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Hypertrophic scars
HYPERTROPHIC SCARS
By RAINSFORDMOWLEM,F.R.C.S. From the Plastic Unit, Hill End Hospital, St Albans
A TYPICALhypertrophic scar passes through a well-defined series of phases, which seem to indicate the existence of a cycle of cellular activity both within and deep to the skin. The length of time the cycle will occupy and the amplitude of the response may vary considerably, but the overall pattern is constant. It is best seen in incised wounds, but it occurs equally frequently after almost any type of skin damage or loss. When primary healing is complete, say between the third and fifth days, the scar is a faintly pink narrow line, on a level with the surrounding skin surface. Within the next twenty to thirty days the width and prominence of the scar increase and the pink colour, instead of fading, becomes more marked. The surface is shiny and "juicy " in appearance and is usually very irritable. In this stage the scar is indistinguishable from a true keloid, and it possesses identical histological appearances. Indeed, the differentiation between the two conditions is entirely clinical and depends on the fact that the keloid maintains or slowly increases its volume and extent over an almost indefinite period, whereas the hypertrophic scar passes into a phase of regression. This stage is initiated by a loss of the moist appearance, and soon afterwards the colour begins to fade. During this process the prominence and the bulk of the scar slowly decrease, and when in six to sixty months the cycle is complete the scar is thin, white, and flat. It is much wider than in its original state, and it possesses no elasticity whatever. The plastic surgeon is called upon to treat these hypertrophic scars when tl~ey result from burns or lacerations, but he also lives under the threat that they may jeopardise his reconstructive efforts. When he is confronted with a patient who already shows such scars he is forewarned, but there are occasions when he has no such indication of the response of the skin to injury. He has probably been taught that " r e d heads," patients with thyroid dysfunction, and negroes are particularly prone to produce poor scars, but he has learned that many who do not fall into these groups are equally likely to present the same problem. There are many factors which mitigate against the healing of a wound with minimal scarring, and to some of these has been ascribed the responsibility for "hypertrophy." Infection.--Gross infection will, of course, delay healing and will produce the inflammatory changes which end in the laying down of massive fibrous tissue. The result will be an irregular thickened scar invading the surrounding subcutaneous tissues, but it will not show the cyclical change so typical of a hypertrophic scar. It has been suggested that sub-clinical infection may be an entity in the production of "hypertrophy " - - b u t this is a condition which has not so far been capable of bacteriological proof, and it is one in which it is difficult to believe if one possesses the average surgeon's faith in the efficiency of the body's protective mechanisms. 2C
Ix3
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JOURNAL
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SURGERY
M o v e m e n t and Tension are well recognised factors in producing thickened scars, but I think it will be found that these differ in many respects from the true hypertrophy. They are raised above the surface, particularly when they cross a concavity. They do not tend to be grossly vascular, and they never regress to the papyraceous state. Rather do they remain as thickened cords of adult fibrous tissue covered by a flaking keratotic epithelium which is likely to ulcerate at points of flexion with the resultant creation of still more fibrosis and still more keratosis. It would seem that such a condition is well explained, firstly by the known tendency for fibroblasts to orientate themselves in parallel to a line of tension and, secondly, by the damage inflicted upon these cells, and upon the " scar epithelium " which covers them, by repeated movement. So far, therefore, we have no adequate explanation of the occurrence of scar hypertrophy, as it may occur in a surgical wound on the face or after, say, a relatively superficial burn of the chest wall. Seven or eight years ago the help of the Strangeways Institute at Cambridge was enlisted, and as the result of the work of Fell and Glficksmann we were presented with a probability apparently so simple that it was almost unbelievable. Since that time, therefore, scars have been carefully examined on their hypothesis, and it would appear to me to fit the observable facts to a nicety. I feel we owe both Miss Fell and Dr Gliicksmann an apology for failing earlier to co-operate in publication, but I think the prolonged clinical investigation has done so much to substantiate their histological hypothesis that the delay seems iustified. The histological material we provided consisted of hypertrophic scars in all stages of development derived from patients presenting burns, war iniuries, surgical wounds, and grafted areas. In a proportion of this material Glficksmann (i95 I) demonstrated foreign bodies in the non-encysted state. These included cotton-wool fibres and silicates from road and bomb