Hyperbaric oxygen therapy (HBO2) is a useful, and often underutilized, treatment modality for a variety of conditions. Providing 100% oxygen at increased atmospheric pressures oxygenates ischemic tissues, decreases edema, lessens reperfusion injury, stimulates angiogenesis, promotes wound healing, and improves fibrosis of irradiated tissues. As a result, HBO2 may significantly improve patient outcomes in carbon monoxide poisoning, crush injury and impending compartment syndrome, bone and soft tissue necrosis secondary to delayed radiation injury, problem wounds, central retinal artery occlusion, and idiopathic sudden sensorineural hearing loss. Given the likelihood of initial patient presentation or necessity of expedient intervention, it is imperative for physicians and surgeons to be able to recognize such opportunities where HBO2 referral is appropriate. Timely referral is important for successful outcomes.
hyperbaric oxygen; hyperbaric medicine; Carbon Monoxide; Central retinal artery occlusion; Idiopathic sudden sensorineural hearing loss.
Doctors and other providers should be aware of the utility of hyperbaric oxygen therapy for the following conditions:
- Carbon Monoxide Poisoning
- Crush Injury and Skeletal Muscle Compartment Syndrome
- Delayed effects of therapeutic radiation including osteoradionecrosis, radiation cystitis, enteritis, proctitis and skin wounds in irradiated fields.
- Central Retinal Artery Occlusion
- Sudden Sensorineural Hearing Loss
- Problem wounds due to diabetes and vascular disease
Hyperbaric oxygen therapy (HBO2) as defined by the Undersea & Hyperbaric Medical Society (UHMS), is “an intervention in which an individual breathes near 100% oxygen intermittently while inside a hyperbaric chamber that is pressurized to greater than sea level pressure (1 atmosphere absolute, or ATA)”  Patients are enclosed within a chamber that is pressurized up to three times normal atmospheric pressure. HBO2 is commonly known by health care providers for treating decompression sickness (“the bends”) in divers; however, there are a total of fourteen indications approved by the Undersea & Hyperbaric Medical Society (UHMS) and generally reimbursed by The Centers for Medicare & Medicaid Services (CMS) and other insurers in the USA.
These indications are:
- Gas Embolism
- Carbon Monoxide Poisoning
- Clostridial Myositis and Myonecrosis (Gas Gangrene)
- Crush Injury, Compartment Syndrome and Other Acute Traumatic Ischemia’s
- Decompression Sickness
- Arterial Insufficiencies including:
- Problem Wounds
- Central Retinal Artery Occlusion
- Severe Anemia
- Intracranial Abscess
- Necrotizing Soft Tissue Infections
- Osteomyelitis (Refractory)
- Delayed Radiation Injury (Soft Tissue and Bony Necrosis)
- Compromised Grafts and Flaps
- Acute Thermal Injury
- Idiopathic Sudden Sensorineural Hearing Loss
Physicians and surgeons encounter a broad spectrum of patients that may need referral for hyperbaric therapy, either as the primary treatment modality or as an adjunct to pharmacologic or surgical interventions. Out of the fourteen indications for HBO2, we have decided to focus on the following based on the likelihood of initial patient presentation or necessity of expedient intervention.
Additional information and resources may be found at the Undersea & Hyperbaric Medical Society: https://www.uhms.org/
Carbon Monoxide Poisoning
Carbon Monoxide (CO) is a colorless, odorless gas that can be inhaled when an individual is exposed to combustion products in a poorly ventilated or enclosed area. CO poisoning is a clinical diagnosis, based upon the patient’s history and reported symptoms. Carboxyhemoglobin (COHb) may be used to confirm exposure, but the relatively short half-life of COHb may result in normal COHb levels [2-4].
The cardiovascular and central nervous systems are the most susceptible following CO exposure, resulting in cardiac injury and often long-lasting neurological sequelae including motor weakness, peripheral neuropathies, hearing and vision changes, and Parkinsonian-like syndromes [5-7]. Infants, children, pregnant women, elderly, and those with heart disease are particularly at risk for more serious illness.
