficial-vein thrombosis in the legs. |
Surgery_Schwartz_6773 | Surgery_Schwartz | thrombophlebitis of the leg. Cochrane Database Syst Rev. 2013(4):CD004982. 86. Decousus H, Prandoni P, Mismetti P, et al. Fondaparinux for the treatment of superficial-vein thrombosis in the legs. N Engl J Med. 2010;363(13):1222-1232. 87. Lohr JM, McDevitt DT, Lutter KS, et al. Operative manage-ment of greater saphenous thrombophlebitis involving the saphenofemoral junction. Am J Surg. 1992;164:269-275. 88. Ascer E, Lorensen E, Pollina RM, et al. Preliminary results of a nonoperative approach to saphenofemoral junction thrombo-phlebitis. J Vasc Surg. 1995;22:616-621. 89. Horne MK III, May DJ, Alexander HR, et al. Venographic surveillance of tunneled venous access devices in adult oncol-ogy patients. Ann Surg Oncol. 1995;2:174-178. 90. Landry GL, Liem TK. Endovascular management of Paget-Schroetter syndrome. Vascular. 2007;15:290-296. 91. Rhee RY, Gloviczki P, Jost C, et al. Acute mesenteric venous thrombosis. In: Gloviczki P, Yao JST, eds. Handbook of Venous Disorders. New York: | Surgery_Schwartz. thrombophlebitis of the leg. Cochrane Database Syst Rev. 2013(4):CD004982. 86. Decousus H, Prandoni P, Mismetti P, et al. Fondaparinux for the treatment of superficial-vein thrombosis in the legs. N Engl J Med. 2010;363(13):1222-1232. 87. Lohr JM, McDevitt DT, Lutter KS, et al. Operative manage-ment of greater saphenous thrombophlebitis involving the saphenofemoral junction. Am J Surg. 1992;164:269-275. 88. Ascer E, Lorensen E, Pollina RM, et al. Preliminary results of a nonoperative approach to saphenofemoral junction thrombo-phlebitis. J Vasc Surg. 1995;22:616-621. 89. Horne MK III, May DJ, Alexander HR, et al. Venographic surveillance of tunneled venous access devices in adult oncol-ogy patients. Ann Surg Oncol. 1995;2:174-178. 90. Landry GL, Liem TK. Endovascular management of Paget-Schroetter syndrome. Vascular. 2007;15:290-296. 91. Rhee RY, Gloviczki P, Jost C, et al. Acute mesenteric venous thrombosis. In: Gloviczki P, Yao JST, eds. Handbook of Venous Disorders. New York: |
Surgery_Schwartz_6774 | Surgery_Schwartz | syndrome. Vascular. 2007;15:290-296. 91. Rhee RY, Gloviczki P, Jost C, et al. Acute mesenteric venous thrombosis. In: Gloviczki P, Yao JST, eds. Handbook of Venous Disorders. New York: Arnold; 2001:244. 92. Morasch MD, Ebaugh JL, Chiou AC, et al. Mesenteric venous thrombosis: a changing clinical entity. J Vasc Surg. 2001;34:680-684. 93. James AW, Rabl C, Westphalen AC, et al. Portomesenteric venous thrombosis after laparoscopic surgery: a systematic literature review. Arch Surg. 2009;144:520-526. 94. Bach AM, Hann LE, Brown KT, et al. Portal vein evaluation with US: comparison to angiography combined with CT arte-rial portography. Radiology. 1996;201:149-154. 95. Burkitt DP. Varicose veins, deep vein thrombosis, and haem-orrhoids: epidemiology and suggested aetiology. Br Med J. 1972;2:556-561. 96. Brand FN, Dannenberg AL, Abbott RD, et al. The epidemiol-ogy of varicose veins: the Framingham Study. Am J Prev Med. 1988;4:96-101. 97. Gibson K, Kabnick L, Varithena 013 Investigator G. A | Surgery_Schwartz. syndrome. Vascular. 2007;15:290-296. 91. Rhee RY, Gloviczki P, Jost C, et al. Acute mesenteric venous thrombosis. In: Gloviczki P, Yao JST, eds. Handbook of Venous Disorders. New York: Arnold; 2001:244. 92. Morasch MD, Ebaugh JL, Chiou AC, et al. Mesenteric venous thrombosis: a changing clinical entity. J Vasc Surg. 2001;34:680-684. 93. James AW, Rabl C, Westphalen AC, et al. Portomesenteric venous thrombosis after laparoscopic surgery: a systematic literature review. Arch Surg. 2009;144:520-526. 94. Bach AM, Hann LE, Brown KT, et al. Portal vein evaluation with US: comparison to angiography combined with CT arte-rial portography. Radiology. 1996;201:149-154. 95. Burkitt DP. Varicose veins, deep vein thrombosis, and haem-orrhoids: epidemiology and suggested aetiology. Br Med J. 1972;2:556-561. 96. Brand FN, Dannenberg AL, Abbott RD, et al. The epidemiol-ogy of varicose veins: the Framingham Study. Am J Prev Med. 1988;4:96-101. 97. Gibson K, Kabnick L, Varithena 013 Investigator G. A |
Surgery_Schwartz_6775 | Surgery_Schwartz | FN, Dannenberg AL, Abbott RD, et al. The epidemiol-ogy of varicose veins: the Framingham Study. Am J Prev Med. 1988;4:96-101. 97. Gibson K, Kabnick L, Varithena 013 Investigator G. A mul-ticenter, randomized, placebo-controlled study to evaluate the efficacy and safety of Varithena(R) (polidocanol endove-nous microfoam 1%) for symptomatic, visible varicose veins with saphenofemoral junction incompetence. Phlebology. 2017;32(3):185-193. 98. Witte ME, Reijnen MM, de Vries JP, Zeebregts CJ. Mechano-chemical Endovenous Occlusion of Varicose Veins Using the ClariVein(R) Device. Surg Technol Int. 2015;26:219-225. 99. Proebstle TM, Alm J, Dimitri S, et al. The European multi-center cohort study on cyanoacrylate embolization of refluxing great saphenous veins. J Vasc Surg Venous Lymphat Disord. 2015;3(1):2-7. 100. Lurie F, Creton D, Eklof B, et al. Prospective randomized study of endovenous radiofrequency obliteration (closure) versus ligation and vein stripping (EVOLVeS): two-year follow-up. | Surgery_Schwartz. FN, Dannenberg AL, Abbott RD, et al. The epidemiol-ogy of varicose veins: the Framingham Study. Am J Prev Med. 1988;4:96-101. 97. Gibson K, Kabnick L, Varithena 013 Investigator G. A mul-ticenter, randomized, placebo-controlled study to evaluate the efficacy and safety of Varithena(R) (polidocanol endove-nous microfoam 1%) for symptomatic, visible varicose veins with saphenofemoral junction incompetence. Phlebology. 2017;32(3):185-193. 98. Witte ME, Reijnen MM, de Vries JP, Zeebregts CJ. Mechano-chemical Endovenous Occlusion of Varicose Veins Using the ClariVein(R) Device. Surg Technol Int. 2015;26:219-225. 99. Proebstle TM, Alm J, Dimitri S, et al. The European multi-center cohort study on cyanoacrylate embolization of refluxing great saphenous veins. J Vasc Surg Venous Lymphat Disord. 2015;3(1):2-7. 100. Lurie F, Creton D, Eklof B, et al. Prospective randomized study of endovenous radiofrequency obliteration (closure) versus ligation and vein stripping (EVOLVeS): two-year follow-up. |