iniuries, but in a considerably higher proportion of cases they consisted of hair follicles and sebaceous glands or their remnants. These were associated with a constant histological picture which appeared significant. In coniunction with Miss Fell, therefore, a series of animal experiments were carried out. They consisted of the implantation of small autogenous grafts beneath the skin and a study of the results. It was found that so long as the keratin produced by the graft and its contained hair follicles remained encysted, no tissue response to the presence of the implant was discernible. As soon, however, as the cyst wall perforated, exposing the subcutaneous tissues to the effects of the keratin, there was a dilatation of those vessels in the immediate neighbourhood. As these vessels break up into smaller branches nearer the skin surface, the area of involvement was roughly pyramidal with the apex down at the point of contact with the keratin and the base on the skin surface. Throughout this pyramid, pervascular extravasation of round cells occurred until the tissues within the area became crowded with them. The process continued until the keratin had been removed by the normal scavenging mechanisms. After this phase there was gradual regression of the dilatation followed by a slow resorption of the fibrosis caused by the initial changes. The various phases of this same cycle were observed in the human histological material, and the picture became coherent. The histological changes accord so well with the observed clinical cycle of
HYPERTROPHIC
SCARS
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scar hypertrophy that it has formed the basis of our subsequent clinical examinations of scars. It is, of course, obvious that if hypertrophy is a reaction to, or a sensitivity to, foreign material and to keratin in particular, there are two primary factors. The first is systemic, but the second must be local. It is possible that the number of wounds which do not at some stage contain some foreign material may be very small, but not every patient develops a hypertrophic scar. Whilst there must be variations in the amount of buried keratin, it is probable that there are individual systemic variations in the amount of reaction such keratin will cause. In any given patient, however, this general systemic factor will be constant, but there may be variations in the local factors which are the activating causes. In other words, two scars on the same patient will not necessarily produce similar and equal responses. With keratin, therefore, in mind as the important element, it may be of interest to review scars which become hypertrophic to see whether there are any relatively constant features of importance in determining their incidence. It would seem that the amount of keratin in any wound must determine the magnitude of the response, for although there is an element of systemic sensitivity in the reaction, the local response is confined to the area of the blood-vessels which are immediately exposed to the effect of the keratin. The actual amount of buried keratin, therefore, is of importance. It can be derived from hair follicles or from sebaceous glands, and the skin most likely to produce hypertrophic scars should possess some or all of the following characteristics :-. I. The Presence of Lanugo.--These hairs are slow-growing, are not very robust, and are often present in very great numbers. Any wound is likely to submerge an appreciable number of follicles beneath the skin surface. In view of their obliquity of growth, the difference between an incision parallel to, and one at right angles to, their general direction may be very considerable. In the former case a minimal number of follicles will be divided--in the latter the number will be maximal. The hair of the beard or scalp is of a much more rapidly growing type, and the density of such hair in any given area is much less than lanugo. The rate of growth is almost sufficient on its own to ensure that any follicle buried beneath the skin is only temporarily isolated from the surface. 2. Sebaceous Glands.--These, too, can be a source of keratin, and it might be expected that areas of most profuse sweating would be most likely to produce hypertrophic scars. 3. Skin Thickness.--It seems probable that the likelihood of isolating either hair follicles or sweat glands is increased in proportion to the thickness of the skin through which the incision is made. The types of patient generally supposed, therefore, to have " b a d skins " from the scar point of view, i.e., those with red hair and fair complexions and those suffering from thyroid disturbances, may therefore be reclassified, the former invariably having a generous distribution of lanugo and the latter having either a coarse skin with an excessive distribution of terminal hair or, alternatively, an active sebaceous mechanism. The negro presents a thick skin with many active sweat glands, but, in addition to this, the common tendency to the use of ornamental
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JOURNAL
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SURGERY