CO induced injuries are due to hypoxic stress from COHb formation as well as systemic oxidative stress . However, it is important to keep in mind that COHb levels are not correlated with symptomatology or very predictive of the development of central nervous system sequelae and long-term patient outcome [9-12]. Therefore, COHb should not be used alone to determine necessity of hyperbaric referral.
Signs and symptoms may present long-after the initial exposure. Patients may complain of nonspecific symptoms, such as: headaches, dizziness, fatigue, and sleep disturbances. In addition, neurological symptoms including neuropsychological and affective symptoms may arise. This symptomatology can present weeks to months later and patients may have deficits lasting for years. Therefore, patient follow-up is crucial .
Patients with signs or symptoms of CO poisoning should be placed on supplemental oxygen to increase tissue oxygenation and hasten the dissociation of CO from hemoglobin . The addition of hyperbaric oxygen accelerates this dissociation, treats tissue hypoxia, reduces the harmful inflammatory response that can occur in damaged tissue, and protects against oxidative stress [14,15]. Despite various findings in differing studies and reviews such as the Cochrane review, which discusses a trial that has been under scrutiny for using inadequate dosing of HBO2, HBO2 has been shown to decrease the incidence of cognitive and cerebrovascular abnormalities and improve long term neurological outcomes [16-19]. This treatment is recommended by the UHMS and is rated as a Class I – Strong recommendation (American Heart Association Classification) .
HBO2 consultation should be considered in patients with signs of significant CO poisoning (e.g. severe acidosis, cardiovascular dysfunction or injury, loss of consciousness, neurological problems, or COHb ≥ 25%), with the optimal benefit occurring with the least delay [20-22]. The most optimal time to HBO2, to prevent delayed neurologic sequence, is within 48 hours of exposure .
Crush Injury and Skeletal Muscle Compartment Syndrome
For both crush injuries and skeletal muscle compartment syndrome, trauma and subsequent tissue hypoxia are involved in a vicious cycle that ultimately lead to limb threatening damage. Following the initial insult, bleeding or edema within the compartment can collapse the microcirculation leading to tissue ischemia and hypoxia. Hypoxic cells leak intracellular water leading to further edema and third spacing of fluid. This ischemia-edema cycle continues until compartment syndrome is fully established and emergent fasciotomy is needed.
If delivered early, HBO2 may benefit the patient through several mechanisms. First, HBO2 offsets tissue hypoxia by increasing oxygen tensions in plasma as well as tissue fluids. This increases the diffusion distance of oxygen from the capillary to the cell [24,25]. Secondly, HBO2 reduces edema by inducing vasoconstriction, reducing capillary inflow and decreasing hydrostatic pressure in the capillary bed. It does this while maintaining fluid outflow with resorption of fluid at the capillary level further reducing fluid built up within the compartment [26-31]. Lastly, HBO2 can mitigate oxidative reperfusion injury by interfering with neutrophil adhesion to the endothelium and providing an oxygenated environment to produce oxygen radical scavengers that are responsible for reducing reactive oxygen species [32,33].
The best argument can be made for patients in the impending compartment syndrome stage. When the patient begins to develop signs and symptoms associated with compartment syndrome (e.g. pain, hyperesthesia, weakness, discomfort with passive stretching of toes, or tautness of the compartment) compartment pressure measurements should be made by the provider caring for the patient in any location (e.g. covering in an Emergency Department in a rural facility). In the impending stage, the patient has not reached the threshold requiring fasciotomy. Consideration and consultation for HBO2 should be made at this time, given the opportunity to intervene in the edema-ischemia cycle and potentially prevent the compartment syndrome advancing to requiring fasciotomy [34,35].
Additionally, the cost effectiveness of HBO2 is evident. It has been reported that when HBO2 was started during the impending stage of compartment syndrome, the total costs were 75 percent less than having to complete HBO2 following a fasciotomy procedure . It is estimated that the cost savings for one patient to undergo a fasciotomy in the impending stage would be equivocal to ten patients undergoing HBO2 in the impending stage and halting their progression . In addition, following crush injury, the same mechanisms may reduce healthcare costs through decreasing complications, reducing tissue loss, and morbidity. This can then improve patient outcomes, mental outlook, and ability to function [13,36].
