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David H. Ahrenholz, MD, Matthew C. Clayton, MD & Lynn D. Solem, MD
Few life events compare with the immediate and long-term effects of a burn injury. Initial effects include marked pain and anxiety and, with large burns, extreme metabolic changes. Patients with permanent scars are emotionally affected for life8 and are the victims of subtle discrimination on many levels.
Definition of thermal burns
Humans are warm-blooded creatures who rigorously maintain their body temperature in a narrow range between 95oF and 105oF. Core temperatures outside this range are poorly tolerated and have adverse effects on the subject. Although patients have survived with a measured core temperature below 65oF under extreme circumstances,31 elevations of the core temperature above 110oF are rapidly fatal.40
The skin is more tolerant of temperature extremes. Cryopreserved cadaver skin can survive many months at -260oF when preserved with glycerol to minimize the effects of ice crystal formation.3 In contrast, Moritz and Henriques28 demonstrated a doubling of cellular destruction rates for each degree rise in temperature between 111oF and 124oF, and clinical burns occur rapidly above 134oF.
Traditional thermodynamics describe heat energy transfer to tissue by radiation, evaporation-condensation, convection and conduction. Heat is transferred by electromagnetic energy such as microwaves and infrared light, and by contact with the molecules of hot gases (flame injuries), hot liquids (scalds) or hot solid objects (contact or branding injuries). Sunburn is a typical, because this first-degree burn is caused by the ionization effects of certain wavelengths of ultraviolet light, without a significant rise in tissue temperature. Similarly, electromagnetic radiation, including X-rays and gamma rays, and high-energy particles such as protons, neutrons, electrons and alpha particles, cause damage by tissue ionization rather than thermal effects.38 Chemical, electrical, high-energy radiation and cold injuries18 are beyond the scope of this paper.
Thermal injuries occur only when sufficient thermal energy is applied to human tissue to produce cell injury or death. The thermodynamics of heat transfer are very complex.14 For example, it is possible for a person to pass a finger through a candle flame (which has a temperature of 1800oF at the apex) without becoming burned yet to be instantly burned by hot water at 180oF. One must remember that the terms heat and temperature are not interchangeable. Heat is the quantity of energy contained in an object. Specific heat is the amount of energy required to raise the temperature of a gram of material by one degree of temperature. Thus, temperature is a measure of the vibratory speed of the molecules in a heated substance. If only a few molecules are present, the temperature rise is very rapid as heat energy is added. Water at 180oF contains much more energy per unit of volume than air heated at the same temperature and pressure.
The skin temperature achieved by a given heat exposure is determined by the rate of heat addition, the duration of exposure, the heat capacity (specific heat) of the tissue, the blood flow through the tissue, the rate of heat transfer to deeper tissues and the rate of heat loss back out through the skin. The total heat energy added is of little consequence if dissipation by conduction to surrounding tissue, washout by local tissue blood flow or radiation of heat energy from the skin back to the environment keeps the tissue below the critical temperature. Branding injuries temporarily reduce local blood flow, producing deeper burns.10
Response to thermal injury
The initial response to an increase in skin temperature is the sensation of local heat. This is received by specific warmth receptors in the skin, and the sensation is not painful unless the initial skin temperature is below normal.12 As the skin temperature rises above 113oF, the warmth receptors cease their discharge, and a set of pain receptors called heat nociceptors are stimulated. After burn injury, these pain receptors remain stimulated when skin temperature returns to normal. In the very deepest burns, the receptors are destroyed, and the burns are painless.
Thermal injury to the skin triggers an inflammatory response. A variety of local cytokines13 cause a rapid accumulation of extravascular fluid, which may cause lethal hypovolemia in major burns. Early fluid resuscitation is life-saving, but local edema in the neck can produce airway obstruction and death. This risk exists even if there is no evidence of inhalation injury and the head and neck tissues are unburned. Many patients with head and neck burns, and most patients with major burns (>40 percent body surface area), require endotracheal intubation during the resuscitative phase to protect the airway.41 Tissue swelling peaks in the first 48 hours and then slowly abates.
Experimental data indicate that the profound metabolic responses to a major thermal burn are aborted by early removal of eschar.27 Early administration of prostaglandin inhibitors such as ibuprofen can also reduce local inflammation.15
Rapid cooling (within 90 seconds) has a number of beneficial effects.37 Heated human cells die rapidly, principally from denaturation of native protein and disruption of cell membranes. Experimentally, immediate cooling of proteins can allow refolding of denatured protein into the native state.4 These proteins regain their preinjury properties and biochemically appear unaltered. Heat applied to skin is conducted at a relatively slow rate to deeper tissue. If a cool material is applied quickly, much of the heat energy is removed, and the deeper tissue levels remain below the critical temperature for injury.