keloids may have led, as the result of marital selection, to an accentuation of the systemic factors necessary to produce hypertrophy. In the light, therefore, of the foreign body hypothesis, it is interesting to try to correlate the work done by Levitt (1951) on the control of hypertrophic scars by X-radiation. His technique requires the use of small doses of radiation to a hypertrophic area either as a method of hastening regression or, if preceding and following surgical excision, as a method of controlling the hypertrophic reaction of the skin to the new wound. The effects of these small doses of radiation are known to be threefold. .... " ~'~ Firstly, the endothelium of the subcutaneous vessels is damaged, with the result that intravascular clotting may occur, so that within the first seven to fourteen days there is decreased vascularity in the area. Secondly, there is a reduction in histiocyte formation. Thirdly, degenerative changes are induced in the epithelium of the hair follicles and the sweat glands. The pathologist therefore states that buried hair follicles or sweat glands can induce a vascular dilatation with pervascular transudation of round cells. The radiologist employs a technique which damages the hair follicles and sweat Fro. i glands--which renders vascular response less A typical road abrasion. Note that the likely and which reduces the numbers of at parallel scars o n t h e c h i n are o f two types : least one type of round cell which normally t h e one on t h e left is p i g m e n t e d , b u t soft passes through the vessel wall. a n d supple. Its n e i g h b o u r is p i g m e n t e d The clinician can perhaps add his quota at each end, b u t t h e deeper central area is hypertrophic, tO the picture. Incised W o u n d s . - - T h e grazing injury commonly seen on the malar, lip, and chin regions following a fall from a cycle almost invariably presents scars of two kinds (Fig. I). When the injury has extended through only part of the thickness of the skin the scar may be pigmented, but it is not hypertrophic. No skin elements have been isolated from their connection with the surface, and none have been buried in the subdermal area. There has therefore been no subdermal vascular response to cause hypertrophy. An adjacent scar may well have been fractionally deeper--skin elements have been buried in the subdermal region and gross hypertrophy is present. In the one case only the skin is damaged and there is no abnormal response. In the other the skin has been perforated, and surface elements may have been carried into the subdermal areas to initiate the response. The scars may be only ~ in. apart, and differences in tension or infection would seem irrelevant. We have all seen the child upon whom an operation for cleft lip within the first few months of life has left an almost invisible scar. We have too often seen a secondary operation at the age of 5 or 6, carried out to correct some minor irregularity, result in a hypertrophic scar which will never attain the linear
HYPERTROPHIC
SCARS
117
proportions of the earlier one. Is this likely to be due to the absence of lanugo hair in the small child and its presence at the age o f 5 ? We have all had experience of operating on the adolescent girl with a peach-like complexion and producing a raised red hypertrophic scar (Fig. 2), even though there has been careful attention to every detail of surgical technique. We have all operated upon the bearded face of the adult male and we have not produced bad scars. Does the difference lie in the liability in the one case of burying keratin-bearing structures, whilst in the other the growth capacity of the beard is such that it refused to stay buried ?
A FIG. 2 B A patient aged 20. Dark hair but a fine skin well endowed with lanugo hair. A, The result of an attempt to pierce the lobule of the ear. B, The result of a minor operation on the breast. Both procedures were carried out one year prior to the photograph, and neither was complicated by clinical infection. On the whole, I think it true to say that the certainty of producing perfect scars increases with the age of the patiem, and it is equally true that with increasing years the hair-bearing capacity of the skin becomes progressively less and the activity of the sweat glands is similarly decreased. Skin losses are perhaps best examined in burns. Superficial loss of a minor degree is seen at the margins of most heat burns. The area is originally only reddened with minimal blistering (Fig. 3). Healing is rapid and leaves only a very slight change in the surface texture, with the orifices of the glands and hair follicles visible as minute pits. Hypertrophy is never seen. Partial losses may extend as deeply as the middle layers of the dermis. These, in the untreated state, are slow to heal, and are commonly followed by the typical hypertrophic scar. Chemicals are an outstanding cause of burns which heal spontaneously with a grossly hypertrophic scar. The depth of penetration of the burn is frequently
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limited by the action of the chemical itself in producing a protective surface coagulum. After this separates, the dermis (deep to which lie many o f the hair follicles and sweat glands) is exposed. Healing is always delayed, and during this stage it is by no means unlikely that at least some of the keratin-bearing structures will lose their continuity with the surface. The repeated dressings and the presence of low-grade infection may aggravate matters by allowing the inclusion of exogenous foreign bodies.
