Annals of Burns and Fire Disasters - vol. XIII - n. 4 - December 2000


Dyakov R.

Clinic of Paediatric Burns and Plastic Surgery, N.I. Pirogov Medical Institute, Sofia, Bulgaria

SUMMARY. During the 10-yr period 1989-98, 2261 burned children were observed at the Clinic of Paediatric Burns and Plastic Surgery of the N.I. Pirogov Medical Institute, Sofia, Bulgaria. Out of the total number of burned children, 1401(61.96%) underwent a surgical intervention. Of these 1401 children, 1149 (82.01 %o) were covered with free flaps after chemical escharectomy or spontaneous biological detachment of the necroses. Surgical escharectomy was performed in only 213 cases (17.99%), with the patients being autografted in one or more stages. Out of all the cases (whether operated upon or not) with IIB degree burns who epithelialized spontaneously, 1843 developed hypertrophic scars and keloids. Surgical procedures were undertaken in 1415 (76.77%) of the cases. We recommend the following steps in order to prevent pathological cicatrization: 1. adequate infusion therapy; 2. appropriate local treatment with preparations containing silver sulphadiazine or 10% povidone-iodine (this stops bacterial contamination, which is an important factor in the prevention of the formation of severe cicatrices in donor sites as well as spontaneously epithelialized sites); 3. early surgical treatment on day 1-8; 4. early and timely rehabilitation. The injection of corticosteroids under and marginally to the grafts prevented cicatrization. Plate devices were used to compress the scars and reduce blood flow. Elastic bandages and underwear also exerted compressive action. All three methods were applied during the whole period of scar maturation, e.g. 8-10 months, and in some cases longer. Reviewing the effects of the complex treatment implemented and the extended prophylaxis model, we can define the results as very good in 941 children (51.05%), good in 812 (44.07%0), and unsatisfactory in 90 (4.88%).


Cicatrices are a major disease condition secondary to burns. In 1953 Lagrot called the condition "the illness of cicatrization", while in 1967 Ranev defined it as a separate phase of the burn disease.The treatment and prophylactics of post-burn cicatrization in childhood is a complex process that depends on a number of factors. It should not become a permanent problem of children. In this light we review and analyse our experience with the complex model of its prophylactics and treatment.

Materials and methods

Over a 10-yr period (1989-1998) 2261 burned children were observed at the N.I. Pirogov Clinic of Paediatric Burns and Plastic Surgery of Medical Institute, Sofia, Bulgaria. Out of the total number of burned children, 1401 (61.96%) underwent surgical intervention. The remaining 860 children (38.04%) were treated conservatively, epithelializing spontaneously. Of the 1401 children subjected to surgical intervention, 1149 (82.01%) were covered with free flaps after chemical escharectomy or spontaneous biological detachment of the necroses. Surgical escharectomy was performed in only 213 cases (17.99%), with the patients being covered with autografts in one or more stages. Prophylaxis of cicatrization began at the moment of the patient's admission to the unit. The prophylactic measures can be divided into three groups, according to the method of treatment:
1. Before operative treatment

  • Adequate resuscitation infusion therapy

  • Declive position of lower limbs in order to avoid tissue oedema

  • Appropriate local treatment in order to prevent bacterial contamination

2. After initiation of operative treatment
2.1 Rapid removal of necrotic tissues and allo- or autografting
An important factor in the prevention of severe cicatrization is the deadline for operative autograft coverage. For this reason we prefer early surgical treatment on days 1-8 and allo- or autografting. This depends on the estimation of the burned child's complex condition. Third-month grafts after early surgical treatment resemble 2-yr-old grafts after post-granulation treatment. The reason for this is the lack of the granulation phase. Early operative treatment/surgical escharectomy employs the following techniques:

  1. tangential escharectomy in IIB degree burns combined with 0.15 mm alto- or autografting
  2. total necrectom_v in the full thickness of the corium, reachinff the fat tissue. and immediate coverage with 0.20-0.30 mm autografts
  3. total necrectomy to the vital tissues in the event of underlying anatomical structure damage; wound covered also in this case with allo- or autografts

Surgical escharectomy is performed on days 1-8 and does not exceed 15%c TBSA at any one time. If we cover the wound with autografts in one stage the surface should not be larger than 7-8 1~-c TBSA. If a greater percentage of escharectomy is necessary, we prefer allografting or mixed allo- and autografting. The "sandwich" technique is also sometimes employed. The subsequent stages of escharectomy follow on day ? or 3 after surgery but no later than day 8. After day 8ywe prefer 30(1c benzoic acid unffuent chemical necrectomy with consequential autografting.