Surgery_Schwartz_6776 | Surgery_Schwartz | F, Creton D, Eklof B, et al. Prospective randomized study of endovenous radiofrequency obliteration (closure) versus ligation and vein stripping (EVOLVeS): two-year follow-up. Eur J Vasc Endovasc Surg. 2005;29:67-73. 101. Darwood RJ, Theivacumar N, Dellagrammaticas D, et al. Ran-domized clinical trial comparing endovenous laser ablation with surgery for the treatment of primary great saphenous varicose veins. Br J Surg. 2008;95:294-301. 102. Falanga V. Venous ulceration. J Dermatol Surg Oncol. 1993;19:764-771. 103. Phillips T, Stanton B, Provan A, et al. A study of the impact of leg ulcers on quality of life: financial, social, and psychologic implications. J Am Acad Dermatol. 1994;31:49-53. 104. Skin Substitute Consensus Development Panel. Nonoperative management of venous ulcers: evolving role of skin substi-tutes. Vasc Surg. 1999;33:197. 105. Abenhaim L, Kurz X. The VEINES study (VEnous Insuffi-ciency Epidemiologic and Economic Study): an international cohort study on chronic | Surgery_Schwartz. F, Creton D, Eklof B, et al. Prospective randomized study of endovenous radiofrequency obliteration (closure) versus ligation and vein stripping (EVOLVeS): two-year follow-up. Eur J Vasc Endovasc Surg. 2005;29:67-73. 101. Darwood RJ, Theivacumar N, Dellagrammaticas D, et al. Ran-domized clinical trial comparing endovenous laser ablation with surgery for the treatment of primary great saphenous varicose veins. Br J Surg. 2008;95:294-301. 102. Falanga V. Venous ulceration. J Dermatol Surg Oncol. 1993;19:764-771. 103. Phillips T, Stanton B, Provan A, et al. A study of the impact of leg ulcers on quality of life: financial, social, and psychologic implications. J Am Acad Dermatol. 1994;31:49-53. 104. Skin Substitute Consensus Development Panel. Nonoperative management of venous ulcers: evolving role of skin substi-tutes. Vasc Surg. 1999;33:197. 105. Abenhaim L, Kurz X. The VEINES study (VEnous Insuffi-ciency Epidemiologic and Economic Study): an international cohort study on chronic |
Surgery_Schwartz_6777 | Surgery_Schwartz | role of skin substi-tutes. Vasc Surg. 1999;33:197. 105. Abenhaim L, Kurz X. The VEINES study (VEnous Insuffi-ciency Epidemiologic and Economic Study): an international cohort study on chronic venous disorders of the leg. VEINES Group. Angiology. 1997;48:59-66. 106. Clarke H, Smith SR, Vasdekis SN, et al. Role of venous elasticity in the development of varicose veins. Br J Surg. 1989;76:577-580. 107. Nicolaides AN, Hussein MK, Szendro G, et al. The relation of venous ulceration with ambulatory venous pressure measure-ments. J Vasc Surg. 1993;17:414-419. 108. Christopoulos DG, Nicolaides AN, Szendro G, et al. Air-pleth-ysmography and the effect of elastic compression on venous hemodynamics of the leg. J Vasc Surg. 1987;5:148-159. 109. van Bemmelen PS, Bedford G, Beach K, et al. Quantitative segmental evaluation of venous valvular reflux with duplex ultrasound scanning. J Vasc Surg. 1989;10:425-431. 110. Nehler MR, Porter JM. The lower extremity venous system. Part II: the | Surgery_Schwartz. role of skin substi-tutes. Vasc Surg. 1999;33:197. 105. Abenhaim L, Kurz X. The VEINES study (VEnous Insuffi-ciency Epidemiologic and Economic Study): an international cohort study on chronic venous disorders of the leg. VEINES Group. Angiology. 1997;48:59-66. 106. Clarke H, Smith SR, Vasdekis SN, et al. Role of venous elasticity in the development of varicose veins. Br J Surg. 1989;76:577-580. 107. Nicolaides AN, Hussein MK, Szendro G, et al. The relation of venous ulceration with ambulatory venous pressure measure-ments. J Vasc Surg. 1993;17:414-419. 108. Christopoulos DG, Nicolaides AN, Szendro G, et al. Air-pleth-ysmography and the effect of elastic compression on venous hemodynamics of the leg. J Vasc Surg. 1987;5:148-159. 109. van Bemmelen PS, Bedford G, Beach K, et al. Quantitative segmental evaluation of venous valvular reflux with duplex ultrasound scanning. J Vasc Surg. 1989;10:425-431. 110. Nehler MR, Porter JM. The lower extremity venous system. Part II: the |
Surgery_Schwartz_6778 | Surgery_Schwartz | Quantitative segmental evaluation of venous valvular reflux with duplex ultrasound scanning. J Vasc Surg. 1989;10:425-431. 110. Nehler MR, Porter JM. The lower extremity venous system. Part II: the pathophysiology of chronic venous insufficiency. Perspect Vasc Surg. 1992;5:81-97. 111. Beidler SK, Douillet CD, Berndt DF, et al. Multiplexed analy-sis of matrix metalloproteinases in leg ulcer tissue of patients with chronic venous insufficiency before and after compres-sion therapy. Wound Repair Regen. 2008;16:642-648. 112. Beidler SK, Douillet CD, Berndt DF, et al. Inflammatory cyto-kine levels in chronic venous insufficiency ulcer tissue before and after compression therapy. J Vasc Surg. 2009;49:1013-1020. 113. Nehler MR, Moneta GL, Woodard DM, et al. Perimalleolar subcutaneous tissue pressure effects of elastic compression stockings. J Vasc Surg. 1993;18:783-788. 114. Dinn E. Treatment of venous ulceration by injection sclero-therapy and compression hosiery: a 5-year study. | Surgery_Schwartz. Quantitative segmental evaluation of venous valvular reflux with duplex ultrasound scanning. J Vasc Surg. 1989;10:425-431. 110. Nehler MR, Porter JM. The lower extremity venous system. Part II: the pathophysiology of chronic venous insufficiency. Perspect Vasc Surg. 1992;5:81-97. 111. Beidler SK, Douillet CD, Berndt DF, et al. Multiplexed analy-sis of matrix metalloproteinases in leg ulcer tissue of patients with chronic venous insufficiency before and after compres-sion therapy. Wound Repair Regen. 2008;16:642-648. 112. Beidler SK, Douillet CD, Berndt DF, et al. Inflammatory cyto-kine levels in chronic venous insufficiency ulcer tissue before and after compression therapy. J Vasc Surg. 2009;49:1013-1020. 113. Nehler MR, Moneta GL, Woodard DM, et al. Perimalleolar subcutaneous tissue pressure effects of elastic compression stockings. J Vasc Surg. 1993;18:783-788. 114. Dinn E. Treatment of venous ulceration by injection sclero-therapy and compression hosiery: a 5-year study. |
Surgery_Schwartz_6779 | Surgery_Schwartz | pressure effects of elastic compression stockings. J Vasc Surg. 1993;18:783-788. 114. Dinn E. Treatment of venous ulceration by injection sclero-therapy and compression hosiery: a 5-year study. Phlebology. 1992;7:23-26. 115. Mayberry JC, Moneta GL, Taylor LM, Jr, et al. Fifteen-year results of ambulatory compression therapy for chronic venous ulcers. Surgery. 1991;109(5):575-581. This review highlights the impact of compression therapy in venous ulcer therapy. 116. Falanga V, Margolis D, Alvarez O, et al. Rapid healing of venous ulcers and lack of clinical rejection with an allergenic cultured human skin equivalent. Human Skin Equivalent Investigators Group. Arch Dermatol. 1998;134:293-300. 117. Phillips TJ. New skin for old: developments in biological skin substitutes [editorial; comment]. Arch Dermatol. 1998;134:344. 118. Motykie GD, Caprini JA, Arcelus JI, et al. Evaluation of therapeutic compression stockings in the treatment of chronic venous insufficiency. Dermatol Surg. | Surgery_Schwartz. pressure effects of elastic compression stockings. J Vasc Surg. 1993;18:783-788. 114. Dinn E. Treatment of venous ulceration by injection sclero-therapy and compression hosiery: a 5-year study. Phlebology. 1992;7:23-26. 115. Mayberry JC, Moneta GL, Taylor LM, Jr, et al. Fifteen-year results of ambulatory compression therapy for chronic venous ulcers. Surgery. 1991;109(5):575-581. This review highlights the impact of compression therapy in venous ulcer therapy. 116. Falanga V, Margolis D, Alvarez O, et al. Rapid healing of venous ulcers and lack of clinical rejection with an allergenic cultured human skin equivalent. Human Skin Equivalent Investigators Group. Arch Dermatol. 1998;134:293-300. 117. Phillips TJ. New skin for old: developments in biological skin substitutes [editorial; comment]. Arch Dermatol. 1998;134:344. 118. Motykie GD, Caprini JA, Arcelus JI, et al. Evaluation of therapeutic compression stockings in the treatment of chronic venous insufficiency. Dermatol Surg. |