A
FIG. 3
B
A b u r n o f t h e chest, a r m s , neck, a n d face caused b y clothes catching fire. A, T o w a r d s the e n d of t h e stage of p r i m a r y epithelialisation, b o t h as t h e result o f s p o n t a n e o u s healing a n d of grafting. H y p e r t r o p h y is b e g i n n i n g in t h e chin a n d neck a n d sternal areas. Elsewhere it is less marked. N o t e its absence on t h e left s h o u l d e r a n d a r m w h e r e t h e b u r n was a partial destruction a n d w h e r e t h e scar shows a white stippling only. B, N i n e m o n t h s later. H y p e r t r o p h y is m o r e m a r k e d in the neck a n d sternal areas a n d at t h e junction lines o f t h e grafts on t h e breasts, t h o u g h in all areas it has passed t h r o u g h t h e phase of m a x i m a l vascularity a n d is b e g i n n i n g to regress. N o t e t h e left shoulder area retains t h e characteristics seen in A.
A similar grossly hypertrophic scar may occasionally follow the cutting of a fairly thick graft with a dermatome, and the causal mechanism is probably identical. Full-thickness losses but seldom produce gross hypertrophy if spontaneous healing is allowed, though they may apparently do so if grafted. According to G10cksmann, this is due to the reintroduction of keratin-bearing structures in the graft. Full-thickness burns causing complete destruction of all skin elements may be produced by the passage of electric current or by molten metal. Though spontaneous healing is very slow and may therefore produce a thick scar, it will not produce a typically hypertrophic scar. There is little reason why it should,
A
B
C FIG. 4 D An extensive laceration involving the full thickness of the cheek associated with fractures of the mandible, occurring in a boy of 17. He has dark hair and a fresh complexion. A, The initial lesion. B, The appearance twenty-one days later. C, Scar hypertrophy seventeen months later. The position and direction of the neck scar is that which would normally be chosen to ensure a good result. D, To show the heavy lanugo distribution not only in the beard area but also on the cheeks and forehead. I19
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for no skin elements remain. The same behaviour is seen in tropical and varicose ulcers and in those embolic skin losses sometimes occurring in the exanthemata. It seems, therefore, that the possibility of the occurrence of hypertrophy can be predicted on the local factors present in any wound (Fig. 4). Whether these factors will produce an actual hypertrophy must also depend on the systemic response they may initiate. Control of hypertrophy would seem therefore to be capable of achievement by two methods. The first is by desensitisation to the local foreign body. If it is accepted that the commonest foreign body is keratin (which is an almost insoluble substance), t&is approach must be fraught with difficulties. The second is by reduction of the activating factors : (a) Exogenous foreign material must be mainly derived from the dressings employed. Short staple cotton as gauze and cotton wool seem to be obvious offenders; (b) endogenous material can be reduced in deep partial thickness losses by excision prior to grafting. This is a procedure not uncommonly employed in any case, but it may deserve greater consideration than it often receives. When the probability of the inclusion of endogenous material in a surgical wound is obvious from an inspection of the skin, a hypertrophic wound can be forecast. In young boys and, indeed, in some young girls it may be desirable to defer an unimportant operation until after puberty, when the skin characteristics, particularly in males, will change. In other cases, however, it is advisable to warn the patient and to adopt the only method of control which is at present available-radiotherapy. It will be obvious, however, that this method of treatment is highly specialised, and haphazard use of therapy is better avoided. SUMMARY I. The behaviour of a hypertrophic scar is outlined, and it is differentiated from fibrosis arising from other causes. 2. The histological characteristics in relation to causation are described. Both exogenous and endogenous foreign bodies are shown to produce a primary vascular response, which is the basis of the hypertrophy. 3. The histological cycle is correlated with the known clinical picture. 4. The importance of keratin-bearing structures of the skin in relation to hypertrophic scar is stressed, and their distribution is discussed. 5. The histological effects of X-ray on normal tissues are correlated with the histological picture as it occurs in scar hypertrophy. 6. The clinical picture of the behaviour of various types of lesion is given. 7. Some possibilities of control of the hypertrophic reaction are outlined. It is obvious that without the co-operation of Miss Fell, Dr Gliicksmann, and Dr Levitt the material for this paper would not have been available. In addition, most of the work and a considerable proportion of the enthusiasm which went into the inception of the investigation lie to the credit of Mr J. N. Barron. The photography was the responsibility of Miss N. Walker. To each and all of them I am glad to acknowledge my indebtedness. REFERENCES
GLOCKSMANN,A. (1951). Brit. J. Plastic Swrg., 4, 88. LEVITT,W. i . (1951). Brit. J. Plastic Surg., 4, lO4.