2.2Early rehabilitation in order to prevent muscular atrophy, articulation immobilization, and contractures
Passive remobilization of operated limbs and neck starts on day 8 post-surgery and active remobilization after day 12-14, under the protection of an elastic compression of 15-40 mm. Once the autografts and donor sites are stable. the use of corticosteroid unguents is initiated. These are applied by gentle massage. When the grafts are fully adherent. after day 20. a corticosteroid solution (triancinolone acetonite 40 mg) diluted to 5 or lOcc with saline is marginally injected. This medication is performed only in patients who have undergone neck, face. and back-ofthe-hand surgery. In other cases. we have to wait for the result of the cicatrization process and the corticosteroid is injected afterwards. After day 20-25 Nye begin using additional medical preparations that contribute to the better final outcome, e.g., Contractubex, Madecassol, hydrating crearns. etc., applied by simple spreading or by phonophoresis. The pathological fibroblastic growth is thus reduced, inflammation is inhibited. and local scar irritation is relieved. When the grafts are completely stable. balneotherapy is also indicated. To suppress fibroblastic activity. eye use corticosteroids such as triamcinolone, Kenalog. or Kenakort injected marginally or under the Grafts themselves. Plastic plates are also used in orderyto reduce blood circulation within the scar. The cicatrices thus regress faster. We use silicone plates as well. but the mechanism of silicone action on scars is still unclear. Elastic dressings and elastic underwear also exert a compressive effect. All three methods are applicable during the whole period of scar maturation, e.g. 8-10 months, and sometimes longer. After day 30. w hen the Grafts are already stable and the donor sites have epithelialized successfully-. patients are advised to visit a specialized health resort.

3. Patients epitheliali-ing spontaneously without surgical intervention
All of the above preventive methods are used.After dismissal from hospital. both operated and unoperated children receive a follow-up on a monthly basis. They carry out a home rehabilitation programme to protect grafted and donor sites.


Out of all the cases (both operated upon or not) with IIB degree burn who epithelialized spontaneously. 1843 patients developed hypertrophic scars and keloids. Keloids were found in 218 patients (11.83% ), hypertrophic scars in 1214 (65.87%), and both types in 411 (22.30% ). Surgical procedures were followed in 1415 cases (76.77~c ). Several surgical techniques were applied. depending on the type of scar and functional disability:

  1. resurfacing of entire affected cicatricial area with normal skin using expanders

  2. local skin flaps

  3. pedicled distant flaps

  4. rotation of cutaneous, fasciocutaneous or musculocutaneus flaps

  5. mixed technique: free flaps and local skin flaps

  6. partial excision and suture

  7. total excision and Oraftina with full-thickness or split-thickness skin grafts

The present study does not trace the results of the different operative methods separately. Cicatrices were marginal to the skin grafts in 612 of all cases (33.20% ). They appeared to develop after partial excision of IIB stage wound edge and spontaneous healing. In 112 cases (22.35%), cicatrization was explained by- the lateness of operative treatment, e.g. after day 20-25, when a granulating wound had alreadv formed. This is the moment when fibroblastic activity and collagen production are most extensive. Elastic fibres were greatly reduced or absent. The autograft goffered and contracted the area. This aggressive behaviour of the connective tissue often reduced or halted the development of surrounding or underlying anatomical structures. This was most frequently- observed on the back of the hand (2-1.35 % ). mainly in children up to 3 years of age. the elbow fold (20.99%), axilla (16.02%). neck (13.9017% ), foot (11.77% ), and remaining anatomical areas - sternal. inguinal, femoral, crural, cervical. dorsal. and gluteal (13.07%). Similar cicatrices also formed on donor sites. especially when the skin was infected or when grafts were taken at a split-thickness level in the deep layers of the stratum reticulare of the corium. On the basis of our findings we recommend that the following requirements should be fulfilled in order to prevent pathological cicatrization:

  • adequate infusion therapy, especially in children admitted with thermal shock. This contributes to faster recovery and timely early operative treatment/ surgical necrectomy. This is a factor in the prevention of severe cicatrization, since the wound heals primarily under the graft, without infection and without the granulation phase, fibroblast activation, and poor epithelialization of the edges;

