Table of Contents

HK J Paediatr (New Series)
Vol 8. No. 4, 2003

HK J Paediatr (New Series) 2003;8:272-282

Paediatric Surgical Forum

Changing Perspectives in Paediatric Burns Care

A Burd, A Zeng


The care of Paediatric Burns patients presents many challenges. Prevention of the injuries has to be a priority but the responsibility of developing and implementing preventive programmes involves many groups. The provision of care is best centralised to optimise the resource allocation and concentrate expertise. Infection remains a major threat in the acute phase and the Intensive Care management of the extensively burned child is extremely demanding. The psychological management of both patients and relatives can be particularly difficult especially when health professionals have little exposure to major paediatric burns. In this case the support must encompass the entire burns team including the patient. Changing surgical strategies have merged the distinction between acute care and reconstruction. With advances in tissue engineering and molecular manipulation the prospect of tissue regeneration with minimal scarring is now the goal of contemporary burns care.

Keyword : Accidents; Burns; Child abuse; Intensive care; Rehabilitation

Abstract in Chinese


Over the past twenty-five years there have been tremendous advances in the evolution of paediatric burn care. The global challenges of prevention, survival and reduction of scarring remain and are being addressed in many different ways in both the developed and developing world. The frontiers of paediatric burns care in Western-based medical practice are continually being extended by the four Shriners burns institutes in North America.1 Unfortunately the overwhelming majority of children do not have access to the best practice standards defined in these Units. Indeed, in most parts of the world, paediatric burns care is not even regarded as a speciality in its own right. In Hong Kong, burns care is still very much evolving; there are current initiatives to rationalise facilities and resource distribution to optimise the delivery of burns care overall but paediatric burn care has not been specifically addressed. We can, however, be proud of the fact that the incidence of paediatric burns is one of the lowest in the world. This is due to a number of factors: demographic, with a falling birth rate; cultural, with an increasing number of single child families and the ever present presence of child minders, either as extended family or domestic workers; tribute must also be paid to the government for its sponsoring of legislation to reduce the possibility of burn accidents and also the very positive and constructive role of the media.2

The spectrum of paediatric burns care as a speciality is extremely wide and is truly holistic. The dimensions are political and ethical as well as medical and biological. This review focuses on just a few aspects of paediatric burns care (Table 1). The cases of six children are presented to illustrate how perceptions and practices are changing.

Table 1 Aspects of care illustrated in review
  • Prevention
  • Organisation of Paediatric Burns Care
  • Medical Challenges: i) Toxic Shock
  • Medical Challenges: ii) Burns Toxaemia Revisited
  • Psychological Challenges: The Massive Burn
  • Combining the Acute and Reconstructive Phases of Treatment
  • Towards Scarless Healing: Regeneration

Burns Prevention, Burns Care and Preventing Burns Morbidity and Mortality

This first case concerns a child who sustained burns by pulling on a kettle flex. This accident occurred in the UK in 1998 and although theoretically an eminently survivable burn, this child died.

Case 1

SV was a ten-month-old girl who sustained 20% BSA burns when she pulled on a kettle flex spilling boiling water over her arm, chest and back. She was given appropriate first aid and taken to the nearest hospital where resuscitation was commenced. She was stabilised and transferred to the regional burns hospital where she was admitted to a general children's ward. The burns were dressed and resuscitation continued. The following day she was bright, alert and stable and the parents were counselled as to the outline treatment plan, which would involve an EUA the following day.

The child was subsequently reviewed by the anaesthetist at 7 pm on that day, post burn injury day one, and pronounced fit for general anaesthetic. Her mother took her into bed with her and gave her a bottle of milk to settle her. At 11 pm her mother woke up to find the child vomiting and then she started to convulse. It took some thirty minutes to control the convulsions and the child was transferred to the Hospital ICU where the Intensivists made the working diagnosis of fitting related either to a febrile convulsion or secondary to toxic shock.

The child needed inotropic support for profound hypotension, ventilatory support for repeated episodes of desaturation and was commenced on broad spectrum antibiotic therapy. The previous partial thickness burns converted to full thickness burns. The ventilatory pressures increased and eventually she was transferred to the regional Paediatric Intensive Care Unit in another hospital to be treated using an oscillating ventilator. Despite continuing efforts to ventilate the child she became increasingly anoxic

and died on the 9th day post burn. Of note Staphylococcus aureus was isolated from a wound swab taken a PBD2 but this was negative for TSST-1, enterotoxins and exfoliative toxin genes A and B. A positive blood culture was grown from one of two bottles established on post burn day two but this was Staphylococcus epidermidis and was considered to be a contaminant. A postmortem was performed but the parents only allowed an external examination and the death was attributed to burns. A coroner's inquest returned a verdict of accidental death.

