Epidemiology of Burn Injury

The American Burn Association (ABA) has led an effort to catalogue burn injuries through a burn registry project. Between 1995 and 2005, burn centers in the United States and Canada contributed information to the National Burn Repository (NBR). From approximately 126,000 records, several conclusions could be drawn about burn injury in North America. Specifically, most burn patients are male (70%) with a mean age of 33 years. Most burn injuries covered less than 10% of the total body surface area (TBSA). The most common etiologies of burn injuries were flames and scalds. Approximately 95% of patients survived their hospitalization.¹¹⁵ Burn centers, however, also reported admitting patients with unusual burn etiologies such as radiation. Skin diseases make up a small number of admissions to burn centers, and the complexity of diseases such as Stevens-Johnson syndrome and necrotizing fasciitis add to the complexity of care in the burn unit.^43,115

Several negative predictors have been noted for survival after burn injury. Increasing age, burn injury over a higher TBSA, and the presence of inhalation injury are all significantly associated with increased mortality.^115,170

Increasing TBSA is associated with higher mortality rates, especially in patients older than 60 years of age and even more so in patients older than 70.¹¹⁵ In elderly patients the presence of medical comorbidities, inhalation injury, and burn size best predict mortality within 1 year of burn injury (Figures 58-1 and 58-2).¹⁰⁸

FIGURE 58-1 Effect of age on percent mortality at three discrete burn sizes.

(From Pruitt BA Jr, Goodwin CW, Mason AD: Epidemiological, demographic, and outcome characteristics of burn injury. In Herndon DN, editor: Total burn care, ed 2, New York, 2002, Saunders, with permission.)

FIGURE 58-2 Changes in the LD₅₀ in patients 21 years of age over time, illustrating the increased survival of individuals with large burns.

(From Pruitt BA Jr, Goodwin CW, Mason AD: Epidemiological, demographic, and outcome characteristics of burn injury. In Herndon DN, editor: Total burn care, ed 2, New York, 2002, Saunders, with permission.)

With the large majority of burn patients surviving their hospital stay, however, a shift away from mortality as a primary outcome measure toward measurements of quality of life and function has been advocated by burn practitioners.¹³⁴ The National Institute on Disability and Rehabilitation Research (NIDRR) has funded the Burn Model Systems project⁹² to further research the long-term outcomes of burn survivors.

Timing of Physiatric Assessment of the Patient With a Burn

A continuum of care model has been established by the North Texas Burn Rehabilitation Model System to emphasize early and regular assessment by a physiatrist and the rehabilitation team. In this model, an attending physiatrist reviews each patient admitted to the burn center. The physiatrist also participates in weekly team rounds and burn interdisciplinary team meetings. The physiatrist provides burn consultation both at the tertiary burn center and in a burn rehabilitation clinic in a rural setting. Although this model is not typical around the country, it might be useful to use it as a model of how the physiatrist can better integrate with the burn team. Most physiatrists in the United States currently see burn patients only if they are transferred to an inpatient rehab unit.

Acute Physiatric Assessment of the Burn Patient

The size and location of the burn injury are important for several reasons. Larger burn injuries are associated with higher mortality and also are more likely to be associated with significant complications.^13,78,106 Relative proportions of the TBSA made up by the head and limbs can be different by age. Estimations of the TBSA burned can be calculated using a tool such as the Lund and Browder chart (Figure 58-3). Other estimators of burn size can be made by following the “rule of nines” or estimating that the palm of the patient’s hand is approximately 1% of the TBSA.⁷⁴

FIGURE 58-3 The Lund and Browder method for calculation of burn size is reliable for different body proportions in children.

(From Artz CP, Moncrief JA, Pruitt BA: Burns: a team approach, Philadelphia, 1979, Saunders, with permission.)

The initial depth of burn injury is estimated by examination. Burns can be divided into superficial, partial-thickness, and full-thickness injuries. Superficial wounds are typically red and painful and have little or no exudate. This depth of burn injures the epidermis only, and healing typically occurs within 7 days. They do not require dressings or surgical interventions, and the risk of scarring is very low. A typical example of a superficial burn is sunburn.

