Effect of hyperbaric oxygen therapy and corticosteroid therapy in military personnel with acute acoustic trauma.

INTRODUCTION: Acute acoustic trauma (AAT) is a sensorineural hearing impairment due to exposure to an intense impulse noise which causes cochlear hypoxia. Hyperbaric oxygen therapy (HBO) could provide an adequate oxygen supply. The aim was to investigate the effectiveness of early treatment with combined HBO and corticosteroid therapy in patients with AAT compared with corticosteroid monotherapy. METHODS: A retrospective study was performed on military personnel diagnosed with AAT between November 2012 and December 2017. Inclusion criteria for HBO therapy were hearing loss of 30 dB or greater on at least one, 25 dB or more on at least two, or 20 dB or more on three or more frequencies as compared with the contralateral ear. RESULTS: Absolute hearing improvements showed significant differences (independent t-test) between patients receiving HBO and the control group at 500 Hz (p=0.014), 3000 Hz (p=0.023), 4000 Hz (p=0.001) and 6000 Hz (p=0.01) and at the mean of all frequencies (p=0.002). Relative hearing improvements were significantly different (independent t-test) at 4000 Hz (p=0.046) and 6000 Hz (p=0.013) and at all frequencies combined (p=0.005). Furthermore, the percentage of patients with recovery to the functional level required by the Dutch Armed Forces (clinical outcome score) was higher in the HBO group. CONCLUSIONS: Early-stage combination therapy for patients with AAT was associated with better audiometric results at higher frequencies and better clinical outcome score.

Markers of Pulmonary Oxygen Toxicity in Hyperbaric Oxygen Therapy Using Exhaled Breath Analysis.

INTRODUCTION: Although hyperbaric oxygen therapy (HBOT) has beneficial effects, some patients experience fatigue and pulmonary complaints after several sessions. The current limits of hyperbaric oxygen exposure to prevent pulmonary oxygen toxicity (POT) are based on pulmonary function tests (PFT), but the limitations of PFT are recognized worldwide. However, no newer modalities to detect POT have been established. Exhaled breath analysis in divers have shown volatile organic compounds (VOCs) of inflammation and methyl alkanes. This study hypothesized that similar VOCs might be detected after HBOT. METHODS: Ten healthy volunteers of the Royal Netherlands Navy underwent six HBOT sessions (95 min at 253 kPa, including three 5-min "air breaks"), i.e., on five consecutive days followed by another session after 2 days of rest. At 30 min before the dive, and at 30 min, 2 and 4 h post-dive, exhaled breath was collected and followed by PFT. Exhaled breath samples were analyzed using gas chromatography-mass spectrometry (GC-MS). After univariate tests and correlation of retention times, ion fragments could be identified using a reference database. Using these fragments VOCs could be reconstructed, which were clustered using principal component analysis. These clusters were tested longitudinally with ANOVA. RESULTS: After GC-MS analysis, eleven relevant VOCs were identified which could be clustered into two principal components (PC). PC1 consisted of VOCs associated with inflammation and showed no significant change over time. The intensities of PC2, consisting of methyl alkanes, showed a significant decrease (p = 0.001) after the first HBOT session to 50.8%, remained decreased during the subsequent days (mean 82%), and decreased even further after 2 days of rest to 58% (compared to baseline). PFT remained virtually unchanged. DISCUSSION: Although similar VOCs were found when compared to diving, the decrease of methyl alkanes (PC2) is in contrast to the increase seen in divers. It is unknown why emission of methyl alkanes (which could originate from the phosphatidylcholine membrane in the alveoli) are reduced after HBOT. This suggests that HBOT might not be as damaging to the pulmonary tract as previously assumed. Future research on POT should focus on the identified VOCs (inflammation and methyl alkanes).

Hyperbaric oxygen therapy for sudden sensorineural hearing loss in divers.