The dangers of the electric kettle flex have been raised by Tempest over fifty years ago.3 In 1985 AB co-authored a short study looking at the electric kettle flex, concluding that the conventional flex presented a hazard. It was observed that passive prevention, warning of the dangers of dangling kettle leads, is of limited efficacy and suggested that legislation to control the type of lead sold with new kettles would jointly focus attention on the hazard of the conventional long lead, and, if 'curly' cables (our proposed alternative) were made compulsory, make the home a safer place for children.4 Legislation does exist influencing domestic burn incidence and again our senior colleagues have remarked on the effectiveness of, for example, the control of the design of heating appliances and the sale of flammable night wear in reducing domestic burns from specific causes.5 The problem with kettle flexes is that legislation to control their design would be very difficult to pass and the manufactures, motivated by unit costs and profit, would not voluntarily modify their product. It is evident that prevention is a continual challenge and each new generation of parents has to learn how vulnerable their children can be. The debate regarding the responsibility for the safety of children, particularly infants can lead to strong emotions being expressed. George and Ebrahim present a provocative perspective in their letter "Infant Scald Burns: a case of negligence?" suggesting that any parent of a child under twelve months who sustains a burn is guilty of criminal negligence.6 Burns prevention is a global issue but the tragedy in this case is that despite the accident being preventable so was the death.

There is the growing awareness that burns care requires expertise, personnel, and equipment that are not cost-effectively maintained in low volume programmes.7 In addition when resource allocation is limited paediatric burn care is not high on the list of health care priorities. It is unfortunate that the policy of senior nurse managers not only in the UK but also in other parts of the world have been promoting the concept of the generic nurse. Whilst it is possible to recognise the problems of providing adequate nursing cover with global recruitment problems, to suggest that generic nurses can effectively look after paediatric burns patients indicates a dangerously naive lack of appreciation of the particular needs and demands of such patients. SV had been placed on a busy general paediatric surgical ward with night staff not experienced in paediatric burns care. The level of supervision of care of this patient was not adequate. That cannot be a criticism of the front-line nursing staff but of their managers and the system of care, which exposes patients to unnecessary risk.

It is not just the nursing cover that is open to scrutiny. In the case of SV the designated senior medical cover was being provided by a Plastic Surgeon with no burns interest. In this case the junior staff did not even call him at the time of the crisis but contacted a Senior Intensivist. The immediate transfer to the general ICU was absolutely appropriate, but when the child was reviewed the following morning by a Paediatric Burn specialist the request to transfer the child to a Paediatric Intensive Care at another hospital was challenged and obstructed. By the time the child was transferred it was too late and the child succumbed.

This tragic incident occurred in the UK where there has for some time been a realisation that all was not well in the provision of burns care. A National Burn Care Review was published in 2000 highlighting the need for stratification of care and rationalising resources.8 The separate needs of the adult and paediatric burns care services was recognised and in particular the need for concentrating care of paediatric burns into dedicated units with PICU support. The medical rationalisation however needs political support and at present in Hong Kong the reality of a single Children's hospital which would also provide such a burns service for the entire territory, whilst an inevitability, is some distance in the future.

Accidents and Death

Prevention has to be the number one priority of those involved in burns care. Nevertheless, no matter how well educated the population, no matter how enlightened the preventive legislation, accidents will happen. As such, paediatric burns will always be with us and we need to provide for their care. Whilst the body of knowledge in burns care may be constantly growing, for individuals, the acquisition of expertise and skills is time and experience related. The experience of seeing a child die following a burn can be very difficult for the junior staff and inevitably raises very complex issues of guilt and grief within the parents. Death can be particularly difficult to cope with when the cause is not understood.

Case 2

Jonathan was twenty-two months old. He had an older brother aged four. They lived in a comfortable house with loving parents and enjoyed the comfort and security of routines. One such routine was the nightly bath. Mum would take both the boys upstairs and heard them laughing and joking into the bathroom. Clean pyjamas, fresh towels, soaps, shampoos, toothpaste and toys, high-spirited boys and a rather tired Mum. She turned the taps on, hot and cold together and began to undress the boys. And then the phone rang.