Partial-thickness burn injuries are divided into superficial partial thickness and deep partial thickness. Superficial partial-thickness burns have mild to moderate wound exudate. This depth of burn injures the superficial layers of the dermis. Loose or tense blisters can be filled with serous fluid. These wounds are painful but typically heal within 7 to 14 days. The risk of scarring from this injury is low, but there might be pigmentation changes in the skin in the long term.

Deep partial-thickness burn injuries have fewer blisters than superficial partial-thickness injuries. These wounds have moderate to extensive exudates. This depth of burn injures the deeper layers of the dermis. These wounds are painful but might heal within 14 to 21 days. Some deep partial-thickness injuries, however, do not heal in this time frame. The prolonged inflammatory wound healing seen in deep partial-thickness burn injuries significantly increases the risk of scarring.

Full-thickness burn injuries damage the epidermis and all of the dermis, and can extend into deeper structures. The area of the burned skin might not be directly painful to palpation or pin prick, but there can be pain from underlying necrotic tissue, surrounding burns, or damage to nearby structures. These wounds typically appear pale with minimal exudate. Significant scarring is almost certain from full-thickness burn injuries.

A summary of burn depth and skin sections is shown in Figures 58-4 and 58-5.

FIGURE 58-4 A superficial (first-degree) burn involves only the epidermis. A partial-thickness burn (second degree) involves the superficial or deep dermis, and a full-thickness burn (third degree) extends to subdermal tissues.

(From Achauer BM, Eriksson E: Plastic surgery indications, operations and outcomes, St Louis, 2000, Mosby, with permission.)

FIGURE 58-5 Cross-section of normal skin, illustrating the epidermis, the dermis, and the epidermal appendages (hair follicles, sweat, and sebaceous glands).

(From Achauer BM, Eriksson E: Plastic surgery indications, operations and outcomes, St Louis, 2000, Mosby, with permission.)

Acute Surgical Procedures in Burn Injuries

In full-thickness burn injuries, the damaged tissues are adherent to underlying structures. With the development of wound edema, combined with the fluids required for resuscitation after burn injury, there is a risk for development of compartment syndromes in the limbs. Thick eschar in the trunk region can inhibit respiration. The surgical team can perform escharotomy, which is a surgical incision through the eschar, to relieve this pressure. The pattern of the incision can be important in avoiding future contractures from the resulting scar. Escharotomies in the limbs and trunk typically are left open in the acute phase.⁷⁴ Limbs requiring escharotomies should be elevated and splinted in a neutral position for 24 hours before initiating passive range of motion.

Early excision and autologous skin grafting has greatly improved survival after burn injury. This reduces the inflammatory stimulation from the burn eschar and reduces the risk of infection. The entire devitalized tissue is removed by the surgical team with tangential excision, followed by split-thickness autologous skin grafting. Donor skin is removed from an unburned area of skin through the use of a powered dermatome (Figure 58-6). The donor skin is then prepared and placed on the surgically prepared wound bed. The donor skin is held in place by staples, sutures, or, in some cases, dermal glues.¹²⁶ A compressive postoperative dressing is then applied to the skin graft area, and an appropriate dressing is applied to the skin graft donor site. Because the donor skin is typically partial thickness, the donor site heals spontaneously, usually over 2 weeks. Although hypertrophic scarring is not usually seen in the donor site, hyperpigmentation and hypertrophic scarring might be seen.

FIGURE 58-6 Donor skin is removed from an unburned area of skin through the use of a powered dermatome.

The donor skin can be prepared by meshing to broaden the area of wound covered. Meshing also allows for any blood or wound exudates to escape from underneath the skin graft. The donor skin can be applied as a sheet over areas of special function such as the hands and face. Sheet grafts generally do not scar as much as meshed grafts and can result in improved function.⁸⁹ Because there is no route of escape from beneath the unmeshed sheet graft, however, seromas or hematomas can form and even cause loss of the skin graft.