By RAINSFORDMOWLEM,F.R.C.S. From the Plastic Unit, Hill End Hospital, St Albans
A TYPICALhypertrophic scar passes through a well-defined series of phases, which seem to indicate the existence of a cycle of cellular activity both within and deep to the skin. The length of time the cycle will occupy and the amplitude of the response may vary considerably, but the overall pattern is constant. It is best seen in incised wounds, but it occurs equally frequently after almost any type of skin damage or loss. When primary healing is complete, say between the third and fifth days, the scar is a faintly pink narrow line, on a level with the surrounding skin surface. Within the next twenty to thirty days the width and prominence of the scar increase and the pink colour, instead of fading, becomes more marked. The surface is shiny and "juicy " in appearance and is usually very irritable. In this stage the scar is indistinguishable from a true keloid, and it possesses identical histological appearances. Indeed, the differentiation between the two conditions is entirely clinical and depends on the fact that the keloid maintains or slowly increases its volume and extent over an almost indefinite period, whereas the hypertrophic scar passes into a phase of regression. This stage is initiated by a loss of the moist appearance, and soon afterwards the colour begins to fade. During this process the prominence and the bulk of the scar slowly decrease, and when in six to sixty months the cycle is complete the scar is thin, white, and flat. It is much wider than in its original state, and it possesses no elasticity whatever. The plastic surgeon is called upon to treat these hypertrophic scars when tl~ey result from burns or lacerations, but he also lives under the threat that they may jeopardise his reconstructive efforts. When he is confronted with a patient who already shows such scars he is forewarned, but there are occasions when he has no such indication of the response of the skin to injury. He has probably been taught that " r e d heads," patients with thyroid dysfunction, and negroes are particularly prone to produce poor scars, but he has learned that many who do not fall into these groups are equally likely to present the same problem. There are many factors which mitigate against the healing of a wound with minimal scarring, and to some of these has been ascribed the responsibility for "hypertrophy." Infection.--Gross infection will, of course, delay healing and will produce the inflammatory changes which end in the laying down of massive fibrous tissue. The result will be an irregular thickened scar invading the surrounding subcutaneous tissues, but it will not show the cyclical change so typical of a hypertrophic scar. It has been suggested that sub-clinical infection may be an entity in the production of "hypertrophy " - - b u t this is a condition which has not so far been capable of bacteriological proof, and it is one in which it is difficult to believe if one possesses the average surgeon's faith in the efficiency of the body's protective mechanisms. 2C
Ix3
II 4
BRITISH
JOURNAL
OF
PLASTIC
SURGERY
M o v e m e n t and Tension are well recognised factors in producing thickened scars, but I think it will be found that these differ in many respects from the true hypertrophy. They are raised above the surface, particularly when they cross a concavity. They do not tend to be grossly vascular, and they never regress to the papyraceous state. Rather do they remain as thickened cords of adult fibrous tissue covered by a flaking keratotic epithelium which is likely to ulcerate at points of flexion with the resultant creation of still more fibrosis and still more keratosis. It would seem that such a condition is well explained, firstly by the known tendency for fibroblasts to orientate themselves in parallel to a line of tension and, secondly, by the damage inflicted upon these cells, and upon the " scar epithelium " which covers them, by repeated movement. So far, therefore, we have no adequate explanation of the occurrence of scar hypertrophy, as it may occur in a surgical wound on the face or after, say, a relatively superficial burn of the chest wall. Seven or eight years ago the help of the Strangeways Institute at Cambridge was enlisted, and as the result of the work of Fell and Glficksmann we were presented with a probability apparently so simple that it was almost unbelievable. Since that time, therefore, scars have been carefully examined on their hypothesis, and it would appear to me to fit the observable facts to a nicety. I feel we owe both Miss Fell and Dr Gliicksmann an apology for failing earlier to co-operate in publication, but I think the prolonged clinical investigation has done so much to substantiate their histological hypothesis that the delay seems iustified. The histological material we provided consisted of hypertrophic scars in all stages of development derived from patients presenting burns, war iniuries, surgical wounds, and grafted areas. In a proportion of this material Glficksmann (i95 I) demonstrated foreign bodies in the non-encysted state. These included cotton-wool fibres and silicates from road and bomb iniuries, but in a considerably higher proportion of cases they consisted of