Who can really say what happened? The memory is unclear. Perhaps the taps were not turned off completely. She had left for just a minute and then that horror that every parent fears and dreads; the scream of their child in pain, horrendous pain. Mum rushed in to find Jonathan, still wearing his nappy, clawing at the side of the bath, trying to get out as his burnt and blistering skin began to peel from his feet.

Mum did all the right things. She pulled Jonathan out, removed his nappy, wrapped him in a towel soaked in cold water. She called the ambulance; called a neighbour to look after Jonathan's brother. She comforted and caressed Jonathan and holding him in her arms told him he would be all right. The ambulance arrived quickly and everything went smoothly, efficiently and within ninety minutes of the accident Jonathan was admitted to the regional burns center in the nearby city. He had 40% BSA partial thickness burns, intravenous fluids using a colloid based formula were commenced and his clinical parameters were monitored, vital signs, capillary haematocrit every 4 hours and urine output. Forty-eight hours after the burn we had a bright eyed, well hydrated, responsive, pain free child. Three days later Jonathan was dead. He died with an absolutely exhausted Paediatrician giving adrenaline directly into his heart. This very experienced Paediatrician had never seen such a sick child, with so few clues as to why he went from life to death in such a relentlessly, devastating fashion. This all happened in 1984.

In the foregoing account we have focused perhaps more on the human aspects of the case than the medical aspects. When Jonathan was admitted it was very easy to identify with the account of the accident and to be aware of the guilt the mother was feeling. The staff did their best to reassure her and explained all that was going to happen and that her son was in the best of hands and was going to be all right. The words she used to her son were echoed. But he was not all right and the catastrophic deterioration had a profound effect on the medical staff as well as the parents. It was the combination of helplessness and then hopelessness that can seriously call into question the reality and effectiveness of our Western Medicine. Leading authorities in the UK burns field were consulted at that time and the consensus was that sometimes children with relatively small burns do just die and we do not know why. Of note this was in 1984 and it was the following year that one possible explanation for some of these deaths was revealed.

In 1985, Frame et al published the first series of Staphylococcal toxaemia in burns patients.9 Since that first report there have been may others worldwide. The susceptibility of burned patients to toxic shock syndrome (TSS) is thought to be because the majority of cases of TSS are related to Staphylococcus Aureus which is the most frequent pathogen colonising the burn wound. Approximately 20% of the S. Aureus strains produce toxic shock syndrome toxin-1 (TSST-1) which is the most commonly implicated toxin in the development of TSS, although there have been reported cases associated with other staphylococcal toxins, namely enterotoxins A, B, and C (SEA-C). The management of the burn wound and the subsequent development of TSS appears to be unrelated.10 The role of prevention is controversial. TSS was not clinically recognised when children were routinely resuscitated using FFP, however anecdotal accounts from surgeons of that period suggest that the clinical picture now associated with toxic shock was rare with patients resuscitated with FFP. The use of flucloxacillin given prophylactically for 5 days to all children with burns is now an established practice in many UK burns units but the evidence that such a practice is associated with a true decrease in incidence of TSS is still not available. One recent report did describe a case that developed once the course of prophylactic antibodies had stopped.11 The diagnosis of TSS follows several established criteria (Table 2), which are based on Chesney's review in 1984.12 These criteria are very exacting and a simplified grouping of signs and symptoms (Table 3) were proposed by Cole and Shakespeare.13

Table 2 Criteria for diagnossi toxic shock syndrome
  1. Fever: temperature >38.9°C.
  2. Rash: diffuse macular erythroderma.
  3. Desquamation: one to two weeks after onset of illness, particularly of palms, soles, fingers, and toes.
  4. Hypotension and poor peripheral perfusion.
  5. Involvement of three or more of the following organ systems:
    1. Gastrointestinal: vomiting or diarrhoea at onset of illness.
    2. Muscular: severe myalgia or creatinine phosphokinase activity more than twice the upper limit of reference range.
    3. Mucous membranes: vaginal, oropharyngeal, or conjunctival hyperaemia.
    4. Renal: blood urea concentration or creatinine phosphokinase activity more than twice the upper limit of reference range, or >5 white blood cells/high power field in the absence of a urinary tract infection.
    5. Hepatic: total bilirubin concentration, or alanine or aspartate aminotransferase activities more than twice the upper limit of reference range.
    6. Haematological: platelets <=100 x 109/1.
    7. Central nervous system: disorientation or alterations in consciousness without focal neurological signs when fever and hypotension are absent.

