Another characteristic of the osteoporosis of burns that seems to set it apart is its persistence, not just until restoration of the anabolic state, but for months and years after the burn has healed (Fig. 48.2). This phenomenon may be most clearly observed in patients who have survived 90% burns, but Klein records less than normal bone among even moderately burned children as long as 17 months after injury.² Muscle atrophy and/or the failure or inability of the person to return to the preburn level of physical activity may account in part for this protracted state of reduced bone mineralization.

Figure 48.2 (a) Advanced osteoporosis in the hands of a 14-year-old male 9 months after 100% TBSA burn. All growth plates are open. (b) At 24 months after injury, osteoporosis persists and there is irregular closure of metacarpal and phalangeal growth plates. (c) At 8 months after injury, growth plates of distal tibiae and fibulae remain open. (d) At 24 months after injury, distal growth plates of tibiae and fibulae are closed. Other major growth plates remain open. Osteoporosis is unchanged.

There is no way to prevent osteoporosis in a patient whose burn is of such severity as to require an extended period of bed confinement. On the other hand, the advance of bone atrophy can at least be favorably modified even among patients with large burns if mobilization and active exercise are initiated soon after the burn. The bones of the axial skeleton, the pelvis, and the lower extremities are most efficiently stressed by weight bearing. Thus, standing is a priority measure, and it is common practice now to walk patients to tolerance prior to permanent wound cover. Muscle contraction alone may help forestall bone atrophy and bone is better stressed if the contraction is resisted. Incrementally increasing resistance during motion or at the termination of an arc of motion or to muscle contraction in an extremity that may not be moved can be supplied by anyone who attends a responsive patient. Isometric muscle contraction can be exacted from even extensively burned patients and is important for bone stress, for maintaining muscle tone and bulk, and for the patient’s continuing ready identification of the affected extremity. Passive motion has no effect on bone and thus does not figure in the prevention of osteoporosis. Other preventive measures, e.g. closure of the wound and maintenance of nutrition, are routine in critical burn care. Treatment of established osteoporosis involves the more aggressive employment of measures for prevention. There are no long-term comparative studies, however, that persuasively measure the effectiveness of exercise, diet, medication, or modality in the treatment of osteoporosis in any state.

Osteomyelitis

In burns, bones can become infected by exposure of bone by the burn; by an open fracture accompanying the burn; by extension of infection from a septic joint; by introduction of organisms along traction pins or internal fracture fixation devices; or by blood-borne organisms of bacteremia. Considering the apparent great liability for seriously burned patients to develop osteomyelitis, it is surprising that it does not regularly occur. As it turns out, clinically significant osteomyelitis in burned patients is rare. Antibiotics given for the general state may prevent seeding of the bone or may repress any small focus of bone infection.

The cortex of long bones is a good barrier to surface organisms. Even exposure of cortex will have little adverse effect if the blood supply of the bone remains intact. Prolonged exposure will kill the outer layer of the cortex, which will in time sequestrate, separating at a well-defined fissure between dead and living bone. With minor or moderate exposure, the bone will usually survive long enough for bordering granulation tissue to cover it. For large defects, it may be useful to drill closely spaced holes through the exposed cortex so as to encourage buds of granulation tissue to emerge from the still vascular medullary canal. Another way to encourage granulation tissue formation over exposed bone is with superficial decortication with an osteotome or burr to expose the capillaries of the inner cortex. With these practices, there is little risk for infecting the bone. It may be that there is sufficient centripetal pressure to discourage the invasion of organisms when the holes are fresh and that the holes are rapidly sealed by blood clot and advancing tissue. There are no reports of deep bone infection related to cortex drilling.