Surgery_Schwartz_6780 | Surgery_Schwartz | comment]. Arch Dermatol. 1998;134:344. 118. Motykie GD, Caprini JA, Arcelus JI, et al. Evaluation of therapeutic compression stockings in the treatment of chronic venous insufficiency. Dermatol Surg. 1999;25:116-120. 119. Lippmann HI, Fishman LM, Farrar RH, et al. Edema control in the management of disabling chronic venous insufficiency. Arch Phys Med Rehabil. 1994;75:436-441. 120. Rubin JR, Alexander J, Plecha EJ, et al. Unna’s boot vs. polyurethane foam dressings for the treatment of venous ulceration. A randomized prospective study. Arch Surg. 1990;125:489-490. 121. O’Meara S, Cullum NA, Nelson EA. Compression for venous leg ulcers. Cochrane Database Syst Rev. 2009;1:CD000265. 122. Vernick SH, Shapiro D, Shaw FD. Legging orthosis for venous and lymphatic insufficiency. Arch Phys Med Rehabil. 1987;68:459-461.Brunicardi_Ch24_p0981-p1008.indd 100622/02/19 3:01 PM 1007VENOUS AND LYMPHATIC DISEASECHAPTER 24 123. Sibbald RG. Apligraf living skin equivalent for healing venous and | Surgery_Schwartz. comment]. Arch Dermatol. 1998;134:344. 118. Motykie GD, Caprini JA, Arcelus JI, et al. Evaluation of therapeutic compression stockings in the treatment of chronic venous insufficiency. Dermatol Surg. 1999;25:116-120. 119. Lippmann HI, Fishman LM, Farrar RH, et al. Edema control in the management of disabling chronic venous insufficiency. Arch Phys Med Rehabil. 1994;75:436-441. 120. Rubin JR, Alexander J, Plecha EJ, et al. Unna’s boot vs. polyurethane foam dressings for the treatment of venous ulceration. A randomized prospective study. Arch Surg. 1990;125:489-490. 121. O’Meara S, Cullum NA, Nelson EA. Compression for venous leg ulcers. Cochrane Database Syst Rev. 2009;1:CD000265. 122. Vernick SH, Shapiro D, Shaw FD. Legging orthosis for venous and lymphatic insufficiency. Arch Phys Med Rehabil. 1987;68:459-461.Brunicardi_Ch24_p0981-p1008.indd 100622/02/19 3:01 PM 1007VENOUS AND LYMPHATIC DISEASECHAPTER 24 123. Sibbald RG. Apligraf living skin equivalent for healing venous and |
Surgery_Schwartz_6781 | Surgery_Schwartz | Rehabil. 1987;68:459-461.Brunicardi_Ch24_p0981-p1008.indd 100622/02/19 3:01 PM 1007VENOUS AND LYMPHATIC DISEASECHAPTER 24 123. Sibbald RG. Apligraf living skin equivalent for healing venous and chronic wounds. J Cutan Med Surg. 1998;3(suppl 1): S1-24-8. 124. Linton R. The communicating veins of the lower leg and the operative technique for their ligation. Ann Surg. 1938;107:582-593. 125. Gloviczki P, Bergan JJ, Rhodes JM, Canton LG, Harmsen S, Ilstrup DM. Mid-term results of endoscopic perforator vein interruption for chronic venous insufficiency: lessons learned from the North American Subfascial Endoscopic Perforator Surgery Registry. The North American Study Group. J Vasc Surg. 1999;29(3):489-502. This study reviews registry outcomes following subfacial endoscopic perforator surgery performed across 17 centers in North America. 126. Vashist MG, Malik V, Singhal N. Role of subfascial endo-scopic perforator surgery (SEPS) in management of perfora-tor incompetence in varicose | Surgery_Schwartz. Rehabil. 1987;68:459-461.Brunicardi_Ch24_p0981-p1008.indd 100622/02/19 3:01 PM 1007VENOUS AND LYMPHATIC DISEASECHAPTER 24 123. Sibbald RG. Apligraf living skin equivalent for healing venous and chronic wounds. J Cutan Med Surg. 1998;3(suppl 1): S1-24-8. 124. Linton R. The communicating veins of the lower leg and the operative technique for their ligation. Ann Surg. 1938;107:582-593. 125. Gloviczki P, Bergan JJ, Rhodes JM, Canton LG, Harmsen S, Ilstrup DM. Mid-term results of endoscopic perforator vein interruption for chronic venous insufficiency: lessons learned from the North American Subfascial Endoscopic Perforator Surgery Registry. The North American Study Group. J Vasc Surg. 1999;29(3):489-502. This study reviews registry outcomes following subfacial endoscopic perforator surgery performed across 17 centers in North America. 126. Vashist MG, Malik V, Singhal N. Role of subfascial endo-scopic perforator surgery (SEPS) in management of perfora-tor incompetence in varicose |
Surgery_Schwartz_6782 | Surgery_Schwartz | performed across 17 centers in North America. 126. Vashist MG, Malik V, Singhal N. Role of subfascial endo-scopic perforator surgery (SEPS) in management of perfora-tor incompetence in varicose veins: a prospective randomized study. India J Surg. 2014;76(2):117-123. 127. van Gent WB, Hop WC, van Praag MC, et al. Conservative versus surgical treatment of venous leg ulcers: a prospective randomized, multicenter trial. J Vasc Surg. 2006;44:563-571. 128. Gohel MS, Barwell JR, Taylor M, et al. Long term results of compression therapy alone versus compression plus surgery in chronic venous ulceration (ESCHAR): randomized controlled trial. BMJ. 2007;335:83. 129. Sottiurai VS. Surgical correction of recurrent venous ulcer. J Cardiovasc Surg. 1991;32:104-109. 130. Raju S, Fredericks R. Valve reconstruction procedures for non-obstructive venous insufficiency: rationale, techniques, and results in 107 procedures with twoto eight-year follow-up. J Vasc Surg. 1988;7:301-310. 131. Raju S, Darcey | Surgery_Schwartz. performed across 17 centers in North America. 126. Vashist MG, Malik V, Singhal N. Role of subfascial endo-scopic perforator surgery (SEPS) in management of perfora-tor incompetence in varicose veins: a prospective randomized study. India J Surg. 2014;76(2):117-123. 127. van Gent WB, Hop WC, van Praag MC, et al. Conservative versus surgical treatment of venous leg ulcers: a prospective randomized, multicenter trial. J Vasc Surg. 2006;44:563-571. 128. Gohel MS, Barwell JR, Taylor M, et al. Long term results of compression therapy alone versus compression plus surgery in chronic venous ulceration (ESCHAR): randomized controlled trial. BMJ. 2007;335:83. 129. Sottiurai VS. Surgical correction of recurrent venous ulcer. J Cardiovasc Surg. 1991;32:104-109. 130. Raju S, Fredericks R. Valve reconstruction procedures for non-obstructive venous insufficiency: rationale, techniques, and results in 107 procedures with twoto eight-year follow-up. J Vasc Surg. 1988;7:301-310. 131. Raju S, Darcey |
