Acute Thermal Burns 2015-11-15T16:00:11+00:00

The use of hyperbaric oxygen therapy in the treatment of thermal burns began in 1965 when Ikeda and Wada observed more rapid healing of second-degree burns in a group of coal miners who were being treated for carbon monoxide poisoning. They followed this serendipitous observation with a series of animal experiments that demonstrated a reduction of edema and improved healing. The Japanese experience stimulated interest in other countries, and there followed a series of reports of uncontrolled clinical experience with favorable results. In 1970 Gruber, working at a U.S. Army biophysics laboratory at the Edgewood Arsenal in Maryland, devised a series of experiments placing rats in a hyperbaric chamber breathing 100 percent oxygen at sea level and at 2 and 3 atmospheres (ATA) of oxygen, respectively. He demonstrated that the area subjacent to a third-degree burn was hypoxic when compared to normal skin and that the tissue oxygen tension could only be raised by oxygen administered at pressure. This important study suggested that HBOT could have a direct effect on the pathophysiology of the burn wound.

Subsequent studies demonstrated that hyperbaric oxygen therapy, when used as an adjunct in a comprehensive program of burn care, can significantly improve morbidity and mortality, reduce length of hospital stay, and lessen the need for surgery. It has been demonstrated to be safe in the hands of those thoroughly trained in rendering HBOT in the critical care setting and with appropriate monitoring precautions. Successful, cost-effective outcomes result from careful patient selection and screening.

Pathophysiology and Hyperbaric Effects

The burn wound is a complex and dynamic injury characterized by a central zone of coagulation surrounded by an area of stasis and bordered by an area of erythema. The zone of coagulation or complete capillary occlusion may progress by a factor of 10 during the first 48 hours after injury. Ischemic necrosis quickly follows. Hematologic changes, including platelet microthrombi and hemoconcentration, occur in the postcapillary venules. Edema forms rapidly in the area of the injury but also develops in distant, uninjured tissue. There are also changes occurring in the distal microvasculature where red cell aggregation, white cell adhesion to venular walls, and platelet thromboemboli occur. This progressive ischemic process, when set in motion, may extend damage dramatically during the early days after injury. The ongoing tissue damage seen in thermal injury arises from the failure of surrounding tissue to supply borderline cells with oxygen and nutrients necessary to sustain viability. The impediment of circulation below the injury leads to desiccation of the wound as fluid cannot be supplied via the thrombosed or obstructed capillaries. Topical agents and dressings may reduce but cannot prevent dessication of the burn wound and the inexorable progression to deeper layers.

Regeneration cannot take place until equilibrium is reached; hence, healing is retarded. Prolongation of the healing process may lead to excessive scarring. Hypertrophic scars are seen in about four percent of cases taking 10 days to heal, in 14 percent of cases taking 14 days or less, in 28 percent of cases taking 21 days, and up to 40 percent of cases taking longer than 21 days to heal. Therapy of burns, then, is directed towards minimizing edema, preserving marginally viable tissue, protecting the microvasculature, enhancing host defenses, and providing the essential substrate necessary to sustain viability.

Infection

Susceptibility to infection is greatly increased owing to the loss of the integumentary barrier to bacterial invasion, the ideal substrate present in the burn wound, and the compromised or obstructed microvasculature which prevents humoral and cellular elements from reaching the injured tissue. Additionally, the immune system is seriously affected, demonstrating decreased levels of immunoglobulins and serious perturbations of polymorphonuclear leukocyte (PMNL) function, including disorders of chemotaxis, phagocytosis, and diminished killing ability. These functions greatly increase morbidity and mortality; infection remains the leading cause of death from burns.

Experimental Evidence

A significant body of animal data support the efficacy of HBOT in the treatment of thermal injury. Ikeda noted a reduction of edema in burned rabbits. Ketchum in 1967 reported an improvement in healing time and reduced infection in an animal model. He later demonstrated dramatic improvement in the microvasculature of burned rats treated with hyperbaric oxygen therapy. Working in Germany, in 1974 Hartwig reported very similar findings and additionally noted less inflammatory response in those animals that had been treated with hyperbaric oxygen. He suggested at that time that hyperbaric oxygen might be a useful adjunct to the technique of early debridement. Wells and Hilton, in a carefully designed and controlled experiment, reported a marked increase in extravasation of fluid in a series of dogs with 40 percent flame burns.