With open fractures at the base of a major soft tissue burn wound, bone infection is probably inevitable. Even so, the infection tends to remain at the fracture site and not to involve the rest of the bone, so that local debridement and stabilization of the soft tissue wound are all that are required for treatment. Dowling reported osteomyelitis of the tibia related to an open bimalleolar fracture in an extensively burned extremity.⁸ On the other hand, osteomyelitis developed in neither of the two open fractures reported separately by Choctaw⁹ and Wang.¹⁰ We treated three patients in whom open fractures of the femur complicated thigh burns. Each case required aggressive and repeated debridement. One fracture was treated in traction, while the other two were treated with external fixators. In one of the patients, who was admitted 8 months after acute burn, there was established osteomyelitis of the femur in relation to the exposed fracture. Osteomyelitis did not develop in either of the other patients; in the end, all three had sound femurs.

When traction pins are directed through burned skin for the treatment of fractures or for suspension of a burned extremity, the factors favoring development of infection along the pin track and the formation of cigarette sequestra are:

• the introduction or migration of organisms from the burn wound;

• linear pressure of the traction pin;

• prolonged traction;

• excessive movement of the extremity leading to loosening of the pin;

• sealing of the pin sites.

For traction or suspension, pins may be inserted through acutely burned skin, through eschar, through granulation tissue, or later through ischemic burn scar, which may be colonized with uncommon and antibiotic-resistant organisms. No amount of local cleaning is likely to sterilize the surface through which the pin must pass, yet it seems that organisms in sufficient numbers to colonize are rarely introduced in this manner.

Local low-grade infections usually resolve when pins are removed if the pin sites are vigorously curetted of granulation tissue. In one case in which a four-pin custom external fixator was used in the treatment of an open infection of the elbow, there resulted diffuse osteomyelitis of the humerus and radius. The infection was controlled with antibiotics and without surgery after the pins were removed. This case was included in Barret’s report of skeletal pinning in 41 severely burned children.¹¹ In experience with the Ilizarov system for correction of skeletal deformity in burns, one patient developed a pin track infection of such severity as to require removal of the pin, curettage, and intravenous antibiotics for control of methicillin-resistant Staphylococcus.¹²

Hematogenous osteomyelitis and that due to spread from an infected joint are rare. There is no report of the occurrence of either entity in association with burns. Were bone infection of this sort to be recognized, effective treatment would depend upon the identification of the offending organisms for organism-specific antibiotic regimens.

Pathological fractures were at one time common in burn management because of the practice of delayed excision of eschar and of keeping patients in bed until wounds were completely covered. During that time, fractures occurred because of bone collapse when patients first stood or walked or when stiff joints were manipulated (Fig. 48.3).¹³ The bones most commonly affected were the femur at its distal metaphysis and the tibia at its proximal one. The only treatment required was support of the extremity until the fracture consolidated, usually in 4–6 weeks. Children were more often affected than adults and the fractures usually compressed one cortex, producing an angular deformity that rapidly corrected with growth. Klein’s study² strongly suggests that fractures occur more frequently in burned children than in a matched normal population even months after the acute burn. Now, however, in acute burn management the most frequently seen fractures are those occurring at the time of, or in association with, the burn injury. Falls or violent trauma account for many of the fractures, and the sites are those common to the causes, bearing no relation to the burn itself.

Figure 48.3 Pathological fracture of the osteoporotic femur of a 9-year-old girl sustained on the first day she stood after 5 weeks of confinement for 40% TBSA burn.

