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Holzheimer RG, Mannick JA, editors. Surgical Treatment: Evidence-Based and Problem-Oriented. Munich: Zuckschwerdt; 2001.

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Surgical Treatment: Evidence-Based and Problem-Oriented.

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Current therapy of burns

, M.D. and , M.D.

Shriners Burn Hospital, Galveston, Texas, U.S.A.

The current therapy of the acutely burned patient is based on adequate resuscitation, early wound debridement and closure, support of post burn hypermetabolic response and control of infection.

Specialized burn centers have developed for the provision of care to acutely injured patients, but providers who are often intimidated and overwhelmed by such injury usually administer the initial care. The American Burn Association has developed criteria for recommendations for transfer to a specialized burn center (table I).

Table I. Criteria for transfer of care to a specialized burn unit.

Table I

Criteria for transfer of care to a specialized burn unit.

Treatment begins by removing the victim from the continuing source of injury.

Evacuation from proximity to flame, extinguishing flames, removal of clothing, continued lavage of chemical agent off the patient to the ground and removal from contact with electrical circuits are used to stop the initial process of a burn. Subsequently, treatment follows the principles of management of airway; breathing and circulation of trauma care resuscitation. Patients do not expire from undressed wounds during the initial assessment but are at genuine risk from loss of the airway, hypovolemia and hypothermia. Ensuring the patency of the airway with intubation or circothyroidotomy is necessary if there is any possibility of inhalation injury before massive edema develops. Burned facial structures can be suggestive of inhalation injury; stridor, inspiratory grunting, wheezing or tachypnea signal impending airway loss. Carbon monoxide binds to hemoglobin, falsely elevating measurements with oxygen saturation monitors. Oxygen at 100% is administered from the scene of the accident to increase the rate of dissociation of CO from hemoglobin. Any suggestion of smoke inhalation should be investigated with an arterial blood gas determination. Use of the high frequency percussive ventilator has been shown to reduce mortality in inhalation injury (1) with further human trials ongoing.

Fluid resuscitation is aimed at restoring circulating intravascular volume.

Venous access is best obtained via two large bore peripheral IV's, although alternate methods are sometime necessary, such as central access, venous cutdowns or interosseous infusions. Delay in administration of resuscitation has been shown to have a direct negative correlation with survival (2). Commonly used resuscitations administer between 2 to 4 cc/kg body weight/% body surface are burned of Lactated Ringer's solution. This predicts the fluid needs over the first 24 hours post injury, with half of the budgeted volume administered during the first 8 hours and the remainder over the following 16 hours, measured from the time of the injury. It can not be stressed enough that these formulas provide only a “budget” for required fluids and must be adjusted based on objective parameters, urine output (0.5 cc/kg for adults or 1.0 cc/kg for children) or persistent metabolic acidosis. Young children have different body proportions and a greater percentage body water; hence evaporative losses can be greater, so the needs are estimated using the Galveston Formula of 5000 cc/m2 burned and 2000 cc/m2 total burned surface area. The same administration plan as for adults is used, with the first one half of the volume given over 8 hours and the remainder over the next 16 hours, again with urine output as the ultimate guide to adequacy of resuscitation. Body surface area charts are available to draw the areas of burn and provide the percentage of the body burned. Maintenance Dextrose is administered in children under two years to prevent hypoglycemia with their relatively diminished Glycogen stores. Hypertonic saline solutions have been advocated at some centers to resuscitate burn patients, but recent studies have not been able to demonstrate clearly decreased fluid requirements or decreased percent weight gain with hypertonic saline compared to Ringer's lactate (3). After a burn injury, the ensuing shock results from alterations in microvascular permeability and fluids shifts that result in tissue edema, reaching a maximum at between 8 and 48 hours post injury. The use of albumin is not advised in the early post burn resuscitation period when the increased albumin would simply pass out into the tissues and cause greater edema. Later use of albumin replacement is still undergoing evaluation, but not definite answer has been found (4).

Burn wounds can be classified as first; second or third degree based on surface appearance.

