Eur J Vasc Surg 6, 427-429 (1992)
SURGICAL PRACTICE
Hypothesis: Why Venous Oedema Causes Ulcers and Lymphoedema Does Not A. D. B. Chant
Royal South Hampshire Hospital, Graham Road, Southampton, U.K. A biomec,hanicalhypothesis is put forward to explain why venous oedema causes ulcers while Iymphoedema does not. Key Words: Venous oedema; Lymphoedema.
There is evidence which suggests that oedema is associated with increased tissue pressure (Pt) in the upright position, that the consequent high pressure increases skin tension and that this increased tension subsequently predisposes to ulceration. 1 The counter argument to this theory suggests that skin is elastic and in any case certain patients, e.g. those with lymphoedema, despite the oedema, do not ulcerate. 2 The purpose of this article is to show how the mechanical hypothesis for venous ulceration can account for the inconsistencies outlined above, to explain how the ischaemic phenomena previously noticed can be accounted for 3 and finally to suggest new areas of research emphasis. The argument which follows is summarised in Figure 1. The cross sectional area of tissues at the ankle is notable for its high bone/soft tissue ratio, thus in contrast to the calf for example, increasing oedema cannot be easily accommodated. The radius (R) at the ankle is therefore relatively fixed so that in the vertical position when Pt rises, the Laplace relationship (T = PR) can only be maintained by an increase in skin tension (T). It is this high tension which appears eventually to cause the skin disruption; the mechanism for this disruption appears to be ischaemia. Figure 2 illustrates my point, showing a thermographic record of skin under two tensions; not unexpectedly (the point is easily confirmed using one's own skin) the increased tension is associated with a 0950-821X/92/040427+03 $03.00/0 © 1992 Grune & Stratton Ltd.
cooling effect due to decreased blood flow which in turn may well disturb tissue nutrition. Turning now to lymphoedema and its lack of ulceration, evidence now exists (and indeed can be easily illustrated on computed tomography scanning) that the degree of hydration of skin in lymphoedema is greater than in controls or in those with venous oedema. Evidence also suggests that the biomechan-
Oedema
P, rises
Skin inelastic (venous)
Skin elastic (lymphoedema)
1,
Tension rises
Tension does not rise
Ischaemia
Ulceration
Fig. 1. Summary of why venous oedema causes ulceration while lymphoedema does not.
428
A . D . B . Chant
Fig. 2. Thermographicpicture of skin unstretched (top) and stretched (bottom). Note the obviouscoolingeffectdue to decreasedblood flow.
ical characteristics of skin in lymphoedema differ reduction of oedema by various means. There is (for markedly from controls and patients with ulcers. 4 the most part anecdotal) evidence regarding the use The skin is therefore likely to be more pliable and less of plastic surgery with a view to physically changing the characteristics of ulcer prone areas but as far as I likely to cause ischaemia. If this hypothesis is correct, then it explains why am aware, relatively little is written about drugs and healing of leg ulcers should be improved by the re- tissue compliance. I hope that the new biomechanical duction of Pt and oedema, why increasing the soft explanation of venous ulceration set out here will tissue/bone ratio (skin grafting) in vulnerable areas is serve as a new impetus to look at an old problem useful, and finally why the use of drugs which affect from a different perspective. New techniques and the rheological properties of blood in small bore treatments should be judged by their capability to alter the underlying biomechanical problems rather vessels 5 has also proved useful. The surgical literature is full of guidance on the than secondary events such as ischaemia. Eur J VascSurgVol6, July1992
Venous Ulceration
Acknowledgement My thanks to Kim Adams for help in preparation of this manuscript.
References 1 CHANT ADB. Tissue pressure, posture and venous ulceration. Lancet 1990; 336: 1050-1051.
429
2 CHANT ADB. Tissue, pressure, posture and venous ulceration. (Letter). Lancet 1990; 337: 338. 3 BROWSE NL, BURNAND KG. The cause of venous ulceration. Lancet 1982; 11: 243-254. 4 MOURAD MM, EDWARDS C, MARKS R. Skin extensibility and the gravitational syndrome. Bioeng Skin 1988; 4: 199-215. 5 SCOTT HJ, MULLIN GM, COLERIDGE-SMITH PD, SCURRJH. Aetiology of venous ulceration. Phlebology 1989; 4: 217-222.
