Rapid Responses to:

CLINICAL REVIEW: A Bayat, D A McGrouther, and M W J Ferguson Skin scarring BMJ 2003; 326: 88-92 [Full text]

Rapid Responses: Submit a response to this article

Rapid Responses published:

IS BOTULINUM TOXIN [BOTOX] OUR NEXT WEAPON TO COMBAT FACIAL SCARRING?

Y.C. Chan   (13 January 2003)

Entitlement to scar reduction treatment

Sarah L Davies   (15 January 2003)

Response to "Skin Scarring" by Bayat , McGrouther and Ferguson

Brian C Sommerlad   (17 January 2003)

Familial scarring

Nigel P Burrows   (7 February 2003)

Prevention of Scarring

Sharon J Williams   (5 June 2003)

Raising the wound pO2 to prevent scarring.

Richard G Fiddian-Green   (6 June 2003)

The wound gurus did not take the fly.

Richard G Fiddian-Green   (11 June 2003)

IS BOTULINUM TOXIN [BOTOX] OUR NEXT WEAPON TO COMBAT FACIAL SCARRING? 13 January 2003
Y.C. Chan, SpR in General Surgery, South-East Thames Deanery Department of Surgery, King's College Hospital, Denmark Hill, London SE5 9RS. Send response to journal: Re: IS BOTULINUM TOXIN [BOTOX] OUR NEXT WEAPON TO COMBAT FACIAL SCARRING?	The excellent review by Bayat et al. (1) has once again highlighted the many variables which can affect the severity of scarring, including the size, depth, and location of the wound, the blood supply to the area, the thickness and colour of the skin, and the direction of the scar. Recently, there are several reports in the literature to suggest that immediate injection of botulinum toxin into the muscles underlying a wound can improve the cosmetic outcome of cutaneous scar (2). This is because one of the major factors in determining the final cosmetic appearance of a cutaneous scar is the tension acting on the wound edges during the healing phase. By injecting through the skin into the underlying muscle, botulinum toxin paralyzes the muscles and relieves the tension (3). As a result of the chemo-denervation, more aesthetic scar can thus be achieved. Using primate models, Gassner et al. at the Mayo Clinic has shown that surgical wounds that had been immobilized with botulinum toxin were rated as significantly better in appearance than the control wounds (4). This adds to the list of wide variety of clinical applications of botulinum toxin, and may be our next weapon in combating facial scarring. References 1. Bayat A, McGrouther DA, Ferguson MWJ. Skin scarring. BMJ 2003; 326: 88-92 ( 11 January ). 2. Sherris DA, Gassner HG. Botulinum toxin to minimize facial scarring. Facial Plast Surg 2002; 18: 35-39. 3. Wieder JM, Moy RL. Understanding botulinum toxin. Surgical anatomy of the frown, forehead, and periocular region. Dermatol Surg 1998; 24: 1172-1174. 4. Gassner HG, Sherris DA, Otley CC. Treatment of facial wounds with botulinum toxin A improves cosmetic outcome in primates. Plast Reconstr Surg 2000; 105: 1948-1953; discussion 1954-1955. Competing interests:   None declared
Entitlement to scar reduction treatment 15 January 2003
Sarah L Davies, N/A M15 5FP Send response to journal: Re: Entitlement to scar reduction treatment	I noted with interest that Bayat et al did not mention scarring caused by self-harm. It is estimated that self-harm affects nearly half a million people in the UK(1). Is their absence an oversight or a reflection of the general medical attitude towards self-inflicted injury and entitlement to treatment? 1. The Mental Health Foundation. About mental health: Self harm.http://www.mhf.org.uk/ Competing interests:   None declared
Response to "Skin Scarring" by Bayat , McGrouther and Ferguson 17 January 2003
Brian C Sommerlad, Consultant Plastic Surgeon Great Ormond Street Hospital for Children, London WC1N 3JH Send response to journal: Re: Response to "Skin Scarring" by Bayat , McGrouther and Ferguson	I would like to point out a small but significant error in the review on skin scarring by Bayat, McGrouther and Ferguson (1). In the study referred to (2), scars which stretch were found to do so mainly in the first three months (not three weeks as stated) after surgery. In fact, expressed as a percentage of the width at one year, scars had stretched to 36% at three weeks, 66% at three months and 93% at nine months. Interestingly, if scars were taped and remained narrow for three months they had caught up by six months, suggesting that scars have to be exposed to stresses to develop tensile strength which will resist stretching. (1) Bayat A, McGrouther D A, Ferguson M W J. "Skin scarring" BMJ 2003; 326: 88-92 (2) Sommerlad B C, Creasey J M. "The stretched scar: a clinical and histological study". Br J Plast Surg 1978; 31: 34-45 Competing interests:   None declared
Familial scarring 7 February 2003
