Journal of the American Academy of Dermatology
488 C7orrespondence tent periulcer venous channels in deep venous insuffi.ciency significantly enhanced ulcer healing. As emphasized by the authors, it is important to exclude arterial disease in the ulcer patient. In this regard, they appropriately discuss the ankle-brachial index, although they fail to mention that this index may be falsely normal in diabetic patients because ofvessel wall stiffness. In such cases, one should be familiar with arterial waveform abnormalities. Regarding the microcirculation, the authors state that "high venous pressure is associated with capillary proliferation." Franzeck et a1.,6 using videomicroscopy, have shown that capillarydensity is reduced in extremities with advanced chronic venous insufficiency. These authors suggest that the tortuosity of the affected capillaries may result in a falsely high capillary count in histologic section and account for previous conclusions about capillary proliferation. The specifics of how the microcirculatory abnormalities produce ulceration remain to be elucidated. As mentioned by the authors two current theories are the fibrin cuff theory (oxygen diffusion barrier) and the white cell trapping theory (perfusion defect). Several recent articles have cast doubt on the hypothesis that pericapillary fibrin cuffs act as an oxygen diffusion barrier.7- IO In conclusion, although compression should serve as the cornerstone of treatment in venous ulcers, one must define the basic underlying abnormality of the venous system to form a rational individualized management plan. Steven E. Zimmet, MD Austin Regional Clinic 3708 Jefferson St. Austin, TX 78731
REFERENCES 1.
2. 3. 4. 5. 6.
7. 8.
Christopoulous D, Nicolaides AN. Noninvasive diagnosis and quantitation of popliteal reflux in the swollen and ulcerated leg. J Cardiovasc Surg 1988;29:535-9. Hanrahan LM, Araki CT, Rodriguez AA, et a1. Distribution of valvular incompetence in patients with venous stasis ulceration. J VascSurg 1991;13:805-11, Hoare MC, Nicolaides AN, Miles CR, et a1. The role of primary varicose veins in venous ulceration. Surgery 1982; 92:450-3. Stemmer R. Sclerotherapy of varicose veins. St. Gallen: Oanzoni & Cie, 1990:32. Queral LA, Criado FJ, Lilly MP, et a1. The role of sclerotherapy as an adjunct to Unna's boot for treating venous ulcers: a prospective study. J Vasc Surg 1990;11:572-5. Franzeck UK, BollingerA, Hasch R, et a1. Transcutaneous oxygen tension and capillary morphologic characteristics and density in patients with chronic venous insufficiency. Circulation 1984;70:806-11. Stibe E, Cheatle TR, Coleridge Smith PD, et a1. Liposclerotic skin: A diffusion block or perfusion problem? Phlebology 1990;5:231-6. Cheatle TR, McMullin OM, Farrah J, et a1. Skin damage in chronic venous insufficiency: Does an oxygen diffusion barrier really exist? J R Soc Med 1990;83:48-9.
9. Michel CC. Oxygen diffusion in oedematous tissue and through pericapillary fibrin cuffs. Phlebology 1990;5:22330. 10. C1audy AL, Mirshahi M, Suria C, et a1. Detection of undegraded fibrin and tumor necrosis factor-a in venous leg ulcers. JAM ACAD DERMATOL 1991;25:623-7.
Leg ulcers To the Editor: In their otherwise excellent review of the management of leg ulcers (J AM ACAD DERMATOL 1991;25:961-87),Phillips and Dover neglected to mention the importance of sodium restriction and the use of diuretics in the management of edema from stasis. Certainly, patients with mild edema will often respond to elevation and compression, in combination with dietary restriction of salt. Patients with more severe and advanced disease benefit from pharmacologic management directed toward edema control. This is especially true in patients who suffer from both arterial and venous insufficiency in whom vasodilator therapy is contemplated because these patients are predisposed to secondary volume retention. I believe that the neglect of any discussion of diuretic therapy, even brief, is an important omission in an otherwise valuable article. David L. Swanson, MD 500 Janalyn Circle Golden Valley, MN 55416
Reply To the Editor: We thank Drs. Zimmett and Swanson for their letters. Dr. Zimmett elegantly describes calf muscle pump dysfunction. The pathophysiologic mechanism of venous ulcers is complex and not yet fully understood. As we stated in our article, venous ulcers are usually associated with deep venous insufficiency, and, as Hanrahan et al. l demonstrated, multisystem incompetence is the most common finding. Although phlebologists may use sclerotherapy to treat venous ulcers, most vascular surgeons find this approach controversial. Prospective studies have shown that surgeryachieves significantly better results. 2 Dr. Zimmett's comment about the ankle-brachial index in diabetic patients underscores our discussion about this problem. As we stated in our article, the systolic blood pressure at the ankle studied with a Doppler flowmeter can sometimes be misleadingly high in the diabetic patient because of medial calcification of the arteries. In these patients, measurement of pulse amplitude with an oscillometer or plethysmograph is helpful. We agree that the role of resting and ambulatory venous function, calf muscle pump function, lymphatic
488 C7orrespondence tent periulcer venous channels in deep venous insuffi.ciency significantly enhanced ulcer healing. As emphasized by the authors, it is important to exclude arterial disease in the ulcer patient. In this regard, they appropriately discuss the ankle-brachial index, although they fail to mention that this index may be falsely normal in diabetic patients because ofvessel wall stiffness. In such cases, one should be familiar with arterial waveform abnormalities. Regarding the microcirculation, the authors state that "high venous pressure is associated with capillary proliferation." Franzeck et a1.,6 using videomicroscopy, have shown that capillarydensity is reduced in extremities with advanced chronic venous insufficiency. These authors suggest that the tortuosity of the affected capillaries may result in a falsely high capillary count in histologic section and account for previous conclusions about capillary proliferation. The specifics of how the microcirculatory abnormalities produce ulceration remain to be elucidated. As mentioned by the authors two current theories are the fibrin cuff theory (oxygen diffusion barrier) and the white cell trapping theory (perfusion defect). Several recent articles have cast doubt on the hypothesis that pericapillary fibrin cuffs act as an oxygen diffusion barrier.7- IO In conclusion, although compression should serve as the cornerstone of treatment in venous ulcers, one must define the basic underlying abnormality of the venous system to form a rational individualized management plan. Steven E. Zimmet, MD Austin Regional Clinic 3708 Jefferson St. Austin, TX 78731
REFERENCES 1.