Cold application can also reduce inflammation to a minor degree.32 Cold packs markedly reduce local pain by inducing local numbness of the thermal nociceptors, especially if ice is applied; prolonged application can induce a local freeze injury or systemic hypothermia.
Clinical classification of burns
Traditionally, physicians refer to three depths of burn wound injury. First-degree burns are the most superficial and damage only epidermis. They are red, painful and not blistered. The pain and redness resolve in three to five days, and the epidermis often flakes off in the subsequent week or two. Severe sunburn (the most common first-degree burn) increases the lifelong risk of skin cancer6 but rarely requires hospitalization.
Second-degree burns blister and are very painful. When the blisters rupture or are debrided, superficial second-degree burns have a bright red base that is moist and weeps easily. Such burns treated with an antibiotic ointment subsequently accumulate a tightly adherent fibrin layer that, to the uninitiated, resembles burn eschar. Spontaneous separation of the fibrin layer occurs as the wound heals over one or two weeks.
Deep second-degree burns have a very pale white or mottled base beneath the blisters, indicating a more severe injury to the dermis. The burns take three or more weeks to heal and are associated with severe hypertrophic scar formation if not grafted.
Third-degree burns rarely blister. The skin surface is dry and insensate and may feel leathery. The full thickness of the dermis, extending into the subcutaneous fat, has been destroyed. Third-degree burns, especially those located on critical areas such as the face and hands, benefit from early split-thickness skin grafting.
Determining depth of burn injury is easy only for very superficial and very deep burns. Most second-degree burns initially are wet and weeping. Over succeeding days, the progressive changes in the dermis appear that indicate the depth of dermal injury.
Initial evaluation of head & neck burns
Patients sustaining head and neck burns are first evaluated for other injuries, using advanced trauma life support (ATLS) protocols.1 Airway, breathing and circulation must be evaluated first, followed by a secondary survey to exclude other traumatic injuries. Blood counts, chemistries and appropriate radiographs are ordered. The thermal injury can be ignored until all life-threatening injuries are treated.
The stable burn patient is then completely undressed, and the percentage of the body surface burned is calculated. Resuscitation begins with placement of large-bore venous catheters and infusion of lactated Ringer's solution according to the Parkland resuscitation formula (4 ml/ kg/% burn, half infused in the first eight hours and the remainder in the next 16 hours).29 A Foley catheter is used to monitor urine output. Patients with extensive burns or burns of critical areas are routinely stabilized and transferred to a burn center for definitive care, according to American Burn Association transfer criteria.24
Circumferential third-degree burns impair blood supply to distal tissue, because swelling occurs beneath the eschar during fluid resuscitation. Escharotomy is performed by incising the burned dermis with a scalpel to expose subcutaneous fat, a painless procedure in areas of third-degree burn. Alternatively, a collagenase enzyme such as sutilains (Travase), which Iyses only nonviable tissue, can be applied within the first few hours.
Some associated injuries are commonly encountered. Persons burned in an enclosed space have a risk of inhalation injury, manifested as respiratory failure in the first 24 hours. Patients with suspected inhalation injury or with massive burns that may lead to airway obstruction from tissue swelling are intubated and given supplemental oxygen.41 Tracheostomy is reserved for patients requiring more than three weeks of intubation,43 because of the increased risk of pulmonary infections associated with tracheostomy.
Admission arterial blood gas and carbon monoxide levels are obtained in patients with facial burns. Elevated carbon monoxide levels are treated with administration of 100% oxygen for four to six hours. Those with severe carbon monoxide poisoning may benefit from hyperbaric oxygen treatment.
An ophthalmologist should examine any patient with burns around the eyes in the first few hours after injury. The most common injury is a corneal abrasion, which will resolve with topical antibiotics and an eye patch once any foreign bodies are removed. Explosions occasionally cause acoustic trauma such as tympanic membrane rupture and permanent hearing loss.
Management of thermal injuries
First-degree (unblistered) burns are painful but heal without scarring. Most patients benefit from oral ibuprofen every four hours for two to five days to reduce pain and inflammation.5 In extensive sunburn, supplemental oral narcotics are also required. Patients are instructed to apply hand lotion four or more times per day until the symptoms resolve. Preparations containing aloe vera or vitamin E are acceptable and well tolerated, but topical antibacterial agents are unnecessary on unbroken skin.
Appropriate wound management for superficial second-degree burns protects the exposed dermis from desiccation or infection until reepithelialization can occur. Small blisters need not be removed, but large bullae are debrided early. Many wounds heal if protected from drying by an occlusive dressing of petrolatum gauze.