Negative results on the following tests:

  1. Blood, throat, or cerebrospinal fluid cultures. Blood cultures may grow S. aureus.
  2. Serological tests for Rocky Mountain spotted fever, leptospirosis, or measles.


Table 3 Simplified criteria for diagnosing TSS in children
  • Pyrexia >39°C
  • Rash
  • Shock
  • Diarrhoea and/or vomiting
  • Irritability
  • Lymphopenia

Because of the potentially serious nature of the condition the index of suspicious has to be low. McAllister et al14 describe a typical prodromal period of 24-48 hours with diarrhoea, vomiting, general malaise, pyrexia, tachycardia and tachypnoea with a fall in white cell count and haemoglobin before the shock phase which develops 3-4 days post burn. Once 'shock' has occurred the mortality is approximately 50%. In view of this, treatment should begin early. The outline of treatment is shown in Table 4. This is based on published15 and personal experience. The single most important measure is to deliver a specific antitoxin to TSST-1 either as human immunoglobulin or pooled fresh frozen plasma or fresh whole blood thereby producing a state of passive immunity in the recipient.16 One point of local interest is that the incidence of toxic shock syndrome seems to be low in Hong Kong. The reasons for this need to be explored but certainly do not relate to prophylactic antibiotic use.

Table 4 Outline management of TSS
  1. Inspect wound and change dressings.
  2. Open treatment or if closed - frequent wound care.
  3. Intravenous fluids including fresh frozen plasma.
  4. Antistaphylococcal antibiotic given intravenously → Clindamycin 25-40 mg/kg/d IV divided q6-8h.
  5. Immunoglobulin given intravenously 400 mg/kg IV as single dose administered over several hours.
  6. Careful monitoring.

Non-accidental Injury, Burns Toxemia and the Resilience of Children

The next case is very different and occurred over eighteen years later and in Hong Kong. It was a case with all the classical features of non-accidental injury and after a delayed presentation a very sick child was admitted. She suffered two cardiac arrests but eventually survived.

Case 3

J was twenty-three months old and suffered a 35% BSA scald injury. Her initial presentation to hospital had been delayed and by the time she was transferred to the regional burns center she was hypotensive, oliguric and acidotic. Her intravenous fluids were increased and she was commenced on inotropic support. By post burn day three her acidosis and renal function were normalising and she was on a decreasing inotropic support. The burn was assessed to be intermediate partial thickness and porcine, biological, dressings were applied. The following day her general condition began to deteriorate. Following an episode of desaturation, the ventilatory pressures increased, the patient become hypotensive, developed runs of supraventricular tachycardias, twice arrested and was twice resuscitated. The inotropic support was increased to 120 mcg of noradrenaline and broad-spectrum intravenous antibiotic were commenced. The porcine skin was removed and the burn wound was reassessed as 67% BSA and Acticoat (a sustained release silver dressing17) was applied (Figure 1). Intravenous immunoglobulin was also given together with Clindamycin.

Over the following days the condition stabilised and began to improve. The inotrope support was reduced and ventilatory pressures again were reduced. Wound cultures from the critical period grew pseudamonas, acinitobacter and non-toxin producing Staphylococcus aureus. The wounds were healing under the Acticoat dressing. The burn on the scalp appeared to have converted to full thickness but was dry. On day 15 post burn the child was extubated. The full-thickness scalp burn was excised and a split thickness graft applied on day 25 and the child eventually discharged on day 54 post burn.

Figure 1 A critically ill child on the Intensive Care Unit covered in sustained release silver dressing. One particular advantage of this dressing in this situation is that it remains active for seven days and does not need changing.

