Hyperbaric Oxygen Therapy
For over hundreds of years the use of increased atmosphere pressure and higher oxygen concentration for what has intrigued many scientists, physicians and people at large. In 1662, Henshaw built the first sealed chamber with compressed air with 21% oxygen. It was used to treat different illnesses such as inflammation, scurvy, arthritis and rickets. Others used similar chambers or rooms to treat chronic diseases like Leprosy. In the early 1930s, Junod reported improvement in patients with cardio-respiratory illnesses when treated in high pressure chambers. Since then many others used such techniques for the treatment of variety of illnesses. Some people even opened spas to cater "health-conscious people". But the organized development of hyperbaric medicine had to wait until Dr. I Boerema in Holland, who in 1956 reported that such a form of therapy aids heart and lung surgery. His colleague, W. H. Brummelkamp, reported in 1959 that anaerobic infections were inhibited by hyperbaric therapy. Since then the use of hyperbaric oxygen expanded and developed to its current potential and has been used in many countries worldwide.
Mechanism of Action
Hyperbaric oxygen therapy (HBOT) is a mode of treatment in which the patient breathes 100% oxygen at pressures greater than the normal atmospheric pressure. In contrast with attempts to force oxygen into tissues by topical applications at levels only slightly higher than atmospheric pressure, HBOT involves the systemic delivery of oxygen at levels 2-3 times greater than atmospheric pressure. Either alone, or more commonly in combination with other medical and surgical procedures, the HBOT serves to enhance the healing process of many treatable conditions. The following are the main mechanisms by which the HBOT works:
Hyperoxygenation (increased oxygen supply) provides immediate support to poorly perfused tissue in areas of compromised blood flow. The elevated pressure within the hyperbaric chamber results in a 10-15 fold increase in plasma oxygen concentration. This translates to arterial oxygen values of more than 1,500 mmHg, thereby producing a four-fold increase in the diffusing distance of oxygen from the capillaries. While this form of therapy is only a temporary measure, it will often serve to buy valuable time and maintain tissue viability until corrective measures can be implemented or a new blood supply established.
Neovascularization or growth of new blood vessels represents an indirect and delayed response to hyperbaric oxygen. Therapeutic effects include enhanced fibroblast (?) division, formation of new collagen, and growth of new capillaries (minute blood vessels) in areas of sluggish tissues such as late radiation damaged tissue, refractory osteomyelitis (?) and chronic ulcerations e.g. Diabetic foot.
Antimicrobial activities (killing of bacteria) by high levels of oxygen have been demonstrated at a number of degrees. Hyperbaric oxygen causes toxin inhibition and toxin inactivation such as in Clostridial perfringens infections (gas gangrene). Hyperoxia enhances the white blood cells' ability to kill bacteria faster, and has been shown to enhance antibiotic activity. Recent research has demonstrated prolonged post-antibiotic effects when hyperbaric oxygen is combined with many antibiotics.
Direct pressure of HBOT utilizes the concept of Boyle's Law to reduce the volume of intravascular or other free gas. For more than a century this mechanism has formed the basis for hyperbaric oxygen therapy as the standard care for decompression sickness and cerebral arterial gas embolism (CAGE). Commonly associated with divers, CAGE is a frequent iatrogenic event in modern medical practice. It results in significant morbidity and mortality and remains grossly under-diagnosed or unrecognized in many instances.
Vasoconstriction (narrowing of blood vessel) is another important mechanism caused by hyperoxia. It occurs without component hypoxia, and is helpful in managing intermediate compartment syndrome and other acute ischemias in injured extremities, and reducing interstitial edema in grafted tissues. Studies in burn wound applications have indicated a significant decrease in fluid resuscitation requirements when hyperbaric oxygen therapy is added to standard burn wound management protocols.
Attenuation of reperfusion injury is the most recent mechanism to be discovered. Much of the damage associated with reperfusion is brought about by the inappropriate activation of leukocytes. Following an ischemic interval, the total injury pattern is the result of two components: a direct irreversible injury component from hypoxia, and an indirect injury which is largely mediated by the inappropriate activation of leukocytes. Hyperbaric oxygen reduces the indirect component of injury by preventing such activation. The net effect is the preservation of marginal tissues that may otherwise be lost to ischemia-reperfusion injury.
Oxygen, when breathed under increased atmospheric pressure, is a potent drug. Besides the beneficial effects discussed above, hyperbaric oxygen can produce noticeable toxic effects if administered indiscriminately. Safe time-dose limits have been established for hyperbaric oxygen exposure, and these profiles form the basis for today's treatment protocols. It is only quite recently that disease-specific hyperoxic dosing has been introduced. Hyperbaric oxygen therapy is administered in pressurized chambers. There are three distinct types of chambers currently available for use in medical practice.