To improve adherence of the skin graft to the donor site, the grafted site is typically immobilized in the immediate postoperative phase. The immobilization phase time is now shorter than in the past because early initiation of therapies and mobilization improve patient function and reduce length of hospital stay.²⁴

Presence of Inhalation Injury

Inhalation injury associated with burns is a significant risk factor for morbidity, especially in children and older adults.^{68,108,129,170} Little has been documented regarding the incidence of hypoxic brain injury in burn patients with inhalation injury, but the reduction of available oxygen, combined with toxic smoke components such as carbon monoxide and cyanide, puts the burn patient with inhalation injury at risk for brain injury.⁴ Burn patients with inhalation injuries are at risk for developing pneumonia, adult respiratory distress syndrome, and multisystem organ failure during the acute periods of recovery.⁷⁵ Early tracheostomy in patients likely to require prolonged intubation has not been shown to change pulmonary outcomes, but it does offer advantages for oral hygiene and preventing of microstomia.¹³⁹ It is not known whether inhalation injury predisposes burn patients to pneumonia in the rehabilitation setting, and as a result, routine oxygen monitoring during therapies varies among practitioners.

Polytrauma and Burns

Approximately 5% of all trauma patients will also have some degree of burn injury.¹⁴⁷ Fractures outside of the burned area can be treated with standard fracture care. An individualized approach is adopted, however, when the fractures occur in regions that also have burn injury.⁹¹ Patients with a history of major trauma can have delayed diagnoses, including fractures or other neurologic and musculoskeletal injuries, which the physiatrist should consider during the assessment of the burn patient.^22,42

Peripheral Neuropathies

Approximately 10% of burn patients will develop peripheral neuropathies from a variety of etiologies, such as direct thermal injury, electrical current, compression, and metabolic derangements.⁹⁷ The patients most likely to develop neuropathies with electrical injuries include those with a history of alcohol abuse and long stays in the intensive care unit.⁹⁷ Several patterns of neuropathy are seen, including mononeuropathies, peripheral polyneuropathies, and patterns that resemble mononeuritis multiplex.^97,106 Deeper and larger TBSA burns are more associated with axonal rather than demyelinating neuropathies.¹⁰⁶

The physiatrist performing electrodiagnostic testing on burn patients should be mindful that the changes after burn injury can alter the results of both nerve conduction testing and electromyography. The increased skin thickness seen with hypertrophic burn scars can have an inverse relationship with the amplitude of the responses seen in nerve conduction testing.⁷⁰ After large burn injuries there can be up-regulation of nicotinic acetylcholine receptors in the muscle cell membrane that results in electrodiagnostic features suggestive of membrane instability or acute denervation.^79,111 As a result, electromyographic studies must be interpreted with caution in the burn patient because these neuromuscular changes can be indistinguishable from true neuropathic changes.

Median sensory neuropathies are the most common peripheral nerve abnormality after burn injury. Conservative electrodiagnostic studies can help to define the extent of nerve injuries in burn patients. Over the course of approximately 1 year, repeated nerve conduction tests typically show improvement in burn-related neuropathy without requiring intervening surgical treatments.⁶¹

Catabolism and Metabolic Abnormalities

In all patients with burn injuries greater than 30% TBSA, the physiatrist should anticipate a significant metabolic abnormality that results in loss of bone mineral density and lean body mass and increased insulin resistance.^73,82,84 These metabolic abnormalities mean that patients with large burn injuries have increased caloric and nutritional needs that should be addressed with early enteral feeding.²⁶ Progressive loss of lean body mass is associated with increasing loss of function and an increased incidence of medical complications, such as pneumonia and poor wound healing.³⁷

The management of the hypermetabolic state in large burn patients has been improved with the use of anabolic agents, β-blockers, and exercise. Oxandrolone is a synthetic testosterone analogue that has been shown to reduce mortality and length of hospital stay.^135,184 Lean body mass and bone mineral density might be improved by maintaining patients on oxandrolone beyond their hospital discharge because the hypermetabolic state can persist beyond the time of wound closure. The typical dosage of oxandrolone for burn patients is 10 mg twice a day.^114,117 Although human growth hormone (HGH) has shown some promise as an additional anabolic agent in burn injury, reports of increased mortality with the use of HGH in critically ill adults have limited research into the use of HGH.^83,165