Silver sulfadiazine, applied to the burn once daily to prevent wound infection, is rather expensive but alleviates pain and prevents drying. With head and neck burns, the patient must wear a mummy mask to contain the cream, which liquefies at body temperature and turns yellow as it mixes with serum. A gray residue of elemental silver appears if silver sulfadiazine is incompletely removed with dressing changes. More commonly, we apply bacitracin ointment to the exposed second-degree burns of the face three to six times per day. This ointment is cheaper than silver sulfadiazine and is equally effective. It is washed off completely once daily to debride accumulating crusts. Male patients are encouraged to shave face burns daily to reduce infections and maintain good hygiene.
Many patients can receive outpatient care once pain is controlled with oral narcotics. Aspirin-containing products are contraindicated because of their prolonged blockade of platelet function in burn patients, who may require excision and grafting. We routinely prescribe oral codeine with acetaminophen for small burns and oxycodone-acetaminophen for more extensive injuries. Patients with exceptional pain or a history of substance abuse do very well with oral methadone, which provides long-duration pain relief without the euphoria-dysphoria of many other narcotics.11
Inpatients receive oral methadone and supplemental parenteral morphine, often administered through a patient-controlled analgesia device.30 Benzodiazepines reduce anxiety about burn cares, especially when combined with active patient intervention such as self-guided imagery, selfhypnosis, relaxation exercises and meditation. A facilitating psychologist or trained nurse can be very helpful at stressful times, especially during debridement or painful burn therapy sessions.17
Large third-degree burns will never heal, but even deep second-degree burns that spontaneously heal can produce unacceptable scarring. Therefore, we excise and autograft burns that will take longer than three weeks to heal. The procedure is usually performed 10 to 14 days after burn, when edema has resolved and areas of superficial second-degree burn have healed (Figs. 1A and 2A).
The surgical treatment of head and neck burns is not a trivial exercise, even for experienced surgeons.45 Excision must be more extensive than elsewhere, to include all dermal elements, especially in hair-bearing areas. Frequently, transfusion of one unit of packed cells is required for each percent of body surface excised from the head.25 Even the most uniform sheet grafts of the face can develop severe hypertrophic burn scar, and wrinkling of neck grafts is a perplexing problem. The American Burn Association recommends that head and neck burns be treated by experienced burn surgeons willing to provide the years of postoperative treatment required for an optimal outcome.29
Preoperatively, the areas of excision are examined, and suitable donor sites are discussed with the patient. The best donor skin match is from adjacent tissue, especially scalp.30 Many patients are initially unwilling to permit shaving of the scalp as a donor site. They should be advised that skin from more caudad donor sites provides a less acceptable color match.
The patient is informed that blood transfusions are anticipated, so that directed donor units can be obtained, if desired. We also place a feeding tube to eliminate the need for chewing until the grafts have stabilized. The need for postoperative bed rest and possibly a halo traction device for graft immobilization are also detailed.23
In the surgical suite, the patient is positioned in reverse Trendelenburg position to facilitate access to the burned areas and reduce venous blood loss. Saline containing dilute epinephrine is injected beneath the eschar before excision.22 Full-thickness excision of the deeply burned skin and all dermal elements, including hair follicles and sweat glands, is performed (Fig. 2B). Remaining hair or sebaceous glands would lift the skin graft or produce confluent sebaceous cysts, which become secondarily infected. Hemostasis is obtained with topical thrombin and pads soaked in 1:100,000 topical epinephrine. The electrocautery is used judiciously to prevent excessive damage to the excised wound bed.
When hemostasis is complete, we initially apply sheets of cadaver allograft skin secured with surgical staples for 24 to 72 hours (see Figs. 1C and 2B). During this time, accumulating edema fluid or blood is removed from beneath the cadaver graft. When the patient returns to the surgical suite, this graft is tightly adherent to the viable burn wound bed.
The cadaver skin is removed, and any questionable areas are reexcised. Sheets of autograft 0.014 to 0.018 inch thick are harvested from donor sites elevated by saline infused subcutaneously with a pressure irrigation system (Davol). Previous authors have emphasized the importance of grafting areas of the face defined as "cosmetic units.17,33." When extensive facial grafts are performed, it is critical to place the seams in normal skin-fold areas to minimize subsequent contractures. Grafts are secured by a combination of small surgical skin staples (usually removed on the third or fourth postgraft day) and 5-0 fast-absorbing gut suture to approximate graft edges. This suture is absorbed in a few days, and the cosmetic result is very acceptable. Any movement of the newly applied graft results in graft loss. Therefore, when grafts are applied to the neck, we use halo skeletal traction or a Risser vest (see Fig. 1D).23 The patient is transferred to the bed under anesthesia and awakened in traction.