This child appeared to have an intermediate depth partial thickness burn. After 48 hours of antibacterial dressing she was dressed with a biological dressing. Subsequently she became catastrophically unwell. This was not the classical picture of toxic shock but the patient certainly appeared to be toxic. Burns toxaemia is not commonly seen in an era when silver based topical preparations are so widely used in burns dressings. Silver nitrate solution, silver sulphadiazine cream and silver impregnated dressing all are responsible for the dramatic decrease in Pseudomonas related sepsis.18 Pseudomonas may not be cultured in the blood but a topical colonisation can interact with burns tissue to produce the devastating clinical picture of 'Septic Shock'. This patient was treated with broad spectrum antibiotics, topical wound therapy and anti-toxin treatment with pooled fresh frozen plasm and immunoglobulin and survived. The massive doses of inotropes did cause an extensive conversion of the burn wound so that areas that had been assessed to be erythema with reversible damage on admission became partial thickness burns and an area of the scalp converted to full-thickness injury. It is important for medico-legal reasons to appreciate the effects of hypotension secondary to sepsis and also systemic inotropic support on the burn wound. In determining the likely mechanism of injury, forensic burns specialists will refer to nomograms which relate temperature of water, duration of contact and depth of injury. The reason to do this is to see whether the injuries sustained are compatible with the account of the adult carer. Another important point to take from this case is that it is essential never to give up in the treatment of a child with burns. When a critical clinical condition is related to sepsis very aggressive therapy should be instituted and maintained until there is complete and irreversible multiple organ failure.19 To this extent acute renal failure is no indication for withdrawing support in the extensively burned child and there is now increasing support for instituting extra-corporeal membrane oxygenation (ECMO) in post-burn respiratory failure which is particularly difficult to manage in the combined inhalational and cutaneous burn.20

Massive Burn Survival, Professional Communication and Psychological Support

The following case illustrates a newer challenge in paediatric burns care, which results from the combination of medical and surgical treatment of children with massive burns. In particular it illustrates how important it is that the burns team are all included in the debate about the application of new technology and understand what the outcomes of treatment can be, if that treatment is successful.

Case 4

Matthew was five years old and sustained 90% BSA full thickness burn in a house fire. He was intubated and resuscitation commenced at a peripheral hospital and transferred by helicopter to the regional burns center. Between the initial phone call and the arrival of Matthew the senior intensivist, anaesthetist and burns surgeon discussed a management strategy for what was an unprecedented burn in that unit. The medical staff were aware of the results coming from the Shriners Burns Institutes in North America and appreciated the underlying message; this was a potentially survivable burns but needed aggressive treatment. It was decided that excisional surgery would be performed on admission. Matthew was transferred from the helicopter-landing pad to the Burn theatre. He was thoroughly assessed including lines, fluids, and ventilation and then surgical removal of the burn commenced. After thirteen hours of meticulous diathermy, excision of 70% BSA burn had been achieved and the surgical wound covered with glycerolized cadaver skin. A split thickness biopsy of unburned skin had been taken for cell culture. The surgery had been uneventful apart from the need to perform an emergency tracheostomy. The uncuffed tube had been taped to the cheek and the developing oedema had caused it to become dislodged. A new endotrached tube could not be replaced and so a tracheostomy performed. At the completion of the first day of surgery the full thickness burn of the face and scalp remained intact (Figure 2a). Matthew was transferred to the Intensive Care Unit where he remained remarkably haemodynamically stable and there was no evidence of developing sepsis. An indication of his stability is that he did not require any inotropic support despite the 90% BSA burn. The next phase in the surgery was to excise the head and neck burn and it was decided to cover the surgical defect with Integra? (This will be discussed in more detail in the next case)

On day four post burn Matthew was taken to theatre for another extensive procedure. The skin of the face and anterior skull was removed by diathermy excision and then the Integra was carefully, and meticulously applied and stitched in place (Figure 2b). The Integra was applied in aesthetic units and seams closed with running sutures. By the completion of the operation Matthew had undergone a transformation from a burned child with a grossly oedematous face to a new age vision, the like of which we had never seen before (Figure 2c). Nevertheless, the operation had gone extremely well and Matthew was returned to the ICU. What subsequently happened should perhaps have been predicted but was overlooked in the 'heroic' efforts to save the life of this child. The nursing staff on the ICU at that hospital had never encountered a child with such extensive burns. Children and indeed adults with that degree of burns had died. The nurses, and of note this was a general ICU catering for many different types of patients, had previously had the experience of the long, slow, lingering death of patients with extensive burns who become more and more septic and after several weeks even months of physically and emotionally draining care would die. The nursing staff were considering the effects of this on the parents. But in addition there was the extensive nature of the burn. The result could only be extensive scarring, disfigurement, deformity. The question of withdrawal of care was raised. Such issues cause intense professional conflict/discussion and the relatives were finding it difficult to make sense out of the mixed messages they were receiving. Survivors of major burns came to counsel the parents but in the event a fulminating pneumococcal septicaemia led to a sudden death of the patient.