2. 3. 4. 5. 6.
7. 8.
Christopoulous D, Nicolaides AN. Noninvasive diagnosis and quantitation of popliteal reflux in the swollen and ulcerated leg. J Cardiovasc Surg 1988;29:535-9. Hanrahan LM, Araki CT, Rodriguez AA, et a1. Distribution of valvular incompetence in patients with venous stasis ulceration. J VascSurg 1991;13:805-11, Hoare MC, Nicolaides AN, Miles CR, et a1. The role of primary varicose veins in venous ulceration. Surgery 1982; 92:450-3. Stemmer R. Sclerotherapy of varicose veins. St. Gallen: Oanzoni & Cie, 1990:32. Queral LA, Criado FJ, Lilly MP, et a1. The role of sclerotherapy as an adjunct to Unna's boot for treating venous ulcers: a prospective study. J Vasc Surg 1990;11:572-5. Franzeck UK, BollingerA, Hasch R, et a1. Transcutaneous oxygen tension and capillary morphologic characteristics and density in patients with chronic venous insufficiency. Circulation 1984;70:806-11. Stibe E, Cheatle TR, Coleridge Smith PD, et a1. Liposclerotic skin: A diffusion block or perfusion problem? Phlebology 1990;5:231-6. Cheatle TR, McMullin OM, Farrah J, et a1. Skin damage in chronic venous insufficiency: Does an oxygen diffusion barrier really exist? J R Soc Med 1990;83:48-9.
9. Michel CC. Oxygen diffusion in oedematous tissue and through pericapillary fibrin cuffs. Phlebology 1990;5:22330. 10. C1audy AL, Mirshahi M, Suria C, et a1. Detection of undegraded fibrin and tumor necrosis factor-a in venous leg ulcers. JAM ACAD DERMATOL 1991;25:623-7.
Leg ulcers To the Editor: In their otherwise excellent review of the management of leg ulcers (J AM ACAD DERMATOL 1991;25:961-87),Phillips and Dover neglected to mention the importance of sodium restriction and the use of diuretics in the management of edema from stasis. Certainly, patients with mild edema will often respond to elevation and compression, in combination with dietary restriction of salt. Patients with more severe and advanced disease benefit from pharmacologic management directed toward edema control. This is especially true in patients who suffer from both arterial and venous insufficiency in whom vasodilator therapy is contemplated because these patients are predisposed to secondary volume retention. I believe that the neglect of any discussion of diuretic therapy, even brief, is an important omission in an otherwise valuable article. David L. Swanson, MD 500 Janalyn Circle Golden Valley, MN 55416
Reply To the Editor: We thank Drs. Zimmett and Swanson for their letters. Dr. Zimmett elegantly describes calf muscle pump dysfunction. The pathophysiologic mechanism of venous ulcers is complex and not yet fully understood. As we stated in our article, venous ulcers are usually associated with deep venous insufficiency, and, as Hanrahan et al. l demonstrated, multisystem incompetence is the most common finding. Although phlebologists may use sclerotherapy to treat venous ulcers, most vascular surgeons find this approach controversial. Prospective studies have shown that surgeryachieves significantly better results. 2 Dr. Zimmett's comment about the ankle-brachial index in diabetic patients underscores our discussion about this problem. As we stated in our article, the systolic blood pressure at the ankle studied with a Doppler flowmeter can sometimes be misleadingly high in the diabetic patient because of medial calcification of the arteries. In these patients, measurement of pulse amplitude with an oscillometer or plethysmograph is helpful. We agree that the role of resting and ambulatory venous function, calf muscle pump function, lymphatic
