Volume 27 Number 3 September 1992
Correspondence 489
function, and arteriovenous connections all demand consideration along with the status of the valvular system to adequately evaluate the leg ulcer patient. 1 We appreciate Dr. Swanson's comments regarding elevation, compression, and dietary salt restriction in the management of edema from venous insufficiency. In patients with edema caused by systemic disease such as cardiac failure, diuretic therapy is appropriate. However, we do not advocate the use ofdiuretics in patients with edema from local causes.
Tania J. Phillips, MD, and Jeffrey S. Dover, MD Dept. ofDermatology Boston University School ofMedicine 80 E. Concord St. Boston, MA 02118-2394
REFERENCES 1. Hanrahan LA, ArakiCT, Rodriguez AA, et al. Distribution of valvular incompetence in patients with venous stasis ulceration. J Vasc Surg 1991;13:805-12. 2. Hobbs JT. The management of varicose veins. Surg Annu 1980;12:169.
Leg ulcers To the Editor: We were pleased to see the interest your journal has taken in undertaking to enlighten its readers on the unglamorous subject of leg ulcers (Phillips TJ, Dover JS. J AM ACAD DERMATOL 1991;25:965-87). However, we are concerned by the inaccuracies and omissions in this article, which leave the reader completely uninformed of the enormous progress in this field during the past two decades. First, the authors ignore the possibility that leg ulceration may occur as a result of superficial venous incompetence alone. This fact has been amply demonstrated in numerous publications that suggest that between 20% and 50% of patients with venous ulcers can be shown to have superficial venous disease only.I-3 As approximately 90% of leg ulcers are believed to be venous in origin, the implication is that 18% to 45% ofall ulcers are completely curable if the cause (Le., superficial venous disease) is dealt with. Darke and Penfold4 have recently proved this very point, achieving healing rates of 90%, during a mean follow-up of 3.5 years, after saphenofemoral junction ligation alone in patients with long saphenous vein incompetence and ulceration. To assume that all venous ulcers are secondary to previous deep vein thrombosis is to adhere to concepts disproved many years ago. Second, the authors claim that venous incompetence is a result of failure of the valves within the perforating veins. Such sentiments, although applauded in the 1940s, are not shared by phlebologists today. Controlled clinical trials have found disappointing results after ligation of
these "incompetent" perforators, with high rates of ulcer recurrence, even in cases in which phlebography had clearly shown the perforating veins to be "incompetent."S.9 Zukowski et al. to have suggested that so-called "incompetence" of perforators is usually secondary to undetected deep venous disease; therefore it is not surprising that surgical treatment of "perforators" does not reduce recurrence of ulcers. Third, in dealing with the hypothesis ofstasis as a cause of Ulceration, the authors correctly point out the literature showing that stasis does not occur and thus conclude that "... the popular term stasis is a misnomer." Therefore we were surprised to find the authors using this quaint misnomer themselves (p. 980). Fourth, when discussing the "fibrin cuff" hypothesis, Phillips and Dover claim that venous hypertension is associated with capillary proliferation. Although it is true that capillary proliferation was reported in the histologic studies of Whimster ll in the 1950s, subsequent studies have failed to confirm this. In fact, Fagrell 12 has convincingly shown that there is a reduction in the actual numbers of capillaries in the gaiter area of patients with deep venous insufficiency, the remaining capillaries being widely dilated and coiled. 12. 13 The explanation of this anomaly is that when histologic sections (two-dimensional) are taken through a coiled capillary, several cuts through the same convoluted capillary may erroneously be interpreted as an increased number of capillaries. Finally, the authors appear to be convinced that peri~ capillary fibrin cuffs cause a diffusion barrier to oxygen and nutrients. No direct measurement of tissue P02 has ever been made. Serious doubt has now been raised regarding the validity of the studies that initially suggested the concept of "diffusion barrier." The positron emission study takes no account of the heterogeneity of skin blood flow and used the apparently normal contralaterallimb as control. 14 The authors will acknowl~ge that this is inappropriate, as they will be aware that the "normal" limb in patients with venous disease often has unsuspected abnormalities such as low skin transcutaneous oxygen pressure (tcPo 2) reading and increasedvenous refilling times after exercise. ls Similarly, although several studies demonstrate reduced levels of tcPo2 over the lipodermatoscIerotic skin of patients with venous disease,I6-20 this "measurement" does not reflect tissue oxygen tension. The technique of tcP02 measurement depends on the ability to cause maximal vasodilatation by heating the skin to 43° or 44° C, and Cheatle et al. 21 have recently demonstrated that capillaries in lipodermatoscIerotic skin of patients with venous disease may not dilate to the same extent as capiIIaries in normal skin in response to heating. When the tcP02 has been measured at 37° C instead of 43 ° C, the oxygenation of the skin of patients with venous disease appear to be higher than in normal controls. 22 For an article of such length, we believe the authors
Journal of the American Academy of Dermatology
490 Correspondence should· have dealt with these concepts of etiology and treatment more accurately, especially considering that venous ulcers constitute the highest proportion of leg ulcers and many are completely curable. Exhaustive detailing of symptomatic tre~tment (e.g., which dressing is "best") is futile when the cause of disease is ignored and does nothing to improve the patient's lot.