Delayed Radiation Injury – Soft Tissue and Bony Necrosis
Radiation therapy is associated with several acute, subacute, and delayed complications following treatment. Many of the acute and subacute complications are self-limiting in nature or are treated symptomatically . The delayed complications of radiation therapy may develop months or even years following radiation exposure. These delayed injuries may be precipitated by an additional insult such as surgery within the irradiated area . These injuries, especially those that manifest months to years later with bony or soft tissue necrosis, require multi-disciplinary management in which medical providers play a crucial role in identifying patients at risk.
The mechanism of delayed radiation injury is not well understood at this time. However, it manifests itself as vascular obliteration and stromal fibrosis in the irradiated field . HBO2’s ability to combat these changes following radiation is multifactorial. Mechanisms include stimulating angiogenesis, recruiting stem cells, improving oxygenation, and reducing fibrosis of irradiated tissues [40-42].
The largest and best studied application for HBO2 in radiation injury is in the treatment and prevention of osteoradionecrosis of the mandible. In osteoradionecrosis of the mandible, tooth extraction is a common precipitating factor and can necessitate subsequent mandibular resection and reconstruction. Pre- and post-surgical HBO2 has been shown to drastically decrease the occurrence and severity of mandibular necrosis and is an opportunity for providers to recommend a consult for HBO2 [43-45]. Recently this practice has come into question in the HOPON Trial, however, the study displayed low incidence and was performed on patients receiving lower doses of radiation than in previous literature . Additionally, HBO2 has been considered and utilized for radiation injury at other soft tissue sites, including injuries to the head and neck, radiation cystitis, and radiation proctitis . Early utilization of HBO2 for delayed radiation effects is important for best outcomes.
Given that the sequelae of radiation injury manifest themselves months to years following exposure, practitioners should be cognizant of the advantages of hyperbaric oxygen in the treatment and prevention of complications secondary to radiation therapy.
Enhancement of Healing in Selected Problem Wounds- Arterial Insufficiencies
Non-healing, problem wounds (e.g., arterial insufficiency ulcers, pressure ulcers, and venous stasis ulcers) are an ever-growing challenge for healthcare providers. The chronicity, recurrence rates, and subsequent complications from these wounds represent an increased cost and burden to healthcare systems . The addition to HBO2 to standard wound-care management optimizes the environment for improved healing by reducing the microcirculation impairment and optimizing the local inflammatory response.
The positive healing effect has been best studied and widely implemented in the treatment of infected, ischemic diabetic foot ulcers. Hyperbaric oxygen can mitigate the hypoperfusion, hypoxia, and prevalence of infection that is common in these non-healing wounds . It does this by increasing the partial pressure of oxygen dissolved in the plasma, which subsequently increases the diffusion distance of oxygen at the tissue level. This increase in available oxygen reduces tissue hypoxia and provides an oxygen-rich environment optimal for neutrophils, fibroblasts, and macrophages to carry out necessary repair or immune functions [50-55]. In addition, hyperbaric oxygen has been shown to stimulate angiogenesis and promote tissue growth [56-61].
This practice has been studied for more than 50 years and has continued to be evaluated. Despite varying outcomes in wound healing, promising results have continued to prevail and HBO2 has shown to decrease amputation [62-64]. Therefore, patients with problematic hypoxic lower-extremity wounds (i.e. wound PO2 < 40 mmHg) such as diabetic foot ulcers, hyperbaric oxygen is a valid adjunctive therapy and referral to HBO2 should be strongly considered.
Central Retinal Artery Occlusion
Central retinal artery occlusion (CRAO) is an emergent condition resulting in sudden, painless vision loss that is associated with an overall poor prognosis.
