As with most medical treatments, absolute and relative contraindications exist with the use of hyperbaric oxygen therapy (HBOT).
. Absolute Contraindications to Hyperbaric Oxygen Therapy
|Necessary Conditions Prior to HBOT
|No treatment for extended time from use of medication
|Impaired wound healing
|No treatment for extended time from use of medication
|Blocks superoxide dismutase, which is protective against oxygen toxicity
|Impaired wound healing
|Discontinue and remove medication
Relative Contraindications to Hyperbaric Oxygen Therapy
|Necessary Conditions Prior to HBOT
|Air trapping upon ascent leading to pneumothorax
|Must be well controlled with medications
|Treatment with benzodiazepines
|None; HBOT for emergencies only
|Chronic obstructive pulmonary disease (COPD)
|Loss of hypoxic drive to breathe
|Observation in chamber
|Eustachian tube dysfunction
|Barotrauma to tympanic membrane
|Training, PE tubes
|Higher risk of seizures
|Pacemakers or epidural pain pump
|Malfunction or deformation of device under pressure
|Ensure company has pressure-tested device and learn to what depth
|Unknown effect on fetus (Previous studies from Russia suggest HBOT is safe.)
|None, but HBOT may be used in emergencies
|May have lower seizure threshold
|Should be stable on medications; may be treated with benzodiazepines
|Upper respiratory infection (URI)
|Resolution of symptoms or decongestants
Decompression Sickness and Air Embolism
Decompression Sickness Decompression 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.[24, 25] DCS can occur after scuba diving, ascent with flying, or hypobaric or hyperbaric exposure.
DCS can be broken down into the following 3 types:
Type I involves musculoskeletal, skin, and lymphatic tissue, and often has accompanying fatigue.
Type II includes neurologic systems (either CNS or peripheral), cardiorespiratory, audiovestibular, and shock.
Type III DCS describes a syndrome that presents with symptoms that progress to a spinal deficit that may 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.[26, 27]
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.[25, 26] 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.
Air embolism refers to bubbles in the arterial or venous circulation. Venous bubbles can result from compressed gas diving (such as scuba) but are often filtered through the pulmonary capillary bed. If a large volume of bubbles is noted, they may overwhelm the pulmonary filter and enter the arterial circulation. Arterial gas emboli (AGE) can also result from pulmonary barotrauma or accidental intravenous air injection or some surgical procedures.[31, 32, 33, 34, 35] Symptoms usually occur within seconds to minutes of the event and can include loss of consciousness, confusion, neurological deficits, cardiac arrhythmias, or cardiac arrest.
The treatment of choice is recompression therapy. Gas embolism used to be treated with US Navy Treatment Table 6A, which required a pressure of 6 ATA. The rationale was that the larger volume of gas warranted increased pressure to force bubble redistribution or elimination. No conclusive evidence shows that this offers superior treatment to the US Navy Treatment Table 6 for most cases; however, if complete relief is not achieved after initial recompression, deeper recompression may be needed.
Carbon Monoxide Poisoning
Carbon monoxide (CO) poisoning, whether intentional or accidental, occurs when one inhales the colorless and odorless carbon monoxide gas. Despite improved awareness and sensory alarms, multiple deaths occur each year.
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.[39, 37, 40, 41, 42]
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.[18, 43, 44] 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;[45, 37, 46] 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.
Enhancement of Healing in Selected Problem Wounds
Normal wound healing proceeds through stages of hemostasis, removal of infectious agents, resolution of the inflammatory response, reestablishment of a connective tissue matrix, angiogenesis, and resurfacing. Problem (or chronic) wounds are those which do not proceed completely through this process because of any number of local and systemic host factors. For this reason, chronic wounds are often categorized as diabetic wounds, venous stasis ulcers, arterial ulcers, or pressure ulcers.