Surgery_Schwartz_6783 | Surgery_Schwartz | procedures for non-obstructive venous insufficiency: rationale, techniques, and results in 107 procedures with twoto eight-year follow-up. J Vasc Surg. 1988;7:301-310. 131. Raju S, Darcey R, Neglen P. Unexpected major role for venous stenting in deep reflux disease. J Vasc Surg. 2010;51:401-408. 132. Masuda EM, Kistner RL. Long-term results of venous valve reconstruction: a fourto twenty-one-year follow-up. J Vasc Surg. 1994;19:391-403. 133. Rockson SG, Miller LT, Senie R, et al. American Cancer Soci-ety Lymphedema Workshop. Workgroup III: diagnosis and management of lymphedema. Cancer. 1998;83:2882-2885. 134. Yasuhara H, Shigematsu H, Muto T. A study of the advan-tages of elastic stockings for leg lymphedema. Int Angiol. 1996;15:272-277. 135. Feldman JL, Stout NL, Wanchai A, et al. Intermittent pneu-matic compression therapy: a systematic review. Lymphology. 2012;45:13-25. 136. Vodder E. Le Drainage Lymphatique, une Novelle Méthode Thérapeutique. Paris: Santé pour tous; | Surgery_Schwartz. procedures for non-obstructive venous insufficiency: rationale, techniques, and results in 107 procedures with twoto eight-year follow-up. J Vasc Surg. 1988;7:301-310. 131. Raju S, Darcey R, Neglen P. Unexpected major role for venous stenting in deep reflux disease. J Vasc Surg. 2010;51:401-408. 132. Masuda EM, Kistner RL. Long-term results of venous valve reconstruction: a fourto twenty-one-year follow-up. J Vasc Surg. 1994;19:391-403. 133. Rockson SG, Miller LT, Senie R, et al. American Cancer Soci-ety Lymphedema Workshop. Workgroup III: diagnosis and management of lymphedema. Cancer. 1998;83:2882-2885. 134. Yasuhara H, Shigematsu H, Muto T. A study of the advan-tages of elastic stockings for leg lymphedema. Int Angiol. 1996;15:272-277. 135. Feldman JL, Stout NL, Wanchai A, et al. Intermittent pneu-matic compression therapy: a systematic review. Lymphology. 2012;45:13-25. 136. Vodder E. Le Drainage Lymphatique, une Novelle Méthode Thérapeutique. Paris: Santé pour tous; |
Surgery_Schwartz_6784 | Surgery_Schwartz | et al. Intermittent pneu-matic compression therapy: a systematic review. Lymphology. 2012;45:13-25. 136. Vodder E. Le Drainage Lymphatique, une Novelle Méthode Thérapeutique. Paris: Santé pour tous; 1936. 137. Ko DS, Lerner R, Klose G, et al. Effective treatment of lymph-edema of the extremities. Arch Surg. 1998;133:452-458. 138. Stevens DL, Bisno AL, Chambers HF, et al. Practice guide-lines for the diagnosis and management of skin and soft tissue infections. Clin Infect Dis. 2005;41:1373-1406. 139. Miller TA, Wyatt LE, Rudkin GH. Staged skin and subcutane-ous excision for lymphedema: a favorable report of long-term results. Plast Reconstr Surg. 1998;102:1486-1501. 140. Baumeister RG, Siuda S. Treatment of lymphedema by micro-surgical lymphatic grafting: what is proved? Plast Reconstr Surg. 1990;85:64-74. 141. Bernas MJ, Witte CL, Witte MH. The diagnosis and treatment of peripheral lymphedema: draft revision of the 1995 Con-sensus Document of the International Society of Lymphology | Surgery_Schwartz. et al. Intermittent pneu-matic compression therapy: a systematic review. Lymphology. 2012;45:13-25. 136. Vodder E. Le Drainage Lymphatique, une Novelle Méthode Thérapeutique. Paris: Santé pour tous; 1936. 137. Ko DS, Lerner R, Klose G, et al. Effective treatment of lymph-edema of the extremities. Arch Surg. 1998;133:452-458. 138. Stevens DL, Bisno AL, Chambers HF, et al. Practice guide-lines for the diagnosis and management of skin and soft tissue infections. Clin Infect Dis. 2005;41:1373-1406. 139. Miller TA, Wyatt LE, Rudkin GH. Staged skin and subcutane-ous excision for lymphedema: a favorable report of long-term results. Plast Reconstr Surg. 1998;102:1486-1501. 140. Baumeister RG, Siuda S. Treatment of lymphedema by micro-surgical lymphatic grafting: what is proved? Plast Reconstr Surg. 1990;85:64-74. 141. Bernas MJ, Witte CL, Witte MH. The diagnosis and treatment of peripheral lymphedema: draft revision of the 1995 Con-sensus Document of the International Society of Lymphology |
Surgery_Schwartz_6785 | Surgery_Schwartz | 1990;85:64-74. 141. Bernas MJ, Witte CL, Witte MH. The diagnosis and treatment of peripheral lymphedema: draft revision of the 1995 Con-sensus Document of the International Society of Lymphology Executive Committee for discussion at the September 3–7, 2001, XVIII International Congress of Lymphology in Genoa, Italy. Lymphology. 2001;34:84-91.Brunicardi_Ch24_p0981-p1008.indd 100722/02/19 3:01 PM | Surgery_Schwartz. 1990;85:64-74. 141. Bernas MJ, Witte CL, Witte MH. The diagnosis and treatment of peripheral lymphedema: draft revision of the 1995 Con-sensus Document of the International Society of Lymphology Executive Committee for discussion at the September 3–7, 2001, XVIII International Congress of Lymphology in Genoa, Italy. Lymphology. 2001;34:84-91.Brunicardi_Ch24_p0981-p1008.indd 100722/02/19 3:01 PM |
Surgery_Schwartz_6786 | Surgery_Schwartz | Brunicardi_Ch24_p0981-p1008.indd 100822/02/19 3:01 PMThis page intentionally left blank | Surgery_Schwartz. Brunicardi_Ch24_p0981-p1008.indd 100822/02/19 3:01 PMThis page intentionally left blank |
Surgery_Schwartz_6787 | Surgery_Schwartz | SURGICAL ANATOMYThe esophagus is a muscular tube that starts as the continu-ation of the pharynx and ends as the cardia of the stomach. When the head is in a normal anatomic position, the transi-tion from pharynx to esophagus occurs at the lower border of the sixth cervical vertebra. Topographically this corresponds to the cricoid cartilage anteriorly and the palpable transverse process of the sixth cervical vertebra laterally (Fig. 25-1). The esophagus is firmly attached at its upper end to the cricoid cartilage and at its lower end to the diaphragm; during swal-lowing, the proximal points of fixation move craniad the dis-tance of one cervical vertebral body.The esophagus lies in the midline, with a deviation to the left in the lower portion of the neck and upper portion of the thorax, and returns to the midline in the midportion of the tho-rax near the bifurcation of the trachea (Fig. 25-2). In the lower portion of the thorax, the esophagus again deviates to the left and anteriorly | Surgery_Schwartz. SURGICAL ANATOMYThe esophagus is a muscular tube that starts as the continu-ation of the pharynx and ends as the cardia of the stomach. When the head is in a normal anatomic position, the transi-tion from pharynx to esophagus occurs at the lower border of the sixth cervical vertebra. Topographically this corresponds to the cricoid cartilage anteriorly and the palpable transverse process of the sixth cervical vertebra laterally (Fig. 25-1). The esophagus is firmly attached at its upper end to the cricoid cartilage and at its lower end to the diaphragm; during swal-lowing, the proximal points of fixation move craniad the dis-tance of one cervical vertebral body.The esophagus lies in the midline, with a deviation to the left in the lower portion of the neck and upper portion of the thorax, and returns to the midline in the midportion of the tho-rax near the bifurcation of the trachea (Fig. 25-2). In the lower portion of the thorax, the esophagus again deviates to the left and anteriorly |