hair follicles and sebaceous glands or their remnants. These were associated with a constant histological picture which appeared significant. In coniunction with Miss Fell, therefore, a series of animal experiments were carried out. They consisted of the implantation of small autogenous grafts beneath the skin and a study of the results. It was found that so long as the keratin produced by the graft and its contained hair follicles remained encysted, no tissue response to the presence of the implant was discernible. As soon, however, as the cyst wall perforated, exposing the subcutaneous tissues to the effects of the keratin, there was a dilatation of those vessels in the immediate neighbourhood. As these vessels break up into smaller branches nearer the skin surface, the area of involvement was roughly pyramidal with the apex down at the point of contact with the keratin and the base on the skin surface. Throughout this pyramid, pervascular extravasation of round cells occurred until the tissues within the area became crowded with them. The process continued until the keratin had been removed by the normal scavenging mechanisms. After this phase there was gradual regression of the dilatation followed by a slow resorption of the fibrosis caused by the initial changes. The various phases of this same cycle were observed in the human histological material, and the picture became coherent. The histological changes accord so well with the observed clinical cycle of
HYPERTROPHIC
SCARS
115
scar hypertrophy that it has formed the basis of our subsequent clinical examinations of scars. It is, of course, obvious that if hypertrophy is a reaction to, or a sensitivity to, foreign material and to keratin in particular, there are two primary factors. The first is systemic, but the second must be local. It is possible that the number of wounds which do not at some stage contain some foreign material may be very small, but not every patient develops a hypertrophic scar. Whilst there must be variations in the amount of buried keratin, it is probable that there are individual systemic variations in the amount of reaction such keratin will cause. In any given patient, however, this general systemic factor will be constant, but there may be variations in the local factors which are the activating causes. In other words, two scars on the same patient will not necessarily produce similar and equal responses. With keratin, therefore, in mind as the important element, it may be of interest to review scars which become hypertrophic to see whether there are any relatively constant features of importance in determining their incidence. It would seem that the amount of keratin in any wound must determine the magnitude of the response, for although there is an element of systemic sensitivity in the reaction, the local response is confined to the area of the blood-vessels which are immediately exposed to the effect of the keratin. The actual amount of buried keratin, therefore, is of importance. It can be derived from hair follicles or from sebaceous glands, and the skin most likely to produce hypertrophic scars should possess some or all of the following characteristics :-. I. The Presence of Lanugo.--These hairs are slow-growing, are not very robust, and are often present in very great numbers. Any wound is likely to submerge an appreciable number of follicles beneath the skin surface. In view of their obliquity of growth, the difference between an incision parallel to, and one at right angles to, their general direction may be very considerable. In the former case a minimal number of follicles will be divided--in the latter the number will be maximal. The hair of the beard or scalp is of a much more rapidly growing type, and the density of such hair in any given area is much less than lanugo. The rate of growth is almost sufficient on its own to ensure that any follicle buried beneath the skin is only temporarily isolated from the surface. 2. Sebaceous Glands.--These, too, can be a source of keratin, and it might be expected that areas of most profuse sweating would be most likely to produce hypertrophic scars. 3. Skin Thickness.--It seems probable that the likelihood of isolating either hair follicles or sweat glands is increased in proportion to the thickness of the skin through which the incision is made. The types of patient generally supposed, therefore, to have " b a d skins " from the scar point of view, i.e., those with red hair and fair complexions and those suffering from thyroid disturbances, may therefore be reclassified, the former invariably having a generous distribution of lanugo and the latter having either a coarse skin with an excessive distribution of terminal hair or, alternatively, an active sebaceous mechanism. The negro presents a thick skin with many active sweat glands, but, in addition to this, the common tendency to the use of ornamental
II6
BRITISH
JOURNAL
OF
PLASTIC
SURGERY