(a) (b) (c)
Figure 2. a) The markedly swollen 'fish-face' typical of the full-thickness burn; b) Integra?is 'tailored' to fit the face in cosmetic units and sutured in place; c) This is the face of a child covered with Integra? This was the first time Integra?had been used on the face and lessons learnt in the application proved of critical value in subsequent cases.

This case illustrates a number of issues related to paediatric burns care. There are now reports of increasing survival amongst patients with extensive burn. In the Shriners Burns Hospital in Galveston between 1982 and 1995, 103 patients with 80% or more total body surface area burns with 70% being full thickness were treated. Sixty-seven percent of the patients survived.21 Sheriden concludes in a paper published in 2000 that 'Survival rates after burns have improved significantly for children. At present, most children, even young children and children with large burns, should survive'.22 With such numbers of children surviving massive burns it is imperative to look at the outcome to see if it is justified in humanitarian terms. As such the American Burn Association and Shriners Hospital set out to develop a Children Burn Outcome Questionnaire.23 This concentrated on children aged 5-18. A subsequent outcome questionnaire has been developed for infants and children under 5.24 Whilst the preliminary studies used to validate these outcome assessments do indicate that children who survive massive burn do tend to score lower as quality of life assessments than normal children, the scores are still within the two standard deviations of the normal indicating that the outcomes are not dramatically adverse.

Whilst the evidence is accumulating that children with massive burns cannot only survive but also enjoy a good quality of life it is important to discuss this with all those involved in the potential care of such patients. There are strong emotional reactions to disfigurement and it is essential to discuss these emotions openly and constructively not only with the patients and their families but also the staff involved in the care of the patients. Effective communication in the Healthcare team does take time and effort but is well rewarded in terms of enhanced patient care.25

Reconstruction in the Acute Phase Using Tissue Engineering

This case illustrates the changing strategy to deal with the acute burn wound and improve the functional outcome of the acute stage of treatment.

Case 5

Keiron suffered 60% body surface area scald burns following a bath immersion incident. Thirty percent of the burns were full thickness (Figure 3a). The full thickness burns were excised (Figure 3b) and a tissue engineered, dermal regeneration template was used to close the wound (Figure 3c). Keiron went on to heal and was discharged and subsequently has a number of secondary scar releases to axillae and neck but otherwise he has done well (Figure 3d).

For the paediatric burns surgeon the question of survival is no longer the big issue. It is quality of survival. This is determined by the scar. Scar tissue is responsible for deformity, scar tissue is responsible for disability. And yet scar tissue is the natural response to connective tissue injury. Thus any burn involving the dermis will result in scarring. The process of scar involves a cellular cascade conducted by the macrophage and mediated through cytokines. The outcome of this macrophage-effected, fibroproliferative response is the deposition of collagen in a random array that can never be fully organised to recreate the high degree of uninjured tissue architecture. Burke, a burns surgeon and Yannis, a Polymer chemist, sought to address this and developed a material we now know as Integra?26 This material is basically a construct of bovine Type I collagen and shark glycosaminoglycans chondroitin-6-sulphate. These elements have been extracted, highly purified and then reconstructed to form a three dimensional matrix over which a silicone membrane is layered. The material is placed into a full thickness wound defect and the matrix is biodegraded but replaced with a directed auto-collagenous neomatrix formation with a high degree of organisation. This matrix is vascularised and the silicone removed and the epidermis replaced with an ultra thin autograft. Another advantage of this approach is the rapid wound closure which results in shorter hospital stay.27 The outcome is a close similarity to dermal regeneration; although the lack of skin appendageal structures underlines the fact that this is not a true regeneration.28 With improvements in surgical technique and post-operative care the results can only improve and the prospect of treating extensively burnt children and achieving a fully functional recovery is a reality.29 Further work is underway to combine skin composites and Integra30 and to pre-seed Integra with viable keratinocytes to make a one, rather than a two stage procedure.31

Towards Scarless Healing: Regeneration

This final case illustrates another approach towards the challenge of scarring.

Case 6

The patient was a 6-year-old girl who sustained burns over approximately 40% of her body surface area from hot soup when she was 4 years old. She had sustained burns to her right arm, right and left buttocks and posterior thighs, and right lateral thigh. She was treated with skin grafting procedures to the right hand and right forearm and was treated conservatively with biological (pigskin) dressings to the other burns.