Surgery_Schwartz_6788 | Surgery_Schwartz | returns to the midline in the midportion of the tho-rax near the bifurcation of the trachea (Fig. 25-2). In the lower portion of the thorax, the esophagus again deviates to the left and anteriorly to pass through the diaphragmatic hiatus.Esophagus and Diaphragmatic HerniaBlair A. Jobe, John G. Hunter, and David I. Watson 25chapterSurgical Anatomy1009Physiology1015Swallowing Mechanism / 1015Physiologic Reflux / 1017Assessment of Esophageal Function1018Tests to Detect Structural Abnormalities / 1018Tests to Detect Functional Abnormalities / 1019Videoand Cineradiography / 1028Tests to Detect Increased Exposure to Gastric Juice / 1028Tests of Duodenogastric Function / 1030Gastroesophageal Reflux Disease1031The Human Antireflux Mechanism and the Pathophysiology of Gastroesophageal Reflux Disease / 1032Complications Associated With Gastroesophageal Reflux Disease / 1033Metaplastic (Barrett’s Esophagus) and Neoplastic (Adenocarcinoma) Complications / 1035Respiratory Complications / | Surgery_Schwartz. returns to the midline in the midportion of the tho-rax near the bifurcation of the trachea (Fig. 25-2). In the lower portion of the thorax, the esophagus again deviates to the left and anteriorly to pass through the diaphragmatic hiatus.Esophagus and Diaphragmatic HerniaBlair A. Jobe, John G. Hunter, and David I. Watson 25chapterSurgical Anatomy1009Physiology1015Swallowing Mechanism / 1015Physiologic Reflux / 1017Assessment of Esophageal Function1018Tests to Detect Structural Abnormalities / 1018Tests to Detect Functional Abnormalities / 1019Videoand Cineradiography / 1028Tests to Detect Increased Exposure to Gastric Juice / 1028Tests of Duodenogastric Function / 1030Gastroesophageal Reflux Disease1031The Human Antireflux Mechanism and the Pathophysiology of Gastroesophageal Reflux Disease / 1032Complications Associated With Gastroesophageal Reflux Disease / 1033Metaplastic (Barrett’s Esophagus) and Neoplastic (Adenocarcinoma) Complications / 1035Respiratory Complications / |
Surgery_Schwartz_6789 | Surgery_Schwartz | Disease / 1032Complications Associated With Gastroesophageal Reflux Disease / 1033Metaplastic (Barrett’s Esophagus) and Neoplastic (Adenocarcinoma) Complications / 1035Respiratory Complications / 1035Surgical Therapy for Gastroesophageal Reflux Disease / 1038Primary Antireflux Repairs / 1040Giant Diaphragmatic (Hiatal) Hernias1045Incidence and Etiology / 1045Clinical Manifestations / 1047Diagnosis / 1047Pathophysiology / 1048Treatment / 1048Diaphragmatic Repair / 1048The Short Esophagus and PEH / 1049Results / 1049Schatzki’s Ring1049Scleroderma1050Eosinophilic Esophagitis1051Symptoms / 1051Signs / 1051Pathology / 1051Treatment / 1051Motility Disorders of the Pharynx and Esophagus1052Clinical Manifestations / 1052Motility Disorders of the Pharynx and Upper Esophagus—Transit Dysphagia / 1052Diagnostic Assessment of the Cricopharyngeal Segment / 1052Motility Disorders of the Esophageal Body and Lower Esophageal Sphincter / 1055Operations for Esophageal Motor Disorders and | Surgery_Schwartz. Disease / 1032Complications Associated With Gastroesophageal Reflux Disease / 1033Metaplastic (Barrett’s Esophagus) and Neoplastic (Adenocarcinoma) Complications / 1035Respiratory Complications / 1035Surgical Therapy for Gastroesophageal Reflux Disease / 1038Primary Antireflux Repairs / 1040Giant Diaphragmatic (Hiatal) Hernias1045Incidence and Etiology / 1045Clinical Manifestations / 1047Diagnosis / 1047Pathophysiology / 1048Treatment / 1048Diaphragmatic Repair / 1048The Short Esophagus and PEH / 1049Results / 1049Schatzki’s Ring1049Scleroderma1050Eosinophilic Esophagitis1051Symptoms / 1051Signs / 1051Pathology / 1051Treatment / 1051Motility Disorders of the Pharynx and Esophagus1052Clinical Manifestations / 1052Motility Disorders of the Pharynx and Upper Esophagus—Transit Dysphagia / 1052Diagnostic Assessment of the Cricopharyngeal Segment / 1052Motility Disorders of the Esophageal Body and Lower Esophageal Sphincter / 1055Operations for Esophageal Motor Disorders and |
Surgery_Schwartz_6790 | Surgery_Schwartz | / 1052Diagnostic Assessment of the Cricopharyngeal Segment / 1052Motility Disorders of the Esophageal Body and Lower Esophageal Sphincter / 1055Operations for Esophageal Motor Disorders and Diverticula1060Long Esophageal Myotomy for Motor Disorders of the Esophageal Body / 1060Myotomy of the Lower Esophageal Sphincter (Heller Myotomy) / 1063Open Esophageal Myotomy / 1065Laparoscopic Cardiomyotomy / 1065Per Oral Endoscopic Myotomy (POEM) / 1065Outcome Assessment of the Therapy for Achalasia / 1065Esophageal Resection for End-Stage Motor Disorders of the Esophagus / 1068Carcinoma of the Esophagus1068Clinical Manifestations / 1068General Approach to Esophageal Cancer / 1069Staging of Esophageal Cancer / 1069Clinical Approach to Carcinoma of the Esophagus and Cardia / 1070Palliation of Esophageal Cancer / 1074Surgical Treatment / 1074Comparative Studies of Esophagectomy Technique / 1077Alternative Therapies / 1077Sarcoma of the Esophagus1078Benign Tumors and Cysts1080Leiomyoma / | Surgery_Schwartz. / 1052Diagnostic Assessment of the Cricopharyngeal Segment / 1052Motility Disorders of the Esophageal Body and Lower Esophageal Sphincter / 1055Operations for Esophageal Motor Disorders and Diverticula1060Long Esophageal Myotomy for Motor Disorders of the Esophageal Body / 1060Myotomy of the Lower Esophageal Sphincter (Heller Myotomy) / 1063Open Esophageal Myotomy / 1065Laparoscopic Cardiomyotomy / 1065Per Oral Endoscopic Myotomy (POEM) / 1065Outcome Assessment of the Therapy for Achalasia / 1065Esophageal Resection for End-Stage Motor Disorders of the Esophagus / 1068Carcinoma of the Esophagus1068Clinical Manifestations / 1068General Approach to Esophageal Cancer / 1069Staging of Esophageal Cancer / 1069Clinical Approach to Carcinoma of the Esophagus and Cardia / 1070Palliation of Esophageal Cancer / 1074Surgical Treatment / 1074Comparative Studies of Esophagectomy Technique / 1077Alternative Therapies / 1077Sarcoma of the Esophagus1078Benign Tumors and Cysts1080Leiomyoma / |
Surgery_Schwartz_6791 | Surgery_Schwartz | of Esophageal Cancer / 1074Surgical Treatment / 1074Comparative Studies of Esophagectomy Technique / 1077Alternative Therapies / 1077Sarcoma of the Esophagus1078Benign Tumors and Cysts1080Leiomyoma / 1081Esophageal Cyst / 1083Esophageal Perforation1083Diagnosis / 1083Management / 1084Mallory-Weiss Syndrome1085Caustic Injury1086Pathology / 1086Clinical Manifestations / 1086Treatment / 1086Acquired Fistula1088Techniques of Esophageal Reconstruction1089Partial Esophageal Resection / 1089Reconstruction After Total Esophagectomy / 1089Composite Reconstruction / 1090Vagal Sparing Esophagectomy With Colon Interposition / 1090Brunicardi_Ch25_p1009-p1098.indd 100901/03/19 6:01 PM 1010abcdeA BKey Points1 Benign esophageal disease is common and is best evaluated with thorough physiologic testing (high resolution esopha-geal motility, 24-hour ambulatory pH measurement, and/or esophageal impedance testing) and anatomic testing (esoph-agoscopy, video esophagography, and/or computed | Surgery_Schwartz. of Esophageal Cancer / 1074Surgical Treatment / 1074Comparative Studies of Esophagectomy Technique / 1077Alternative Therapies / 1077Sarcoma of the Esophagus1078Benign Tumors and Cysts1080Leiomyoma / 1081Esophageal Cyst / 1083Esophageal Perforation1083Diagnosis / 1083Management / 1084Mallory-Weiss Syndrome1085Caustic Injury1086Pathology / 1086Clinical Manifestations / 1086Treatment / 1086Acquired Fistula1088Techniques of Esophageal Reconstruction1089Partial Esophageal Resection / 1089Reconstruction After Total Esophagectomy / 1089Composite Reconstruction / 1090Vagal Sparing Esophagectomy With Colon Interposition / 1090Brunicardi_Ch25_p1009-p1098.indd 100901/03/19 6:01 PM 1010abcdeA BKey Points1 Benign esophageal disease is common and is best evaluated with thorough physiologic testing (high resolution esopha-geal motility, 24-hour ambulatory pH measurement, and/or esophageal impedance testing) and anatomic testing (esoph-agoscopy, video esophagography, and/or computed |