The effect was clearly related to oxygen and not simply increased pressure. They also reported a reduction in hemoconcentration and improved cardiac output in treated dogs. Nylander, using a well-accepted animal model, showed that hyperbaric oxygen therapy reduced the generalized edema associated with burn injury.

Using an India ink technique in 1977, Korn and colleagues showed an early return of capillary patency in hyperbaric-treated animals. He also demonstrated survival of the dermal elements and more rapid epithelialization from these regenerative sites. He suggested the decreased desiccation of the wound he observed was a function of subjacent capillary integrity noted in the HBOT treated animals. Saunders and colleagues have recently done similar studies with similar results. They have also reported an improvement in collagen synthesis in HBOT treated animals. Perrins failed to show a beneficial effect in a small scald wound in a pig model treated with HBOT. In 1977, Niccole reported that HBOT offered no advantage over topical agents in controlling wound bacterial counts. He proposed that HBOT acted as a mild antiseptic. His data, however, supported the observation of improved healing of partial thickness injury noted by earlier investigators. Stewart and colleagues have shown preservation of adenosine triphosphate (ATP) in areas subjacent to partial thickness in burns in hyperbaric treated rats.

These studies may relate directly to the preservation of energy sources for the sodium pump. Failure of the sodium pump is felt to be a major factor in two processes: the ballooning of the endothelial cells that occurs after burn injury and the subsequent massive fluid losses. Both groups in Stewart’s study received identical treatment with topical antibiotic agents. In a very large 1973 controlled series, Bleser reported reduction of burn shock and a fourfold increased survival in 30 percent burned animals versus controls. Reduction of PMNL killing ability in hypoxic tissue has been well documented by Hohn, et al. Mader demonstrated the increased ability of PMNL killing in an O2 enriched animal model suggesting that this may be an additional benefit of HBOT. Thus, the overwhelming evidence in a large number of controlled animal studies suggests that hyperbaric oxygen produces numerous beneficial effects. These include reducing edema, preventing conversion of partial to full thickness injury, preserving the microcirculation, preserving adenosine triphosphate (ATP) (and perhaps secondarily the sodium pump), and improving survival. HBOT may eventually be proven to also enhance PMNL killing.

Human Experience

Beginning with the reports of Wada in 1965 and continuing with Ikeda, Lamy, and Tabor, reports of clinical series began to accumulate. In 1974 Hart reported a controlled, randomized series showing a reduction of fluid requirements, faster healing, and reduced mortality when his patients were compared to controls and to U.S. National Burn Information Exchange standards. Waisbren in 1982 reported a reduction in renal function, a decrease in circulating white blood cells, and an increase in positive blood cultures in a retrospective series of patients who had received HBOT. He stated he could demonstrate neither a salutary nor deleterious effect; however, his data showed a 75 percent decrease in the need for grafting in the hyperbaric-treated group. Grossman and colleagues have reported a very large clinical series showing improved healing, reduced hospital stay, and reduced mortality. Merola’s 1978 randomized study revealed faster healing of partial thickness burns in 37 patients treated with HBOT versus 37 untreated controls. Niu and his associates from the Naval Burn Center in Taiwan recently reported a very large clinical series showing a statistically significant reduction in mortality in 266 seriously burned patients who received adjunctive HBOT when compared to 609 control patients who did not receive HBOT. Hammarlund and colleagues have reported a reduction of edema and wound exudation in a carefully controlled series of human volunteers with ultraviolet irradiated blister wounds.

One hospital has shown a significant reduction in length of hospital stay in burns of up to 30 percent of the total body surface area (TBSA).