OBJECTIVE: Sudden sensorineural hearing loss in divers may be caused by either inner-ear barotrauma or inner-ear decompression sickness. There is no consensus on the best treatment option. This study aimed to evaluate the therapeutic value of hyperbaric oxygen therapy for sudden sensorineural hearing loss in divers. METHOD: A literature review and three cases of divers with sudden sensorineural hearing loss treated with hyperbaric oxygen therapy are presented. RESULTS: Hyperbaric oxygen therapy resulted in hearing improvement in 80 per cent of patients: 39 per cent had hearing improvement and 41 per cent had full recovery. CONCLUSION: Hyperbaric oxygen therapy improved hearing in divers with sudden sensorineural hearing loss.

Hyperbaric oxygen diving affects exhaled molecular profiles in men.

Exhaled breath contains volatile organic compounds (VOCs) that are associated with respiratory pathophysiology. We hypothesized that hyperbaric oxygen exposure (hyperoxia) generates a distinguishable VOC pattern. This study aimed to test this hypothesis in oxygen-breathing divers. VOCs in exhaled breath were measured in 10 male divers before and 4h after diving to 9msw (190kPa) for 1h. During the dive they breathed 100% oxygen or air in randomized order. VOCs were determined using two-dimensional gas chromatography with time-of-flight mass spectrometry. Compared to air dives, after oxygen dives there was a significant increase in five VOCs (predominately methyl alkanes). Furthermore, a strong, positive correlation was found between increments in 2,4-dimethyl-hexane and those of 4-ethyl-5-methyl-nonane. Although non-submerged hyperoxia studies on VOCs have been performed, the present study is the first to demonstrate changes in exhaled molecular profiles after submerged oxygen diving. The pathophysiological background might be attributed to either a lipid peroxidation-induced pathway, an inflammatory pathway, or to both.

Nitric oxide and carbon monoxide diffusing capacity after a 1-h oxygen dive to 9 m of sea water.

INTRODUCTION: To prevent extensive pulmonary lesions in submerged oxygen divers lung function like the forced vital capacity (FVC) or the diffusing capacity for carbon monoxide (DL,co) are used to monitor pulmonary oxygen toxicity (POT). As the diffusing capacity for nitric oxide (DL,no) measures more accurately the membrane diffusing capacity compared to DL,co we hypothesized that DL,no is superior in monitoring the onset of physiological changes indicative of POT as compared to DL,co or FVC. METHOD: 26 healthy divers (mean age 30.7 ± 6.2 years) made two submerged dives to 190 kPa for 1 h on two randomized separate days, whilst breathing 100% oxygen or compressed air. FVC, DL,no, DL,co and alveolar volume (VA ) were measured 6 times during a 26-h period. RESULTS: Up to 8 h no significant differences in outcomes were found between the oxygen and air dives. However, at 8 h after the oxygen dives there was a significant reduction in DL,no, DL,co and VA as compared with air dives. In contrast, the reduction in FVC was significantly greater after the air dive. At 22 h there were no longer differences in outcomes between the dives. CONCLUSIONS: These data show that DL,no and DL,co are significantly reduced 8 h after submerged oxygen dives as compared to similar air dives. Together with the reduction in VA this may be indicative of interstitial edema as an early sign of POT. Our data warrant validation of the superiority of DL,no and DL,co over FVC in the practical monitoring of divers.

Assessment of pulmonary oxygen toxicity: relevance to professional diving; a review.

When breathing oxygen with partial oxygen pressures PO2 of between 50 and 300 kPa pathological pulmonary changes develop after 3-24h depending on the PO2. This kind of injury (known as pulmonary oxygen toxicity) is not only observed in ventilated patients but is also considered an occupational hazard in oxygen divers or mixed gas divers. To prevent these latter groups from sustaining irreversible lesions adequate prevention is required. This review summarizes the pathophysiological effects on the respiratory tract when breathing oxygen with PO2 of 50-300 kPa (hyperoxia). We discuss to what extent the most commonly used lung function parameters change after exposure to hyperoxia and its role in monitoring the onset and development of pulmonary oxygen toxicity in daily practice. Finally, new techniques in respiratory medicine are discussed with regard to their usefulness in monitoring pulmonary oxygen toxicity in divers.

