BURNS

 

Caveat

  • The following list provides a 'knowledge share base' working to collaborate and promote the benefits of Hyperbaric Oxygen Therapy.

  • Australia is not a leader in this field but lagging behind the rest of the world in relationship to the wider applications of modern Hyperbaric Oxygen Therapy using different 'pressure protocols for different conditions'. 

  • The information provided does not constitute a medical endorsement or recommendation. It is intended for informational purposes only, and no claims, either real or implied, are being made. 

Hyperbaric Oxygenation In The Management of Thermal Burns

 

Burns are very common, sometimes fatal, and have a high impact on the wellbeing of those affected. Recovery is often slow and complicated by infection and scarring. 

 

Hyperbaric Oxygen Therapy (HBOT) is a treatment designed to increase the supply of Oxygen to the compromised region, and improve healing responses. HBOT involves the patient breathing 100% Oxygen in a specially designed chamber. Hyperbaric chambers may be either monoplace (single occupancy) commonly in private medical facilities or larger multiplace chambers typically within hospitals.

 

Undersea Hyperb Med. 2013 Jan-Feb;40(1):89-108.

Adjunctive hyperbaric oxygen therapy in the treatment of thermal burns.

Cianci P, Slade JB Jr, Sato RM, Faulkner J.

Source

Department of Hyperbaric Medicine, Doctors Medical Center San Pablo, Calif, USA. pecianci@aol.com

Abstract

A significant and consistently positive body of evidence from animal and human studies of thermal injury support the use of hyperbaric oxygen as a means of preventing dermal ischemia, reducing edema, modulating the zone of stasis, preventing partial- to full-thickness conversion, preserving cellular metabolism and promoting of healing. The vast majority of clinical reports have shown reduction in mortality, length of hospital stay, number of surgeries and cost of care. Hyperbaric oxygen has been demonstrated to be safe in the hands of those thoroughly trained in rendering therapy in the critical care setting and with appropriate monitoring precautions. Careful patient selection is mandatory. HBOT is recommended at 2 ATA for 90-minutes twice daily.  

 

 

During the first 24-hours

  • HBOT counteracts vasodilation and exudation of plasma by its vasoconstricting effect, and prevent burns shock

  • HBOT inhibits wound infection

  • HBOT promotes epithelialization of the wound

  • HBOT is a useful adjunct to survival of skin grafts and flaps

  • HBOT is effective against serious problems accompanying serious burns, such as smoke inhalation and CO poisoning

  • HBOT counteracts ischemia of the tissues

  • HBOT helps to maintain the integrity of the wound by minimizing RBS aggregation and platelet thrombi and their propagation from the zone of heat coagulation

 

After 24-hours

  • HBOT relieves paralytic ileus

  • HBOT has a beneficial effects on stress ulceration of the stomach (Curling’s ulcers)

  • HBOT counteracts burns encephalopathy/cerebral edema

  • HBOT reduces the length of hospitalisation

  • HBOT reduces the need for surgical procedures

 

Conclusions

There are considerable studies to support the benefit of HBOT combined with appropriate medical strategies in the treatment and management of thermal burns. The Undersea and Hyperbaric Medical Society approves treatment of patients with burns by HBOT provided the treatment is carried out in an approved facility.

 

The Effects of Hyperbaric Oxygen Therapy (HBOT) on Acute Thermal Burns

Introduction

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 observation with a series of animal experiments that demonstrated a significant 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 but with favourable 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 (HBOT). 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. HBOT used as an adjunct to comprehensive management of patients with burns has resulted in a statistically significant 25% reduction in the length of hospital stay (p<0.012) and 19% reduction in overall cost of care (Cianci et al 1989, 1990).

 

Basic Considerations

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 desiccation 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 defences, and providing the essential substrate necessary to sustain viability.  

 

Infection

Susceptibility to infection is greatly increased owing to the loss of barrier integrity to bacterial invasion. Infection susceptibility is fostered by 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 animal studies

A significant body of animal data support the efficacy of HBOT in the treatment of thermal injury. Ikeda 1967, 1970 noted a reduction of edema in burned rabbits. Ketchum 1967 reported a 30% 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.  

Hartwig 1974 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 1977 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 1984 demonstrated that hyperbaric Oxygen therapy reduced the generalized edema associated with burn injury.

 

Korn 1977, 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 was a function of subjacent capillary integrity noted in the HBOT treated animals. Saunders 1989 demonstrated similar clinical results and reported an improvement in collagen synthesis in HBOT treated animals.  

Not all studies have been supportive; Perrins 1970 failed attempt to limit tissue destruction in scalds with hyperbaric Oxygen in a pig model. Niccole 1977 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 1989 has 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 1976. Mader 1980 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

Wada 1965, observed that coal miners with CO poisoning treated with HBOT appeared to de better than those treated conventionally. Their wounds dried earlier, had fewer infections and healed faster.  

In 1974 Hart reported a randomised double-blinded study of 191 burn patients. They concluded that application of HBOT within the first 24-hours decreases healing time, morbidity and mortality significantly when compared to controls and to U.S. National Burn Information Exchange standards. Hart recommended a monoplace chamber as a safe and economical and convenient means of HBOT for burns patients. Hart et al, concludes HBOT as an adjunctive measure in the treatment and management of burns patients; it does not replace resuscitative, topical and or surgical care; and it is not a panacea.  

Waisbren 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. Waisbren 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 1978 reported a very large clinical series of in excess of 800 burns patients treated using HBOT during a 6-year period at Sherman Oaks Community Hospital in California .

