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Hyperbaric Complications

Editor: Jeffrey S. Cooper Updated: 6/2/2025 10:19:37 PM

Introduction

Hyperbaric oxygen therapy is considered a safe treatment for various conditions. However, as with virtually all medical treatments, there is a potential for adverse effects. A thorough understanding of these risks enables clinicians to both minimize the potential for some adverse effects and discuss the risks and benefits when offering treatment to patients.

A study involving patients treated in monoplace chambers from 2009 to 2010 revealed an estimated incidence of adverse effects of around 0.4%. Among these, ear pain accounted for nearly 50% of the cases, whereas around 25% were classified as confinement anxiety. 

Complications associated with hyperbaric oxygen therapy can be classified into 2 categories—pressure-related or oxygen-related adverse effects. Pressure-related complications primarily involve barotrauma, which can impact any closed, air-filled cavity, including the ears, sinuses, teeth, lungs, and bowel. Oxygen-related adverse effects can be further subdivided into 3 categories—pulmonary, neurological, and ophthalmological.

Alternatively, complications can be classified as primary effects—resulting from pressure and hyperoxia—or secondary effects, stemming from controlled oxidative stress mediated by reactive oxygen and nitrogen species.

Confinement anxiety is caused by the physical space of the chamber and is not considered a true complication of hyperbaric oxygen therapy.[1][2][3]

Additional considerations include elevated blood pressure, cardiogenic pulmonary edema, hypoglycemia, and risks of increased toxicity with specific chemotherapeutic agents, such as bleomycin and doxorubicin.[4]

Issues of Concern

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Issues of Concern

Effects of Pressure

Barotrauma can best be understood through Boyle's Law: P1V1 = P2V2. As pressure increases, volume decreases, and vice versa. Barotrauma results from an inability to equalize pressure between the environment and the air-filled space in the body, resulting in a squeeze. This process requires equalization to minimize risks to the hyperbaric patient.

Middle ear barotrauma: The middle ear is the most frequently affected site of barotrauma, with severity ranging from mild hyperemia to actual rupture of the tympanic membrane. The severity of barotrauma injuries, regardless of the cause, can be graded using the TEED scale. A TEED 0 indicates symptoms with a normal physical examination, whereas a TEED 5 denotes rupture of the tympanic membrane. In addition, the more recently introduced O'Neill Grading System is specifically designed for patients undergoing hyperbaric oxygen therapy. This system is somewhat simplified, using scores of 0 (symptoms without anatomical change), 1 (fluid or erythema), or 2 (bleeding behind the tympanic membrane or perforation), to ensure greater consistency.[5] For patients who are unable to equalize due to poor technique or intubation and sedation, a myringotomy may be indicated before treatment can proceed.[6][7][8][9]

Gases expand when the hyperbaric chamber is depressurized during a diver's ascent. This expansion can cause noticeable pressure on the tympanic membranes in the middle ear. Typically, the expanded air escapes through the eustachian tubes. However, significant eustachian tube swelling due to barotrauma during descent or a misinformed patient performing a forceful Valsalva maneuver during their ascent can cause trauma to the tympanic membrane or the round or oval window of the inner ear.

Sinus and dental barotrauma: Gas-filled spaces contract during the pressurization of a hyperbaric chamber, which occurs during a patient's descent. Under normal conditions, air moves freely in and out of the sinuses but can become trapped. Air trapping in the sinuses is typically secondary to a mechanical obstruction, such as polyps or inflammation. Sinus barotrauma typically results in sinus pain and swelling. However, more significant sequelae, including cranial nerve symptoms, have been reported. Consequently, patients with active upper respiratory tract infections are advised to delay hyperbaric treatment until symptoms have resolved.

Dental barotrauma, also known as tooth squeeze, is an uncommon condition that can occur when an air pocket in the tooth is formed by dental decay, a temporary cap, or a filling. This condition can be quite painful.

Pulmonary barotrauma: Pulmonary barotrauma is the most severe and deadly type of barotrauma. Anything that leads to pulmonary overpressurization can rupture the alveoli, including air trapping in the lungs, breath holding during depressurization, severe bronchospasm, or a closed glottis during a coughing fit or seizure. The resulting complication depends on where the escaped air travels once the rupture occurs; possible avenues include the mediastinum (pneumomediastinum), visceral pleura (pneumothorax), or vasculature (arterial gas embolism). These complications are rare but can be severe, particularly if left untreated or unrecognized. A pneumothorax has the potential of becoming a tension pneumothorax, particularly during depressurization, which can lead to cardiovascular collapse and death.

Pulmonary conditions increase the risk of pulmonary barotrauma, including chronic obstructive pulmonary disease, asthma, pulmonary fibrosis, pulmonary bullae or cysts, lung tumors, and bronchiectasis. A pulmonary evaluation should be performed for patients with these (or similar) conditions, and individually tailored discussions on the risk versus benefit of hyperbaric oxygen therapy should be undertaken. 

Device-related considerations: Implanted devices must be given special consideration, as not all are adequately pressure-tested. These devices include cardiac implants such as pacemakers, defibrillators, and left ventricular assist devices; implanted or external breast prostheses; and orbital implants.

Oxygen Toxicity

Clinicians must understand that oxygen functions like a drug. Even at normobaric pressures, O2 administration can have adverse effects. At high pressures, oxygen can cause pulmonary, neurological, and ophthalmological issues.