Severe spinal cord decompression illness after an uneventful North Sea dive.

The aim of this case report is to illustrate that, even under moderate conditions, a dive can result in spinal cord decompression illness (DCI). The diver in question completed five dives with the same profile. The first four included substantial physical strain, while the final dive was for observation only, without physical strain. The spinal cord was the target organ for DCI. We discuss the roles of various diver-related risk factors and of factors related to the dive itself. Older divers have a higher risk for decompression incidents. The nature of the dive profile is a major factor in the uptake and release of inert gas. Physical exertion during pressure-exposure boosts the inert gas load, increases bubbling in tissues and raises the risk of DCI in the decompression phase of the dive. We discuss the causal involvement of such risk factors in this case, given the characteristics of the diver and the circumstances of the dive. Finally, we want to express our concern for physical fitness and smoking habits, especially for divers over the age of 40.

Lung function before and after oxygen diving: a randomized crossover study.

RATIONALE: Breathing oxygen with a partial pressure of > 50 kPa can cause pulmonary oxygen toxicity (POT). Diffusing capacity for carbon monoxide (DL(CO)) is thought to be a more sensitive indicator of POT than vital capacity (VC). Because diffusing capacity can be measured more specifically using nitric oxide (DL(NO)), we hypothesized that DL(NO) is better able to monitor and exclude POT than DL(CO). OBJECTIVE: To compare changes in lung function after oxygen and air dives which include measurement of DL(NO) and DL(CO). METHOD: Eleven healthy male divers (mean age 27.5 +/- 3.1 years) made two immersed dives to 150 kPa for three hours on two separate days, during which they randomly breathed 100% oxygen or air. VC, DL(NO) and DL(CO) were measured six times during a 26-hour period on both days and on a third non-diving day. RESULTS: There were no significant changes in DL(CO), DL(NO) or other diffusing capacity or spirometric parameters after either type of dive. CONCLUSION: Lung function after a single three-hour oxygen dive at a pO2 of approximately 150 kPa is comparable to that after an air dive at the same depth and duration. This suggests that such an oxygen dive does not induce detectable signs of POT. Our hypothesis that DL(NO) is more sensitive than DL(CO) for detection of POT could not be tested because the oxygen exposure did not affect either parameter.

Differences in spirometry and diffusing capacity after a 3-h wet or dry oxygen dive with a PO(2) of 150 kPa.

RATIONALE: Breathing oxygen with a partial pressure of >50 kPa causes pulmonary oxygen toxicity (POT), resulting in a decrease in vital capacity (VC) and in diffusing capacity for carbon monoxide (DLco). As submersion is thought to potentiate POT, we hypothesized that submerged oxygen divers are at increased risk for POT. OBJECTIVE: To compare changes in lung function after submerged (wet) and non-submerged (dry) oxygen dives. METHOD: Thirteen healthy male divers (mean ± SD: 25 ± 2 years, 184 ± 7 cm, 85 ± 10 kg) made a dry and a wet dive to 150 kPa for 3 h, during which they breathed 100% oxygen. At baseline, within 1 and 4 h after their dives, spirometry and diffusing capacity were measured. Data were analysed with ANOVA using Bonferroni correction and paired t-tests. RESULTS: Compared with baseline, there was a significant reduction in DLco (-1·6 mmol kPa(-1) min(-1)) after a wet oxygen dive but not after a dry dive. In addition, relative to baseline, there was a significant difference in ΔDLco and ΔVC when comparing wet and dry oxygen dives. CONCLUSION: Diffusing capacity is more impaired after a wet oxygen dive than after a dry one. This suggests that wet oxygen divers are at increased risk for POT. Monitoring studies during daily practice of professional divers are mandatory to determine the exact operational relevance of the present findings.