keloids may have led, as the result of marital selection, to an accentuation of the systemic factors necessary to produce hypertrophy. In the light, therefore, of the foreign body hypothesis, it is interesting to try to correlate the work done by Levitt (1951) on the control of hypertrophic scars by X-radiation. His technique requires the use of small doses of radiation to a hypertrophic area either as a method of hastening regression or, if preceding and following surgical excision, as a method of controlling the hypertrophic reaction of the skin to the new wound. The effects of these small doses of radiation are known to be threefold. .... " ~'~ Firstly, the endothelium of the subcutaneous vessels is damaged, with the result that intravascular clotting may occur, so that within the first seven to fourteen days there is decreased vascularity in the area. Secondly, there is a reduction in histiocyte formation. Thirdly, degenerative changes are induced in the epithelium of the hair follicles and the sweat glands. The pathologist therefore states that buried hair follicles or sweat glands can induce a vascular dilatation with pervascular transudation of round cells. The radiologist employs a technique which damages the hair follicles and sweat Fro. i glands--which renders vascular response less A typical road abrasion. Note that the likely and which reduces the numbers of at parallel scars o n t h e c h i n are o f two types : least one type of round cell which normally t h e one on t h e left is p i g m e n t e d , b u t soft passes through the vessel wall. a n d supple. Its n e i g h b o u r is p i g m e n t e d The clinician can perhaps add his quota at each end, b u t t h e deeper central area is hypertrophic, tO the picture. Incised W o u n d s . - - T h e grazing injury commonly seen on the malar, lip, and chin regions following a fall from a cycle almost invariably presents scars of two kinds (Fig. I). When the injury has extended through only part of the thickness of the skin the scar may be pigmented, but it is not hypertrophic. No skin elements have been isolated from their connection with the surface, and none have been buried in the subdermal area. There has therefore been no subdermal vascular response to cause hypertrophy. An adjacent scar may well have been fractionally deeper--skin elements have been buried in the subdermal region and gross hypertrophy is present. In the one case only the skin is damaged and there is no abnormal response. In the other the skin has been perforated, and surface elements may have been carried into the subdermal areas to initiate the response. The scars may be only ~ in. apart, and differences in tension or infection would seem irrelevant. We have all seen the child upon whom an operation for cleft lip within the first few months of life has left an almost invisible scar. We have too often seen a secondary operation at the age of 5 or 6, carried out to correct some minor irregularity, result in a hypertrophic scar which will never attain the linear
HYPERTROPHIC
SCARS
117
proportions of the earlier one. Is this likely to be due to the absence of lanugo hair in the small child and its presence at the age o f 5 ? We have all had experience of operating on the adolescent girl with a peach-like complexion and producing a raised red hypertrophic scar (Fig. 2), even though there has been careful attention to every detail of surgical technique. We have all operated upon the bearded face of the adult male and we have not produced bad scars. Does the difference lie in the liability in the one case of burying keratin-bearing structures, whilst in the other the growth capacity of the beard is such that it refused to stay buried ?
A FIG. 2 B A patient aged 20. Dark hair but a fine skin well endowed with lanugo hair. A, The result of an attempt to pierce the lobule of the ear. B, The result of a minor operation on the breast. Both procedures were carried out one year prior to the photograph, and neither was complicated by clinical infection. On the whole, I think it true to say that the certainty of producing perfect scars increases with the age of the patiem, and it is equally true that with increasing years the hair-bearing capacity of the skin becomes progressively less and the activity of the sweat glands is similarly decreased. Skin losses are perhaps best examined in burns. Superficial loss of a minor degree is seen at the margins of most heat burns. The area is originally only reddened with minimal blistering (Fig. 3). Healing is rapid and leaves only a very slight change in the surface texture, with the orifices of the glands and hair follicles visible as minute pits. Hypertrophy is never seen. Partial losses may extend as deeply as the middle layers of the dermis. These, in the untreated state, are slow to heal, and are commonly followed by the typical hypertrophic scar. Chemicals are an outstanding cause of burns which heal spontaneously with a grossly hypertrophic scar. The depth of penetration of the burn is frequently
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limited by the action of the chemical itself in producing a protective surface coagulum. After this separates, the dermis (deep to which lie many o f the hair follicles and sweat glands) is exposed. Healing is always delayed, and during this stage it is by no means unlikely that at least some of the keratin-bearing structures will lose their continuity with the surface. The repeated dressings and the presence of low-grade infection may aggravate matters by allowing the inclusion of exogenous foreign bodies.