In patients who present with sudden painless vision loss, evaluation of visual acuity along with fundoscopic exam should be performed and documented. In addition, an ophthalmologist should be consulted emergently. Additional diagnostic work-up is necessary to screen and identify predisposing conditions that may help guide further decision making. However, prompt supplementation of oxygen to ischemic retina is of the utmost importance and should not be delayed while awaiting the arrival of consultations or further diagnostic testing [13,65].
If oxygen supplementation at normal atmospheric pressure is ineffective at restoring vision, HBO2 consultation and hyperoxygenation via HBO2 should be initiated. The timing of reoxygenation is essential in CRAO, with improved outcomes in patients who receive proper treatment within 90 minutes of symptom onset. Although, good outcomes have been reported as late as 24 hours after vision loss [66-71]. However, even with optimal treatment, the patient outcome is largely dependent upon the severity of the CRAO, the vessel occluded, the degree and location of the occlusion, as well as the underlying etiology of the occlusion [72,73]. Overall, recent publications have displayed improvement in visual acuity with timely HBO2 onset [74,75].
Idiopathic Sudden Sensorineural Hearing Loss
Idiopathic sudden sensorineural hearing loss (ISSHL) is defined as a loss of ≥ 30 dB occurring within three days over at least three contiguous frequencies . This may present as a patient who complains of sudden unilateral hearing loss, tinnitus, aural fullness, and vertigo [77,78].
The etiology and pathophysiology of ISSHL remains unclear; however, it is now known that perilymphatic oxygen tension is significantly decreased in patients who present with ISSHL. This results in decreased oxygen delivery to the cochlea and associated structures (in particular, the stria vascularis and the organ of Corti) [79,80]. The need for improved oxygen delivery is the primary rational for utilizing HBO2 in treating ISSHL. HBO2 greatly increases arterial perilymphatic oxygen concentration, increasing oxygen delivery to the cochlea and associated structures [80-82]. In addition, there are other potential benefits of HBO2 including blunting of ischemia-reperfusion injury, edema reduction, and anti-inflammatory effects.
Patients who present with sudden sensorineural hearing loss should be evaluated by an otolaryngologist and audiologist in a timely manner. Those determined to have ISSHL may benefit from the addition of an HBO2 consultation and HBO2 as adjunctive therapy, with the best outcomes within two weeks of symptom onset and initiated as soon as possible .
Author disclosure of interest
The authors report no conflict of interest. Conflicts may include, but are not limited to, personal, professional, or financial relationships with manufacturers of products mentioned in the manuscript or manufacturers of competing products. No such potential, perceived, or real conflicts of interest exist for either author.
Authors have full access to and control of this paper. The decision to submit this manuscript for publication rests with the authors and no others. No organizations provided support for this effort.
- Indications for Hyperbaric Oxygen Therapy (2020).
- Peterson J, Stewart R (1970) Absorption and elimination of carbon monoxide by inactive young men. Arch Environ Health 21: 165-171. [Crossref]
- Weaver LK, Howe S, Hopkins R, Chan KJ (2000) Carboxyhemoglobin half-life in carbon monoxide-poisoned patients treated with 100% oxygen at atmospheric pressure. Chest 117: 801-808. [Crossref]
- Pace N, Strajman E, Walker E (1950) Acceleration of carbon monoxide elimination in man by high pressure oxygen. Science 111: 652-654. [Crossref]
- Gorman DF, Clayton D, Gilligan JE, Webb RK (1992) A longitudinal study of 100 consecutive admissions for carbon monoxide poisoning to the Royal Adelaide Hospital. Anaesth Intensive Care 20: 311-316. [Crossref]
- Hardy KR, Thom SR (1994) Pathophysiology and treatment of carbon monoxide poisoning. J Toxicol Clin Toxicol 32: 613-629. [Crossref]
- Thom S, Taber R, Mendiguren I, Clark J, Hardy K, et al. (1995) Delayed neuropsychologic sequelae after carbon monoxide poisoning: prevention by treatment with hyperbaric oxygen. Ann Emerg Med 25: 474-480.
- Penney D, Benignus V, Kephalopoulos S, Kotzias D, Kleinman M, et al. (2010) Carbon monoxide. WHO guidelines for indoor air quality: selected pollutants. Bonn, Germany: WHO Regional Office for Europe.