Nigel P Burrows, Consultant Dermatologist Dept Dermtology, Addenbrookes Hospital, Hills Rd, Cambridge CB2 2QQ Send response to journal: Re: Familial scarring	Bayat et al (1) have provided a comprehensive review of cutaneous scarring. Whilst the importance of both a personal or family history of scarring was noted the article failed to highlight one of the commonest inherited disorders of connective tissue which has scarring as a cardinal feature. The Ehlers-Danlos syndrome (EDS) is a heterogeneous group of disorders characterised by skin fragility, atrophic scars, bruising and joint laxity (2). The ‘cigarette paper’ like scars are most common over accident prone sites such as elbows, knees and face and become apparent as soon as the affected child starts to crawl or walk. Scar revision in EDS patients is usually disappointing due to the propensity for the scars to stretch. EDS can be associated with fatal vascular or bowel rupture in Type IV (vascular EDS) and clinicians should be aware of this diagnosis as non essential surgical procedures should not be undertaken in this subgroup. The diagnosis of EDS is based on clinical features, pattern of inheritance and in some cases biochemical or genetic testing. The true incidence is not known but may be as common as 1:5000 (3). Up to 9% of adult general dermatology patient have been found to have a mild variant of classical EDS and it may be important to identify such individuals prior to skin surgery so that they can be counselled regarding the possible increased risk of a poor cosmetic outcome (4). (1) Bayat A McGrouther DA, Ferguson MWJ. Skin scarring. Br Med J 2003;326:88-92 (2) Beighton P. The Ehlers–Danlos syndromes. In: Beighton, ed. McKusick’s Heritable Disorders of Connective Tissue, 5th edn. St Louis: CV Mosby, 1993: 189–251. (3) Steinmann B, Royce PM, Superti-Furga A. The Ehlers–Danlos Syndrome. In: Royce PM, Steinmann B, eds. Connective Tissue and its Heritable Disorders. New York: Wiley-Liss, 1993: 351–407. (4) Holzberg M, Hewan-Lowe KO, Olansky AJ. The Ehlers-Danlos syndrome: recognition, characterization, and importance of a milder variant of the classic form. J Am Acad Dermatol 1998; 19: 656-66 Competing interests:   None declared
Prevention of Scarring 5 June 2003
Sharon J Williams, Retired Registered Nurse N/A Send response to journal: Re: Prevention of Scarring	The following method reduces the incidence of unsightly scarring, especially on the face. I have had numerous skin cancers removed from my face by curretting, liquid nitrogen and plastic surgery. My skin is prone to scarring even from mosquito bites or minor abrasions. This method has left me with little or no scarring on my face. 1. Clean the wound gently with witch hazel; never use soap or alcohol. Soap is alkaline and destroys the natural acid mantle of the skin. Alcohol toughens the skin. Use a facial tissue, clean cotton cloth or gauze; avoid anything with the potential to leave lint in the wound. Blot, don't wipe. 2. Apply Polysporin or Bacitracin ointment to the pad of a bandaid before applying to affected area. Once daily treatment is sufficient as long as there is no sign of infection. 3. As soon as the raw wound has filled in with normal skin tissue, apply Vitamin E 400 IU to the area once or twice a day and cover with a bandaid to avoid accidental scratching. Use a sterilized, glass-headed pin to poke a hole in the Vitamin E capsule, squeeze a little Vitamin E on the wound and replace the pin in the hole in the capsule. Competing interests:   None declared
Raising the wound pO2 to prevent scarring. 6 June 2003
Richard G Fiddian-Green, None None Send response to journal: Re: Raising the wound pO2 to prevent scarring.	Tom Hunt, the wound-healing guru at UCSF, observes that collagen synthesis is inversely related to the ambient wound tissue pO2 (1). He further observes that healing wounds consume little oxygen but large amounts of lgucose and produce large amounts of lactate. They rely, therefore, upon ATP generated by anaerobic rather than by aerobic metabolism. The consumption of lactate by normally oxygenated tissues allows anaerobic glycolysis to proceed uninhibited by the accumulation of lactate in accordance with the law of mass action. Raising the pO2 in wounds has two potentially benefical effects. It enhances the oxidative killing powers of wound leukocytes and impairs collagen synthesis. Raising wound pO2 does not impair wound healing. The inference is that keloid formation is a product of persistent wound hypoxia possibly fueled by low grade 2. infection and persistent cytokine release. Cytokines uncouple oxidative phosphorylation (2), deplete tissues of NAD(+)/NADH and decrease oxygen consumption (3) thereby impairing ATP resynthesis by aerobic means. Might the scarring of wounds be prevented by running a small Silastic tube, permeable to O2 and CO2, under the wound and passing oxygen through it? [This proposal could form the basis of an intellectual property disclosure which could form the basis of both device and method patents]. 1. Hunt TK, Hopf HW, Mueller RV. Wound healing in Scientific Foundations of Trauma. Cooper GJ, Dudley HAF, Gann DS, Little RA, Maymnard RL, Eds. Butterworth/Heinemann, Oxford. 1997, Chapter 39, pp530-550. 2. Lassus P, Opitz-Araya X, Lazebnik Y. Requirement for caspase-2 in stress-induced apoptosis before mitochondrial permeabilization. Science. 2002 Aug 23;297(5585):1352-4. 3. Khan AU, Delude RL, Han YY, Sappington PL, Han X, Carcillo JA, Fink MP. Liposomal NAD(+) prevents diminished O(2) consumption by immunostimulated Caco-2 cells. Am J Physiol Lung Cell Mol Physiol. 2002 May;282(5):L1082-91. Competing interests:   None declared