  • proper local treatment with, preparations containing silver sulphadiazine or 10% povidone-iodine. Epithelium-stimulating unguents are indicated only in superficial burns that are not very likely to produce extensive cicatrices. The local use of silver- and iodine-containing medicines prevents bacterial contamination below 10' per g tissue. This is an important factor for the prevention of the formation of severe cicatrices on donor sites as well as spontaneously epithelializing sites. Prolonged infection aggravates primary lesions. There is an additional requirement for donor sites: when a split-thickness graft is taken it should not affect the deep layers of the stratum reticulare. Epithelialization is slow, poor, and unstable and there are conditions for bacterial contamination. Fibroblasts thus activate significantly, leading to pathological cicatrization;

  • early rehabilitation and prompt complex preventive therapy. Having reviewed the effects of the implemented complex treatment and extended model of prophylaxis of pathological cicatrization in the 1843 cases evaluated, we can report very good results in 941 children (51.05%), good results in 812 (44.07%), and unsatisfactory results in 90 (4.88%). Complications were observed in 2 patients (0.1 %): postinjection abscess formed after corticosteroid application. The patients whose results were considered unsatisfactory in the follow-up period are still liable to additional treatment, mainly surgical.


The healing of burn wounds is accomplished in two ways - complete regeneration (restitution) and substitution. Restitution is possible only if the skin is burned as deep as the stratum papillare and all the specialized cells of the organ are preserved. If the skin is affected deeper in the zone of the stratum reticulare, the defect is covered by substitutive unspecialized connective tissue. The final result is demonstrated by a lesser or more extensive formation of the cicatrix. In the first case, a normotrophic scar is formed; in the second, a hypertrophic scar or a keloid is present. The process depends on the depth of stratum reticulare damage. The basic mechanism is identical in both cases and the differences are quantitative, not qualitative. Keloids and hypertrophic scars are a frequent consequence after deep burns heal and represent the most important disorder in the process of scar formation.Morphologically vast areas of fibroblasts with constant collagen and glycoprotein production and few or no elastic fibres represent both scar types. Apart from these common features, there are considerable clinical and morphological differences. The clinical signs of both scar types are well known and easily distinguished. Microscopic studies show that the fibroblast count in keloids is from 60 to 150 per optic field, i.e. 2 or 3 times the amount in hypertrophic scars and 3 to 5 times that in normal scar tissue. Mast cell numbers, mucin, and water content are significantly higher in keloids. In all three types of scars fibroblasts acquire the structure and functions of smooth muscle cells and contribute to wound contraction.2 The resulting differences are quantitative. Keloids and hypertrophic scars contain large quantities of type III collagen. This is related to tissue resistance and stretch ability, and creates differences in the elasticity of normal skin and the burned area. The newly synthesized collagen is unevenly distributed within the scar. The cross-bindings are formed rapidly and the fibrils become highly stretch-resistant.' This leads to rigidity of the affected area, graft goffering, and contractures. The main reasons for abnormal (pathological) post-burn scar formation are:

  • physical - related to the presence of local infection, as described by ourselves and many other researchers;

  • local - lymph stasis of the affected area, together with a topical predilection for the shoulder, sternum, and retroauricular area

  • mechanical - increased tension of wound edges;' thus, when granulating burn wounds are treated operatively, fibrous tissues are excised completely and the graft lies free the edges. It is believed that when incisions follow Langer's lines there is less possibility of a keloid forming

  • individual and racial factors - keloids and hypertrophic scars are more likely to be seen in the Negroid race and Mediterranean and red-haired people. However, no gene has been discovered that is responsible for the formation of keloids and there is no significant correlation between the HLA system and their occurrence

Most of the clinically orientated physicians who deal with the problem of cicatrization agree that the accent should fall on prophylactics and that this should be part of the treatment from the very beginning. In this context we point out two basic rules:

    1. increased capillary permeability and resulting local oedema should be reduced;

    2. the formation of fibroblasts and collagen fibres should be inhibited.