- Winter PM, Miller JN (1976) Carbon monoxide poisoning. JAMA 236: :1502-1504.
- Choi IS (1983) Delayed neurologic sequelae in carbon monoxide intoxication. Arch Neurol 40: 433-435. [Crossref]
- Min SK (1986) A brain syndrome associated with delayed neuropsychiatric sequelae following acute carbon monoxide intoxication. Acta Psychiatr Scand 73: 80-86. [Crossref]
- Smith G, Sharp GR (1960) Treatment of carbon-monoxide poisoning with oxygen under pressure. Lancet 276: 905-906.
- Moon RE (2019) Hyperbaric Oxygen Therapy Indications 14th Edition. North Palm Beach: Best Publishing Company.
- Thom SR, Ohnishi ST, Fisher D, Xu Y, Ischiropoulos H (1999) Pulmonary vascular stress from carbon monoxide. Toxicol Appl Pharmacol 154: 12-19.
- Piantadosi CA, Zhang J, Demchenko IT (1997) Production of hydroxyl radical in the hippocampus after CO hypoxia or hypoxic hypoxia in the rat. Free Radic Biol Med 22: 725-732.
- Buckley NA, Juurlink DN, Isbister G, Bennett MH, Lavonas EJ (2011) Hyperbaric oxygen for carbon monoxide poisoning. Cochrane Database Syst Rev 2011: CD002041. [Crossref]
- Birmingham CM, Hoffman RS (2011) Hyperbaric oxygen therapy for acute domestic carbon monoxide poisoning: two randomized controlled trials. Intensive Care Med 37: 1218.
- Thom SR (1993) Leukocytes in carbon monoxide-mediated brain oxidative injury. Toxicol Appl Pharmacol 123: 234-247. [Crossref]
- Ischiropoulos H, Beers MF, Ohnishi ST, Fisher D, Garner SE, et al. (1996) Nitric oxide production and perivascular nitration in brain after carbon monoxide poisoning in the rat. J Clin Invest 97: 2260-2267. [Crossref]
- Thom SR (2002) Hyperbaric-oxygen therapy for acute carbon monoxide poisoning. N Engl J Med 347: 1105-1106.
- Hampson NB, Dunford RG, Kramer CC, Norkool DM (1995) Selection criteria utilized for hyperbaric oxygen treatment of carbon monoxide poisoning. J Emerg Med 13: 227-231. [Crossref]
- Goulon M, Barios A, Rapin M, Nouaihat F, Grosbuis S, et al. (1986) Carbon monoxide poisoning and acute anoxia due to breating coal gas and hydrocarbons. J Hyperb Med 1: 23-41.
- Liao SC, Mao YC, Yang KJ, Wang KC, Wu LY, et al. (2019) Targeting optimal time for hyperbaric oxygen therapy following carbon monoxide poisoning for prevention of delayed neuropsychiatric sequelae: A retrospective study. J Neurol Sci 396: 187-192. [Crossref]
- Krogh A (1919) The number of distribution of capillaries in muscle with calculation of the oxygen pressure head necessary for supplying the tissue. J Physiol 52: 409-415. [Crossref]
- Pierce E (1969) Pathophysiology, apparatus, and methods, including the special techniques of hypothermia and hyperbaric oxygen. Extracorporeal Circulation for Open-Heart Surgery. Springfield.
