B58-19 Oxidative Stress and Anti-inflammatory Response in Spinal Cord Decompression Sickness: A Prospective Case-control Study

Abstract Rationale Spinal cord decompression sickness represents the most severe neurological diving injury, affecting 30-40% of decompression sickness cases with 10% experiencing permanent disability. The spinal cord appears particularly vulnerable due to its unique vascular anatomy with watershed areas in the mid-thoracic region and limited collateral circulation. While traditionally attributed to gas bubble formation, emerging evidence suggests secondary inflammatory and oxidative mechanisms contribute to tissue damage. We investigated oxidative stress biomarkers and inflammatory cytokines in spinal cord decompression sickness patients to elucidate pathophysiological mechanisms. Methods This prospective, monocentric case-control study enrolled 35 consecutive recreational divers (28 males, 7 females; mean age 47±11 years) with spinal cord decompression sickness (37 sample observations) admitted within 24 hours of symptom onset and 15 healthy volunteer divers (26 sample observations) as controls performing standardized air dives to 30 meters for 20 minutes. Blood samples were collected before and after hyperbaric oxygen therapy administered according to standard treatment protocols. Oxidative stress markers (thiobarbituric acid-reactive substances TBARS, reduced ascorbic acid RAA) and inflammatory cytokines (IL-6, IL-1β, TNF-α, IL-10, IL-2) were measured using spectrophotometric assays and ELISA. Clinical outcomes were assessed after first table. Mann-Whitney U tests compared spinal cord decompression sickness patients versus controls and complete recovery versus residual deficits groups, with Bonferroni correction (α = 0.007) applied for multiple comparisons. Results Spinal cord decompression sickness patients demonstrated significantly elevated oxidative stress markers: TBARS (2.24±0.35 vs 0.99±0.16 μmol/L, p = 0.002, r = 0.415) and RAA (201.81±11.68 vs 157.48±4.09 μmol/L, p = 0.003, r = 0.396) compared to controls. Unexpectedly, the anti-inflammatory cytokine IL-10 was markedly elevated (26.26±9.72 vs 2.25±0.47 pg/mL, p 0.001, r = 0.478), representing an 11-fold increase. Proinflammatory cytokines (IL-6, IL-1β, TNF-α) showed no significant differences between groups (all p 0.130). No biomarkers predicted clinical outcomes after first table (complete recovery: n = 17, 50%; residual deficits: n = 17, 50%). Hyperbaric oxygen therapy significantly reduced IL-6 (p 0.001, r = 0.652) and TNF-α (p = 0.006, r = 0.454) while increasing IL-10 (p 0.001, r = 0.662), but did not immediately affect oxidative stress markers (Figure). Conclusions Spinal cord decompression sickness is characterized by significant oxidative stress and a prominent anti-inflammatory response dominated by IL-10 elevation, challenging traditional inflammatory models. The absence of elevated proinflammatory cytokines suggests complex immunoregulatory mechanisms. While biomarkers lacked prognostic value, hyperbaric oxygen therapy’s modulation of cytokine profiles supports anti-inflammatory mechanisms in its therapeutic effect. These findings reveal unique pathophysiological characteristics of spinal cord decompression sickness warranting further investigation into IL-10’s compensatory role and potential therapeutic targeting. This abstract is funded by: None