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Hyperbaric Oxygen Therapy Contraindications

Editor: Jeffrey S. Cooper Updated: 5/13/2025 5:09:57 PM

Introduction

Hyperbaric oxygen therapy (HBOT) involves exposing the body to a pressurized environment at a minimum of 1.4 atmospheres absolute (ATA) with 100% oxygen inspiration.[1] Selecting an appropriate treatment plan requires considering both the potential risks and benefits.[2] Although HBOT is generally well tolerated, candidates, especially those with chronic medical conditions, should undergo thorough evaluation before initiating treatment.

Function

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Absolute Contraindications

The only absolute contraindication to HBOT is an untreated pneumothorax. Placing a patient in a chamber and altering ambient pressure can precipitate a life-threatening tension pneumothorax during ascent. Patients with pneumothorax must receive appropriate treatment, such as thoracostomy tube insertion, before undergoing HBOT.

Relative Contraindications

Certain conditions previously regarded as absolute contraindications to HBOT have been reclassified as relative contraindications based on evolving evidence. These conditions include:

  • Concurrent use of doxorubicin and HBOT may increase the risk of doxorubicin-mediated cardiotoxicity. However, this risk can be mitigated by discontinuing doxorubicin at least 24 hours before HBOT, enabling treatment while minimizing potential adverse effects.
  • Treatment with bleomycin, which is associated with interstitial pneumonitis and fibrosis, was previously considered an absolute contraindication to HBOT due to studies suggesting an increased risk of adverse effects with supplemental oxygen. However, recent research indicates that many patients can safely undergo HBOT, especially if bleomycin exposure occurred more than 6 months prior. A thorough pretreatment evaluation, including a physical examination, radiography, blood gas analysis, and spirometry, is necessary to assess the safety of HBOT in these patients.
  • Disulfiram inhibits superoxide dismutase, thereby increasing the risk of oxygen toxicity, which may manifest as seizures or pulmonary complications. To minimize this risk, the medication should be discontinued before HBOT to allow for adequate clearance. Additionally, careful monitoring for early signs of toxicity and adjusting oxygen exposure parameters can further enhance patient safety.
  • Cisplatin use is considered a relative contraindication due to its potential to impair wound healing, which may reduce the effectiveness of HBOT in treating wounds and late radiation effects. However, no evidence suggests an increased risk or severity of adverse effects with cisplatin, and its use remains acceptable in emergent HBOT applications.
  • Mafenide increases local carbon dioxide production, which may potentially lead to acidosis. Discontinuing the medication before HBOT can enhance patient safety. However, no significant adverse effects have been well-documented from the concurrent use of this medication.[3]

Several conditions have traditionally been considered relative contraindications to HBOT, necessitating a comprehensive evaluation of individual risk factors and potential benefits to determine whether proceeding with this intervention is appropriate. These conditions include:

  • Chronic obstructive pulmonary disease is a relative contraindication to HBOT due to the risk of hypercarbia. Increased oxygen levels can lead to oxygen-induced hypoventilation and exacerbate ventilation/perfusion (V/Q) mismatch.
  • Asthma can lead to air trapping and pulmonary barotrauma. Similarly, asymptomatic pulmonary blebs, bullae, and pulmonary sequestrations identified on imaging are considered relative contraindications due to the risk of air trapping, which may lead to pneumothorax.[4]
  • Implanted devices should be pressure-tested to ensure their functionality in a high-pressure environment. Most devices can withstand 100 feet of seawater (4 ATA), but confirmation from the manufacturer is recommended. Although no cases of internal cardiac defibrillators triggering a fire in the hyperbaric chamber have been reported, disabling the device during treatment may be considered if the risk of dysrhythmia is deemed acceptable. Emergent treatment with HBOT may still be reasonable for patients with implanted defibrillators, as ex vivo data support its safety.[5]
  • Epidural pain pumps may malfunction or become deformed under pressure. Thus, it is crucial to contact the manufacturer to determine the device-specific pressure limitations.
  • Pregnancy has traditionally been considered a relative contraindication to HBOT due to unknown fetal effects. However, recent studies suggest that HBOT may be beneficial in specific cases, such as carbon monoxide poisoning. Given the high affinity of fetal hemoglobin for oxygen and carbon monoxide, HBOT can improve fetal outcomes in cases of severe maternal hypoxia, such as in carbon monoxide poisoning.
  • High fever and epilepsy can lower the seizure threshold, increasing the risk of oxygen toxicity. The likelihood of HBOT-induced seizures in patients with a seizure history or recent brain surgery remains uncertain. However, the use of antiepileptic medications and appropriate fever management can help mitigate this risk.
  • Difficulty equalizing ear or sinus pressure—due to prior surgery, radiation, or an acute upper respiratory infection—can result in pain or barotrauma. A history of ear conditions requiring surgery, such as otosclerosis, may also pose challenges. Patients with nasal congestion or mild difficulty clearing their ears may benefit from phenylephrine nasal spray. If this is ineffective or if there is a significant history of ear disease, tympanostomy tube placement should be considered before initiating HBOT.
  • Eustachian tube dysfunction increases the risk of tympanic membrane barotrauma. Affected patients should undergo pressure equalization training or have tympanostomy tubes placed before initiating HBOT.
  • Claustrophobia may be a contraindication to HBOT, depending on its severity, the patient's response to anxiolytics, and the size of the chamber. In severe cases, it may be considered an absolute contraindication if the patient poses a risk to themselves or the chamber operator.
  • A history of eye surgery may contraindicate HBOT if any air or gas remains trapped in the eye, as pressure changes can cause expansion or contraction, potentially resulting in ocular damage.
  • A history of thoracic surgery can elevate the risk of atelectasis and pneumothorax during HBOT, thereby necessitating a thorough pretreatment evaluation.
  • A history of spontaneous pneumothorax is a relative contraindication and requires further assessment before initiating HBOT.[6]
  • Active upper respiratory tract infections and severe sinus infections increase the risk of sinus and inner ear barotrauma, potentially causing complications and significant discomfort. Similarly, uncontrolled high fevers (>39 °C) are considered a relative contraindication and warrant clinical evaluation to determine the underlying infection.
  • Asymptomatic pulmonary lesions identified on chest radiographs should be assessed before proceeding with HBOT.
  • A history of optic neuritis or sudden blindness has traditionally been considered a relative contraindication to HBOT. However, limited studies have evaluated the safety and efficacy of HBOT in these patients. Notably, HBOT has shown therapeutic benefits in several ophthalmological conditions, including radiation-induced optic neuritis, central retinal artery occlusion, retinal vein occlusion, and macular edema. A thorough clinical evaluation is essential to assess the potential risks and benefits for patients with a history of ocular pathology.

  • Insulin-dependent diabetes mellitus and acute hypoglycemia are considered relative contraindications to HBOT due to the risk of therapy-induced hypoglycemia. However, with point-of-care glucose monitoring and frequent nursing assessments, HBOT can typically be administered safely in patients with diabetes mellitus.
  • Nicotine and caffeine use are contraindicated before HBOT due to their vasoconstrictive effects, which can reduce treatment efficacy. Similarly, the use of illicit vasoconstricting agents, such as cocaine and amphetamines, is contraindicated for the same reason.
  • Congenital spherocytosis has been considered a potential contraindication to HBOT due to the risk of hemolysis from increased oxygen partial pressure. However, case reports indicate that some patients with this hematological condition have tolerated HBOT without complications.
  • Perilymph fistulas, which result from inner ear barotrauma, can cause vestibular symptoms, such as vertigo. HBOT may exacerbate these symptoms by forcing gas into the cochlea.[7] The condition must be carefully assessed before treatment to prevent complications. Vestibular symptoms must be closely monitored during HBOT, with pressure changes adjusted as needed.
  • HBOT may trigger the reactivation of tuberculosis. High-risk patients should undergo a tuberculin skin test or interferon γ-release assay before HBOT to detect latent tuberculosis.[8]

Exposure to HBOT-related oxidative stress may have significant implications for ocular diseases such as age-related macular degeneration and keratoconus. These conditions should be carefully evaluated when assessing the risks and benefits of treatment.[9] In patients with glaucoma, elevated oxygen concentrations in the aqueous humor may increase the risk of trabecular meshwork damage, particularly when the anterior ocular surface is directly exposed to hyperbaric oxygen in a hood or monoplace chamber. Using a mask for HBOT delivery may offer a safer alternative.[10]

Active Cancer—Not a Contraindication

Active cancer was once hypothesized to be a contraindication to HBOT due to concerns that it might stimulate the release of vascular endothelial growth factor (VEGF) and promote tumor progression. However, differences in tumor growth cycles compared to wound healing, along with a literature review, suggest a net neutral effect on gene expression related to cancer progression.

Issues of Concern

Hyperbaric Oxygen—A Driver of Cancer Progression? 

