The purpose of this hyperbaric oxygen therapy module is to inform nurses about the availability and use of hyperbaric oxygen therapy and the implications for patients and healthcare providers. After studying the information presented here, you will be able to:
Describe how hyperbaric oxygen therapy (HBOT) works.
Name six conditions that HBOT benefits.
Discuss measures to prevent complications of hyperbaric treatments.
Jimmy Speer was visiting a friend with a French bulldog when it happened. “I was just playing with the dog, and he turned and snapped,” the 8-year-old said. The dog bit off almost the entire tip of Jimmy’s nose. After plastic surgery to reattach the skin flap, Jimmy’s physician worried there was insufficient blood flow through the flap for proper healing. Jimmy had four hyperbaric oxygen treatments. “This gives extra oxygen to the area to help it survive and heal,” said physician Richard Stack, MD, of Mercy San Juan Medical Center in Carmichael, Calif. Jimmy’s mother, Rachael Speer, said, “The treatments prevented years of painful plastic surgery.”1
Hyperbaric medicine is a relatively new branch of medical science. Experiments have taken place for years, but its scientific foundation has been established in only the past few decades. Now hyperbaric oxygen therapy, or HBOT, is increasingly accepted as the treatment of choice or an important adjunctive therapy in a number of medical conditions.
The Undersea and Hyperbaric Medical Society, or UHMS, definition of HBOT is a treatment in which a patient breathes 100% oxygen while inside a chamber at a pressure higher than one atmosphere absolute (1 ATA), sea level pressure.2,3 The society, the Centers for Medicare and Medicaid Services and other third- party carriers state that breathing 100% oxygen at 1 ATA or exposing isolated parts of the body to 100% oxygen does not constitute HBOT.3,4
HBOT began in 1664, when a British clergyman advocated treating acute and chronic inflammatory diseases by increasing atmospheric pressure. He built a sealed room called a domicilium and pressurized it with a system of organ bellows. In 1877, Paul Bert demonstrated that oxygen at increased pressure was toxic and suggested using pure oxygen for medical treatments at atmospheric pressure only. A French surgeon built the first mobile hyperbaric chamber in 1879 and performed a number of operations under pressure with positive results. In 1889, J. Lorrain Smith demonstrated that breathing oxygen at surface pressure for prolonged periods caused pulmonary toxicity and that increased pressure hastened its onset. Smith also found pulmonary toxicity was reversible by reducing oxygen levels or exposure times. Orville Cunningham built a steel ball hospital in Cleveland, Ohio, in 1928. This hospital was a giant hyperbaric chamber six stories high and 64 feet wide that could be pressurized to 3 ATA or 66 feet of sea water. No scientific evidence existed to support its use at that time, and it was dismantled.
The first systematic studies to define the physiological effects of HBOT on humans were conducted in the early 1930s. The first clinical use of HBOT was by the U.S. Navy, which published procedures for the treatment of decompression sickness in 1943. By the mid-1960s, this treatment became the gold standard of care. In 1960, physicians reported treating the first patient with an anaerobic infection with HBOT. Since 1962, the positive effects of HBOT on aerobic/anaerobic infections and on wound healing have been demonstrated in animal and human models with volumes of level A evidence to support its use.5-7
HBOT is administered in a monoplace chamber (having room for one person) or a multiplace chamber (with room for two or more people). Both are designed to withstand increased internal pressure. In the monoplace chamber, the patient rests in a semi-reclining or flat position while the chamber is pressurized with 100% oxygen to a maximum of 3.0 ATA. A communication system allows the patient and the hyperbaric nurse to converse. Ventilator connections and IV lines are placed outside the chamber and connected to the patient. Multiplace chambers are compressed with air, typically to a maximum pressure of 6.0 ATA. In these chambers a patient breathes 100% oxygen through a head tent, tight-fitting mask or endotracheal tube. Critical care patients can be safely treated in both types of chambers.6-8
Two other chambers are used but not considered HBOT, which by definition requires that 100% oxygen be inhaled in a pressurized chamber. During topical oxygen therapy, oxygen is administered via a small chamber with an extremity placed in it or by a bag placed over a wound. This has limited effect and is not covered by insurance or endorsed by Medicare or the UHMS. The other chamber is the portable soft or “bag”- type hyperbaric chamber made of lightweight materials, such as plastics. The chambers can be pressurized to 1.3 or 1.7 ATA and only with air. The FDA approves some of these for immediate onsite treatment of altitude sickness. These bag chambers are used for several off-label indications, but are not Medicare approved.4
HBOT is beneficial for a variety of diseases. Many of HBOT’s effects are based on one or more of the following mechanisms of action:3,6,7
Hyperoxygenation: Under pressure, oxygen is forced into blood plasma. At 3 ATA of pressure, plasma carries more dissolved oxygen than hemoglobin does. The dissolved oxygen in plasma at this pressure is capable of sustaining life without negative results even in the absence of hemoglobin. This hyperoxygenation accounts for HBOT’s usefulness in treating acute blood loss or severe anemia when a blood transfusion is not possible. This also explains why it is the treatment of choice in acute carbon monoxide poisoning.