Chervenkov et al.b developed an extended prophylactic scheme:

  • hypergranulation suppression with corticosteroids
  • measures against tissue oedema by means of the decliveposition of affected areas, early rehabilitation, and compressive dressings
  • fibroblastic growth reduction by phonophoresis with cytostatic medicines (prorezid)
  • measures against bacterial infection
  • early surgical treatment

Early surgical treatment in terms of surgical escharectomy, as a means of cicatrix prevention, is confirmed by many researchers. It is closely related to early rehabilitation, which is most effective in optimal therapeutic terms. When combined with physiotherapy it greatly improves tissue elasticity. Severe cicatricial contractures that considerably hinder childhood development are thus unlikely to appear.Besides early surgical interventions to prevent cicatrization, we also pay great attention to adjuvant therapy (complex additional therapy). The main practical trends are:

  • reduction of scar irritation - pain and severe itching accompany a great number of keloids and hypertrophic scars. Antihistamines can influence these symptoms in some patients. There is evidence that antihistamines can inhibit in vitro proliferation of keloid fibroblast cultures. The relief of local symptoms decreases scar irritation. It probably stops mediator liberation by mastocytes or other additional factors that are capable of provoking a new onset of scar growt

  • compressive therapy - elastic bandages, underwear, and devices like clips and plates are worn for a period of 4-6 months, sometimes for a year. These exert a pressure greater than 24 mm Hg, e.g. higher than the capillary pressure, and are to be worn 24 h a day with intervals of no more than 30 min for personal hygiene. These findings are confirmed by a number of researchers

  • corticosteroid application under grafts and in areas undergoing cicatricial transformation. Various other researchers observe the positive effect of this medication

  • use of medical preparations that decrease scar growth and development (such as Contractubex, Madecassol, ete.). Our clinical findings together with their use are not described in the present paper

An effective method, which we implemented not long ago and is particularly suitable for patients with hand and neck lesions, is the use of silicone plates. Some researchers propose the use of silicone gel; however, the mechanism of silicone action remains unclear.Other reports describe the use of human interferon-' since it has been proved that interferon gamma decreases collagen synthesis in fibroblast cultures. Granstein tested it intracicatricially in a limited group of patients and reported very good results.'- Reich reported that cicatrices were infuenced positively by electrostimulation but further research is necessary in this the field.-' We have not made any observations of the effects of the last two methods, of which we have no experience.

RESUME. Pendant la période décennale 1989-98 1'Auteur a observe 2261 enfants brfilés à la Clinique des Brulures Pédiatriques et de Chirurgie Plastique à 1'Institut Medical N.I. Pirogov, Sofia, Bulgarie. Sur le numéro total de ces enfants br6lés, 1401 (61,96%) ont subi une intervention chirurgicale. De ces 1401 enfants, 1149 (82,01 %o) ont été couverts avec des lambeaux libres après 1'escarrectomie chimique ou la separation spontanée des necroses. L'escarrectomie chirurgicale a été effectuée dans seulement 213 cas (17,99%), quand les patients ont été traités avec autogreffe dans une ou plusieurs phases. De toes ces patients (opérés et non) atteints de br6lures de degré IIB, qui ont eu une épithélialisation spontanée, 1843 ont développé des cicatrices hypertrophiques et des chéloîdes, et dans 1415 cas (76,77%) des procedures chirurgicales ont été effectuées. L'Auteur recommande les étapes suivantes pour prévenir la cicatrisation pathologique: 1. thérapie d'infusion adequate; 2. traitement local approprié avec des preparations qui contiennent la sulphadiazine argentée ou la polyvidone iodée à 10% (ceci bloque la contamination bactérienne, qui est un facteur important dans la prevention de la formation des cicatrices sévères dans les sites donneurs comme aussi dans les sites d'épithélialisation spontanée); 3. traitement chirurgical précoce dès les jours 1-8; 4. rééducation précoce et opportune. L'injection de corticostéroîdes au-dessous et à cóté des greffes prévenait la cicatrisation. Des appareils à plaque ont été utilisés pour comprimer les cicatrices et réduire la circulation sanguine. Aussi Femploi de pansements et de sons-vétements élastiques a elercé une action compressive. Toutes les trois méthodes ont été employées pendant toute la période de la maturation des cicatrices. Cest-à-dire 8-10 mois, et dans certains cas méme plus longtemps. Considérant les effets du traitement complexe administré et le modèle de prophylaxe de longue durde. 1'Auteur définit les résultats comme très bons dans 9-11 enfants (51,05%c), bons dans 812 (-14,07~'c) et non satìsfaisants dans 90 (-1,88%).