The wound gurus did not take the fly. 11 June 2003
Richard G Fiddian-Green, None None Send response to journal: Re: The wound gurus did not take the fly.	In my rapid response to this article I provocatively stated that Tom Hunt, the wound guru, had shown that "collagen synthesis is inversely related to the ambient wound tissue pO2". I had expected any wound guru who might have read it to point that out. My statement is exactly the opposite of what Hunt has been saying for almost two decades and illustrated in a graph in his review (1). The point I was making was that Tom Hunt may be wrong for the following reasons. A. Cytokines, released by tissue injury, bacterial toxins and/or sepsis, uncouple oxidative phosphorylation and thereby increase the demand for O2 and generate heat. As Wilmore observes in the chapter preceding that of Tom Hunt's much of the increase in oxygen consumption by a wound can be accounted for by an increase in the generation of heat (2). Furthermore the increased O2 consumption is greatly reduced by preventing the heat loss. B. Wilmore also observes that wound healing is powered by ATP resynthesis by anaerobic and not aerobic metabolism. Hunt acknowledges this fact and the conflict that has created with his conclusions. C. Hunt also acknowledges that the increase in tissue pO2 in response to an increase in FiO2, a measure of tissue perfusion and hence nutrient transport to the wound, is a much better predictor of wound healing than the absolute level of tissue pO2. D. The generation of free radicals during the reperfusion of tissues in a wound might consume large amounts of O2 if it were not for the cytopathic hypoxia probably induced by the reduction in NAD/NADH pool size. Conversely the reduction in this pool size and the rise in wound lactate are established stimuli for collagen synthesis (1) E. Increasing wound pO2 enhances the generation of free radicals by leukocytes and thereby reduces the likelihood of bacterial growth and wound infections (1) Converesly Wound hypoxia and acidosis limit neutrophil bacterial killing mechanisms (3). Supplemental oxygen prevents wound infections after elective surgery (4,5). F. Cytokines may stimulate collagen synthesis and cause pulmonary fibrosis (6). G. Hypoxia co-ordinately up-regulates matrix production and decreases turnover in renal fibroblasts. (7). Conclusion: The positive correlation Hunt shows between pO2 and collagen accumulation in support of his thesis is more likely a reflection of the degree in impairment of O2 uptake, or cytopathic hypoxia, induced by the release of cytokines. The greater the tissue damage, the greater the inflammatory response, the greater the release of cytokines, the greater the degree of cytopathic hypoxia, the greater the likelihood of infection and hence the greater then likelihood of accumulation of excessive collagen and hence scarring. The subcutaneous delivery of oxygen has the potential to limit the infective componant. 1. Hunt TK, Hopf HW, Mueller RV. Wound healing in Scientific Foundations of Trauma. Cooper GJ, Dudley HAF, Gann DS, Little RA, Maymnard RL, Eds. Butterworth/Heinemann, Oxford. 1997, Chapter 39, pp530-550 2. Wilmore DW, Stoner HB. The wound-organ. in Scientific Foundations of Trauma. Cooper GJ, Dudley HAF, Gann DS, Little RA, Maymnard RL, Eds. Butterworth/Heinemann, Oxford. 1997, Chapter 38, pp524-529. 3. Allen DB, Maguire JJ, Mahdavian M, Wicke C, Marcocci L, Scheuenstuhl H, Chang M, Le AX, Hopf HW, Hunt TK. Wound hypoxia and acidosis limit neutrophil bacterial killing mechanisms. Arch Surg. 1997 Sep;132(9):991-6. 4. Greif R, Akca O, Horn EP, Kurz A, Sessler DI. Supplemental perioperative oxygen to reduce the incidence of surgical-wound infection. Outcomes Research Group. N Engl J Med. 2000 Jan 20;342(3):161-7. 5. Gottrup F. Prevention of surgical-wound infections. N Engl J Med. 2000 Jan 20;342(3):202-4. 6. Batra V, Khurana S, Musani AI, Hastie AT, Carpenter KA, Zangrilli JG, Peters SP. Concentration of cytokines and growth factors in BAL fluid after allergen challenge in asthmatics and their effect on alpha-smooth muscle actin and collagen III synthesis by human lung fibroblasts. Chest. 2003 Mar;123(3 Suppl):398S-9S. Review. 7. Norman JT, Clark IM, Garcia PL. Hypoxia promotes fibrogenesis in human renal fibroblasts. Kidney Int. 2000 Dec;58(6):2351-66. Competing interests:   None declared