Direct pressure: HBOT reduces the volume of any free gases circulating in the bloodstream or sequestered in tissue. Gas bubbles become smaller when exposed to increasing pressure. Bubbles are present in both decompression sickness and gas embolism. The quickest way to reduce the size of such bubbles and allow rapid symptom relief is compression in a hyperbaric chamber while breathing 100% oxygen. This mechanism has formed the basis for hyperbaric oxygen therapy as the standard of care for decompression sickness and arterial gas embolisms.
Enhanced antimicrobial activity: High levels of oxygen in blood and tissue help fight infections caused by anaerobic bacteria. As the oxygen tension rises, bacterial replication is inhibited and toxin production ceases. This is helpful in treating patients with Clostridial gas gangrene or other infections caused by anaerobic bacteria. HBOT is bacteriostatic and bactericidal against many other organisms. Increased oxygen tension also potentiates the action of some antimicrobial agents. The ability of white blood cells to kill bacteria increases with higher oxygen levels, which is particularly helpful in areas of marginal perfusion.
Neovascularization and angiogenesis: When oxygen tensions are less than 15 to 30 mmHg, fibroblasts cannot synthesize collagen, migrate or divide. In hypoxic bone, new bone formation cannot take place after injury. HBOT reverses this by increasing oxygen tension, which allows fibroblasts to synthesize collagen and osteoclasts to deposit bone. HBOT also promotes and accelerates angiogenesis, the formation of new blood vessels. This helps treat hypoxic wounds, skin ulcers, osteomyelitis, osteoradionecrosis (radiation necrosis) and marginally surviving skin grafts.
Vasoconstriction: Oxygen is a powerful vasoconstrictor. Breathing oxygen at normal pressure reduces inflow to the capillaries by about 20%, resulting in compromised tissue becoming hypoxic. But in the hyperbaric environment, high plasma oxygen levels can maintain tissue oxygen levels and capillary outflow even with vasoconstriction. The result is a reduction of edema by about 20% due to a decrease in capillary transudation. This vasoconstrictive action is useful in managing intermediate compartment syndrome and other acute ischemic injuries, including reducing interstitial edema in grafted tissue. Even a small reduction in edema results in significantly more oxygen reaching the cell.
Reversal of reperfusion injuries: Most damage from reperfusion is caused by the inappropriate activation of leukocytes. Ischemic hypoxia causes leukocytes to stick to endothelium cell walls, resulting in vessel occlusion. Hyperbaric oxygen reduces this effect, which can last up to eight hours post-treatment. The net effect is the preservation of marginally perfused tissues that may otherwise be lost to an ischemia-reperfusion injury.
The UHMS has established standards and guidelines for HBOT. The society recognizes a number of conditions for which HBOT has substantial scientific support and therapeutic benefit. These indications are considered an appropriate use of HBOT, and most are covered by Medicare or third-party insurers.3,4
Air or gas embolism occurs when gas bubbles are introduced into the vascular system through decompression or by certain medical procedures (such as accidental injection of air into veins, during cardiopulmonary bypass, dialysis or removal of central catheters). Symptoms mimic a myocardial infarction or stroke and can affect any organ system. HBOT provides direct pressure, which reduces or eliminates intravascular and other free gas formations, reduces edema and improves oxygenation to ischemic/hypoxic tissue.