Surgery_Schwartz_6792 | Surgery_Schwartz | testing (high resolution esopha-geal motility, 24-hour ambulatory pH measurement, and/or esophageal impedance testing) and anatomic testing (esoph-agoscopy, video esophagography, and/or computed tomog-raphy [CT] scanning).2 Gastroesophageal reflux disease (GERD) is the most com-mon disease of the gastrointestinal tract for which patients seek medical therapy. When GERD symptoms (heartburn, regurgitation, chest pain, and/or supraesophageal symptoms) are troublesome despite adequately dosed PPI, surgical cor-rection may be indicated.3 Barrett’s esophagus is the transformation of the distal esoph-ageal epithelium from squamous to a specialized columnar epithelium capable of further neoplastic progression. The detection of Barrett’s esophagus on endoscopy and biopsy increases the future risk of cancer by >40x compared to indi-viduals without Barrett’s esophagus.4 Giant hiatal hernia, otherwise known as paraesophageal her-nia, should be repaired when symptomatic or associated with iron | Surgery_Schwartz. testing (high resolution esopha-geal motility, 24-hour ambulatory pH measurement, and/or esophageal impedance testing) and anatomic testing (esoph-agoscopy, video esophagography, and/or computed tomog-raphy [CT] scanning).2 Gastroesophageal reflux disease (GERD) is the most com-mon disease of the gastrointestinal tract for which patients seek medical therapy. When GERD symptoms (heartburn, regurgitation, chest pain, and/or supraesophageal symptoms) are troublesome despite adequately dosed PPI, surgical cor-rection may be indicated.3 Barrett’s esophagus is the transformation of the distal esoph-ageal epithelium from squamous to a specialized columnar epithelium capable of further neoplastic progression. The detection of Barrett’s esophagus on endoscopy and biopsy increases the future risk of cancer by >40x compared to indi-viduals without Barrett’s esophagus.4 Giant hiatal hernia, otherwise known as paraesophageal her-nia, should be repaired when symptomatic or associated with iron |
Surgery_Schwartz_6793 | Surgery_Schwartz | of cancer by >40x compared to indi-viduals without Barrett’s esophagus.4 Giant hiatal hernia, otherwise known as paraesophageal her-nia, should be repaired when symptomatic or associated with iron deficiency anemia. Laparoscopic hiatal hernia repair with fundoplication is the most common approach to repair.5 Achalasia is the most common primary esophageal motor disorder. It is characterized by an absence of peristalsis and a hypertensive nonrelaxing lower esophageal sphincter. It is best treated with laparoscopic Heller myotomy and partial fundoplication.6 Most esophageal cancer presents with dysphagia, at which time it has invaded the muscularis of the esophagus and is often associated with lymph node metastases. The preferred treatment at this stage is multimodality therapy with chemo-radiation therapy followed by open or minimally invasive esophagectomy.Figure 25-1. A. Topographic relationships of the cervical esophagus: (a) hyoid bone, (b) thyroid cartilage, (c) cricoid cartilage, | Surgery_Schwartz. of cancer by >40x compared to indi-viduals without Barrett’s esophagus.4 Giant hiatal hernia, otherwise known as paraesophageal her-nia, should be repaired when symptomatic or associated with iron deficiency anemia. Laparoscopic hiatal hernia repair with fundoplication is the most common approach to repair.5 Achalasia is the most common primary esophageal motor disorder. It is characterized by an absence of peristalsis and a hypertensive nonrelaxing lower esophageal sphincter. It is best treated with laparoscopic Heller myotomy and partial fundoplication.6 Most esophageal cancer presents with dysphagia, at which time it has invaded the muscularis of the esophagus and is often associated with lymph node metastases. The preferred treatment at this stage is multimodality therapy with chemo-radiation therapy followed by open or minimally invasive esophagectomy.Figure 25-1. A. Topographic relationships of the cervical esophagus: (a) hyoid bone, (b) thyroid cartilage, (c) cricoid cartilage, |
Surgery_Schwartz_6794 | Surgery_Schwartz | therapy followed by open or minimally invasive esophagectomy.Figure 25-1. A. Topographic relationships of the cervical esophagus: (a) hyoid bone, (b) thyroid cartilage, (c) cricoid cartilage, (d) thyroid gland, (e) sternoclavicular. B. Lateral radio-graphic appearance with landmarks identified as labeled in A. The location of C6 is also included (f). (Reproduced with permission from Shields TW: General Thoracic Surgery, 3rd ed. Philadelphia, PA: Lea & Febiger; 1989.)Three normal areas of esophageal narrowing are evident on the barium esophagogram or during esophagoscopy. The uppermost narrowing is located at the entrance into the esopha-gus and is caused by the cricopharyngeal muscle. Its luminal diameter is 1.5 cm, and it is the narrowest point of the esopha-gus. The middle narrowing is due to an indentation of the ante-rior and left lateral esophageal wall caused by the crossing of the left main stem bronchus and aortic arch. The luminal diameter at this point is 1.6 cm. The | Surgery_Schwartz. therapy followed by open or minimally invasive esophagectomy.Figure 25-1. A. Topographic relationships of the cervical esophagus: (a) hyoid bone, (b) thyroid cartilage, (c) cricoid cartilage, (d) thyroid gland, (e) sternoclavicular. B. Lateral radio-graphic appearance with landmarks identified as labeled in A. The location of C6 is also included (f). (Reproduced with permission from Shields TW: General Thoracic Surgery, 3rd ed. Philadelphia, PA: Lea & Febiger; 1989.)Three normal areas of esophageal narrowing are evident on the barium esophagogram or during esophagoscopy. The uppermost narrowing is located at the entrance into the esopha-gus and is caused by the cricopharyngeal muscle. Its luminal diameter is 1.5 cm, and it is the narrowest point of the esopha-gus. The middle narrowing is due to an indentation of the ante-rior and left lateral esophageal wall caused by the crossing of the left main stem bronchus and aortic arch. The luminal diameter at this point is 1.6 cm. The |