Grafts are examined hourly, and fluid or blood is meticulously removed. This attention increases the opportunity for complete graft take over the subsequent five days (Fig. 2C). Neck immobilization is maintained until the seventh day,20 by which time a transparent plastic orthosis has been made. Our burn therapist makes a negative mold of the grafted part using dental alginate. A plaster-of-Paris positive cast is then formed from the negative impression. The transparent plastic orthosis is formed from the plaster positive. When the patient tolerates wearing the neck splint four to six hours at a time, the halo traction is removed, and the patient is allowed to ambulate while wearing the splint. Optimal outcomes are achieved when well-fitting splints are worn at least 20 hours per day, in combination with stretching exercises for neck, mouth, and eyelid areas (see Figs. 1E and 1F).
The facial skin is thinnest over the eyelids. Third-degree burns of the eyelids contract the skin, and exposure keratitis can rapidly destroy vision. The corneas are protected from drying with transparent plastic domes until grafting is undertaken.
Intraoperatively, plastic globe protectors are inserted and then removed after the grafts are sewn in place. Excessive excision damages the levator oculi muscles, with subsequent lid ptosis and vision impairment. The thickest practical skin grafts are used for resurfacing the lower eyelids, because subsequent lid contractures with globe exposure are so common. In the most severe cases, surgical tarsorrhaphies protect the corneas while graft healing proceeds (Fig. 3).2
Third degree burns of the ears are a common problem. Past authors have advocated application of antimicrobials and minimal debridement until eschar has spontaneously separated and granulation tissue has formed. This permits maximal preservation of the pinna. Unhealed ears are painful, however, and contact with a pillow disrupts sleep unless an elaborate ear-protective device is worn to bed.
Intraoperatively, the brown necrotic skin and auricular cartilage can be shaved off (Fig. 4A). Bleeding from the earlobe is brisk, but viable cartilage is white and does not bleed. When hemostasis is complete, small sheet grafts are secured with surgical staples. Some patients require a pedicle flap of temporalis fascia for coverage of exposed ear cartilage (Fig. 4B).26
The skin of the lips is thin and easily injured. Typically, we place upper and lower lip grafts to meticulously reconstruct the vermilion border, allowing the vermilion areas to heal spontaneously. The pink color of healed burns is very acceptable in this area. If granulation tissue forms, a superior or inferior mucosal flap can be advanced and sutured to reconstruct the vermilion border.34 Microstomia is a very common problem after extensive facial grafting. Oral orthoses of many kinds can be used beneath the facial orthosis to maintain lateral commissure length. We prefer a dental orthosis with integral wings to stretch the lateral commissures.21 The cheek pouches are stretched daily with a smooth cylinder, such as an empty plastic syringe case.
Grafting around the nose is particularly challenging. There is little soft tissue covering the alar cartilage, which may have a skeletonized appearance after debridement. Carefully crafted grafts usually heal, but flattening of the alar margins often results from scar contraction (Fig. 5)42.
Cellulitis is a common complication of even superficial burns despite topical antibacterial use. It manifests as increased local pain, swelling and a spreading area of redness from the edges of the wound. Treatment of cellulitis consists of rest, elevation of the affected part, and either oral or parenteral cephalosporin antibiotics. Prophylactic penicillin fails to reduce the rate of cellulitis.44
Surgical complications include harvesting skin grafts of the wrong shape or thickness. The depth of hair follicles in the scalp varies from person to person. Even in a single individual, follicle depth varies across the scalp surface. Grafts taken too thick result in transference of hair to the graft site and, in some cases, donor site alopecia. Very thick grafts (more than 0.018 inch) have excellent color and durability, but secondary infection of the donor site can produce hypertrophic scars or scalp alopecia.
Excessive bleeding often requires transfusion, although a postoperative hematocrit of 25 percent to 28 percent is acceptable in otherwise healthy adults. Skin grafts are secured when the wound bed is completely dry. The sheet grafts must be rolled frequently in the postgraft period to express any accumulated blood or serum and thereby prevent graft loss.
Outcomes of thermal injuries
Immediately after a second-degree burn heals, the skin shows pink discoloration. The pink color represents increased blood flow beneath the skin, which remains hyperemic for weeks to months. The color becomes purple with exposure to cold temperatures, dependent positioning or constrictive clothing, and bright red with any vasodilation, triggered by a rise in ambient temperature, exercise, alcohol consumption and so on.