Carbon monoxide/cyanide poisoning occurs when carbon monoxide displaces oxygen on hemoglobin molecules, which normally carry four molecules of oxygen each. Symptoms can range from mild to severe. HBOT is the treatment of choice when carboxyhemoglobin (COHb) is over 25%. Fetal COHb can be 10% to 15% higher than maternal levels, so pregnant women should always be considered for treatment at any level. HBOT hastens the elimination of carbon monoxide from hemoglobin and reduces associated cerebral edema. High tissue levels of oxygen also enhance the dissociation of carbon monoxide and cyanide from peripheral binding sites.
Clostridial myonecrosis (gas cangrene) is a rapid, fulminating infection that threatens life and limb and is most commonly caused by Clostridium perfringens. HBOT is adjunctive to aggressive surgical debridement and provides hyperoxygenation and enhanced white cell function as well as halting the production of alpha toxin.
Crush injuries/compartment syndromes and other acute traumatic ischemias impede blood flow to the extremities due to disrupted arterial flow. HBOT is used with surgical fasciotomy and provides for hyperoxygenation and reduction of edema and compartment pressures.
Decompression sickness is due to the formation of inert gas bubbles in bloodstream and tissue during decompression that occludes blood vessels and can compress nerves. Symptoms can be subtle and diverse. The treatment of choice is HBOT, which provides direct pressure and hyperoxygenation, reduces edema and hastens the elimination of inert gas.
Central retinal artery occlusion is an occlusion of the retinal artery and an emergency. Symptoms are sudden and painless loss of vision. The retina has the highest rate of oxygen consumption of any organ in the body. The treatment of choice is HBOT, which provides hyperoxygenation.
Enhancement of healing in selected problem wounds includes diabetic foot ulcers. HBOT re-establishes a wound’s oxygen gradient by relieving hypoxia, reducing edema and inducing angiogenesis. HBOT also corrects diabetic-induced leukocyte changes and can be used to prepare an ulcer for coverage with a flap or graft. Up to 35% of diabetic foot ulcers cannot be healed with conventional means and may benefit from HBOT.9 HBOT also has been shown to improve the health-related quality of life of patients with diabetes.10 A diabetic foot ulcer must meet the following criteria to qualify for HBOT: The patient must have diabetes and a lower extremity wound due to diabetes; the wound must be classified at Wagner grade 3 or higher; and the patient must have failed a course of standard wound therapy.
In severe anemia, HBOT increases the amount of physically dissolved oxygen concentrations and overcomes hypoxic/ischemic tissue states. Patients with a low hemoglobin level can be maintained with HBOT until definitive treatment is possible.
With an intracranial abscess, HBOT enhances host defenses, reduces perifocal brain edema and augments treatment of anaerobic flora and concomitant skull necrosis.
Necrotizing soft tissue infections are usually a mixed flora infection that can include fungal infections. Typically this type of soft tissue infection is found only in host compromised patients. Primary treatment is surgery and antibiotics, with HBOT used as an adjunctive therapy. HBOT can help demarcate potentially viable from nonviable tissue, preoperatively. Postoperatively, HBOT provides hyperoxygenation and enhanced white cell function with increased bacteriostatic/bactericidal effects.
Refractory osteomyelitis is a chronic infection of the bone that has failed to heal with conventional therapy (surgery and antibiotics). HBOT is used adjunctively to enhance white cell function, osteoclast function and neovascularization.
Delayed radiation injuries include soft tissue radionecrosis and osteoradionecrosis. Radiation causes a progressive obliterative endarteritis that results in hypoxic tissue. HBOT is an essential part of the overall treatment plan. It enhances osteoclast function and neovascularization and provides increased fibroblast activity.
With compromised grafts and flaps, HBOT supports marginally perfused/oxygenated tissue and reverses ischemic-reperfusion injury. It also improves the development of wound granulation tissue and accelerates angiogenesis.