Due to HBOT’s ability to stimulate the regeneration of chronically injured tissue, concerns have been raised about whether increased oxygen delivery could promote cancer growth, particularly in solid tumors with large hypoxic regions. Many HBOT candidates have a prior history of cancer or are actively battling malignancy. However, the concern over accelerating tumor progression remains largely theoretical. Substantial evidence indicates that HBOT has little to no effect on cancer progression.[11][12] On the contrary, the treatment may be a beneficial adjunct to chemotherapy, immunotherapy, and radiation therapy.[13][14] Notably, hypoxia is increasingly recognized as a driver of malignant progression, rather than an inhibitor.[15]

Apprehension about HBOT stimulating cancer progression has persisted for decades, partly fueled by isolated case reports describing rapid tumor progression following treatment.[16] However, these reports do not establish a causal relationship between HBOT and malignancy. In contrast, most studies indicate that HBOT has minimal to no effect on cancer growth or progression.[17][18] A deeper understanding of tumor hypoxia at the molecular and physiological levels further supports these findings.

As mentioned, instead of inhibiting cancer growth, hypoxia is increasingly recognized as a driver of cancer progression and is considered by some to be a hallmark of tumor biology.[19] As growing solid tumors outpace their blood supply, areas of hypoxia develop. To survive, tumor cells release angiogenic signals that stimulate the formation of new blood vessels.

Cancer cells differ significantly from normal cells. Mutations within cancer cells upregulate angiogenic factors, leading to a disorganized and defective vascular network that further exacerbates intratumor hypoxia.[20] Additionally, the rapid proliferation of tumor cells and blood vessels disrupts the basement membrane, increasing the risk of invasion and metastasis. Tumor hypoxia is associated with more aggressive malignant behavior and reduced survival across multiple cancer types.[21]

Under normal physiological conditions, oxygen inhibits neovascularization by promoting the degradation of hypoxia-inducible factor (HIF) proteins. However, this degradation is suppressed in hypoxic environments, allowing HIF proteins to bind to VEGF DNA and enhance protein translation. This dysregulation makes hypoxia a powerful stimulus for angiogenesis. In certain cancers, such as neuroblastoma, mutations in HIF proteins have a central role in tumor pathogenesis.[22]

In addition to dysregulated angiogenesis, hypoxic tumor cells adapt metabolically to survive in low-oxygen conditions. Tumor cells preferentially rely on anaerobic glucose metabolism, a phenomenon known as the Warburg effect. Hypoxia intensifies this effect by upregulating glucose transporters and depriving cells of the oxygen required for normal cellular respiration. Higher levels of HIF have also been shown to enhance the Warburg effect.[23] These anaerobic metabolic adaptations contribute to tumor metastasis, immune evasion, and decreased efficacy of certain chemotherapy drugs, all of which drive cancer progression and increase aggressiveness.

Hypoxia and increased anaerobic respiration also elevate the production of reactive oxygen species (ROS), placing additional stress on tumor cells. In response, tumors upregulate antioxidant defense mechanisms, which can enhance resistance to therapy. Additionally, chronic ROS exposure induces persistent DNA damage, promoting mutational heterogeneity and selecting cells that evade apoptosis, further supporting tumor survival and progression.

Hyperbaric oxygen therapy in malignancy

The mechanisms outlined above highlight the significant impact hypoxia has on tumor cells. However, HBOT counteracts these hypoxia-driven processes rather than promoting cancer growth. Increased oxygen delivery to hypoxic tumor cells enhances the degradation of HIF proteins, leading to reduced VEGF expression and reduced angiogenic signaling.[24] Due to inherent tumor biology, HBOT exposure does not stimulate angiogenesis.

Several in vitro and clinical studies support this conclusion. In a murine model, 4 weeks of HBOT resulted in no significant changes in tumor vascularity, tumor mass, or Ki-67 expression compared to an untreated control group. In human studies, HBOT has been investigated as a pretreatment for chemotherapy, with clinical trials similarly demonstrating no alterations in tumor volume or vascularity as measured by magnetic resonance imaging (MRI).

HBOT alone is ineffective as a standalone cancer treatment. However, this intervention has been explored as an adjunct to radiation and chemotherapy, potentially enhancing treatment efficacy by increasing oxygen availability and promoting the generation of cytotoxic ROS. Additionally, emerging evidence suggests that HBOT may modulate immune responses, potentially improving the efficacy of immunotherapy.[25] These potential applications remain under investigation, and a comprehensive review of ongoing research is beyond the scope of this discussion.

Conclusions on hyperbaric oxygen therapy and cancer

We echo the clinical observation made by Feldmeier et al in 2003 that HBOT does not accelerate the healing of normal wounds.[26] Regardless of concentration, oxygen alone does not enhance cellular growth or division. The benefits of HBOT in wound healing stem from its ability to stimulate angiogenesis, recruit stem cells, and activate other slower-acting mechanisms. However, the tumor microenvironment differs significantly from that of a chronic, nonhealing wound. In tumors, angiogenesis is a response to excessive, dysregulated growth rather than impaired cellular proliferation. As a result, HBOT has little to no effect on tumor progression.