The stress response after burn injury is thought to be mediated by circulating catecholamines. An association of increased cortisol and catecholamine levels with infections and poor wound healing has been demonstrated in children.¹²³ β-Blockade is helpful in managing the increased catecholamines and the stress response to burn injury. The administration of propranolol in doses high enough to reduce resting heart rate by 20% has been shown in children to reduce the metabolic rate and help preserve protein and lean body mass.⁷² β-Blockade might also have benefits for improving wound healing and preventing posttraumatic stress disorder (PTDS) in both adults and children.^157,162

Dysfunction in insulin action is also observed as part of the metabolic response to large burn injury. The mechanism for this is not entirely clear, but it can be related to insulin antagonists emanating from inflammatory cells in the burn region.⁴⁰ Patients with burn injuries greater than 40% TBSA should have close monitoring of blood glucose, with a goal of euglycemia in the acute phase. They might also need glucose monitoring for months to years after injury.⁶² Besides maintaining appropriate blood glucose levels, insulin has an added benefit to improving the metabolic state of the burn patient to help with minimizing lean body mass losses.⁸¹

Mobilization and exercise should be initiated early in the burn patient. An increase over time has occurred in the frequency of active and passive therapeutic interventions by the rehabilitation team in caring for acute care of burn patients.¹⁸⁰ In the acute stages after a large burn, passive therapies, including splinting and positioning, should be initiated to minimize the risk of burn scar contracture, improve respiration, and reduce the risk of ventilator-associated pneumonias.^5,66 As soon as the patient is able, however, active exercise should be started to help maintain function and to address the hypermetabolic state. Exercise is also an essential component for maximizing the benefits of anabolic hormones.¹⁶³

Nutrition and Swallowing in Burns

Enteral feeding should be instituted early for patients unable to feed normally. This helps maintain gut immunity and motility, while providing the necessary calories and nutrients to counter the hypermetabolic response to burn injury.^99,105 The total caloric requirements for adults with burn injuries can be estimated. Daily caloric requirements for an adult patient can be close to 25 kcal/kg plus 40 kcal/1% TBSA burn/day.³³

In addition to the changes in lipid and carbohydrate metabolism seen in patients with a large burn injury, important changes in protein and amino acid metabolism are also of special importance. The administration of glutamine appears to have benefits in patients with large burn injuries and is the subject of ongoing research.¹³³ Using body weight measurement to assess nutritional status can be difficult because of surgical procedures, dressings, and fluid changes. The serum prealbumin level can be very helpful as a marker of protein synthesis.²⁶

Dysphagia can be a barrier to achieving adequate nutrition (see also Chapter 27). Dysphagia can develop from inhaled irritants, mechanical complications of tube placement, or neurologic injury. Larger TBSA burns, higher number of days with a tracheostomy, and higher number of days on a ventilator are all correlated with dysphagia after burn injury.³⁹ An abnormal bedside swallowing assessment is predictive of abnormal barium swallowing studies, but there is still uncertainty regarding the best protocols for assessing swallowing in burn patients.⁴¹ Although some very complex cases might have prolonged dysphagia, studies have described between 42% and 90% of patients having normal swallowing function by the time of hospital discharge.^148,177

Heterotopic Ossification

In patients with burn injuries greater than 30% TBSA, there is a risk of development of heterotopic ossification. The most common site of heterotopic ossification in burn patients is the posterior elbow (Figure 58-7). Heterotopic ossification can develop in an unburned limb but is more common in an affected limb and can be associated with delayed wound closure over the elbow.⁹³

FIGURE 58-7 Heterotopic ossification of the posterior elbow.