  1. Brody G.S.: Keloids and h_ypertrophic scars. Plast. Reconstr. Surg..
    80: 804, 1990
  2. De Santis P., Savoia A.: Denmofunctional treatment of hypertrophic
    burn scars. Ann. Burns and Fire Disasters. 10: 16_'-5. 1997.
  3. Ehrlich H.. Desmouliere A.. Dieeelmann R.. Cohen I.K. et al.: -Morphological and immunochemical differences bemeen keloid and hypertrophic scar. Am. J. Pathol.. 145: 105. 1994.
  4. Murray J.C.: Keloids and hypertrophic scars. Clin. Dean.. 12: 27-37. 1994.
  5. Thomas DAV., Hopkinson I Harding K.G Shepherd J.P.: The 17.pathogenesis of hypertrophic-keloid scan-ing. Int. J. Orol -Nlaxillo
    fac., Surg.. 23: 23_'. 1994.
  6. Chervenkov J.. Shindarski B.I.: "Burn injuries". -Med. Fish.. Sofia.
  7. Berman N.. Duncan -\I.R.: Short-term treatment in vivo with human interferon alpha-'_'b results in a selective and persistent normalization of keloidal fibroblast collagen. elycosaminoalycan. and collagenase production in vitro. J. Am. Acad. Dermatol J. 31: 694.1989
  8. Atanassov N Dyakov R Andreeva D Victorova A.: Evidences for urgent operative treatment of children with burn consequences.J. Emerg. Med. l: 2?-26. 1999.
  9. Hadjiiski O.: Epidemiology and prevention of burns in childhood. 22.First International Symposium on Cardiovascular Prevention and Paediatric Traumatology. Sofia. September 1995.
  10. Hadjiiski O.: No~N-adav treatment of burns in Bulgaria. Seventh 23.National Conference of Burns and Plastic Surgery. Vama. October 1996
  11. Hadjiiski O.. Tzolova N.: Early blood necrectomies in childhood partial dermal burns. Biennial Central European Burns Conference. Slovak Medical Society. Bratislava, Slovak Republic, November 1991
  12. Vaalenova E.: Surgical treatment of extensive and deep burns.Doctorate. Sofia. 1990.
  13. Petrova bl.: The role of rehabilitation in post-burn cicatrix evolution. Reports, "Atone, Seventh National Conference of Bums and Plastic Surgery. 1?1-1?3. Varna, October 1996
  14. Pophristova E.. Nlazealowa J.: Some observations on mast cell numbers in steroid-treated keloids. Ann. Burns and Fire Disasters, 9: 168- î 1. 1996.
  15. Antova K.. Atanassov N.: Compressive therapy for prophylaxis and treatment of burn-induced hypertrophic scars and keloids. Reports, Novelties in Practical Treatment of Burns and Plastic Surgery. `'area. October 1986.
  16. Hadjiiski O.. Atanassov N.. Petrova IVL: Paediatric .bums in Bulgaria. Epidemiology. organization and operative methods. Rehabilitation. First International Congress. Current Concepts in Paediatric Burn Care. Zurich. 1996.
  17. Hirshowitz B.: Treatment of scars and keloids. Br. J. Plast. Surg.. 44: 318. 1991.
  18. Chavrakov G.. Mlazgalova J.: The physicochemical characteristics of keloid collagen before and after clinical treatment with kenacort: A polarizing microscopy study. Ann. Bums and Fire Disasters. 6: 24 7-50. 1993.
  19. Tsur H.. Blankstein A.. Kon hI. et al.: New technique for intralesional steroid injections. Ann. PLast. Surg.. 18: 83-4. 1987.
  20. Sawada Y.. Song K.: Treatment of scars and keloids with a cream containing silicone oil. Br. J. Plast. Sure., 43: 683. 1990.
  21. Larrabee VV.F.. East C.A.. Jaffe H.S.: Intralesional interferon gamma treatment for keloids and hspertrophic scars. Arch. Otolarvn. H.-N, Sure.. 116: 1159. 1990.
  22. Granstein R.D.. Rook A.. Flotte T.J. et al.: A controlled trial of intralesional recombinant interferon gamma in the treatment of keloidal scarring. Arch. Dermatol.. 1-16: 1`_'95. 1990.
  23. Reich J.D.. \l eiss D.. Hertz P.M. et al.: The long-term effect of pulsed electrical stimulation WESi on the prevention of the regrovvth of keloid scars. J. Invest. Dermatol.. 98: 631. 1992


This paper vsas received on 9 february 200

Address correspondence to:
Dr Rumen Dyakov MD, PhD
56 Hristo Botev Blvd., Sofia1000, Bulgaria
tel.: 35988 343206; e-mail:


<% footer %>


Contact Us