M illions of individuals suffer from chronic wounds that will not heal. Often, these wounds won’t heal due to a variety of factors such as obesity, age, diet, circulatory problems, diabetes, arthritis, kidney disease and smoking.

These wounds can become infected, requiring amputation in extreme cases, if not treated in a timely and effective manner.

The life of all muscles, skin, bones and organs depend on the oxygen concentration found within. Oxygen is supplied to these tissues by a person’s blood vessels. But with certain conditions, such as diabetes, prior surgery with scar tissue or radiation therapy for cancer, there is a possibility that microscopic blood circulation can be affected.

If the circulation is affected, the oxygen concentration in certain areas may be low. This greatly reduces the body’s ability to heal itself, especially if the body develops a wound.

Hyperbaric oxygen therapy is a medical treatment in which a patient breathes 100 percent oxygen inside a pressurized treatment chamber. It increases blood and tissue oxygen content.

In other words, this medical treatment “super-oxygenates” wounds, creating new microscopic blood vessel growth to approximately 85 percent of normal tissue. The new growth helps improve oxygen delivery, therefore enhancing wound healing.

During the treatment, a patient lies in a see-through, pressurized chamber while breathing 100 percent oxygen. This helps more oxygen dissolve in a patient’s blood, with the patient receiving the equivalent of 200 to 250 percent oxygen. The high-dose oxygen stimulates certain molecules, creating new microscopic blood vessel growth and faster wound healing.

C arbon monoxide poisoning is caused by exposure to a colorless, odorless gas known as carbon monoxide (CO). CO is found in combustion fumes. CO poisoning is usually caused by car or truck exhaust, wood stoves, and other fuel burning appliances, smoke from a fire or blocked fireplaces, nonelectric heaters, malfunctioning gas appliances, and faulty heating exhaust systems in the home or garage.

Known as a silent killer, CO displaces the oxygen in the bloodstream when the CO is mixed in the normal air you breathe. If a heater's combustion system malfunctions and CO seeps out of it, for example, the gas can kill people while they are asleep. CO poisoning typically occurs at home, in a garage or car, or in another enclosed space like a camper, trailer, or tent.

Everyone is at risk for CO poisoning from combustion fumes, especially during the winter when windows are closed. Some people are more susceptible than others. These include babies, pregnant women, and people with heart problems, breathing problems, or anemia.

CO binds to hemoglobin with 200 times the affinity of oxygen. CO also shifts the oxygen dissociation curve to the left (the Haldane effect), which decreases oxygen release to tissues. CO can also bind cytochrome oxidase aa3/C and myoglobin. Reperfusion injury can occur when free radicals and lipid peroxidation are produced.

The treatment of CO poisoning with hyperbaric oxygen therapy (HBOT) is based upon the theory that oxygen competitively displaces CO from hemoglobin. While breathing room air, this process takes about 300 minutes. While on a 100% oxygen nonrebreather mask, this time is reduced to about 90 minutes. With HBOT, the time is shortened to 32 minutes. HBOT (but not normobaric oxygen) restores cytochrome oxidase aa3/C and helps to prevent lipid peroxidation. HBOT is also used to help prevent the delayed neurologic sequelae (DNS). Treatment instituted sooner is more effective. Multiple papers describe controversial methods and conclusions about the use of HBOT for CO poisoning.

Patients with CO poisoning can present with myriad symptoms that they may not initially attribute to CO poisoning, as CO is considered the “great imitator” of other illnesses. Presentation can include flulike symptoms such as headache, visual changes, dizziness, and nausea. More serious manifestations include loss of consciousness, seizures, chest pain, ECG changes, tachycardia, and mild to severe acidosis.

Candidates for HBOT are those who present with morbidity and mortality risks that include pregnancy and cardiovascular dysfunction and those who manifest signs of serious intoxication, such as unconsciousness (no matter how long a period), neurologic signs, or severe acidosis. CO-hemoglobin (Hgb) level usually does not correlate well with symptoms or outcome; many patients with CO-Hgb levels of 25-30% are treated.

Pregnant females often have a CO level that is 10-15% lower than the fetus. Fetal Hgb not only has a higher affinity for CO but also has a left-shifted oxygen dissociation curve compared with adult hemoglobin. Exposure to CO causes an even farther leftward shift, in both adult and fetal hemoglobin, and decreased oxygen release from maternal blood to fetal blood and from fetal blood to fetal tissues. Pregnant patients with CO-Hgb levels greater than 10% should be treated with HBOT.

HBOT is administered at 2.5-3 ATA for periods of 60-100 minutes. Depending on patient presentation and response, 1-5 treatments are recommended.