When assessed 18 months after the initial burn injury, the scar on the right buttock was remarkable in that it was growing beyond the original area of the burn and was forming an overhanging lip of 2 to 3 cm on the medial margin. The scar on the left buttock/trunk area, however, was softening and becoming paler, as would be expected for a more normal hypertrophic burn scar. The scar in the region of the right popliteal fossa was very rigid, and horizontal fissures were forming when the knee joint was flexed and extended, causing open wounds and discomfort. The scars in the natal cleft were enlarging, forming tail-like appendages that were interfering with personal hygiene.

This child received a number of surgical treatments for her keloid scars including intra and extra lesional excision, excision and reconstruction with Integra?and excision and application of a cultured auto keratinocyte cell suspension. Where the keloid was excised and the bed treated with cell suspension, there has been no recurrence. The follow up has been in excess of two years.

This case has been described in detail elsewhere32 and early results on other cases are promising (Figures 4a & 4b). The hypothesis that is being actively explored is that

(a) (b)
(c) (d)

Figure 3. a) This full thickness burn was the result of a non-accidental immersion in a bath; b) The full thickness burn was excised down to the fascia with the preservation of some fat. 30% of the body surface area burn was excised in one operation; c) The artificial skin was stapled to the patient; d) Six years follow-up with a healthy, happy child with full functional recovery although some texture abnormalities.


(a) (b)

Figure 4 a) An aggressive keloid affecting the right ear of a post burn paediatric patient; b) The keloid was shaved off and cultured keratinocytes applied. The wound re-epithelialised quickly and there has been no early recurrence (four months follow-up).

the keratinocyte does have a major influence on fibroblast behaviour. This influence is exerted through a co-ordinated cytokine cascade. Fibroblasts in the normal wound are acting under the influence of the macrophage and their main response is the abundant depositions of collagen. The application of a keratinocyte cell suspension to a fresh wound will interfere with this response. Indeed the hypothesis to be explored is that the fibroblast responds to the keratinocyte rather than the activated macrophage. The keratinocyte cell suspension does contain a mix of proliferating and terminally differentiating keratinocytes and it is this mix that is potentially critical. The proliferating keratinocyte is essentially an epidermal stem cell and the hypothesis suggests that this cell has a better concept of dermal architecture than the newly recruited fibroblast and the activated macrophage. Thus when the stem cell rich keratinocyte cell suspension is sprayed onto the dermal bed it will establish a program of dermal regeneration as well as epidermal regeneration. The key to scarless healing is to redirect the mechanism of tissue repair to one of tissue regeneration.


Paediatric Burns Care presents many challenges for those dedicated specialists involved in this speciality. The work can be physically and emotionally draining but the rewards can be great in terms of satisfaction and fulfillment. Whilst fire, hot water and children exist there will, unfortunately, be a need for the provision of paediatric burns care facilities. These six cases are all severe burns but any burn in a child benefits from specialist care to achieve the best outcome. The provision of this care cannot be demanded in entirety in a resource restricted health economy but rationalisation and redistribution of resource and the concentration of care in selected centers can go a long way to achieving the best results for Paediatric Burns patients.


1. Burns Care at Shriners Hospitals. (accessed 5/4/2003).

2. Ying SY, Ho WS. Playing with fire - a significant cause of burn injury in children. Burns 2001;27:39-41.

3. Tempest MN. A survey of domestic burns and scalds in Wales during 1955. Br Med J 1956;1:1387.

4. Burd DA, Burd E. The electric kettle flex - a cause for concern. Burns Incl Therm Inj 1985;12:136-8.

5. Colebrook L, Colebrook V, Bull JP, et al. The prevention of burning accidents. Br Med J 1956;1:1379.

6. George A, Ebrahim MK. Infant scald burns: a case of negligence? Burns 2003;29:95.

7. Shiridan RL. Burns. Crit Care Med 2002:30(Suppl);S500-14.

8. Dowloadable from (accessed 7th April 2003)

9. Frame JD, Eve MD, Hackett ME, et al. The toxic shock syndrome in burned children. Burns Incl Therm Inj 1985;11:234-41.

10. Edwards-Jones V, Dawson MM, Childs C. A survey into toxic shock syndrome (TSS) in UK burns units. Burns 2000;26:323-33.