Surgery_Schwartz_6795 | Surgery_Schwartz | is due to an indentation of the ante-rior and left lateral esophageal wall caused by the crossing of the left main stem bronchus and aortic arch. The luminal diameter at this point is 1.6 cm. The lowermost narrowing is at the hiatus of the diaphragm and is caused by the gastroesophageal sphincter mechanism. The luminal diameter at this point varies somewhat, depending on the distention of the esophagus by the passage of food, but has been measured at 1.6 to 1.9 cm. These normal constrictions tend to hold up swallowed foreign objects, and the overlying mucosa is subject to injury by swallowed corrosive liquids due to their slow passage through these areas.Figure 25-3 shows the average distance in centimeters measured during endoscopic examination between the incisor teeth and the cricopharyngeus, aortic arch, and cardia of the stomach. Manometrically, the length of the esophagus between the lower border of the cricopharyngeus and upper border of the lower sphincter varies according to | Surgery_Schwartz. is due to an indentation of the ante-rior and left lateral esophageal wall caused by the crossing of the left main stem bronchus and aortic arch. The luminal diameter at this point is 1.6 cm. The lowermost narrowing is at the hiatus of the diaphragm and is caused by the gastroesophageal sphincter mechanism. The luminal diameter at this point varies somewhat, depending on the distention of the esophagus by the passage of food, but has been measured at 1.6 to 1.9 cm. These normal constrictions tend to hold up swallowed foreign objects, and the overlying mucosa is subject to injury by swallowed corrosive liquids due to their slow passage through these areas.Figure 25-3 shows the average distance in centimeters measured during endoscopic examination between the incisor teeth and the cricopharyngeus, aortic arch, and cardia of the stomach. Manometrically, the length of the esophagus between the lower border of the cricopharyngeus and upper border of the lower sphincter varies according to |
Surgery_Schwartz_6796 | Surgery_Schwartz | aortic arch, and cardia of the stomach. Manometrically, the length of the esophagus between the lower border of the cricopharyngeus and upper border of the lower sphincter varies according to the height of the individual.Brunicardi_Ch25_p1009-p1098.indd 101001/03/19 6:01 PM 1011ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25ABFigure 25-2. Barium esophagogram. A. Posterior-anterior view. White arrow shows deviation to left. Black arrow shows return to midline. B. Lateral view. Black arrow shows anterior deviation. (Reproduced with permission from Shields TW: General Thoracic Surgery, 3rd ed. Philadelphia, PA: Lea & Febiger; 1989.)Pharynx24–26cmUpper sphincter(C6)40cm38cmLower sphincter(T11)15cm14cmAortic arch(T4)25cm 23cmIncisor teethFigure 25-3. Important clinical endoscopic measurements of the esophagus in adults. (Reproduced with permission from Shields TW: General Thoracic Surgery, 3rd ed. Philadelphia, PA: Lea & Febiger; 1989.) Superior pharyngeal constrictor m.Middle pharyngeal | Surgery_Schwartz. aortic arch, and cardia of the stomach. Manometrically, the length of the esophagus between the lower border of the cricopharyngeus and upper border of the lower sphincter varies according to the height of the individual.Brunicardi_Ch25_p1009-p1098.indd 101001/03/19 6:01 PM 1011ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25ABFigure 25-2. Barium esophagogram. A. Posterior-anterior view. White arrow shows deviation to left. Black arrow shows return to midline. B. Lateral view. Black arrow shows anterior deviation. (Reproduced with permission from Shields TW: General Thoracic Surgery, 3rd ed. Philadelphia, PA: Lea & Febiger; 1989.)Pharynx24–26cmUpper sphincter(C6)40cm38cmLower sphincter(T11)15cm14cmAortic arch(T4)25cm 23cmIncisor teethFigure 25-3. Important clinical endoscopic measurements of the esophagus in adults. (Reproduced with permission from Shields TW: General Thoracic Surgery, 3rd ed. Philadelphia, PA: Lea & Febiger; 1989.) Superior pharyngeal constrictor m.Middle pharyngeal |
Surgery_Schwartz_6797 | Surgery_Schwartz | of the esophagus in adults. (Reproduced with permission from Shields TW: General Thoracic Surgery, 3rd ed. Philadelphia, PA: Lea & Febiger; 1989.) Superior pharyngeal constrictor m.Middle pharyngeal constrictor m.Inferior pharyngeal constrictor m.Cricopharyngeus m.EsophagusBAFigure 25-4. External muscles of the pharynx. A. Posterolateral view. B. Posterior view. Dotted line represents usual site of myotomy. (Reproduced with permission from Shields TW: General Thoracic Surgery, 3rd ed. Philadelphia, PA: Lea & Febiger; 1989.)The pharyngeal musculature consists of three broad, flat, overlapping fan-shaped constrictors (Fig. 25-4). The opening of the esophagus is collared by the cricopharyngeal muscle, which arises from both sides of the cricoid cartilage of the lar-ynx and forms a continuous transverse muscle band without an interruption by a median raphe. The fibers of this muscle Brunicardi_Ch25_p1009-p1098.indd 101101/03/19 6:02 PM 1012SPECIFIC CONSIDERATIONSPART IIblend | Surgery_Schwartz. of the esophagus in adults. (Reproduced with permission from Shields TW: General Thoracic Surgery, 3rd ed. Philadelphia, PA: Lea & Febiger; 1989.) Superior pharyngeal constrictor m.Middle pharyngeal constrictor m.Inferior pharyngeal constrictor m.Cricopharyngeus m.EsophagusBAFigure 25-4. External muscles of the pharynx. A. Posterolateral view. B. Posterior view. Dotted line represents usual site of myotomy. (Reproduced with permission from Shields TW: General Thoracic Surgery, 3rd ed. Philadelphia, PA: Lea & Febiger; 1989.)The pharyngeal musculature consists of three broad, flat, overlapping fan-shaped constrictors (Fig. 25-4). The opening of the esophagus is collared by the cricopharyngeal muscle, which arises from both sides of the cricoid cartilage of the lar-ynx and forms a continuous transverse muscle band without an interruption by a median raphe. The fibers of this muscle Brunicardi_Ch25_p1009-p1098.indd 101101/03/19 6:02 PM 1012SPECIFIC CONSIDERATIONSPART IIblend |
Surgery_Schwartz_6798 | Surgery_Schwartz | transverse muscle band without an interruption by a median raphe. The fibers of this muscle Brunicardi_Ch25_p1009-p1098.indd 101101/03/19 6:02 PM 1012SPECIFIC CONSIDERATIONSPART IIblend inseparably with those of the inferior pharyngeal constric-tor above and the inner circular muscle fibers of the esophagus below. Some investigators believe that the cricopharyngeus is part of the inferior constrictor; that is, that the inferior constric-tor has two parts, an upper or retrothyroid portion having diago-nal fibers, and a lower or retrocricoid portion having transverse fibers. Keith in 1910 showed that these two parts of the same muscle serve totally different functions. The retrocricoid portion serves as the upper sphincter of the esophagus and relaxes when the retrothyroid portion contracts, to force the swallowed bolus from the pharynx into the esophagus.The cervical portion of the esophagus is approximately 5 cm long and descends between the trachea and the vertebral column, from | Surgery_Schwartz. transverse muscle band without an interruption by a median raphe. The fibers of this muscle Brunicardi_Ch25_p1009-p1098.indd 101101/03/19 6:02 PM 1012SPECIFIC CONSIDERATIONSPART IIblend inseparably with those of the inferior pharyngeal constric-tor above and the inner circular muscle fibers of the esophagus below. Some investigators believe that the cricopharyngeus is part of the inferior constrictor; that is, that the inferior constric-tor has two parts, an upper or retrothyroid portion having diago-nal fibers, and a lower or retrocricoid portion having transverse fibers. Keith in 1910 showed that these two parts of the same muscle serve totally different functions. The retrocricoid portion serves as the upper sphincter of the esophagus and relaxes when the retrothyroid portion contracts, to force the swallowed bolus from the pharynx into the esophagus.The cervical portion of the esophagus is approximately 5 cm long and descends between the trachea and the vertebral column, from |