In acute thermal burn injury, HBOT is used adjunctively with standard burn care. It limits tissue fluid loss and burn wound extension and conversion by providing hyperoxygenation, vasoconstriction, enhanced white cell function and neovascularization. The UHMS recommends HBOT, but it is not yet covered by Medicare although it is covered by some third-party payers.4 Medicare may elect to cover HBOT for this indication in the future after completion and compilation of ongoing clinical studies.
Like any medical therapy, the risk and benefits of hyperbaric therapy must be carefully weighed with each patient. By appreciating the absolute and relative contraindications to HBOT, most serious complications can be anticipated and avoided.
An untreated pneumothorax is the only absolute contraindication to HBOT. The potential for disaster is obvious. Once the patient is compressed to a given depth, the pressure within the pleural cavity equilibrates with pressure within the chamber. The danger occurs during decompression; for example, decreasing the ambient pressure from 3 ATA to 1 ATA triples the volume of air trapped in the pneumothorax. This could result in fatal cardiopulmonary compromise. Patients with a pneumothorax can be safely treated after chest tubes have been placed.6,7
Many relative contraindications exist to HBOT. The most serious involve patients prone to develop spontaneous pneumothorax or seizures during treatment because of oxygen toxicity. Other relative contraindications center on pressure-related “squeeze” syndromes (barotraumas). Middle ear squeeze is the most common barotrauma. Barotraumas can occur in any enclosed air space in the body, such as in the ear when the eustachian tubes are blocked or in a sinus when the opening is blocked by blood or edema. These conditions must be considered in the HBOT risk-benefit analysis performed on any patient referred for treatment.6,7
Patients and HBOT
Typically, treatments last for 90 to 120 minutes plus about 10 to 15 minutes for compression and decompression. HBOT may be needed twice a day for a few indications early in the treatment plan. As the chamber is compressed, the patient may experience fullness in the ears. The hyperbaric nurse teaches patients how to clear their ears to equalize pressure during compression. The patient will notice the temperature increases slightly as the pressure is increased. Once at treatment pressure, patients can sleep, listen to music or watch television or movies.6,7
Patients are typically not treated if they have a cold or flu symptoms or a fever over 100 F. Some patients receiving HBOT have conditions requiring implanted devices, such as pacemakers and intracardiac defibrillators. HBOT may cause such devices to malfunction or fail. Hyperbaric nurses can determine whether this is a safety issue. Patients must also remove hard contact lenses, loose-fitting dentures, partial plates and jewelry before treatment. Hair and body products, such as deodorant, fragrance, makeup and hairspray, are not allowed in the chambers.
Before treatment, the hyperbaric nurse must evaluate all medication patches and petroleum-based dressings and wound ointments for safety. Patients can wear only facility-owned garments made of 100% cotton or a cotton/polyester blend of at least 50% cotton. A grounding wire must be attached before treatment. These measures reduce the potential for static electricity. Although extremely rare, electrical sparks can cause a fire in the hyperbaric chamber. Nurses should avoid giving injections within 45 minutes of a treatment as changes in pressure can slow absorption.
Patients and families are instructed that flammable items are not allowed in the chamber, such as cigarette lighters and anything with batteries (cell phones, etc.). Visual changes occasionally occur after several treatments. Patients should not buy or change their eyeglass or contact lens prescriptions during HBOT as eyesight will return to normal levels within six to eight weeks. Patients should avoid smoking and drinking caffeine before HBOT. As vasoconstrictors, they may limit the blood and oxygen that reaches tissues during treatment. Some patients with claustrophobia require mild sedation during treatment. Only hyperbaric MDs and RNs should educate patients about HBOT.6,7
HBOT may become more widely used in the future: It is being investigated for conditions including autism, fracture, traumatic brain injury, acute thermal burns, retinitis pigmentosa, glioblastoma, periodontal disease and cerebral palsy. Hyperbaric nursing is an exciting and rapidly-growing field. •
Gannett Education guarantees this educational activity is free from bias.
Connie Goldsmith, RN, MPA, is a freelance medical writer and frequent contributor. James R. Wilcox, RN, BSN, ACHRN, CWCN, CFCN, CWS, WCC, DAPWCA, FCCWS, is director of quality and research for Diversified Clinical Services in Florida and is the president of the Baromedical Nurses Association.