11. Johnson D, Pathirana PD. Toxic shock syndrome following cessation of prophylactic antibiotics in a child with a 2% scald. Burns 2002;28:181-4.

12. Chesney PJ, Bergdoll MS, Davis JP, Vergeront JM. The disease spectrum, epidemiology, and etiology of toxic-shock syndrome. Annu Rev Microbiol 1984;38:315-38.

13. Cole RP, Shakespeare PG. Toxic shock syndrome in scalded children. Burns 1990;16:221-4.

14. McAllister RM, Mercer NS, Morgan BD, Sanders R. Early diagnosis of staphylococcal toxaemia in burned children. Burns 1993;19:251-2.

15. Blomqvist L. Toxic shock syndrome after burn injuries in children. Scand J Plast Reconstr Surg Hand Surg 1997;31:77-81.

16. Edwards-Jones V, Greenwood JE; Manchester Burns Research Group. What's new in burn microbiology? James Laing Memorial Prize Essay 2000. Burns 2003;29:15-24.

17. Yin HQ, Langford R, Burrell RE. Comparative evaluation of the antimicrobial activity of ACTICOAT antimicrobial barrier dressing. J Burn Care Rehabil 1999;20:195-200.

18. Klasen HJ. A historical review of the use of silver in the treatment of burns. II. Renewed interest for silver. Burns 2000;26:131-8.

19. Sheridan RL, Schnitzer JJ. Management of the high-risk pediatric burn patient. J Pediatr Surg 2001;36:1308-12.

20. Pierre EJ, Zwischenberger JB, Angel C, et al. Extracorporeal membrane oxygenation in the treatment of respiratory failure in pediatric patients with burns. J Burn Care Rehabil 1998;19:131-4.

21. Meyers-Paal R, Blakeney P, Robert R, et al. Physical and psychologic rehabilitation outcomes for pediatric patients who suffer 80% or more TBSA, 70% or more third degree burns. J Burn Care Rehabil 2000;21(1 Pt 1):43-9.

22. Sheridan RL, Remensnyder JP, Schnitzer JJ, Schulz JT, Ryan CM, Tompkins RG. Current expectations for survival in pediatric burns. Arch Pediatr Adolesc Med 2000;154:245-9.

23. Daltroy LH, Liang MH, Phillips CB, et al. American Burn Association/Shriners Hospitals for Children burn outcomes questionnaire: construction and psychometric properties. J Burn Care Rehabil 2000;21(1 Pt 1):29-39.

24. Kazis LE, Liang MH, Lee A, et al. The development, validation, and testing of a health outcomes burn questionnaire for infants and children 5 years of age and younger: American Burn Association/Shriners Hospitals for Children. J Burn Care Rehabil 2002;23:196-207.

25. Burd A, Cheung KW, Ho WS, Wong TW, Ying SY, Cheng PH. Before the paradigm shift: concepts and communication between doctors and nurses in a burns team. Burns 2002;28:691-5.

26. Burke JF, Yannas IV, Quinby WC Jr, Bondoc CC, Jung WK. Successful use of a physiologically acceptable artificial skin in the treatment of extensive burn injury. Ann Surg 1981;194:413-28.

27. Ryan CM, Schoenfeld DA, Malloy M, Schulz JT 3rd, Sheridan RL, Tompkins RG. Use of Integra artificial skin is associated with decreased length of stay for severely injured adult burn survivors. J Burn Care Rehabil 2002;23:311-7.

28. Moiemen NS, Staiano JJ, Ojeh NO, Thway Y, Frame JD. Reconstructive surgery with a dermal regeneration template: clinical and histologic study. Plast Reconstr Surg 2001;108:93-103.

29. Dantzer E, Braye FM. Reconstructive surgery using an artificial dermis (Integra): results with 39 grafts. Br J Plast Surg 2001;54:659-64.

30. Boyce ST, Kagan RJ, Meyer NA, Yakuboff KP, Warden GD. The 1999 clinical research award. Cultured skin substitutes combined with Integra Artificial Skin to replace native skin autograft and allograft for the closure of excised full-thickness burns. J Burn Care Rehabil 1999;20:453-61.

31. Jones I, James SE, Rubin P, Martin R. Upward migration of cultured autologous keratinocytes in Integra trade mark artificial skin: a preliminary report. Wound Repair Regen 2003;11:132-8.

32. Burd A, Chan E. Keratinocyte-keloid interaction. Plast Reconstr Surg 2002;110:197-202.


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