Although the role of HBOT as an adjunct to cancer therapy remains under investigation, many cancer patients develop chronic, nonhealing wounds during treatment. HBOT has demonstrated significant benefits for conditions such as radiation cystitis and osteoradionecrosis of the jaw. However, concerns about HBOT potentially accelerating tumor growth or reactivating dormant malignancies often result in treatment denial for these patients. Based on the evidence presented, the risk of HBOT promoting cancer growth is largely theoretical, while the potential benefits for these patients outweigh this minimal risk.

Heart Failure and Hyperbaric Oxygen Therapy

HBOT induces diffuse vasoconstriction, which increases cardiac afterload while simultaneously reducing cardiac output. As a result, a history of heart failure, particularly with reduced ejection fraction, is considered a relative contraindication. However, clinical evidence suggests that HBOT can be safely administered when heart failure is appropriately managed, including the use of diuretics and fluid restriction.[27]

Clinical Significance

HBOT is used in emergent and elective interventions. The primary emergent indication is decompression sickness resulting from gas embolism or decompression illness. The treatment is also used in the acute management of carbon monoxide poisoning, chronic refractory osteomyelitis, radiation-induced soft tissue injuries, and clostridial myonecrosis. However, the quality of supporting evidence varies across these applications. Additionally, HBOT has been utilized for necrotizing wounds, retinal artery occlusion, and acute trauma. HBOT has also been used to treat necrotizing wounds, retinal artery occlusion, and acute trauma, though its efficacy for these conditions remains uncertain. In certain cases, HBOT acts as an adjunct to conventional treatments for conditions that are unresponsive to standard therapies alone.[28]

Additional research suggests that patients recovering from head and neck tumors after radiation and surgical intervention may experience progressive fibrosis of the soft tissue within the jaw. Studies indicate that individuals who receive coadministered HBOT experience better outcomes than those who do not, supporting the referral of irradiated head and neck cancer patients to HBOT centers. Physicians should coordinate this effort with planned surgeries to optimize tissue healing.[29] Delayed radiation sequelae from treatments for neurologic, gynecologic, urologic, and colorectal cancers have also demonstrated responsiveness to concurrent HBOT.[30][31]

HBOT has also been used to treat severe anemia in cases where transfusions are refused (such as by observant Jehovah’s Witnesses) or cannot be safely performed.[32] This application is supported by basic science research and reinforced by clinical case reports. One of the main drawbacks of this treatment is the limited access to HBOT centers. A national shortage of HBOT facilities in the United States restricts the availability of this intervention and hinders further research into its role as a mainstay therapy.

Enhancing Healthcare Team Outcomes

HBOT indications should be carefully evaluated against potential contraindications to ensure that the expected benefits outweigh the associated risks.[33] Interprofessional collaboration is crucial for assessing contraindications and determining whether HBOT is appropriately indicated. HBOT is used in both emergent and elective settings. The roles of healthcare professionals can vary significantly. In emergencies, earlier initiation is associated with improved outcomes.[34] Although emergency physicians typically make the final decision regarding emergent HBOT, nurses, radiologists, emergency medical personnel, and pharmacists play vital roles in identifying contraindications.

Emergency medical personnel are responsible for obtaining the initial history, which may reveal indications for emergent HBOT, such as diving injuries or carbon monoxide toxicity. Radiology staff must review prior imaging for abnormalities, such as pulmonary nodules, that may contraindicate elective HBOT. In emergent situations, radiologists are vital in ruling out tension pneumothorax, the only absolute contraindication to HBOT.

Pharmacists and pharmacy staff are vital in reviewing a patient’s medication regimen to ensure the safe administration of HBOT in conjunction with other medical interventions, such as cancer chemotherapy. Nurses play a crucial role in monitoring patients for adverse reactions and ensuring their safety and well-being throughout the HBOT treatment process.

For elective HBOT, primary care providers must evaluate medical conditions that could serve as relative contraindications, including claustrophobia, upper respiratory infections, diabetes, eustachian tube malformations, and chronic respiratory diseases. Continuous monitoring of comorbidities is necessary to mitigate potential risks associated with HBOT.

The Oxford Centre for Evidence-Based Medicine (CEBM) has established evidence levels for HBOT based on specific conditions, including gas embolism, radiation injury, and refractory osteomyelitis.[35][36][37] This framework allows clinicians to make informed decisions about the use of HBOT, ensuring its appropriate use based on the quality of evidence available for each condition.

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