 

HBOT combined protocol as follow

  • Treatment was given within 4-hours of admission of the patient to the burn unit

  • Treatment given in a monoplace chamber at 2-2.5 ATA (100% Oxygen) for varying periods of time

  • Tissue pO2 was individually monitored. In second-degree burns the tissue pO2 achieved at 2ATA was 1200mmHg, compared with 25mmHg at 1ATA. This value dropped to 40mmHg 2-hours after HBOT. In third-degree burns, the tension achieved at 2ATA was 1500mmHg dropping to 400mmHg 2-hours after HBOT

 

The results observed

  • Reduction in patients’ fluid requirements

  • Reduction in second-degree burn healing time

  • Reduction in eschar separation time

  • Reduction in donor graft harvesting time

  • Reduction in hospital stay

  • Reduction in associated complications – ulcers, infections, pulmonary emboli etc

  • Reduction in mortality by 10% compared with non-HBOT treated patients

 

Merola 1978, revealed faster healing of partial thickness burns in 37 patients treated with HBOT versus 37 untreated controls. Niu 1987 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. HBOT was recommended at 2.5ATA for a 90-120 minute session which was repeated 2-3 times daily for the initial 24-hours and then 1-2 times per day following. The overall mortality in the HBOT group and non-HBOT group was not different, but in a high-risk group of patients the mortality was reduced considerably. There was less fluid loss and earlier reepithelialization in the HBOT group of treated patients.  

 

Cianci 1989, presented considerable evidence and concluded:

  • In patients with burns involving between 18-39% of the total body surface, there was a 37% reduction in the length of hospital stay

  • In patients with partial to full thickness burns involving 40-80% of the total body surface, there was a reduction of the number of surgical procedures for debridement and grafting

  • HBOT patients showed a reduction of fluid requirements

 

Grossman 1982 presented accumulated experience with 1,130 burn patients and continued to demonstrate merits of HBOT. Hammarlund 1991 reported a reduction of edema and wound exudation in a carefully controlled series of human volunteers with ultraviolet irradiated blister wounds.  

Maxwell 1991 reported 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. 

 

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 1989, University of Chicago Burn Centre reported no evidence of oxidative stress in HBOT treated burn patients, using exhaled products of lipid peroxidation as a marker.  

Ray 1991 analyzed serious burns being treated for concurrent inhalation injury, thermal injury, and adult respiratory distress syndrome. 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 was reported through the use of hyperbaric Oxygen in this study (p<0.05).

 

Surgical Management

The trend continues towards 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, offers 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 intraoperative 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.  

Cianci 1994, reports the mechanisms and healing effects of HBOT for burns, and provide a rationale for its proactive use to treat burn wounds. Cianci clinical data review demonstrates reduced edema, less inflammatory response, reduced hemoconcentration and extravasation, reduced wound surface area, improved dermal survival, enhanced re-epithelialization, reduced need for grafting, decreased hospital stay, and reduced mortality. HBOT-treated patients demonstrated an average savings of US $107K per case. Cianci recommends HBOT be not recommended for trivial burns or when survival chances are minimal, but rather for burns of 20% TBSA or greater, involving hands, face or perineum, and either for partial or full skin thickness burns.  

Juha 2004 concludes hyperbaric Oxygen therapy (HBOT) is an important adjunct in the management of problem wounds, which exist in chronic Oxygen deficiency and in which the local Oxygen tension is below optimal for healing. In the treatment of hypoxic and ischemic wounds, the most important effects of hyperbaric Oxygenation are the stimulation of fibroblast proliferation and differentiation, increased collagen formation and cross-linking, augmented neovascularization, and the stimulation of leukocyte microbial killing. Ischemic soft tissues also benefit from hyperOxygenation through improved preservation of energy metabolism and reduction of edema.  

For an objective assessment of wound perfusion and Oxygenation, transcutaneous oximetry provides a simple, reliable, non-invasive, diagnostic technique. It can be used for assessment of tissue perfusion in the vicinity of the problem wound. Transcutaneous oximetry may be used in the assessment of wound healing potential, selection of amputation level, and patient selection for HBOT. In diabetic patients with chronic foot ulcers peri-wound transcutaneous Oxygen tensions (TcPo2) over 400 mmHg in 2.5 ATA hyperbaric Oxygen or over 50 mmHg in normobaric pure Oxygen predict healing success with adjunct HBOT with high accuracy.  

Jain 2005, Text Hyperbaric Medicine provides an excellent summary for the rationale for HBOT in thermal burns:  

 

During the first 24-hours

  • HBOT counteracts vasodilation and exudation of plasma by its vasoconstricting effect, and prevent burns shock

  • HBOT inhibits wound infection

  • HBOT promotes epithelialization of the wound

  • HBOT is a useful adjunct to survival of skin grafts and flaps

  • HBOT is effective against serious problems accompanying serious burns, such as smoke inhalation and CO poisoning

  • HBOT counteracts ischemia of the tissues

  • HBOT helps to maintain the integrity of the wound by minimizing RBS aggregation and platelet thrombi and their propagation from the zone of heat coagulation

 

After 24-hours

  • HBOT relieves paralytic ileus

  • HBOT has a beneficial effects on stress ulceration of the stomach (Curling’s ulcers)

  • HBOT counteracts burns encephalopathy/cerebral edema

  • HBOT reduces the length of hospitalisation

  • HBOT reduces the need for surgical procedures

 

Conclusions

There are considerable studies to support the benefit of HBOT combined with appropriate medical strategies in the treatment and management of thermal burns. The Undersea and Hyperbaric Medical Society approves treatment of patients with burns by HBOT provided the treatment is carried out in an approved facility with appropriate medical supervision. HBOT is recommended at 2 ATA for 90-minutes twice daily.  

HBOT as an adjunctive to comprehensive management of patients has resulted in a statistically significant 25% reduction in the length of hospital stay (p<0.012), and 19% reduction in the overall cost of care (Cianci et al 1989, 1990)