Table 1

Comparison of Factors in HBOT and Non-HBOT Groups
In Patients With 18-39 Percent Total Body Surface Area Burns

Variable   HBOT Control
  (n =8) (n=12)
Age
Average 29.5 30.9
Range 16-47 18-42 p<0.57 NS
Standard Deviation 9.6 8.5
Total BodySurface Burn (%)
Average 24.0 25.8
Range 20-33 18-39 p<0.91 NS
Standard Deviation 04.3 07.6
Full Thickness Injury
Average 5.2 5.6
Range 0-18 0.20 p<0.96 NS
Standard Deviation 06.1 06.2
Surgeries
Average 1.3 1.7
Range 0-2 0.3 p<0.42 NS
Standard Deviation 0.88 1.2
DaysHospitalized
Average 20.8 33.0
Range 16-33 16.58 p<0.012*
Standard Deviation 06.7 13.1
Cost ofBurn Care $44,838 $55,650
Average $27,600- $21,500- p<0.47 NS
Range $75,500 $98,700
Standard Deviation $9,200 $11,300

NS, Not Significant; *p<.012, significant (Mann-Whitney U test)

 

Reduced Surgical Requirements

Surgical Therapy

Brookside group has additionally reported a reduction in the need for surgery, including grafting, in a series of patients with burns up to 80 percent of total body surface area (TBSA) when they were compared to non-HBOT treated controls.

HBOT treated patients in this study experienced an average medical savings of $95,000 per case. In a series of patients with burns of up to 50 percent TBSA, averaging 28 percent total body surface area injury, similar results were obtained  In a retrospective, blinded review by the same group, researchers examined resuscitative fluid requirements in a group of severely burned patients. A 25 percent reduction in resuscitative fluid administration and a statistically significant reduction in maximum weight gain and percent weight gain was noted in the HBOT treated group versus the controls. Maxwell and colleagues in 1991 reported a small controlled series showing a reduction of surgery, resuscitative weight gain, intensive care days, total hospitalization time, wound sepsis, and cost of hospitalization in the group treated with HBOT. Recent data demonstrate continuing improvement in outcome of large burns. The number of surgeries was reduced 85 percent (p<0.03).

Improved Inhalation Function

Considerable attention has been given to the use of HBOT in inhalation injury. There is currently a fear that it may cause worsening of pulmonary damage, particularly in those patients maintained on high levels of inspired O2. Grim and colleagues from the University of Chicago Burn Center reported no evidence of oxidative stress in HBOT treated burn patients, using exhaled products of lipid peroxidation as a marker. Ray and colleagues have analyzed serious burns being treated for concurrent inhalation injury, thermal injury, and adult respiratory distress syndrome. She noted no deleterious effect in those patients on continuously high-inspired oxygen. More rapid weaning from the ventilator was possible in the HBOT treated group (p<0.05). A significant savings in cost of care ($60,000) was achieved through the use of hyperbaric oxygen in this study (p<0.05). There is presently no evidence to controvert these data.

Surgical Management

Over the past 20 years, the pendulum swung to an aggressive surgical management of the burn wound, i.e., tangential excision and early grafting of the deep second-degree, probable third-degree burns, especially to functionally important parts of the body. Hyperbaric oxygen, as adjunctive therapy, has offered the surgeon yet another modality of treatment for these deep second-degree burns to the hands and fingers, face and ears, and other areas where the surgical technique of excision and coverage is often imprecise. These wounds, not obvious third degree, are then best treated with topical antimicrobial agents, bedside debridement, and adjunctive HBOT, allowing the surgeon more time for healing to take place and to better define the extent and depth of injury. Adjunctive HBOT has drastically reduced the healing time in the major burn injury, especially if the wounds are deep second degree.

There is some theoretical benefit of hyperbaric oxygen therapy for obviously less well-defined third-degree burns. Fourth-degree burns, most commonly seen in high voltage electrical injuries, benefit from several pro­cesses, including reduced fascial compartmental pressures, reduced swelling of injured muscle due to preservation of aerobic glycolysis, and greatly reduced anaerobic infection.

Finally, reconstruction utilizing flaps and composite grafts, e.g., ear to nose grafts, has been greatly facilitated with HBOT. Often the decision to use HBOT has been made intraoperatively because a surgeon is concerned about a compromised cutaneous or musculocutaneous flap. The patient is, in many instances, prepared pre-operatively about the possibility of receiving this post-surgical adjunctive therapy.

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