Surgery_Schwartz_6799 | Surgery_Schwartz | to force the swallowed bolus from the pharynx into the esophagus.The cervical portion of the esophagus is approximately 5 cm long and descends between the trachea and the vertebral column, from the level of the sixth cervical vertebra to the level of the interspace between the first and second thoracic verte-brae posteriorly, or the level of the suprasternal notch anteriorly. The recurrent laryngeal nerves lie in the right and left grooves between the trachea and the esophagus. The left recurrent nerve lies somewhat closer to the esophagus than the right, owing to the slight deviation of the esophagus to the left, and the more lateral course of the right recurrent nerve around the right sub-clavian artery. Laterally, on the left and right sides of the cervi-cal esophagus are the carotid sheaths and the lobes of the thyroid gland.The thoracic portion of the esophagus is approximately 20 cm long. It starts at the thoracic inlet. In the upper portion of the thorax, it is in intimate | Surgery_Schwartz. to force the swallowed bolus from the pharynx into the esophagus.The cervical portion of the esophagus is approximately 5 cm long and descends between the trachea and the vertebral column, from the level of the sixth cervical vertebra to the level of the interspace between the first and second thoracic verte-brae posteriorly, or the level of the suprasternal notch anteriorly. The recurrent laryngeal nerves lie in the right and left grooves between the trachea and the esophagus. The left recurrent nerve lies somewhat closer to the esophagus than the right, owing to the slight deviation of the esophagus to the left, and the more lateral course of the right recurrent nerve around the right sub-clavian artery. Laterally, on the left and right sides of the cervi-cal esophagus are the carotid sheaths and the lobes of the thyroid gland.The thoracic portion of the esophagus is approximately 20 cm long. It starts at the thoracic inlet. In the upper portion of the thorax, it is in intimate |
Surgery_Schwartz_6800 | Surgery_Schwartz | sheaths and the lobes of the thyroid gland.The thoracic portion of the esophagus is approximately 20 cm long. It starts at the thoracic inlet. In the upper portion of the thorax, it is in intimate relationship with the posterior wall of the trachea and the prevertebral fascia. Just above the tracheal bifurcation, the esophagus passes to the right of the aorta. This anatomic positioning can cause a notch indentation in its left lateral wall on a barium swallow radiogram. Immediately below this notch, the esophagus crosses both the bifurcation of the trachea and the left main stem bronchus, owing to the slight deviation of the terminal portion of the trachea to the right by the aorta (Fig. 25-5). From there down, the esophagus passes over the posterior surface of the subcarinal lymph nodes (LNs), and then descends over the pericardium of the left atrium to reach the diaphragmatic hiatus (Fig. 25-6). From the bifurcation of the trachea downward, both the vagal nerves and the esophageal | Surgery_Schwartz. sheaths and the lobes of the thyroid gland.The thoracic portion of the esophagus is approximately 20 cm long. It starts at the thoracic inlet. In the upper portion of the thorax, it is in intimate relationship with the posterior wall of the trachea and the prevertebral fascia. Just above the tracheal bifurcation, the esophagus passes to the right of the aorta. This anatomic positioning can cause a notch indentation in its left lateral wall on a barium swallow radiogram. Immediately below this notch, the esophagus crosses both the bifurcation of the trachea and the left main stem bronchus, owing to the slight deviation of the terminal portion of the trachea to the right by the aorta (Fig. 25-5). From there down, the esophagus passes over the posterior surface of the subcarinal lymph nodes (LNs), and then descends over the pericardium of the left atrium to reach the diaphragmatic hiatus (Fig. 25-6). From the bifurcation of the trachea downward, both the vagal nerves and the esophageal |
Surgery_Schwartz_6801 | Surgery_Schwartz | (LNs), and then descends over the pericardium of the left atrium to reach the diaphragmatic hiatus (Fig. 25-6). From the bifurcation of the trachea downward, both the vagal nerves and the esophageal nerve plexus lie on the muscular wall of the esophagus.Dorsally, the thoracic esophagus follows the curvature of the spine and remains in close contact with the vertebral bod-ies. From the eighth thoracic vertebra downward, the esopha-gus moves vertically away from the spine to pass through the hiatus of the diaphragm. The thoracic duct passes through the hiatus of the diaphragm on the anterior surface of the verte-bral column behind the aorta and under the right crus. In the thorax, the thoracic duct lies dorsal to the esophagus between the azygos vein on the right and the descending thoracic aorta on the left.The abdominal portion of the esophagus is approximately 2 cm long and includes a portion of the lower esophageal sphincter (LES). It starts as the esophagus passes through the | Surgery_Schwartz. (LNs), and then descends over the pericardium of the left atrium to reach the diaphragmatic hiatus (Fig. 25-6). From the bifurcation of the trachea downward, both the vagal nerves and the esophageal nerve plexus lie on the muscular wall of the esophagus.Dorsally, the thoracic esophagus follows the curvature of the spine and remains in close contact with the vertebral bod-ies. From the eighth thoracic vertebra downward, the esopha-gus moves vertically away from the spine to pass through the hiatus of the diaphragm. The thoracic duct passes through the hiatus of the diaphragm on the anterior surface of the verte-bral column behind the aorta and under the right crus. In the thorax, the thoracic duct lies dorsal to the esophagus between the azygos vein on the right and the descending thoracic aorta on the left.The abdominal portion of the esophagus is approximately 2 cm long and includes a portion of the lower esophageal sphincter (LES). It starts as the esophagus passes through the |
Subsets and Splits
No community queries yet
The top public SQL queries from the community will appear here once available.