Wounds that fail to heal are typically hypoxic. Multiple components of the wound healing process are affected by oxygen concentration or gradients, which explains why hyperbaric oxygen therapy (HBOT) can be an effective therapy to treat chronic wounds. Angiogenesis occurs in response to high oxygen concentration. This is likely a multifactorial effect of HBOT. First, fibroblast proliferation and collagen synthesis are oxygen dependent, and collagen is the foundational matrix for angiogenesis. In addition, HBOT likely stimulates growth factors involving angiogenesis and other mediators of the wound healing process. Hyperbaric oxygen also has been shown to have direct and indirect antimicrobial activity; in particular, it increases intracellular leukocyte killing.[13, 14, 12]
Diabetic lower extremity ulcers have been the focus of most wound research in hyperbaric medicine, since the etiology of these wounds is multifactorial, and HBOT can address many of these factors. Several randomized controlled clinical trials have studied HBOT for the treatment of diabetic lower extremity wounds.[49, 50, 51, 52] Additionally, many more prospective, noncontrolled clinical trials and retrospective trials have been completed. Based on the body of evidence, major insurance carriers around the world now endorse the use of HBOT for the treatment of diabetic lower extremity wounds that show evidence of deep soft tissue infection, osteomyelitis, or gangrene. HBOT has been shown to reduce the amputation rate in patients with diabetic ulcers as well.[49, 50, 52]
In an effort to select patients appropriately for HBOT, various objective vascular evaluation methods have been used, including transcutaneous oximetry, capillary perfusion pressure, laser Doppler, and other types of vascular studies. Debate is ongoing regarding which method provides the most reliable data and whether these methods are more useful than other clinical markers of wound failure.
Note that HBOT should be used in conjunction with a complete wound healing care plan. As with all chronic wounds, other underlying host factors (eg, large vessel disease, glycemic control, nutrition, infection, presence of necrotic tissue, offloading) must be simultaneously addressed in order to have the highest chance of successful healing and functional capacity.
Because the goals of HBOT for wound healing include cellular proliferation and angiogenesis, HBOT is generally performed daily for a minimum of 30 treatments. Treatment is generally at 2 to 2.4 ATA for a total of 90 minutes of 100% oxygen breathing time. Based on the response to therapy, extended courses of therapy may be indicated.
Compromised Skin Grafts and Flaps
Most 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 shown 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 shown 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 showed the greatest improvement.
Human case studies showing 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.
Crush Injury and Compartment Syndrome
Acute 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[58, 59] 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).[15, 16] 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.[61, 58, 62] 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.
Necrotizing Soft Tissue Infections
These 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 the infection and reduce tissue loss. First, HBOT is toxic to anaerobic bacteria. Next, HBOT improves polymorphonuclear function and bacterial clearance.[12, 66] Based on results of work related to CO poisoning, HBOT may decrease neutrophil adherence based on inhibition of beta-2 integrin function.[17, 16] 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.[19, 67] 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 2 studies: 34% (untreated) vs. 11.9% (treated) in one study; 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.
The 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.[72, 73, 74, 75] HBOT can also help reduce increased intracranial pressure (ICP) and its effects are proposed to be more pronounced with perifocal brain swelling.[9, 76, 77] 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. The optimized number of treatments has not been determined.
Delayed Radiation Injury
Radiation 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.
Marx 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.
Soft tissue radionecrosis
While 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, and radiation cystitis may 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 2 largest studies were published by Bevers and Chong.
HBOT and carcinogenesis
Practitioners 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.
Refractory osteomyelitis is defined as acute or chronic osteomyelitis that is not cured after appropriate interventions. More often than not, refractory osteomyelitis is seen in patients whose systems are compromised. This condition often results in nonhealing wounds, sinus tracts, and, in the worst case, more aggressive infections that require amputation.
Mader and Niinikoski showed that hyperbaric oxygen therapy (HBOT) is capable of elevating oxygen tension in infected bone to normal or above normal levels.[86, 12] Since polymorphonuclear (PMN) function requires adequate oxygen concentration, this is a significant mechanism by which HBOT helps to control osteomyelitis, as demonstrated by Mader in the same study.