- Multi-place chambers - These units can accommodate between 2-18 patients, depending upon configuration and size. They commonly incorporate a minimum pressure capability of 6 atmospheres absolute (ATA). Patients are accompanied by hyperbaric staff members, who may enter and exit the chamber during therapy. The multi-place chamber is compressed on air, and patients are provided with oxygen via an individualized internal delivery system. Advantages of this type of chamber include constant patient attendance and evaluation, and multiple patients treated per session. Disadvantages are high capitalization and staffing costs, large space requirements and risk of decompression sickness in the attending staff.
- Duo-place Chambers - Reneau Type (now named Proteus): This system became available during the mid-1980's. The chamber is constructed of stainless steel, and has a capability of 6 ATA. The main compartment accommodates one supine patient. The chamber is compressed with air, and the patient breathes oxygen by an individualized internal delivery system. Advantages of this chamber include constant patient attendance, with access limited to the head and neck. Disadvantages include relatively high capitalization cost for single patient treatments, and risk of decompression sickness in the attending staff.
Sygma II Type:
This system was introduced in the late 1980's. It is constructed of acrylic and steel, with a capability of 3 ATA. One supine or two seated patients can be treated in this chamber. Constant patient attendance is available via an access lock during single patient treatments. Advantages include two patients per session and constant patient attendance. Disadvantages include risk of decompression sickness in attending staff and relatively high capitalization.
3. Mono-place Chambers - These units, first introduced in the 1960's are designed for single occupancy. They are constructed of acrylic, have a pressure capability of 3 ATA. Recent technical innovations have allowed critically-ill patients to undergo therapy in the mono-place chamber. The high flow oxygen requirement is supplied via the hospital's existing liquid oxygen system. Advantages include cost efficient delivery of hyperbaric oxygen, and no risk of decompression sickness. Disadvantages include relative patient isolation and increased fire hazard.
Indications for HOBT
As the medical science advances, the doctors and scientists have discovered many beneficial uses of HBOT. While in some case it is absolutely necessary to apply HBOT, the others also benefit from it when combined with medical and surgical procedures. Based on this concept, the indications for HBOT are divided into groups:
A. Standard of Care
- Acute Carbon Monoxide Poisoning e.g. smoke inhalation; cyanide poisoning
- Cerebral Arterial Gas Embolism e.g. decompression or iatrogenically induced
- Clostridial Myonecrosis e.g. gas gangrene
- Osteo-radionecrosis (radiation induced damage) e.g. mandible
B. Adjunctive Therapy
- Crush Injury: Compartment Syndrome e.g. acute ischemias, traumatic wounds
- Chronic Ulcers e.g. Diabetic foot, atherosclerotic ulcers, Buerger's disease
- Enhancement of Healing e.g. hypoxic wounds, problem wounds
- Radiation Tissue Injury e.g. bone and soft tissue complications
- Necrotizing Soft Tissue Infections e.g. subcutaneous tissue, muscle, fascia
- Thermal Burns e.g. acute management; wound healing support
Carbon Monoxide Poisoning
Smoke inhalation injuries are common in fires and other smoke situations in closed spaces. Carbon monoxide, found in smoke, is the leading cause of deaths in case of fire. Hyperbaric treatment of carbon monoxide poisoning attempts to accelerate the release and subsequent elimination of carbon monoxide from hemoglobin and hyperoxygenated tissues, antagonize brain lipid peroxidation, reactivate cellular enzymes and proteins, and decrease cerebral edema and neuropsychiatric sequelae. Indications for hyperbaric treatment of carbon monoxide poisoning include comatose patients, patients with ischemic changes on ECG, those with abnormal psychological and neurological tests, and those with CO-Hb levels greater than 40%.
Naval investigations and experiments have increased understanding and treatment of severe decompression sickness or "bends", a phenomenon caused by diving. During decompression, gases within the vasculature and other tissues come out of solution and expand to promote a mechanical and pro-inflammatory reaction. The gas bubbles disrupt vascular endothelium and nerve tissue, cause middle ear and cochlear dysfunction, foster edema via vascular and lymphatic occlusion, and promote ischemia by blocking vessels. The brain and other tissues develop micro-hemorrhages. Patients present clinically with joint and/or muscle pain, itching, edema, and mottled skin. More severe and ominous symptoms include upper lumbar cord and brain dysfunction, cardiac irregularities, respiratory problems, and severe abdominal pain. Onset of symptoms usually occurs within the first 30 minutes after diving but can take up to 12 hours. HBOT attempts to reduce the bubble size until the inert gas is eliminated while tissues are hyper-oxygenated.