The best treatment and prevention for heterotopic ossification in burns is still controversial. This is particularly the case regarding the use of bisphosphonates, with some evidence suggesting etidronate is not helpful.^78,154 It is possible that etidronate is ineffective because of the significant postinjury inflammatory state seen in burn injury, and higher potency bisphosphonates might be more effective.¹⁴⁹ Some practitioners might be concerned regarding the potential development of osteonecrosis of the jaw with bisphosphonate administration, but this complication has been described primarily in patients receiving zoledronate or pamidronate in the setting of cancer treatment. No osteonecrosis was reported in osteoporosis trials using risedronate or alendronate.¹⁴³ Therapies should be maintained in limbs affected by heterotopic ossification, and surgical resection should be performed when the bone is mature. Heterotopic ossification can restrict the performance of activities of daily living (see Chapter 26) or result in neurovascular compromise.⁷⁸

Recurrence is common even after resection and the use of postoperative continuous passive motion. The timing of surgical resection is made based on the severity of functional deficit.⁷⁸ Surgical resection, however, might have to be delayed in burns compared with other diagnoses to allow for adequate soft tissue coverage in the proposed surgical site.

Dressing Choices and Hydrotherapy

Patients with burns often continue to have ongoing issues with wound care both in the rehabilitation and outpatient settings. Adequate management of open wounds is important for management of the hypermetabolic response to burn injury, reducing the risk of infection and minimizing the risk of hypertrophic scarring.

In superficial and partial-thickness wounds not treated with tangential excision and skin grafting, there are a large number of products available. Not many high quality studies have been performed on the various types of dressings that can be used for these wounds. There appears, however, to be a trend toward better healing with the use of hydrocolloid, biosynthetic, and antimicrobial dressings rather than with silver sulfadiazine dressings.¹⁷⁸

The use of immersion hydrotherapy in burn wound care is less commonly practiced in today’s burn centers.⁶⁷ Hydrotherapy tanks can be a source of gram-negative bacteria such as Pseudomonas.¹⁵⁵ The minimization of hydrotherapy techniques has been associated with a reduction in serious skin infections in the burn unit.¹¹² Further minimization of hydrotherapy is possible with the use of hydrocolloid and biosynthetic dressings instead of creams such as silver sulfadiazine. On the outpatient side, third-party reimbursement typically does not cover the costs for hydrotherapy. The pain associated with dressing changes can be minimized by adequate analgesia, distraction, and the use of longer-lasting dressings that reduce the frequency of changes.^85,156,185

Hypertrophic Scarring

Hypertrophic scarring is the most common complication after burn injury (prevalence of 67%).¹⁹ Hypertrophic scars and keloids are both dermatoproliferative disorders of the skin. Hypertrophic scars are described as raised, red, painful, pruritic, and contractile. Hypertrophic scars stay within the margins of the original injury.⁴⁴ Keloid scars have some of the same characteristics as hypertrophic scars, but they also extend beyond the original injury and invade into local soft tissues.¹⁵³ Hypertrophic burn scars tend to develop in the first few months of injury, while increasing in volume and erythema. After several months they can regress, becoming less erythematous and flatter, but the skin never returns to its original state.⁴⁴

Although there have been some advances in the prediction of wound healing, there is no accurate predictor of who will develop hypertrophic burn scars.¹⁴⁵ It is thought that younger patients, particularly adolescents and those with darker skin pigmentation, tend to have a higher incidence of hypertrophic scarring.⁴⁴ Wounds with a prolonged inflammatory wound healing phase and wounds that are open longer than 3 weeks are more likely to develop hypertrophic scars (Figure 58-8).¹⁰

FIGURE 58-8 Hypertrophic scarring.

One of the limitations of studying hypertrophic burn scarring is the lack of a widely accepted animal model for burn scarring.⁴⁴ Although some progress has been made in creating thick scars in an excisional porcine wound model, there are no well-validated scar models in other species.⁴⁴

Despite this, some progress has been made in the understanding of the development of hypertrophic burn scars. A key signal in scar development appears to be transforming growth factor–β(TGF-β).¹⁷⁴ TGF-β is a ubiquitous protein and part of a larger family of proteins known as bone morphogenic proteins. It exists in a latent form that can be activated through a variety of inflammatory signals. TGF-β acts through a dimerized cell membrane receptor that activates the Smad signaling proteins to increase the expression of proteins related to increased extracellular matrix production.^10,60 Beyond local inflammatory signals, there also are likely systemic effects on the development of hypertrophic burn scars from bone marrow–derived fibrocytes that become present in burn wounds and scars.¹⁷⁶ Over time, fibroblasts can develop an autocrine feedback loop between TGF-β and the Smad proteins that might perpetuate the excessive production of extracellular matrix.¹⁸⁶

