The primary injury mechanism in decompression sickness (DCS) is the formation of bubble during dives, and it is widely accepted that its definitive treatment consists of hyperbaric oxygen therapy (HBOT) to reduce bubble volume.1

In addition, some published data have reported an increase in oxidative stress in DCS2–4 and that HBOT may influence oxidative stress.2–7 In two previous studies with rats, it was found that DCS increases malondialdehyde (MDA), a lipid hyperoxidation biomarker,8 in spinal cord and brain biopsies, and that the HBOT reduces those levels.2,3 One study reported a subject with DCS who underwent HBOT and showed an increase in salivary reactive oxygen species (ROS), urinary nitric oxide metabolites and urinary 8-isoprostane (a lipid peroxidation biomarker), all of which increased further after HBOT.4 In some studies, with healthy volunteers who underwent HBOT was found after HBOT an increase of ROS and glutathione peroxidase (antioxidant) in lymphocytes,5 of salivary ROS, of urinary 8-isoprostane, of salivary total antioxidant capacity (TAC)6 and of serum superoxide dismutase (antioxidant) and of serum MDA.7 In addition, an increase in oxidative stress has been reported in individuals who practice diving with self-contained underwater breathing apparatus (scuba).4,5,9,10 Therefore, we think that serum MDA levels could be increased in DCS patients.

The novel objectives of our study were to compare serum MDA levels between DCS patients and healthy subjects, and to determine the effect of HBOT on those serum MDA levels in DCS patients.

This prospective observational study was conducted with the approval of the Clinical Research Ethics Committee of the Hospital Universitario de Canarias (HUC), Tenerife, Spain (code CHUC_2023_150; 21st March 2024) and with informed consent signed by scuba divers with DCS and healthy subjects. Patient recruitment was carried out in the hyperbaric section of the Tenerife Medical Institute Limited Company (IMETISA), and its assistance activity is carried out for staff of Intensive Medicine Service of HUC.

Serum samples were obtained from DCS patients (at the time of diagnosis and 12 h after undergoing HBOT) and healthy subjects. We obtained the second blood sample after 12 h of undergoing HBOT because we had observed that most DCS patients needed only one HBOT session and lived far from the hyperbaric chamber; thus, it would have been difficult to obtain a second sample later. Serum MDA concentrations were determined using the thiobarbituric acid-reactive substances (TBARS) method previously described by Kikugawa et al.8

DCS patients received HBOT in a hyperbaric chamber, model IBERCO IB-230 × 6000. We administered HBOT following U.S. Navy recommendations.1 HBOT table 5 was used for the treatment of type I DCS, which involves musculoskeletal pain and skin symptoms, and the patient remains at 2.8 atmospheres absolute (ATA) or 18 m of seawater (msw) or 60 feet of seawater (fsw) for 45 min (40 min with 100% oxygen and 5 min with air at 21% oxygen). HBOT table 6 was used for the treatment of type II DCS, which involves the central nervous system, the inner ear, or the cardiopulmonary system; and the patient remains at 2.8 ATA for 75 min (60 min with 100% oxygen and 15 min with air at 21% oxygen).

There were no significant differences between DCS patients (n = 20) and healthy subjects (n = 17) in age (36 (30–52) vs 36 (28–49) years; p = 0.75) and sex (10 (50%) vs 8 (47%; p = 0.99). We found lower serum MDA levels in healthy controls (0.68 [0.61−0.74] nmol/mL) than in DCS patients at the time of diagnosis (1.38 (1.04–2.12) nmol/mL); p < 0.001) and after first HBOT (1.32 (1.18–1.85) nmol/mL); p < 0.001; n = 17). However, there were no significant differences in serum MDA levels in DCS patients at moment of DCS diagnosis and after first HBOT (p = 0.69).

The characteristics of dives and of HBOT sessions in each DCS patient are shown in Table 1. There were no significant associations between serum MDA levels at the time of DCS diagnosis and type of DCS (p = 0.15), sex (p = 0.40), age (rho = 0.16; p = 0.49), number of dives in previous days (rho = 0.09; p = 0.70), number of dives on the day of the event (rho = 0.32; p = 0.16), time of last immersion (rho = 0.57; p = 0.01), depth of last immersion (rho = 0.13; p = 0.58), time from leaving the water to symptom onset (rho= −0.17; p = 0.48), number of sessions of HBOT (rho = 0.14; p = 0.57), time from HBOT initiation to symptom resolution (rho = 0.06; p = 0.81).

There were no significant associations between laboratory parameters and serum MDA levels at moment of DCS diagnosis (Table 2). No DCS patient needed mechanical ventilation, vasoactive agents, or Intensive Care Unit stay.

We must acknowledge several limitations of our study. First, compounds related to the antioxidant state and other markers of the oxidant state were not reported. Second, we did not collect oxidative stress data in healthy subjects who underwent HBOT, in divers without DCS, or in divers prior to developing DCS. Third, the timing of blood samples differed among patients. Fourth, the type and number of HBOT sessions varied, as they were established based on the type of DCS and the clinical response to HBOT. Fifth, we reported the maximum depth and duration of the dives, but we could not provide other dive-related data (such as ascent profile to assess decompression stress). Sixth, we reported the time from the beginning of HBOT to complete clinical resolution; however, we could not provide information on the resolution time of each individual symptom. Seventh, we have not calculated the sample size; however, it was sufficient to find differences on serum MDA levels between DCS patients and healthy subjects.

In conclusion, to the best of our knowledge, our study is the first series reporting data on oxidative stress in DCS patients and reporting data on the effect of HBOT on oxidative stress in DCS patients. The new findings from our study were that DCS patients showed higher serum MDA levels than health subjects and that those levels remain high after 12 h of the first HBOT session without significant differences in respect to DCS diagnosis. However, further research is necessary to validate these preliminary findings.