Gas gangrene caused by Cl. perfringes is a life-threatening and/or limb-threatening infection that mandates emergent surgical intervention. Use of HBOT in conjunction with surgery may save life or limb. Hyperbaric medicine works by a number of mechanisms to decrease the production of the alpha toxin released from clostridium, limit bacterial replication, and oxygenate tissues.
Radiation injury causes a triad of hypocellularity, hypovascularity, and hypoxia in the tissues subjected to radiotherapy. A progressive tissue fibrosis and capillary loss are noted. The resulting tissue damage may manifest as non-healing ulcers, pigmentary skin changes, tissue indurations, loss of elasticity, and local erythema and tenderness. Bone may progress to an avascular necrosis. The central avascular region of ulcers and osteoradionecrosis is rendered hypoxic, and the surrounding tissues have greater oxygen content. Hyperbaric treatment promotes angiogenesis and hyperoxygenation to the radiated affected tissues, and thereby limits the damage caused by radiation
Chronic Non-healing Wounds
The rationale for treatment of chronic non-healing wounds is to enhance angiogenesis, collagen deposition, re-epithelialization, cellular respiration, as well as oxidative killing of bacteria. Decreased edema noted following hyperbaric treatment allows better diffusion of oxygen and nutrients through tissues while also relieving pressure on surrounding vessels and structures. In this light, HBOT has been used for treating crush injuries, venous and arterial insufficiencies, burn wounds, marginal flaps, and skin grafts.
Foot wounds of patients with diabetes offer a particularly difficult problem. These patients often have an impaired immune system, predisposing them to infections. Blood supply to the wounds is hindered, causing distal ischemia. Neuropathies render the foot insensate and impair motor function. This impaired motor function flattens the foot so that promotes further susceptibility to ulceration via pressure. Recently, a number of randomized prospective studies demonstrated the benefit of hyperbaric therapy in healing foot wounds of patients with diabetes. The mechanism of action is essentially similar to that of other type of chronic ulcers as described above. HBOT may offer added fuel to the overall armamentarium in the treatment of diabetic foot.
Other Useful Applications
Several other applications of HBOT are well documented, notably reperfusion injuries and transcutaneous oxygen. Considering the pros and cons of these applications, further well-organized prospective studies should help identify the appropriate therapeutic benefits of HBOT.
Side-effects of HBOT
Like many other medicines and treatment procedures, HBOT also has side-effects. In most cases patients complain of nausea and vomiting, sweating, dry cough, shortness of breath, chest pain and muscle twitching. Occasionally, some patients develop seizure, vertigo (?), visual changes, tinnitus (ringing in the ear), hiccups, or lung edema (?). Only rarely, some patients develop hallucinations and/or decreased level of consciousness. Most of these side-effects are short lasting and the patients gradually adjust with the procedure.
What does a Patient Say?
Dr. Hasan from Chittagong developed ulcer in his left foot. He has been diabetic for over 12 years. Initially he underwent debridement of the wound and antibiotic treatment. But the wound continued to get worse, affecting his big toe. A local surgeon amputated the great toe and more wound care followed. After about a month, his infection spread to other toes and the sole of the foot, and this time his doctor recommended amputation of the left foot. Dr. Hasan panicked and contacted Dr. Shakti Paul (author) in Bangkok Hospital, who advised him that HBOT might help to save his foot. He rushed to Bangkok Hospital. An Orthopedic surgeon did thorough debridement without amputation and antibiotic therapy but this time he received HBOT at the hospital. "My ulcer improved day by day. I could feel the burning in the foot again which was not there before I started oxygen treatment," says a delighted Dr. Hasan. "The doctors suggested 21 sessions of HBOT, which I completed. The surgeon applied skin graft. The wound healed completely in a month," added Dr. Hasan. "Thank God, my leg and perhaps life was saved," says a much relieved Dr. Hasan.
Hyperbaric Oxygen is not new but remained underutilized for years, perhaps because of the difficulties in its clinical applications. Many medical conditions respond well to HBOT and many more are in the process of development. Notable among HBOT use are: acute carbon monoxide poisoning, decompression sickness, gas gangrene, radionecrosis, crush injuries, chronic ulcer and diabetic foot, necrotizing soft tissue inections etc.
Its use in the future depends on continued enthusiasm, research, and practice based on sound principles. At present wound healing centers may harbor most hyperbaric chambers but it should become part of an integrated health care where many other complicated patients are treated.
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