- Bird AD, Telfer AB (1965) Effect of hyperbaric oxygen on limb circulation. Lancet 1: 355-356. [Crossref]
- Nylander G, Lewis D, Nordstrom H, Larsson J (1985) Reduction of postischemic edema with hyperbaric oxygen. Plas Reconstr Surg 76: 596-603. [Crossref]
- Skylar MJ, Hargens AR, Strauss MB, Gershuni DH, Hart GB, et al. (1986) Hyperbaric oxygen reduces edema and necrosis of skeletal muscle in compartment syndromes associated with hemorrhagic hypotension. J Bone Joint Surg Am 8: 68. [Crossref]
- Strauss MB, Hargens AR, Gershuni DH, Greenberg DA, Crenshaw AG, et al. (1983) Reduction of skeletal muscle necrosis using intermittent hyperbaric oxygen for treatment of a model compartment syndrome. J Bone Joint Surg 65: 656-662. [Crossref]
- Strauss MB, Hargens AR, Gershuni DH, Hart GB, Akeson WH (1986) Delayed use of hyperbaric oxygen for treatment of a model compartment syndrome. J Orthop Res 4: 108-111. [Crossref]
- Sukoff MH, Ragatz RE (1982) Hyperbaric oxygenation for the treatment of acute cerebral edema. Neurosurgery 10: 29-38. [Crossref]
- Burt JT, Kapp JP, Smith RR (1987) Hyperbaric oxygen and cerebral infarction in the gerbil. Surg Neurol 28: 265-268. [Crossref]
- Thomas MP, Brown LA, Sponseller DR, Williamson SE, Diaz JA, et al. (1991) Myocardial infarct size reduction by synergistic effect of hyperbaric oxygen and recombinant tissue plasminogen activator. Am Heart J 120: 791-800. [Crossref]
- Weaver LK (2014) Hyperbaric Oxygen Therapy Indications 13th Edition. North Palm Beach: Best Publishing Company.
- Strauss M (1988) Cost-effective issues in hyperbaric oxygen therapy: Complicated fractures. J Hyperbaric Med 3: 199-205.
- Strauss MB (2012) The effect of hyperbaric oxygen in crush injuries and skeletal muscle-compartment syndromes. Undersea Hyperb Med 39: 847-855. [Crossref]
- Rubin P, Casarrett G (1968) Clinical Radiation Pathology. Philadelphia PA: W. B. Saunders Co.
- Delanian S, Lefaix J (2007) Current management for late normal tissue injury: radiation-induced fibrosis and necrosis. Semin Radiat Oncol 17: 99-107. [Crossref]
- Marx RE (1983) Osteoradionecrosis: a new concept of its pathophysiology. J Oral Maxillofac Surg 41: 283-288. [Crossref]
- Goldstein LJ, Gallagher KA, Bauer SM, Bauer RJ, Baireddy V, et al. (2006) Endothelial progenitor cell release into circulation is triggered by hyperoxia-induced increases in bone marrow nitric oxide. Stem Cells 24: 2309-2318. [Crossref]
- Gallagher KA, Liu Z, Xiao M, Chen H, Goldstein LJ, et al. (2007) Diabetic impairments in NO-mediated endothelial progenitor mobilization and homing are reversed by hyperoxia and SDF-1 alpha. J Clin Invest 117: 1249-1259. [Crossref]
- Marx R (1999) Radiation injury to tissue. In: EP K, ed. Hyperbaric Medicine Practice. 2nd ed. Best; Flagstaff, AZ: Best.
- Bedwinek JM, Shukovsky LJ, Fletcher GH, Daly TE (1976) Osteonecrosis in patients treated with definitive radiotherapy for squamous cell cancers of the oral cavity and naso- and oropharynx. Radiology 119: 665-667. [Crossref]
- Gomez DR, Estilo CL, Wolden SL, Zelefsky MJ, Kraus DH, et al. (1991) Correlation of osteoradionecrosis and dental events with dosimetric parameters in intensity-modulated radiation therapy for head-and-neck cancer. Int J Radiat Oncol Biol Phys 81: e207-e213. [Crossref]
- Feldmeier JJ, Hampson NB (2002) A systematic review of the literature reporting the application of hyperbaric oxygen prevention and treatment of delayed radiation injuries: an evidence based approach. Undersea Hyperb Med 29: 4-30. [Crossref]
- Shaw RJ, Butterworth CJ, Tesfaye B, Bickerstaff M, Dodd S, et al. (2019) HOPON (Hyperbaric Oxygen for the Prevention of Osteoradionecrosis): a randomized controlled trial of hyperbaric oxygen to prevent osteoradionecrosis of the irradiated mandible after dentoalveolar surgery. Int J Radiat Oncol Biol Phys 104: 530-539.