Accepted 10 December 1991
Eur J Vasc Surg Vol 6, July 1992
SURGICAL PRACTICE
Hypothesis: Why Venous Oedema Causes Ulcers and Lymphoedema Does Not A. D. B. Chant
Royal South Hampshire Hospital, Graham Road, Southampton, U.K. A biomec,hanicalhypothesis is put forward to explain why venous oedema causes ulcers while Iymphoedema does not. Key Words: Venous oedema; Lymphoedema.
There is evidence which suggests that oedema is associated with increased tissue pressure (Pt) in the upright position, that the consequent high pressure increases skin tension and that this increased tension subsequently predisposes to ulceration. 1 The counter argument to this theory suggests that skin is elastic and in any case certain patients, e.g. those with lymphoedema, despite the oedema, do not ulcerate. 2 The purpose of this article is to show how the mechanical hypothesis for venous ulceration can account for the inconsistencies outlined above, to explain how the ischaemic phenomena previously noticed can be accounted for 3 and finally to suggest new areas of research emphasis. The argument which follows is summarised in Figure 1. The cross sectional area of tissues at the ankle is notable for its high bone/soft tissue ratio, thus in contrast to the calf for example, increasing oedema cannot be easily accommodated. The radius (R) at the ankle is therefore relatively fixed so that in the vertical position when Pt rises, the Laplace relationship (T = PR) can only be maintained by an increase in skin tension (T). It is this high tension which appears eventually to cause the skin disruption; the mechanism for this disruption appears to be ischaemia. Figure 2 illustrates my point, showing a thermographic record of skin under two tensions; not unexpectedly (the point is easily confirmed using one's own skin) the increased tension is associated with a 0950-821X/92/040427+03 $03.00/0 © 1992 Grune & Stratton Ltd.
cooling effect due to decreased blood flow which in turn may well disturb tissue nutrition. Turning now to lymphoedema and its lack of ulceration, evidence now exists (and indeed can be easily illustrated on computed tomography scanning) that the degree of hydration of skin in lymphoedema is greater than in controls or in those with venous oedema. Evidence also suggests that the biomechan-
Oedema
P, rises
Skin inelastic (venous)
Skin elastic (lymphoedema)
1,
Tension rises
Tension does not rise
Ischaemia
Ulceration
Fig. 1. Summary of why venous oedema causes ulceration while lymphoedema does not.
428
A . D . B . Chant
Fig. 2. Thermographicpicture of skin unstretched (top) and stretched (bottom). Note the obviouscoolingeffectdue to decreasedblood flow.
ical characteristics of skin in lymphoedema differ reduction of oedema by various means. There is (for markedly from controls and patients with ulcers. 4 the most part anecdotal) evidence regarding the use The skin is therefore likely to be more pliable and less of plastic surgery with a view to physically changing the characteristics of ulcer prone areas but as far as I likely to cause ischaemia. If this hypothesis is correct, then it explains why am aware, relatively little is written about drugs and healing of leg ulcers should be improved by the re- tissue compliance. I hope that the new biomechanical duction of Pt and oedema, why increasing the soft explanation of venous ulceration set out here will tissue/bone ratio (skin grafting) in vulnerable areas is serve as a new impetus to look at an old problem useful, and finally why the use of drugs which affect from a different perspective. New techniques and the rheological properties of blood in small bore treatments should be judged by their capability to alter the underlying biomechanical problems rather vessels 5 has also proved useful. The surgical literature is full of guidance on the than secondary events such as ischaemia. Eur J VascSurgVol6, July1992
Venous Ulceration
Acknowledgement My thanks to Kim Adams for help in preparation of this manuscript.
References 1 CHANT ADB. Tissue pressure, posture and venous ulceration. Lancet 1990; 336: 1050-1051.
429
2 CHANT ADB. Tissue, pressure, posture and venous ulceration. (Letter). Lancet 1990; 337: 338. 3 BROWSE NL, BURNAND KG. The cause of venous ulceration. Lancet 1982; 11: 243-254. 4 MOURAD MM, EDWARDS C, MARKS R. Skin extensibility and the gravitational syndrome. Bioeng Skin 1988; 4: 199-215. 5 SCOTT HJ, MULLIN GM, COLERIDGE-SMITH PD, SCURRJH. Aetiology of venous ulceration. Phlebology 1989; 4: 217-222.
Accepted 10 December 1991
Eur J Vasc Surg Vol 6, July 1992
