Hyperbaric Oxygen Therapy is a treatment method applied as breathing %100 oxygen under pressures above 1 absolute atmospheres (ATA) [5]. It increases the oxygen concentration dissolved in the plasma thus maintain increased delivery for the tissues [6]. This effect is profitable in many diseases with hypoxia being the underlying pathophysiology [7]. Hyperbaric Oxygen Therapy is used as a primary indication for this purpose in ophthalmology in retinal arterial occlusions, central retinal vein occlusions, vascular originated cystoid macular edemas like retinal vein branch occlusions, scleral necrosis cases, orbital infections with mycotic and anaerobic origin, non-healing corneal edema and anterior segment ischemia. It can be used as an adjuvant therapy for proliferative vitreoretinopathy due to cycle cell anemia, primary open angle glaucoma, visual area defects following macular hole surgery and optic neuropathies with vascular origin [8]. There are limited number of studies on how hyperbaric oxygen therapy effects intraocular pressure and anterior segment parameters. Gallin-Cohen et al. reported a decrease in IOP in measurements after breathing air under 3 ATA and 1 ATA pressure [4]. Kalthoff and John reported a mean 2–3 mmHg decrease in IOP in a chamber pressurized to 2 and 4 ATA [9].
Hosking et al. studied the changes in IOP following induced hypercapnia and hyperoxia and observed a decrease in IOP values in hyperoxia in both normal people and patients with glacouma [20]. Bojic et al. reported that HBOT (Breathing %100 O2 under 2 ATA) do not effect IOP level in patients with glaucoma [10]. In this study IOP values were determined at 10.00 am before and after HBOT to minimize the error due to diurnal rhythm. A statistictically significant decrease in IOP values was observed after breathing air under 2,4 ATA pressure. The mechanism on how HBOT decreases IOP is unclear. Nevertheless it was submitted that the IOP decrease is due to the choroidal volume decrement which happens after a %40 reduction in intraocular fluid volume and a 3 mmHg decrease in episcleral pressure after the partial oxygen pressure increase with HBOT [4]. In another opinion it was advocated that the increased oxygen concentration [4] and decreased CO2 concentration [11] are responsible for the decrease in IOP. In a study by Marcus et al. the increased partial CO2 pressure during exercise was reported to cause a decrease in blood pH and a simulataneous drop in IOP[11]. Increase in H + ions and low pH was reported among the known effects of HBOT [6]. Thus the active transport mechanism that plays an important role in aqueous humour production is inhibited by the increase in H + ions. This may decrease the aqueous humour production and thus cause a decrease in IOP.
The number of studies on the effects of HBOT on central corneal thickness is limited. Ali Ayata et al. demonstrated a statistically significant decrease in central corneal thickness in non-diabetic patients taking HBOT [12]. Knut Evanger et al. reported that HBOT causes a decrease in both peripheral and central corneal thickness. This decriment was more prominent in peripheral cornea than the central. But the observed decriment was not statistically significant [13]. In another study by Evanger et al. no statistically significant change in central corneal thickness was observed in neither groups of phakic and pseudophakic patients after HBOT[14]. In this study a statistically significant decrease in the central corneal thickness was demonstrated. The underlying mechanism causing a decrease in central corneal thickness is unclear. There no blood vessels in the cornea. It absorbs the oxygen richly from the atmosphere and from the aqueous humour filling the anterior chamber [15]. Fluid and nutrients are slowly dispersed from the tears and the anterior chamber to corneal stroma [15]. Thin endothelial layer forms the deepest layer of the cornea and these cells pumps excess fluid from the stroma towards the anterior chamber to maintain the clarity of the cornea. The endothelial pump function is an energy focused process. HBOT induced hyperoxia may increase corneal metabolism and endothelial pump function. This may explain the changes in corneal thickness observed in our patients.
There are many studies about refractive changes after HBOT. A transient myopic shift is a defined situation in patients taking HBOT [16]. The reason for the refractive change demonstrated in earlier studies about this is the changes in crystalline lens. In a study a transient myopic shift was demonstrated in phakic patients while no change was observed in pseudophakic patients [14]. Myopic shift returns to previous state approximately 10 weeks following the treatment [17]. This should be taken into consideration in patients taking HBOT with a scheduled refractive surgery. No statistically significant changes were observed in this study in refractive measures of keratometry and spheric equivalent values of the patients.
The number of studies on the effects of HBOT on anterior chamber depth is limited. Knut Evanger at al. reported an increase in anterior chamber depth in phakic patients receiving HBOT while no statistically significant changes were observed in pseudophakic patients [14]. In another study by same authors no statistically significant changes were observed in a total number of 20 patients (10 men and 10 women) after 19 sessions of HBOT [19]. In our study a statistically significant decrease was observed in anterior chamber depths of 30 patients after HBOT when compared to values before HBOT. HBOT may be causing a decriment in anterior chamber depth secondary to its effects on aqueous humour [6]. Our study demonstrates the changes after one session of HBOT, while the mentioned studies reports the changes after longer durations of HBOT therapies; this may be the reason why our results are different from the results in the literature.
In conclusion; the acute effects of hyperbaric oxygen on anterior segment morphology and on intraocular pressure were evaluated in this study and a statistically significant decrease in central corneal thickness, intraocular pressure and iridocorneal angle values is demonstrated after one session of HBOT. No difference was observed in refractive error and keratometric values of the patients. These findings of changes stimulated by HBOT on anterior segment morphology and on intraocular pressure should be supported with more studies with larger groups and longer follow-up durations.