  • First-degree wounds are superficial and reddened. They do not require surgical intervention and are generally treated with topical moisturizers and avoidance of recurrent injury. Typically from prolonged sun exposure without blisters.
  • Second-degree burns are deeper, causing a superficial edema deposition between deeper viable tissue and injured, more superficial tissues. The surface appearance is moist with blisters in various degrees of rupture. Treatment involves debridement of intact blisters at risk for rupture to remove the fluid, which contain high concentrations of thromboxanes and coverage with topical antimicrobial agents or synthetic wound dressings. The deeper elements of the skin remain intact and can regenerate the epithelial layer.
  • Third degree wounds are deepest and appear whitened, black, or dry, leather like skin. They require surgical debridement and skin grafting if larger than two centimeters.

Need for surgical intervention/debridement depends on the depth of the injury.

  • Full-thickness burns destroy all of the dermal elements; hence there are no epidermal cells left to regenerate the injured area.
  • Partial thickness injuries allow epidermal cells to survive in the dermal elements, such as sweat glands or hair follicles to repopulate the injured area.

In general, partial thickness and second-degree burns are used interchangeably, while full thickness and third degree are synonymous.

It is generally accepted that early debridement and grafting of wounds requiring surgery reduces hospital stay and morbidity/mortality. Previously wounds became infected and through bacterial action, the eschar would separate leaving a granulating bed for skin grafting. The risk of such management is the development of invasive wound infection and sepsis. By early, aggressive surgical debridement, non-viable tissue is removed and hence the wound bed is relatively infection free. Further, the removal of dead tissue has the potential to reduce the generation of chemical mediators that stimulate the inflammatory cascade leading to remote and multisystem organ failure. Complete debridement should proceed at the earliest possible opportunity, even if donor sites are insufficient to provide total wound coverage. In this case, biological dressings (preferably Cadaver allograft) should be used to cover the remaining wounds. Excision of burn wounds, this requires large volumes of blood for transfusion (approximately 1 cc/cm2 to be excised) (5). Blood loss can be minimized by the use of excision to the level of faschia or tourniquets when performing tangential excisions of the extremities. Tangential excision gives a better cosmetic outcome by leaving subcutaneous fat but blood loss is greater.

After the eschar has been excised, the wound must be closed. In general wounds of 30% total body surface area or less can be closed in a single operation with split thickness skin grafts taken from unburned areas. As the size of injury increases, there is proportionately less donor site for autografting, so alternate techniques are required. Larger expansions of the skin using meshers are available, usually requiring cadaver allograft overgrafting of 4: 1 or greater autograft skin expansion (6). Wounds of greater than 90% may require up to 10 operations for coverage, or use of cultured epithelial autografts (7). Both options have particular advantages and disadvantages (table II).

Table II. Widely expanded meshed autograft vs. cultured epithelial autograft.

Table II

Widely expanded meshed autograft vs. cultured epithelial autograft.

Organ dysfunction associated with the systemic inflammatory response syndrome may occur. Renal failure previously complicated cases of inadequate resuscitation, but increased awareness of its causes (i.e. poor renal perfusion and nephrotoxic drugs) have reduced the frequency of this complicating factor. Pulmonary injury from smoke and toxin inhalation can be minimized by use of aerosolized heparin and mucomyst (8) the High frequency Percussive ventilator, minimizing barotrauma (9), and expeditious removal of the endotracheal tube to allow coughing for pulmonary hygiene. Smoke inhalation injury and Multisystem Organ Failure in association with burns have a mortality as high as 50%.

Patients with severe burns have metabolic rates 100 to 150% higher than normal.

Support of the hypermetabolic response to burns is accomplished by keeping patient rooms warm (80–90 degrees F) and meeting nutritional needs (1500 Kcal/m2 Total body surface area and 1500 Kcal/m2 burned) (10), or the use of hormonal modulation (table III). Without this treatment, increased energy and protein requirements must be met to prevent impaired wound healing, cellular dysfunction and decreased resistance to infection.

Table III. Hormonal modulators of hypermetabolism.

Table III

Hormonal modulators of hypermetabolism.