A unique mechanism by which HBOT is beneficial in osteomyelitis is in promoting osteoclast function. The resorption of necrotic bone by osteoclasts is oxygen-dependent. This has best been demonstrated in animal models of osteomyelitis.
Additionally, as previously mentioned, HBOT facilitates the penetration or function of antibiotic drugs. Other properties of HBOT previously discussed, such as neovascularization and blunting the inflammatory response, likely provide additional benefit.
Convincing animal evidence supports the use of HBOT in the treatment of osteomyelitis. Clinical studies are somewhat problematic, however, because osteomyelitis has so many different presentations that comparisons become difficult. This is compounded by the small study sizes found in the literature; however, these do suggest benefit of HBOT for refractory osteomyelitis in humans.
One specific subset of osteomyelitis that merits special attention is malignant otitis externa. This progressive pseudomonal osteomyelitis of the ear canal can spread to the skull base and become fatal. Davis et al published a study of 17 patients with malignant otitis externa, all of whom showed dramatic improvement with the addition of HBOT to standard surgical debridement and antibiotic therapy.
Thermal burns present a multifactorial tissue injury that culminates in a marked inflammatory response with vascular derangement from activated platelets and white cell adhesion with resultant edema, hypoxia, and vulnerability to severe infection. Poor white cell function caused by the local environment exacerbates this problem. Hyperbaric oxygen therapy (HBOT) addresses each of these pathophysiological derangements, and can, therefore, make a significant difference in patient outcomes. These mechanisms of action have been discussed above.
Multiple animal studies support the utility of HBOT for treatment of thermal burns. Human studies ranging from case series to randomized clinical trials have supported the potential benefit of HBOT in burn treatment. These include a small randomized study by Hart that demonstrated improved healing and decreased mortality. Niezgoda showed increased healing in a standardized human burn model. In a series of publications, Cianci[91, 92] suggests significant reduction in length of hospital stay, need for surgery, and cost.
Because of the goals of therapy, HBOT is begun as soon as possible after injury, with a goal of 3 treatments within the first 24 hours and then twice daily. Length of treatment depends on the clinical impairment of the patient and the extent of and response to grafting. Special attention must be given to fluid management and chamber and patient temperature to avoid undue physiologic stress to the patient as well as potential complications of treatment (ie, oxygen toxicity).
Patients who develop exceptional anemia have lost significant oxygen carrying capacity in the blood. These patients become candidates for hyperbaric oxygen therapy (HBOT) when they are unable to receive blood products because of religious or medical reasons. The major oxygen carrier in human blood is hemoglobin, transporting 1.34 mL of oxygen per gram. Borema performed an experiment in the 1960s in which exsanguinated pigs (who had only plasma in their vasculature) were able to sustain life under hyperbaric conditions.
The body generally uses 5-6 vol% (mL of O2 per 100 mL of blood); under 3 ATA, 6 vol% of molecular oxygen can be dissolved into the plasma. The CNS and cardiovascular systems are the two most oxygen-sensitive systems in the human body.[93, 95] Oxygen debt is one way of determining a patient’s need to start or continue HBOT. A cumulative oxygen debt is the time integral of the volume of oxygen consumption (VO2) measured during and after shock insult minus the baseline VO2 required during the same time interval. Patients who have a debt >33 L/m2 do not survive, whereas patients with debts ≤9 usually recover.
HBOT is administered at 2-3 ATA for periods of up to 4 hours per treatment. As many as 3-4 sessions a day may be necessary, depending on a patient’s clinical picture. Treatments should continue until the patient can receive blood products, no longer demonstrates end stage organ failure, or no longer has a calculated oxygen debt.