Vasodilation is often accompanied by an acute increase in skin dysesthesias, such as itching, pain and "pins-and-needles" sensations. The most prominent is itching, which is also triggered by exposure to dust or volatile chemicals. Uncontrolled scratching leads to blistering of the fragile epidermis and open wounds. Even minor shear forces such as rubbing or scratching can cause blistering of the new epidermis, which is loosely attached to the underlying dermis. With time, the basement membrane matures, and this propensity for blistering disappears.
Antihistamines such as diphenhydramine hydrochloride are routinely administered. Other agents, such as oral hydroxyzine (Vistaril, Atarax), cyproheptadine (Periactin), and doxepin, are useful in selected patients who have intractable itching.19 Lotions containing 5 percent to 10 pecent urea can provide additional relief. Topical doxepin, although rather expensive, is a novel agent for itching as well.
This skin hyperemia persists while the skin undergoes a secondary maturation phase. During this time, the skin is hypersensitive to a variety of normal stimuli. Exposure to heat or cold causes aching pains or other unpleasant sensations. These symptoms, described as heat or cold intolerance, improve after the pink color fades. Treatment is limited to avoidance of temperature extremes.
Sunlight also causes problems with newly healed burns or grafted areas. Exposure to even brief amounts of sunlight causes hyperpigmentation of the hyperemic skin.16 This effect is incompletely prevented by even the most effective sunblock creams. In dark-skinned burn patients, melanin-containing cells located at the basement membrane level that were lost when the skin blisters return at a variable rate, migrating under the new epidermal cells from the wound edges or from deep dermal appendages. Therefore, we recommend no exposure of the pink skin to sunlight until the hyperemia is resolved. Opaque clothing or opaque sunblock agents such as zinc oxide ointment are most effective in preventing hyperpigmentation when sun exposure cannot be avoided.
In areas where dermis was lost, the skin is thinner than normal and never regains normal durability or texture. Areas receiving thick split-thickness skin grafts are most durable, but even the donor sites can develop hypertrophic scarring and ultimately lack durability. Initially, the skin thickness may appear quite normal, but hypertrophic burn scars develop three to six weeks after healing, manifested as increased redness and palpable thickening of the skin. Untreated, this thickened scar tissue grows, frequently causing severe contractures around the neck, mouth, nose, ears and eyes.
Compression of tissue after thermal burn sufficient to cause visible blanching reduces hypertrophic scar formation and itching and protects the skin from heat, cold, sunlight and mechanical abrasion.35 This compression can be achieved with garments, splints, orthoses and even casts.
Optimally, the pressure is maintained around the clock. On a practical basis, the garments are usually removed daily so the patient can bathe and apply lubricating lotions.
Some areas are not amenable to compression with elastic garments. Exceptionally flexible areas such as the neck need special treatment. A rigid transparent plastic orthosis can be fashioned for neck and face burns. The plastic orthoses obtain better and more consistent compression than alternative methods.20 Similarly, natural depressions of the body surface, such as the axillary folds and the adult female sternum, rarely are adequately compressed with garments. Flexible molded silicone inserts beneath custom elastic garments may produce improved results.
Intradermal injection of corticosteroids such as triamcinolone can further hasten softening of rigid scar tissue.9 This therapy is seldom effective unless combined with tissue compression.
The impact of a severe facial burn, especially with noticeable scarring, is hard to overestimate.45 The majority of patients report anxiety, depression and withdrawal that may be life-long. Patients with severe facial burns are rarely noticed in public, because many avoid all outside contact except with family members. Even the arts and literature portray persons with facial burns as emotionally scarred or sinister (c.f. Phantom of the Opera, Nightmare on Elm Street, Darkman, Man Without a Face). Few of us can comprehend the difficulty of reintegrating into society with cosmetically unacceptable facial scars.
Every effort is made to reduce the impact of the burn on the patient. Early education of family members, friends and schoolmates is especially helpful. Some behaviors can reduce the severity of the permanent cosmetic change, such as avoiding sunlight, which causes severe hyperpigmentation, and wearing compression garments or orthoses to minimize hypertrophic scars. When such devices are no longer needed, further corrective surgery can occasionally improve the appearance, although surgery is often not indicated. Trained personnel can instruct patients in the judicious use of camouflage makeup to dramatically improve their appearance.
The evaluation and treatment of head and neck burns remains a challenge to the burn surgeon, because of the long-term emotional and psychologic effects of even the most minor change in facial appearance. Fortunately, the results currently achieved are orders of magnitude better than previously available, but they still remain far below the perfect outcome desired by both the physician and the burn victim.
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