Although fractures complicate burn treatment and occasionally delay mobilization of patients, their management need not be complex. Fractures in extremities not burned can be treated by manipulative reduction and cast immobilization, by open reduction and fixation, with an external fixator, or with skeletal traction (Fig. 48.4). Fractures in extremities with first-degree or superficial second-degree burns can be managed in the same way. Deep second-degree and third-degree burns present a different problem only with respect to the early bacterial colonization of third-degree burns and the degradation of deep second-degree burns to full-thickness burns that will, in turn, become colonized. There is a precious window of time when fractures requiring open reduction and internal fixation can be definitively treated without increased risk for infecting the bone; however, fracture reduction and stabilization are so important in the functional management of a severely burned patient that the risk for bone infection should be acknowledged and shouldered at any post-burn stage. Skeletal traction can often be the management choice, particularly in children and adolescents, even if the treatment protocol requires that the patient be moved from bed for tubbing, dressing change, or additional surgery. The disadvantages of skeletal traction are the confinement to bed and the imposed relatively fixed position of the affected extremity. External fixators have made it possible to align and stabilize fractures in burned extremities without open operation. There is the added functional advantage of patient mobility. Brooker’s extensive favorable experience supports this concept.¹⁴ With both skeletal traction and external fixation, there is an added risk for bone infection because of the path from surface to bone provided by the pins. This is a risk worth taking, and it is minimized by scrupulous pin site care and by removal and replacement of any loosening pin. Frye and Luterman recognized and discussed the specific and continuous difficulties encountered in the management of fractures and burns.¹⁵

Figure 48.4 (a) This 15-year-old male sustained closed fractures of the right femur, left tibia and left humerus at the time of a 46% TBSA burn involving mainly trunk and right lower extremity. The femur and humerus fractures were treated in skeletal traction. Suspension of the right lower extremity aided management of circumferential deep burns of that extremity. Lesser burns of the left leg made it possible to treat the minimally displaced fracture of the left tibia in a circular cast. All fractures consolidated in 6 weeks in satisfactory alignment. (b) Fracture of the left humerus as it appeared at the time of admission to the hospital. (c) At 5 weeks after injury, the fracture shows maturing callus. Traction was discontinued at 6 weeks.

When casts are used for stabilization of fractures in burned extremities, the wound is made inaccessible and there is an abiding fear that the unattended wound will seriously degrade or at best not improve. Such fear may be well founded; however, Wang ¹⁰ showed that a bivalved circular cast could be used effectively for an open comminuted fracture of a proximal tibia with overlying deep burns, and Choctaw⁹ reported successful use of a cast for immobilization of an open comminuted fracture after immediate post-burn grafting of the affected extremity. Common sense should dictate which fractures can be treated with circular or bivalved casts or with splints. If a reduced or moderately displaced but aligned fracture is so stable as to require external support only for maintenance of alignment, then cast or splint immobilization should be all that is needed. On the other hand, if a fracture because of instability, requires maintenance of reduction by three-point pressure or molding of the cast material, it will be better treated by other means.

Dowling ⁸ reported osteomyelitis resulting from open bimalleolar fracture in an extremity with extensive deep burns. In neither of the cases reported by Wang and Choctaw did the bone become infected. There were also no infections among Saffle’s 42 fractures, nine of which were treated by open reduction and internal fixation.¹⁶ With two fractures of the femur, each of which was exposed at the base of a deep chronic burn, aggressive debridement of the wounds and the fracture ends was followed by treatment with skeletal traction in one and by external fixation with the Ilizarov system in the other. Both fractures healed without further complication.

Fractures in burned patients heal quickly. There is no recorded experience that suggests that healing is delayed by the burn. Neither is there any record of failure of union. Callus formation may be abundant.

Among severely burned patients, non-displaced or minimally displaced fractures may not be detected until unusual local pain in an affected extremity prompts radiographic examination. A radiograph obtained for other reasons may reveal a fracture as an incidental finding. These fractures are usually of no functional significance. Modest angular deformity near a joint may be a problem in adults, although not in children. On the other hand, undetected transphyseal fractures in children can be a major functional threat.