D ecompression sickness (DCS) refers to symptoms caused by blocked blood supply, damage from direct mechanical effects, or later biochemical actions from suspected bubbles evolving from inert gas dissolved in blood or tissues when atmospheric pressure decreases too rapidly. DCS can occur after scuba diving, ascent with flying, or hypobaric or hyperbaric exposure.

DCS can be broken down into the following 3 types:

Associated symptoms can last from a few days to a few weeks, depending on the severity and can include:

1. Type I involves musculoskeletal, skin, and lymphatic tissue, and often has accompanying fatigue.
2. Type II includes neurologic systems (either CNS or peripheral), cardiorespiratory, audiovestibular, and shock.
3. Type III DCS describes a syndrome that presents with severe symptoms of DCS as well as AGE. Some of these cases can be refractory to recompression.

The bubbles causing DCS also can injure vessel endothelium, which leads to platelet aggregation, denatured lipoproteins, and activation of leukocytes, causing capillary leaks and proinflammatory events.

Hyperbaric oxygen therapy (HBOT) is used to diminish the size of the bubbles, not simply through pressure, but also by using an oxygen gradient. According to Boyle's law, the volume of the bubble becomes smaller as pressure increases. With a change in 1.8 ATA, this is only about 30%. The bubble causing DCS is thought to be composed of nitrogen. When a tissue compartment is at equilibrium and then ascends to a decreased atmospheric pressure, nitrogen seeps out of blood, tissue, or both, causing a bubble. During HBOT, the patient breathes 100% oxygen, creating oxygen-rich, nitrogen-poor blood. This creates a gradient of nitrogen between the blood and the bubble, causing nitrogen to efflux from the bubble into the bloodstream, which, in effect, makes the bubble smaller.

The treatment of choice is recompression. Although treatment as soon as possible has the greatest success, recompression is still the definitive treatment, and no exclusionary time from symptom onset has been established. DCS Type I can be treated using the US Navy Treatment Table 5: 60 fsw for two 20-min periods, with a slow decompression to 30 fsw for another 20 minutes. For DCS types I, II, and III, the US Navy Treatment Table 6 is a recommended treatment protocol. Patients are placed at 60 fsw (2.8 ATA) for at least three 20-min intervals and then are slowly decompressed to 30 fsw. They remain there for at least another 2.5 hours. The time a patient is kept at 60 or 30 fsw can be extended depending on the patient's symptom response to therapy.

M ost skin grafts and flaps in normal hosts heal well. In patients with compromised circulation, this may not be the case. Patients with diabetes or vasculopathy from another etiology and patients who have irradiated tissue are particularly subject to flap or graft compromise. In these patients, hyperbaric oxygen therapy (HBOT) has been demonstrated to be useful. Unfortunately, if patients are not identified early, the initial flap or graft may be lost. Even in such cases, patients can significantly benefit from HBOT to prepare the wound bed for another graft or flap procedure. The procedure then has a higher chance of success following HBOT.

Over 30 animal studies have documented efficacy of HBOT in preserving both pedicled and free flaps in multiple models. These models looked at arterial, venous, and combined insults in addition to irradiated tissues. While improvement was observed regardless of the type of vascular defect, those with arterial insufficiency and radiation injury demonstrated the greatest improvement.

Human case studies documentng benefit of hyperbaric treatment for flap survival were first reported in 1966. A controlled clinical trial showing improved survival of split skin grafts followed shortly thereafter. This was corroborated by a later clinical trial. Additionally, evidence exists of benefit for flaps in post-irradiated tissue in human subjects.

As the underlying pathophysiology of all compromised grafts and flaps is hypoxia, HBOT benefits patients by reducing the oxygen deficit. A unique mechanism of action of HBOT for preserving compromised flaps is the possibility of closing arteriovenous shunts. Additionally, the same mechanisms of action that improve wound healing, namely, improved fibroblast and collagen synthesis and angiogenesis, also are likely to benefit a compromised graft or flap.

The current standard for HBOT to treat a compromised graft or flap includes twice daily treatment until the graft or flap appears viable and then once per day until completely healed. The initiation of HBOT should be expedited. In general, benefit should be seen by 20 treatments. If it is not, continuation of therapy should be reviewed. However, the cost of creating a complex flap is high, which makes HBOT cost-effective for this diagnosis. Of course, patients with compromised flaps need surgical attention to the arterial and venous supply, appropriate local management, and maximization of medical support.

A cute peripheral traumatic ischemia includes those injuries that are caused by trauma that leads to ischemia and edema; a gradient of injury exists. This category contains crush injuries as well as compartment syndrome. Crush injuries often result in poor outcome because of the body’s attempt to manage the primary injury. The body then develops more injury due to the reperfusion response. Injuries are graded using definite points on a severity scale. The commonly referenced system is the Gustilo classification, but other classification scales are available.