Pulmonary toxicity: Pulmonary oxygen toxicity is believed to be a function of the duration of oxygen exposure and occurs more rapidly at higher pressures. In the setting of hyperbaric oxygen therapy, this condition presents as tracheobronchitis, which initially develops centrally and then spreads outward along the tracheobronchial tree. At the mild end of the spectrum, it presents as a cough. However, tracheobronchitis may progress to substernal burning and, in severe cases, lead to dyspnea with both exertion and at rest. The latter is a rare complication and often resolves within a few days.[10][11] More severe complications of pulmonary oxygen toxicity are possible, but contemporary hyperbaric oxygen therapy regimens do not allow for this progression.

Central nervous system toxicity: The neurologic effects of oxygen toxicity are significantly affected by acute changes in the partial pressure of oxygen, such as a large dose of oxygen. These effects can be remembered by the acronym VENTID—Vision (tunnel vision), Ears (tinnitus), Nausea, Twitching (muscle fasciculation), Irritability, and Dizziness. A generalized tonic-clonic seizure is considered the most concerning neurologic symptom of oxygen toxicity. The incidence of this complication is dose-dependent, occurs once every 5000 to 10,000 treatments, and is more common in individuals with lower seizure thresholds, such as those with epilepsy, diabetes, fever, or alcohol abuse disorder. Acute carbon monoxide poisoning is known to increase the risk of oxygen toxicity seizures, which is an indication of hyperbaric oxygen therapy. Fortunately, oxygen toxicity seizures typically stop after the patient begins breathing normal air; no other intervention is needed. Patients who experience oxygen toxicity seizures are not precluded from having further treatments. However, the addition of more frequent air breaks may be used to decrease the risk of another event. When consenting a patient for hyperbaric oxygen therapy, it should be explained to the patient that if they have an oxygen toxicity seizure, it does not mean that they have developed epilepsy, but that it was a result of the intervention (oxygen therapy).

Ophthalmologic adverse effects: Ophthalmologic adverse effects of hyperbaric oxygen therapy include both temporary complications, such as myopic change, and permanent complications, such as retinopathy of prematurity and cataract formation.

Myopic change is the most common ocular complication of hyperbaric oxygen therapy. Transient myopic change is believed to be due to the increased refractive index of the lens. The exact pathophysiological mechanism remains debatable, but it is likely related to oxidative changes in the crystalline lens. Myopic change is observed more frequently in patients using hoods in the hyperbaric chamber compared to those using a mask, which is likely due to direct exposure of the eye to high partial pressures of oxygen. There are no effects on artificial lenses. This complication is considered fully reversible after the cessation of hyperbaric oxygen therapy, and vision rapidly improves within the first 6 weeks. However, a return to baseline can take up to 1 year.[12]

Retinopathy of prematurity only occurs in neonates and can result in permanent blindness. Exceptional care should be taken in considering risks and benefits in treating premature infants, with explicit discussion regarding retinopathy of prematurity with the parents or guardians. 

Cataract formation tends to occur only after many hyperbaric treatments. One study suggests that de novo cataract formation starts after 150 daily treatments, while another asserts that 300 to 850 hours of exposure are required. Therefore, this complication does not typically occur in patients who receive the standard regimen of 20 to 60 treatments. Despite this, the patient should still be advised if multiple rounds of treatment are indicated. Cataract progression is also possible.[13]

Additional Concerns

Claustrophobia: Although pressure and oxygen are not typically issues, the enclosed area within the chamber can potentially be an issue. Patients should be asked about any known discomfort regarding tight spaces during the initial consultation for hyperbaric oxygen therapy.

Blood pressure effects: Hyperbaric oxygen therapy can cause elevated blood pressure, likely due to vasoconstriction and subsequent increased systemic vascular resistance. However, the clinical significance of this effect remains uncertain.

Cardiogenic pulmonary edema: Given the increase in systemic vascular resistance, patients with known congestive heart failure and low cardiac ejection fractions (<35%) are at a mild risk of developing acute pulmonary edema.[14]

Use of Chemotherapeutic Agents

Bleomycin: The current recommendation is to wait at least 6 months after bleomycin administration before receiving hyperbaric oxygen therapy due to the increased risk of complications associated with pulmonary oxygen therapy. In addition, patients who have received bleomycin at any time in the past should undergo pulmonary investigations before initiating hyperbaric oxygen therapy, given the risk of fibrosis associated with the drug.

Doxorubicin: The current recommendation is to wait at least 24 hours after doxorubicin administration before initiating hyperbaric oxygen therapy.

Clinical Significance

Hyperbaric oxygen therapy is a relatively safe and effective treatment for various conditions, many of which cannot be treated effectively otherwise. However, patients must be made aware of certain risks and complications before initiating therapy. Although most common complications are relatively benign, such as ear and sinus barotrauma, claustrophobia, and transient myopic change, more severe complications are also possible. As with all medical therapies, educating patients on the risks and obtaining informed consent is mandatory.[15][16][14][17][18][19]

Enhancing Healthcare Team Outcomes

Hyperbaric oxygen therapy is a safe and effective treatment for various acute and chronic conditions. However, healthcare professionals need to educate patients about the potential complications associated with this therapy. Although most complications are benign or self-limiting, there can be severe adverse reactions, such as pneumothorax or arterial gas embolism. In addition, patients who undergo multiple therapy sessions may be at risk for developing cataracts. Patients must be informed about these risks before initiating treatment.

References


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