Central Retinal Artery Occlusion
Central retinal artery occlusion (CRAO) is a sudden, painless loss of vision; this is the most recently approved indication by the Undersea and Hyperbaric Medicine Society (UHMS) for HBOT. CRAO is caused by the obstruction of the central retinal artery and, although an infrequent cause of visual loss, leads to permanent visual loss. Current treatment for CRAO consists of attempts to lower intraocular pressure and movement of a potential embolus downstream, ocular massage, anterior chamber paracentesis, and medications (both eye drops and oral); most modalities have proven inefficacious.
A small study by Hertzog et al evaluated HBOT with CRAO. Patients were divided into groups based on time of onset of CRAO to HBOT. The study noted that HBOT was most useful in preserving vision if instituted within 8 hours. Another retrospective study published by Beiran compared patients from a facility where HBOT was available to a facility that did not have HBOT. The patients who received HBOT demonstrated visual improvement (82% HBOT vs 29.7% control).
Patient selection for HBOT should meet the following criteria: < 24 hours of painless vision loss; no history of flashes or floaters prior to vision loss; visual acuity 20/200 or worse, even with pinhole testing; age >40 years; and no recent eye surgery or trauma. Visual improvement has been reported even with delay of HBOT.
HBOT is administered at 2 ATA on 100% oxygen. If no response is noted, pressure should be increased to 2.8 ATA. If vision is still not improved after 20 minutes, US Navy treatment Table 6 is indicated. If vision is improved, continue at treatment depth for 90 minutes bid. Continue daily bid compression until resulting in 3 days without visual improvement. If the patient responds to 100% oxygen via nonrebreather (NRB) mask itself, HBOT is not needed, and the patient should be maintained on surface 100% oxygen for 12 hours.
Complications and Special Concerns
As with any medical therapy, treatment brings both risks and benefits. One of the more frequently seen injuries caused by hyperbaric oxygen therapy (HBOT) is barotrauma (ie, injuries caused by pressure as a result of an inability to equalize pressure from an air-containing space and the surrounding environment).[2, 3]
Table 4. Complications to Hyperbaric Oxygen Therapy (Open Table in a new window)
|Middle ear (URI, Eustachian tube dysfunction)
|Ear pain, fullness
Wait for URI resolution
|Sinus pain or bleeding
Steroid nasal spray
|Replacement of filling or crown (allows trapped air bubble to escape)
Chest pain or burning
Decreased vital capacity
Thoracostomy (if pneumothorax)
Increase decompression time
|Round or oval window blowout
Nystagmus, vertigo, or both
Refer to ENT
|Visual refraction change
|Progressive myopia with prolonged number of treatments
|Most resolve spontaneously when treatment finished
|Clouding of vision
|Prescreen for existing
HBOT does not influence cataract formation
|CNS (Incidence 0.7 per 10,000 treatments at 2.4 ATA)
|Removal from oxygen source
Resume HBOT with shorter oxygen treatment periods
Does not require medication
Treat hypoglycemia if present
Treat fever if present
Chest pain or burning
Decreased vital capacity
|Decrease total oxygen exposure time (including outside HBOT)
Pediatric patients also have special concerns. The proportion of surface area to body mass is much greater in children than in adults. As temperature in the chamber can fluctuate, care must be taken to ensure the child remains warm without causing hyperthermia. This can be more difficult in a monoplace chamber because the patient cannot be physically reached from outside the chamber to provide blankets or warmed water as heat sources. Unless children can focus and equalize their ears, consideration for placement of tympanostomy tubes should be discussed with the parents to prevent middle ear barotrauma.
Oxygen administration is easy in a monoplace chamber because the chamber is pressurized with oxygen. Multiplace chambers can fashion equipment to fit the child. A neck ring can be fitted over the child’s torso, or, if the child is small enough, 2 hoods can be placed together to form a capsule around the child. Care must be taken when treating patients with ductal dependent lesions, as oxygen is a signal for ductus arteriosus closure. This has not been a documented problem in pregnancy. Bronchopulmonary dysplasia in a preterm infant, as is associated
Medical Oxygen Hyperbaric Clinic
4660 South Biltmore La.
Madison, WI 53718