Pediatric Burns
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Pediatric Burns By Bradley J. Phillips

Chapter 1:  Historical Perspective and the Development of Modern Burn Care
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the use of propranolol,107 and the use of insulin,108 insulin-like growth factor,109 or human growth hormone.110

Rehabilitation

As postburn mortality decreased, the problems encountered by burn survivors, particularly those with deep and extensive injuries, became paramount.111 The scientific study of the occupational, physical, and psychosocial rehabilitation of the thermally injured patient is a relatively young field. The Cocoanut Grove monograph briefly states that 6 patients with dorsal hand burns who had been splinted in extension were referred to the Physical Therapy Department after completion of surface healing.112 In the 1950s, Moncrief began rehabilitation soon after admission and resumed it 8 to 10 days after skin grafting.113,114 The advent of heat-malleable plastic (thermoplastic) material made it possible to fabricate increasingly complex and effective positioning devices.115 This was followed by the introduction of pressure to treat hypertrophic scars and the development of customized pressure garments.116 Others reduced or eliminated the delay between skin grafting and ambulation, without deleterious effects on graft take.117,118 In brief, burn rehabilitation is no longer viewed as a “phase” which begins after completion of wound healing, but as a highly specialized process which must begin immediately upon patient admission and often continues for 24 or more months. A recent review noted a need for more research in this area, to include prevention and management of hypertrophic scarring and contractures, pain management, post-traumatic stress disorder, affective disorders, and body-image problems.119

Conclusion

The 1910 edition of the Encyclopedia Britannica stated that death “almost invariably” results when one-third or more of the TBSA is burned.1 For young adults, the 20th century in the West featured an extraordinary diminution in the lethal-area 50% (LA50—that burn size which is lethal for 50% of a given cohort of patients), from 43% TBSA in 1945 through 1957 to 82% in 1987 through 1991.21 At the Galveston Shriners’ Burn Center, the mortality rate in children with 96-100% TBSA burns during 1982 through 1996 was only 69%. This led the authors to conclude that “prompt intravenous access and resuscitation, aggressive operative therapy, and the avoidance of sepsis and organ failure by meticulous critical care should enable any child with almost any burn size to live.” At that hospital120 and others providing comprehensive long-term psychosocial and physical rehabilitation,121 follow-up data indicate that young survivors of massive thermal injury can experience reasonably well-adjusted lives. No one intervention was solely responsible for these improvements; rather, it is the combined effects of fluid resuscitation, wound care, infection control, inhalation injury management, nutritional support, and aggressive rehabilitation. All these interventions, however, were directed in a coordinated fashion at correcting what Burke called “the fundamental defects of burn injury—the destruction of skin and its immediate physiologic effects.”1 This revolution has been possible only because of integrated clinical and laboratory research, carried out by multidisciplinary teams in specialized centers supported by generous public and private funding. New challenges remain—in maintaining and expanding adequate numbers of fully trained nurses, therapists, and physicians,122 in caring for the most severely injured, in facilitating their return to a successful role in society, and in translating the most effective of these advances to that large portion of the world which has not yet adopted them.

Key Points

  • Civilian fire disasters and military conflicts focused attention on the burn problem and motivated the creation of a new type of specialized care facility: the burn unit. The success of these units depends on multidisciplinary teams engaged in closely integrated laboratory and translational research and evidence-based clinical care.
  • Postburn shock is primarily caused by loss of fluid similar to plasma from the blood into the interstitium (edema formation). Fluid resuscitation formulae were developed based on the recognition that these losses are proportional to burn size.
  • Before the development of effective topical antimicrobials, invasive gram-negative burn wound infection was the leading cause of postburn death. The commonly used topical agents are mafenide acetate or some form of the silver cation (silver sulfadiazine, silver-impregnated dressings).
  • Early excision and grafting of deep partial and full-thickness burn wounds has become the standard of care for burn patients.
  • Inhalation injury increases postburn mortality. Effective therapies include not only gentle mechanical ventilation, but also those which maintain small airway patency.
  • Thermal injury causes hypermetabolism and hypercatabolism, which persist to some degree
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