A
FIG. 3
B
A b u r n o f t h e chest, a r m s , neck, a n d face caused b y clothes catching fire. A, T o w a r d s the e n d of t h e stage of p r i m a r y epithelialisation, b o t h as t h e result o f s p o n t a n e o u s healing a n d of grafting. H y p e r t r o p h y is b e g i n n i n g in t h e chin a n d neck a n d sternal areas. Elsewhere it is less marked. N o t e its absence on t h e left s h o u l d e r a n d a r m w h e r e t h e b u r n was a partial destruction a n d w h e r e t h e scar shows a white stippling only. B, N i n e m o n t h s later. H y p e r t r o p h y is m o r e m a r k e d in the neck a n d sternal areas a n d at t h e junction lines o f t h e grafts on t h e breasts, t h o u g h in all areas it has passed t h r o u g h t h e phase of m a x i m a l vascularity a n d is b e g i n n i n g to regress. N o t e t h e left shoulder area retains t h e characteristics seen in A.
A similar grossly hypertrophic scar may occasionally follow the cutting of a fairly thick graft with a dermatome, and the causal mechanism is probably identical. Full-thickness losses but seldom produce gross hypertrophy if spontaneous healing is allowed, though they may apparently do so if grafted. According to G10cksmann, this is due to the reintroduction of keratin-bearing structures in the graft. Full-thickness burns causing complete destruction of all skin elements may be produced by the passage of electric current or by molten metal. Though spontaneous healing is very slow and may therefore produce a thick scar, it will not produce a typically hypertrophic scar. There is little reason why it should,
A
B
C FIG. 4 D An extensive laceration involving the full thickness of the cheek associated with fractures of the mandible, occurring in a boy of 17. He has dark hair and a fresh complexion. A, The initial lesion. B, The appearance twenty-one days later. C, Scar hypertrophy seventeen months later. The position and direction of the neck scar is that which would normally be chosen to ensure a good result. D, To show the heavy lanugo distribution not only in the beard area but also on the cheeks and forehead. I19
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for no skin elements remain. The same behaviour is seen in tropical and varicose ulcers and in those embolic skin losses sometimes occurring in the exanthemata. It seems, therefore, that the possibility of the occurrence of hypertrophy can be predicted on the local factors present in any wound (Fig. 4). Whether these factors will produce an actual hypertrophy must also depend on the systemic response they may initiate. Control of hypertrophy would seem therefore to be capable of achievement by two methods. The first is by desensitisation to the local foreign body. If it is accepted that the commonest foreign body is keratin (which is an almost insoluble substance), t&is approach must be fraught with difficulties. The second is by reduction of the activating factors : (a) Exogenous foreign material must be mainly derived from the dressings employed. Short staple cotton as gauze and cotton wool seem to be obvious offenders; (b) endogenous material can be reduced in deep partial thickness losses by excision prior to grafting. This is a procedure not uncommonly employed in any case, but it may deserve greater consideration than it often receives. When the probability of the inclusion of endogenous material in a surgical wound is obvious from an inspection of the skin, a hypertrophic wound can be forecast. In young boys and, indeed, in some young girls it may be desirable to defer an unimportant operation until after puberty, when the skin characteristics, particularly in males, will change. In other cases, however, it is advisable to warn the patient and to adopt the only method of control which is at present available-radiotherapy. It will be obvious, however, that this method of treatment is highly specialised, and haphazard use of therapy is better avoided. SUMMARY I. The behaviour of a hypertrophic scar is outlined, and it is differentiated from fibrosis arising from other causes. 2. The histological characteristics in relation to causation are described. Both exogenous and endogenous foreign bodies are shown to produce a primary vascular response, which is the basis of the hypertrophy. 3. The histological cycle is correlated with the known clinical picture. 4. The importance of keratin-bearing structures of the skin in relation to hypertrophic scar is stressed, and their distribution is discussed. 5. The histological effects of X-ray on normal tissues are correlated with the histological picture as it occurs in scar hypertrophy. 6. The clinical picture of the behaviour of various types of lesion is given. 7. Some possibilities of control of the hypertrophic reaction are outlined. It is obvious that without the co-operation of Miss Fell, Dr Gliicksmann, and Dr Levitt the material for this paper would not have been available. In addition, most of the work and a considerable proportion of the enthusiasm which went into the inception of the investigation lie to the credit of Mr J. N. Barron. The photography was the responsibility of Miss N. Walker. To each and all of them I am glad to acknowledge my indebtedness. REFERENCES
GLOCKSMANN,A. (1951). Brit. J. Plastic Swrg., 4, 88. LEVITT,W. i . (1951). Brit. J. Plastic Surg., 4, lO4.