The benefits of hyperbaric oxygen therapy (HBOT) for this indication include hyperoxygenation by increasing oxygen within the plasma. HBOT also induces a reduction in blood flow that allows capillaries to resorb extra fluid,resulting in decreased edema. As a gradient of oxygenation is based on blood flow, oxygen tissue tensions can be returned, allowing for the host defenses to properly function. Animal studies suggest that a decreased neutrophil adherence to ischemic venules is observed with elevated oxygen pressures (2.5 ATA). Reperfusion injury is diminished, as HBOT generates scavengers to destroy oxygen radicals.

Compartment syndrome also is a continuum of injury that occurs when compartment pressures exceed the capillary perfusion pressures. The extent to which the injury has affected tissues is unclear, even after surgical intervention. HBOT is not recommended during the “suspected” stage of injury, when compartment syndrome is not yet present but may be impending. HBOT is beneficial during the impending stage, when objective signs are noted (pain, weakness, pain with passive stretch, tense compartment). With these signs, even if surgery is not elected because of compartment pressures or patient stability, HBOT is indicated. Once the patient has undergone fasciotomy, HBOT can be used to help decrease morbidity.

HBOT should be started as soon as is feasible, ideally within 4-6 hours from time of injury. After emergent surgical intervention, the patient should undergo HBOT at 2-2.5 ATA for 60-90 minutes. For the next 2-3 days, perform HBOT 3 times daily, then twice daily for 2-3 days, and then daily for the next 2-3 days.

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hese infections may be single aerobic or anaerobic but are more often mixed infections that often occur as a result of trauma, surgical wounds, or foreign bodies, including subcutaneous and muscular injection of contaminated street drugs. They are often seen in compromised hosts who have diabetes or a vasculopathy of another type. These infections are named based on their clinical presentation and include Necrotizing Fasciitis , Clostridial and nonclostridial myonecrosis , and Fournier Gangrene

Regardless of the depth of the tissue invasion, these infections have similar pathophysiology that includes local tissue hypoxia, which is exacerbated by a secondary occlusive endarteritis. Intravascular sequestration of leukocytes is common in these types of infections, mediated by toxins from specific organisms. Clostridial theta toxin appears to be one such mediator. All of these factors together foster an environment for facultative organisms to continue to consume remaining oxygen, and this promotes growth of anaerobes.

The cornerstones of therapy are wide surgical debridement and aggressive antibiotic therapy. Hyperbaric oxygen therapy (HBOT) is used adjunctively with these measures, as it offers several mechanisms of action to control theinfection and reduce tissue loss. First, HBOT is toxic to anaerobic bacteria. Next, HBOT improves polymorphonuclear function and bacterial clearance. Based on results of work related to CO poisoning, HBOT may decrease neutrophil adherence based on inhibition of beta-2 integrin function. Further investigation is needed to see if this mechanism is at work in necrotizing infections as well. In the case of clostridial myonecrosis, HBOT can stop the production of the alpha toxin. Finally, limited evidence indicates that HBOT may facilitate antibiotic penetration or action in several classes of antibiotics, including aminoglycosides,cephalosporins, sulfonamides and amphotericin.

Multiple clinical studies suggest that HBOT is efficacious in the treatment of necrotizing soft tissue infections. These include case series, retrospective and prospective studies, and non-randomized clinical trials. They suggest significant reductions in mortality and morbidity. The reduction in mortality was remarkably similar in two studies: 34% (untreated) vs. 11.9% (treated) in one study;[68] 38% (untreated) vs. 12.5% (treated) in the other. In another study, the treated group had more patients with diabetes and more patients in shock and still had significantly less mortality (23%) than the untreated group (66%). Clinical studies involving patients with Fournier gangrene treated with HBOT bear similar results.

Initial HBOT is aggressively performed at least twice per day in coordination with surgical debridement. Typically, a treatment pressure ranging from 2.0-2.5 ATA is adequate. However, in the specific case of clostridial myonecrosis, 3 ATA is often used to ensure adequate tissue oxygen tensions to stop alpha toxin production. For the same reason, HBOT should be initiated as quickly as possible in this circumstance and performed 3 times in the first 24 h if at all feasible.

Intracranial Abscess

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T he disorders considered in treatment of intracranial abscesses (ICA) include subdural and epidural empyema as well as cerebral abscess. Studies from around the world have reviewed mortality from ICA with a resulting mortality of about 20%. HBOT has multiple mechanisms that make it useful as an adjunctive therapy for ICA.