Infection remains a significant problem until the integrity of the skin, lungs and gut can be restored and resolution of post burn immunosuppression occurs. Topical antimicrobial therapy (table IV) is used to control localized infection at the wound site, but will not be effective if significant amounts of devitalized tissue remaining. Quantitative wound cultures are useful for surveillance and colony counts of greater than 1 × 105 organisms/gm tissue indicates a wound at risk for invasion. This is best confirmed by histologic examination of a wound biopsy where actual invasion of viable tissue by pathogens in seen. Systemic antibiotics are indicated for perioperative coverage of suspected wound pathogens and gut flora and need not be continued after dressings are taken down and healed wounds exposed. Oral prophylaxis with antifungals has been shown to reduce the incidence of fungal wound infections (11).

Table IV. Common topical antimicrobial agents.

Table IV

Common topical antimicrobial agents.

Burn wound related sepsis is characterized by five signs (table V).

Table V. Signs of burn wound related sepsis.

Table V

Signs of burn wound related sepsis.

Burn wound sepsis is sometimes difficult to assess in the face of the ongoing hypermetabolism. Fever and leucocytosis are commonly see in otherwise healthy burn patients. Bacterial translocation from the gut is a potential source of infection as vasoconstriction results from the burn related shock, stressing the importance of continued trophic enteral feeding.

Rehabilitation begins with wound coverage to prevent burn scar contracture. Aggressive physical and occupational therapy with exercise and splinting in position of function are key. Use of pressure garments has been shown to organize the collagen of a wound more rapidly, but evaluation of its cosmetic and functional advantages are undergoing study currently. Plastic and reconstructive surgeons should be involved early on in hospital course so that future need for releases and surgeries can be planned.

Conclusion

Burn wound mortality and morbidity have steadily decreased over the last 30 years. Recognition of the potential complications, early excision and wound closure has led to these changes.

References

1.
Ciofi W G Jr, Graves T A, McManus W F. et al. High frequency percussive ventilation in patients with inhalation injury. J Trauma. 1989;29:1350–1354.
2.
Wolf S E, Rose J K, Desai M H, Mileski J P, Barrow R E, Herndon D N. Mortality determinants in massive pediatric burns: An analysis of 103 children with >80% TBSA burns (>70% full-thickness) Ann Surg. 1997;225(5):554–569. [PMC free article: PMC1190795] [PubMed: 9193183]
3.
Gunn M L, Hansbrough J F, Davis J W, Furst S R, Field T O. Prospective, randomized trial of hypertonic sodium lactate vs. lactated Ringer's solution for burn shock resuscitation. J Trauma. 1989;29:1261–1267. [PubMed: 2671402]
4.
Greenhalgh D G, Housinger T A, Kagan R J, Rieaman M, James L, Novak S, Farmer L, Warden G D. Maintenance of serum albumin levels in pediatric burn patients: a prospective, randomized trial. J Trauma. 1995;39(1):67–73. [PubMed: 7636912]
5.
Desai M H, Herndon D N, Bromeling L D, Barrow R E, Nichols F J, Rutan R L. Early burn wound excision significantly reduces blood loss. Ann Surg. 1990;211(6):753–762. [PMC free article: PMC1358131] [PubMed: 2357138]
6.
Alexander J W, MacMillan B G, Law E, Kittur D S. Treatment of severe burns with widely meshed skin allografts overlay. J Trauma. 1981;21:433–438. [PubMed: 7230295]
7.
Green H, Kekindle O, Thomas J. Growth of cultured human epidermal cells into multiple epithelia suitable for grafting. Proc Natl Acad of Sci USA. 1979;76:5665–5668. [PMC free article: PMC411710] [PubMed: 293669]
8.
Desai M H, Brown M, Mlcak R. et al. Nebulization treatment of smoke inhalation injury in sheep model with DMSO, heparin, combinations and acetylcysteine. Crit Care Med. 1986;14:321–.
9.
Cortiella J, Mlcak R, Herndon D N. High frequency percussive ventilation in pediatric patients with inhalation injury. J Burn Care Rehabil. 1999;20(3):232–235. [PubMed: 10342478]
10.
Hildreth M A, Herndon D N, Deai M H, Duke M A. Caloric needs of adolescent patients with burns. J Burn Care Rehabil. 1989;10:523–526. [PubMed: 2600100]
11.
Desai M H, Herndon D N, Abston S. Candida infection in massively burned patients. J Trauma. 1981;21(3):237–239.
Copyright © 2001, W. Zuckschwerdt Verlag GmbH.
Bookshelf ID: NBK6954

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