Shukri K. Shami, FRCS, and Sanjeev Sarin, PRCS Department ofSurgery, University College and Middlesex School ofMedicine, The Middlesex Hospital, Mortimer Street, London WIN 8AA, England
REFERENCES 1. Sethia KI
Correspondence 489
function, and arteriovenous connections all demand consideration along with the status of the valvular system to adequately evaluate the leg ulcer patient. 1 We appreciate Dr. Swanson's comments regarding elevation, compression, and dietary salt restriction in the management of edema from venous insufficiency. In patients with edema caused by systemic disease such as cardiac failure, diuretic therapy is appropriate. However, we do not advocate the use ofdiuretics in patients with edema from local causes.
Tania J. Phillips, MD, and Jeffrey S. Dover, MD Dept. ofDermatology Boston University School ofMedicine 80 E. Concord St. Boston, MA 02118-2394
REFERENCES 1. Hanrahan LA, ArakiCT, Rodriguez AA, et al. Distribution of valvular incompetence in patients with venous stasis ulceration. J Vasc Surg 1991;13:805-12. 2. Hobbs JT. The management of varicose veins. Surg Annu 1980;12:169.
Leg ulcers To the Editor: We were pleased to see the interest your journal has taken in undertaking to enlighten its readers on the unglamorous subject of leg ulcers (Phillips TJ, Dover JS. J AM ACAD DERMATOL 1991;25:965-87). However, we are concerned by the inaccuracies and omissions in this article, which leave the reader completely uninformed of the enormous progress in this field during the past two decades. First, the authors ignore the possibility that leg ulceration may occur as a result of superficial venous incompetence alone. This fact has been amply demonstrated in numerous publications that suggest that between 20% and 50% of patients with venous ulcers can be shown to have superficial venous disease only.I-3 As approximately 90% of leg ulcers are believed to be venous in origin, the implication is that 18% to 45% ofall ulcers are completely curable if the cause (Le., superficial venous disease) is dealt with. Darke and Penfold4 have recently proved this very point, achieving healing rates of 90%, during a mean follow-up of 3.5 years, after saphenofemoral junction ligation alone in patients with long saphenous vein incompetence and ulceration. To assume that all venous ulcers are secondary to previous deep vein thrombosis is to adhere to concepts disproved many years ago. Second, the authors claim that venous incompetence is a result of failure of the valves within the perforating veins. Such sentiments, although applauded in the 1940s, are not shared by phlebologists today. Controlled clinical trials have found disappointing results after ligation of
these "incompetent" perforators, with high rates of ulcer recurrence, even in cases in which phlebography had clearly shown the perforating veins to be "incompetent."S.9 Zukowski et al. to have suggested that so-called "incompetence" of perforators is usually secondary to undetected deep venous disease; therefore it is not surprising that surgical treatment of "perforators" does not reduce recurrence of ulcers. Third, in dealing with the hypothesis ofstasis as a cause of Ulceration, the authors correctly point out the literature showing that stasis does not occur and thus conclude that "... the popular term stasis is a misnomer." Therefore we were surprised to find the authors using this quaint misnomer themselves (p. 980). Fourth, when discussing the "fibrin cuff" hypothesis, Phillips and Dover claim that venous hypertension is associated with capillary proliferation. Although it is true that capillary proliferation was reported in the histologic studies of Whimster ll in the 1950s, subsequent studies have failed to confirm this. In fact, Fagrell 12 has convincingly shown that there is a reduction in the actual numbers of capillaries in the gaiter area of patients with deep venous insufficiency, the remaining capillaries being widely dilated and coiled. 12. 13 The explanation of this anomaly is that when histologic sections (two-dimensional) are taken through a coiled capillary, several cuts through the same convoluted capillary may erroneously be interpreted as an increased number of capillaries. Finally, the authors appear to be convinced that peri~ capillary fibrin cuffs cause a diffusion barrier to oxygen and nutrients. No direct measurement of tissue P02 has ever been made. Serious doubt has now been raised regarding the validity of the studies that initially suggested the concept of "diffusion barrier." The positron emission study takes no account of the heterogeneity of skin blood flow and used the apparently normal contralaterallimb as control. 14 The authors will acknowl~ge that this is inappropriate, as they will be aware that the "normal" limb in patients with venous disease often has unsuspected abnormalities such as low skin transcutaneous oxygen pressure (tcPo 2) reading and increasedvenous refilling times after exercise. ls Similarly, although several studies demonstrate reduced levels of tcPo2 over the lipodermatoscIerotic skin of patients with venous disease,I6-20 this "measurement" does not reflect tissue oxygen tension. The technique of tcP02 measurement depends on the ability to cause maximal vasodilatation by heating the skin to 43° or 44° C, and Cheatle et al. 21 have recently demonstrated that capillaries in lipodermatoscIerotic skin of patients with venous disease may not dilate to the same extent as capiIIaries in normal skin in response to heating. When the tcP02 has been measured at 37° C instead of 43 ° C, the oxygenation of the skin of patients with venous disease appear to be higher than in normal controls. 22 For an article of such length, we believe the authors
Journal of the American Academy of Dermatology
490 Correspondence should· have dealt with these concepts of etiology and treatment more accurately, especially considering that venous ulcers constitute the highest proportion of leg ulcers and many are completely curable. Exhaustive detailing of symptomatic tre~tment (e.g., which dressing is "best") is futile when the cause of disease is ignored and does nothing to improve the patient's lot.
Shukri K. Shami, FRCS, and Sanjeev Sarin, PRCS Department ofSurgery, University College and Middlesex School ofMedicine, The Middlesex Hospital, Mortimer Street, London WIN 8AA, England
REFERENCES 1. Sethia KI