The overexpression of extracellular matrix alone does not entirely account for the development of hypertrophic scar. A balance of both extracellular matrix formation and remodeling of the matrix and new skin is necessary for normal wound healing. In dermatoproliferative disorders, an imbalance in both production and breakdown is present. Important components in the balance of burn scarring are likely also derived from keratinocyte signals.⁶⁴ As an example, keratinocyte-derived stratifin has been demonstrated to activate matrix metalloproteinases, which can be an important component of extracellular matrix breakdown and reorganization.⁶³

Many treatment options are available for addressing the symptoms associated with hypertrophic burn scars, but none completely remove the scar. The best treatment is to prevent the scar through adequate wound care. When scars are present, early and aggressive treatment is indicated.

The first-line treatment for any burn scar is regular moisturizer cream, applied several (four to six) times per day, avoidance of mechanical insults, and the minimization of direct heat and sun exposure.¹⁵ Deficiencies in skin, such as sweat and sebaceous glands, can cause scars to be dry and pruritic, and a moisturizer cream is helpful in managing these problems.^15,65 Patients with burn scars should also be instructed to minimize direct sunlight and heat exposure through the use of clothing and sunscreen.¹⁸⁷

Pressure garments have been used in burn scar treatment for decades. They are thought to improve the appearance of burn scars by making the scar flatter and less erythematous and by offering some environmental protection.¹⁷¹ Some evidence exists that pressure aids in remodeling hypertrophic burn scar.³¹ The overall clinical effectiveness overall is controversial, however, and in metaanalysis of research into pressure garment use, the overall effect seems small, with minor benefits on scar height but not necessarily on secondary measures of scar.⁸ If they are used, pressure garments should be prescribed with monitoring by the rehabilitation physician or therapist for adequate fit and wear tolerance because friction in the garment can create or perpetuate superficial wounds in the burn scar.

Silicone gel sheeting can also be used alone or in combination with pressure garments. If worn for several (12 to 24) hours per day, silicone is thought to change hypertrophic burn scars through a combination of temperature and perfusion changes.¹¹⁸ Some evidence exists that silicone sheeting might be helpful in improving the volume in hypertrophic burn scars.¹¹⁶ Reviews indicate that the evidence for the use of silicone sheeting in the treatment or prevention of hypertrophic burn scars, however, is weak.¹²⁴

Intralesional corticosteroid injection can also be of some limited benefit in the treatment of hypertrophic burn scar.⁹⁴ The injections are done with an injection tangential to the skin. The injection is usually painful, and force is necessary to infiltrate the injectate into the fibrotic scar tissue. Some authors combine triamcinolone with other agents such as 5-fluorouracil or add a second modality such as pulsed dye laser treatment to potentiate the effects of the intralesional steroid.^12,34

The use of pulsed dye laser in the treatment of hypertrophic scars is also controversial. In some studies the use of laser resulted in the formation of new wounds and little clinically relevant benefit in the scar.^6,183 Other studies have shown benefit with this type of laser for the treatment of hyperpigmentation in burn scars.²¹ Pulsed dye laser appears to have some benefits compared with carbon dioxide or argon lasers, which have also been used to attempt to obliterate hypertrophic scars and keloids.¹⁸⁸ Significant scar recurrence with carbon dioxide laser has been described.⁹ The use of pulsed dye laser in burn scar treatment is not yet routine in most burn centers in North America. Some early preclinical evidence supports the effect of interferon-α as a promising treatment for hypertrophic burn scars, but larger human studies have yet to be done.^169,175

Massage is routinely applied to hypertrophic burn scars, although the evidence for its effectiveness is lacking.^30,131 Massage of hypertrophic burn scars can be applied by the therapist or patient, but the skin must be monitored for potential development of pain and superficial wounds in the scar.³⁰