- Craighead P, Shea-Budgell MA, Nation J, Esmail R, Evans AW, et al. (2011) Hyperbaric oxygen for late radiation tissue injury in gynecologic malignancies. Curr Oncol 18: 220-227. [Crossref]
- Hopf H, Ueno C, Aslam R, Burnand K, Fife C, et al. (2006) Guidelines for the treatment of arterial insufficiency ulcers. Wound Rep Reg 14: 693-710. [Crossref]
- Wattel F, Mathieu D, Coget J (1990) Prediction of final outcome with transcutaneous oxygen measurements of problem wounds treated with hyperbaric oxygen. Paper presented at: Proceedings, 2nd European Conference on Hyperbaric Medicine, Basel.
- Wattel F, Mathieu D, Fossati P, Neviere R, Coget J (1991) Hyperbaric oxygen in the treatment of diabetic foot lesions search for healing predictive factors. J Hyperbaric Med 6: 263-268.
- Smith BM, Desvigne LD, Slade JB, Dooley JW, Warren DC (1996) Transcutaneous oxygen measurements predict healing of leg wounds with hyperbaric therapy. Wound Repair Regen 4: 224-229. [Crossref]
- Wang C, Lau J (2001) Hyperbaric Oxygen Therapy in Treatment of Hypoxic Wounds. cms.gov. Agency for Healthcare Research and Quality.
- Mandell GL (1974) Bacteriacidal activity of aerobic and anaerobic polymorphonuclear neutrophils. Infect Immun 9: 337-341. [Crossref]
- Mader JT, Brown GL, Guckian JC, Wells CH, Reinarz JA (1980) A mechanism for the amelioration by hyperbaric oxygen of experimental staphylococcal osteomyelitis in rabbits. J Infect Dis 142: 915-922. [Crossref]
- Mader J, Adams K, Sulton T (1987) Infectious diseases: pathophysiology and mechanisms of hyperbaric oxygen. J Hyperbaric Med 2: 133-40.
- Adams K, Mader J (1987) Aminoglycoside potentiation with adjunctive hyperbaric oxygen therapy in experimental Pseudomonas aeruginosa osteomyelitis. Paper presented at: Undersea Hyperbaric Medical Society Annual Scientific Meeting, Baltimore, Maryland.
- Adams K, Sutton T, Mader J (1987) In vitro potentiation of tobramycin under hyperoxic conditions. Paper presented at: Undersea Hyperbaric Medical Society Annual Scientific Meeting, Baltimore.
- Van Unnika (1965) Inhibition of toxin production in Clostridium perfringens in vitro by hyperbaric oxygen. Antonie Van Leeuwenhoek 31: 181-186. [Crossref]
- Luongo C, Imperatore F, Cuzzocrea S, Filippelli A, Scafuro MA, et al. (1998) Effects of hyperbaric oxygen exposure on a zymosan-induced shock model. Crit Care Med 26:1972-1976. [Crossref]
- Zamboni WA, Roth AC, Russell RC, Nemiroff PM, Casas L, et al. (1989) The effect of acute hyperbaric oxygen therapy on axial pattern skin flap survival when administered during and after total ischemia. J Reconstr Microsurg 5: 343-347. [Crossref]
- Zamboni WA, Roth AC, Russell RC, Graham B, Suchy H, et al. (1993) Morphologic analysis of the microcirculation during reperfusion of ischemic skeletal muscle and the effects of hyperbaric oxygen. Plast Reconstr Surg 91: 1110-1123. [Crossref]
- Fedorko L, Bowen JM, Jones W, Oreopoulos G, Goeree R, et al. (2016) Hyperbaric oxygen therapy does not reduce indications for amputation in patients with diabetes with nonhealing ulcers of the lower limb: a prospective, double-blind, randomized controlled clinical trial. Diabetes Care 39: 392–399. [Crossref]
- Londahl M, Katzman P, Nilsson A, Hammarlund C (2010) Hyperbaric oxygen therapy facilitates healing of chronic foot ulcers in patients with diabetes. Diabetes Care 33: 998–1003. [Crossref]
- Santema KTB, Stoekenbroek RM, Koelemay MJW, Reekers JA, van Dortmont LMC, et al. (2018) Hyperbaric Oxygen Therapy in the Treatment of Ischemic Lower- Extremity Ulcers in Patients With Diabetes: Results of the DAMO2 CLES Multicenter Randomized Clinical Trial. Diabetes Care 41: 112–119. [Crossref]
- Murphy-Lavoie H, Butler F, Hagan C. (2012) Central retinal artery occlusion treated with oxygen: a literature review and treatment algorithm. Undersea Hyperb Med 39: 943-953. [Crossref]
- Li HK, Dejean BJ, Tang RA (1996) Reversal of visual loss with hyperbaric oxygen treatment in a patient with Susac Syndrome. Ophthalmology 103: 2091-2098. [Crossref]
- Murphy-Lavoie H, Harch P, VanMeter K (2004) Effect of hyperbaric oxygen on central retinal artery occlusion. Paper presented at: UHMS Scientific Assembly, Sydney, Australia.