HBOT induces high oxygen tensions in tissue, which helps to prevent anaerobic bacterial growth, including organisms commonly found in ICA. HBOT can also help reduce increased intracranial pressure (ICP) and its effects are proposed to be more pronounced with perifocal brain swelling. As discussed earlier, HBOT can enhance host immune systems and the treatment of osteomyelitis. Candidates for adjunctive HBOT are patients who have multiple abscesses, who have an abscess that is in a deep or dominant location, whose immune systems are compromised, in whom surgery is contraindicated, who are poor candidates for surgery, and who exhibit inadequate response despite standard surgical and antibiotic treatment.

HBOT is administered at 2.0-2.5 ATA for 60-90 minutes per treatment. HBOT may be 1-2 sessions per day.

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adiation therapy causes acute, subacute, and delayed injuries. Acute and subacute injuries are generally self-limited. However, delayed injuries are often much more difficult to treat and may appear anywhere from 6 months to years after treatment. They generally are seen after a minimum dose of 6000 cGy. While uncommon, these injuries can cause devastating chronic debilitation to patients. Notably, they can be quiescent until an invasive procedure is performed in the radiation field. Injuries are generally divided into soft tissue versus hard tissue injury Osteoradionecrosis (ORN).

While the exact mechanism of delayed radiation injury is still being elucidated, the generally accepted explanation is that an obliterative endarteritis and tissue hypoxia lead to secondary fibrosis. Hyperbaric oxygen therapy (HBOT) was first used to treat ORN of the mandible. Based on the foundational clinical research of Marx, multiple subsequent studies supported its use. The success of HBOT in treating ORN then led to its use in soft tissue radionecrosis as well.

OSTEORADIONECROSIS

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M arx demonstrated conclusively that ORN is primarily an avascular aseptic necrosis rather than the result of infection. He developed a staging system for classifying and planning treatment, which is largely accepted throughout the oromaxillofacial surgery community.

• STAGE I

Exposed alveolar bone: The patient receives 30 HBOT treatments and then is reassessed for bone exposure, granulation, and resorption of nonviable bone. If response is favorable, an additional 10 treatments may be considered.

• STAGE II

A patient who formerly was Stage I with incomplete response or failure to respond: Perform transoral sequestrectomy with primary wound closure followed by an additional 10 treatments.

• STAGE III

A patient who fails stage II or has an orocutaneous fistula, pathologic fracture, or resorption to the inferior border of the mandible: The patient receives 30 treatments, transcutaneous mandibular resection, wound closure, and mandibular fixation, followed by an additional 10 postoperative treatments.

• STAGE IIIR

Mandibular reconstruction 10 weeks after successful resolution of mandibular ORN: The patient receives 10 additional postoperative HBOT treatments.

The cornerstone of therapy is to begin and complete (if possible) HBOT prior to any surgical intervention and then to resume HBOT as soon as possible after surgery. Only in this way is adequate time allowed for angiogenesis to support postoperative healing. For patients with a history of significant radiation exposure, but no exposed bone, who require oral surgery, many practitioners suggest 20 HBOT treatments prior to surgery and 10 treatments immediately following surgery. Feldmeier has published an excellent review of this literature.

HBOT is administered at 2.0-2.5 ATA for 60-90 minutes per treatment. HBOT may be 1-2 sessions per day.

SOFT-TISSUE RADIONECROSIS

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W hile soft tissue radionecrosis also is rare, it causes significant morbidity, depending on the site of injury. All of these injuries lead to significant local pain. Both Radiation Cystitis. and radiation proctitis can result in severe blood loss with symptomatic anemia. Radiation cystitis may also cause obstructive uropathy secondary to fibrosis and blood clot formation. Radionecrosis of the neck and larynx can lead to dysphagia and respiratory obstruction. Irradiated skin develops painful, necrotic wounds that do not heal with standard wound healing care plans.

For each of these subpopulations of soft tissue radionecrosis, published case series and prospective, nonrandomized clinical trials corroborate one another, providing a degree of external validity. Larger studies are warranted. A national registry is currently being evaluated, from which more powerful conclusions may be forthcoming. Currently, the largest group of reported patients treated with HBOT for soft tissue radionecrosis are those with radiation cystitis. At least 15 publications, representing almost 200 patients, report a combined success rate in the 80% range. The two largest studies were published by Bevers and Chong.

HBOT & CARCINOGENESIS

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P ractitioners and patients are often concerned that HBOT may foster recurrence of malignancy or promote the growth of an existing tumor. This is largely because of the known angiogenic effective of HBOT. Feldmeier has reviewed this subject extensively. Malignant angiogenesis appears to follow a different pathway than angiogenesis related to wound healing. His review of the literature suggests that the risk is low.