Changes involving pericapsular structures

Heterotopic bone

Heterotopic bone formation is a rare but functionally important complication of thermal burns. The incidence in a general burn population is reported to be somewhere between 1% and 3%.^1,¹⁷^–²² In select populations, the incidence may be higher, as it will be if patients with periarticular calcification are included in the statistics. For example, Tepperman et al. reported a 35.3% incidence among patients referred to a tertiary care center for rehabilitation.²³ Jackson made the observation that the incidence of heterotopic bone could be expected to be less in institutions that admit patients with minor burns.²⁴ Munster’s²⁵ radiographic survey of 88 adult and teenaged patients with 160 burned upper extremities yielded a 16% incidence of pericapsular calcification; the 23% incidence reported by Schiele et al.¹ included both heterotopic ossification and calcification. In the early routine radiographic study reported by Evans,¹³ periarticular calcification that did not progress to heterotopic bone was excluded from the final calculation of an incidence of 2%. The 3.3% incidence recorded by Kolar and Vrabec²⁶ included patients with pericapsular calcification. Even if heterotopic bone occurs infrequently in thermal burns, it remains that once it develops it often compromises joint motion and is difficult to treat. In addition, its pathogenesis is still incompletely understood; thus, protocols for prevention may in fact miss the mark.

Pathogenesis

The metabolic changes occurring after thermal burn are increased metabolic rate; protein catabolism; ureagenesis; fat mobilization; glycogenolysis; gluconeogenesis; elevated glucose flow; and eventual total body weight loss.^27,²⁸ There is an accompanying suppression of the immune system that favors wound infection, but at the same time favors survival of skin allografts. Infection, failure of skin graft take, or anything that delays closure of a burn wound will extend the altered metabolic state. Although it might be assumed that there occurs, along with the metabolic upheaval, an adverse change in connective tissue milieu, the exact nature of such a change is not known. It is also not known what the metabolic changes have to do with the development of heterotopic bone, but it is apparent that the burn disease is necessary to its formation. Other factors to be considered in the genesis of heterotopic bone are percentage of burn, location of burn, period of confinement, osteoporosis, superimposed trauma, and genetic predisposition.

Percentage of burn

Most reported cases of heterotopic bone have had a 20% or greater total body surface area burn; however, heterotopic bone has been found in patients with as little as 10% third-degree burn.¹³ Peterson et al.,²⁰ Munster et al.,²⁵ and Elledge et al.¹⁹ have reported affected patients with total body surface area burns of 8%, 14%, and 12%, respectively. In addition, with the now-extensive experience with salvage of patients with 80% or greater burns, it is clear that heterotopic bone occurs no more frequently among these patients than in the general burn population. Thus, the percentage of burn is not a determining factor.

Location of burn

By no means has all of the reported heterotopic bone occurred in joints with overlying burn. In their initial report, Evans and Smith described heterotopic bone occurring a distance from any third-degree burn involvement.²⁹ Johnston noted that in one of his three patients, the skin overlying one affected joint was not even superficially burned.³⁰ If degradation of connective tissue milieu in burns is a total body phenomenon, it follows that heterotopic bone formation need not be burn site dependent. Thus, the location of the burn cannot alone be a determining factor.

Period of confinement

Evans and Smith expressed belief that length of bed confinement was an important factor in the development of heterotopic bone.²⁹ At the time of that report, patients with even moderate burns might be kept in bed for several weeks. The consequences of prolonged confinement were loss of active range of joint motion and bone demineralization; it was thought that each of these adverse changes might contribute to the formation of heterotopic bone. Thus, any maloccurrence that necessitated longer confinement could be a factor in the pathogenesis. Kolar implicated wound sepsis as an independent factor, along with the length of confinement.²⁶ Other investigators have not addressed the period of confinement as specifically as Kolar, and there have been no comparative studies of groups of confined and non-confined patients. Thus, it may never be determined whether the current aggressive practice of early mobilization of patients will have an effect on the incidence of heterotopic bone.

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Musculoskeletal changes secondary to thermal burns

Information

Alterations limited to bone

Alterations involving pericapsular structures

Alterations involving the joint proper

Alterations involving muscles and tendons

Alterations secondary to soft tissue

Soft tissue injury

Abnormalities of growth

Changes confined to bone

Osteoporosis

Osteomyelitis

Fractures