- Anderson B, Saltzman H, Heyman A (1965) The effects of hyperbaric oxygenation on retinal arterial occlusion. Arch Ophthal 73: 315-319.
- Augsburger JJ, Magargal LE (1980) Visual prognosis following treatment of acute central retinal artery obstruction. Br J Ophthalmol 64: 913-917. [Crossref]
- Miyake Y, Horiguchi M, Matsuura M (1987) Hyperbaric oxygen therapy in 72 eyes with retinal arterial occlusion. Undersea and Hyperbaric Medical Society 39: 949-953.
- Hayreh SS, Kolder HE, Weingeist TA (1980) Central retinal artery occlusion and retinal tolerance time. Ophthalmology 87: 75-78. [Crossref]
- Stone R, Zink H, Klingele T, Burde RM (1977) Visual recovery after central retinal artery occlusion: Two cases. Ann Ophthalmol 9: 445-450. [Crossref]
- Hayreh SS, Zimmerman MB (2005) Central retinal artery occlusion: Visual outcome. Am J Ophthalmol 140: 376-391. [Crossref]
- Schmidt I, Walter P, Siekmann U, Plange N, Koutsonas A, et al. (2020) Development of visual acuity under hyperbaric oxygen treatment (HBO) in non arteritic retinal branch artery occlusion. Graefes Arch Clin Exp Ophthalmol 258: 303-310. [Crossref]
- Çevik MÖ, Bagli BS, Çevik SG (2020) Hyperbaric oxygen treatment results in a group of Turkish central retinal artery occlusion patients with a combined presence of thrombophilic mutations. Undersea Hyperb Med 47: 65-73. [Crossref]
- Haberkamp T, Tanyeri H (1999) Management of idiopathic sudden sensorineural hearing loss. Am J Otol 20: 587-592.
- Stachler RJ, Chandrasekhar SS, Archer SM, Rosenfeld RM, Schwartz SR, et al. (2019) Clinical practice guideline: sudden hearing loss. Otolaryngol Head Neck Surg 146: S1-S35. [Crossref]
- Rauch S (2008) Idiopathic sudden sensorineural hearing loss. N Engl J Med 359: 833-840.
- Cavallazzi G (1996) Relations between O2 and hearing function. Paper presented at: Proceedings of International Joint Meeting on Hyperbaric and Underwater Medicine; Milano, Italy.
- Nagahara K, Fisch U, Yagi N (1983) Perilymph oxygenation in sudden and progressive sensorineural hearing loss. Acta Otolaryngol 96: 57-68. [Crossref]
- Lamm C, Walliser U, Schumann K, Lamm K (1988) Oxygen partial pressure measurements in the perilymph and the scala tympani in normo- and hyperbaric conditions. An animal experiment study. HNO 36: 363-366. [Crossref]
- Tsunoo M, Perlman HB (1969) Temporary arterial obstruction. Effects on perilymph oxygen and microphonics. Acta Otolaryngol 67: 460-466.