On beginning a second century of decompression sickness research: where are we and what comes next?

It is just 100 years since the publication of J. S. Haldane's groundbreaking work on the prevention of decompression sickness (DCS). While we still do not know the exact mechanisms that underlie DCS, probabilistic modeling now allows good estimation of risk for a given set of conditions, although reduction of risk to zero remains impractical. Unfortunately, individual monitoring for intravascular bubbles has not proven a good predictor of symptomatic DCS. Current research aims to identify underlying biological factors that, once understood, may allow development of preventive measures and treatment that go beyond recompression. With one or more drugs to combat DCS, we should be able to eliminate the residual risk, extend dive profiles beyond current limits, and rescue people who have exceeded the limits and taken a hit.

Pharmacological interventions to decompression sickness in rats: comparison of five agents.

INTRODUCTION: This research investigated whether decompression sickness (DCS) risk or severity could be reduced using drug interventions that are easier to implement and equal to or more efficacious than recompression therapy. METHODS: Using a rat model of DCS, anti-inflammatory or anticoagulant drugs, including lidocaine, aspirin (ASA), methylprednisolone (MP), alpha-phenyl-N-butylnitrone (PBN), and transsodium crocetinate (TSC) were tested to determine their effect on incidence of DCS, death, and time of symptom onset. Each treatment group consisted of approximately 40 animals that received the drug and approximately 40 controls. Animals were exposed to one of five compression and decompression profiles with pressure ranging from 6.3 ATA (175 fsw) to 8.0 ATA (231 fsw); bottom time was either 60 or 90 min; and decompression rate was either 1.8 or 15 ATA x min(-1). Following decompression, the rats were observed for 30 min while walking on a wheel. DCS was defined as an ambulatory deficit or abnormal breathing. RESULTS: None of the drugs reached statistical significance for all DCS manifestations. Lidocaine post-dive and MP were the only treatments with marginally (P < 0.15) significant differences in DCS outcomes compared to controls. Lidocaine post-dive significantly decreased the incidence of neurological DCS from 73-51%. MP significantly extended the time of onset of death from DCS from 5.4 min to 7.1 min. DISCUSSION: Of the treatments investigated, lidocaine given post-dive has the best chance of success in adjuvant therapy of DCS. Future studies might investigate adjuvant drugs given in combination or during recompression.

Nitrogen load in rats exposed to 8 ATA from 10-35 degrees C does not influence decompression sickness risk.

INTRODUCTION: Environmental temperature is commonly thought to modulate decompression sickness (DCS) risk, but the literature is mixed regarding which conditions elicit the greatest risk. If temperature is a risk factor, then managing thermal exposure may reduce DCS incidence. We analyzed whether hot or cold conditions during or immediately after a hyperbaric exposure altered DCS incidence in a rat model. METHODS: Rats (eight groups of five animals in each of nine conditions; mean body mass +/- SD = 259.0 +/- 9.2 g) were placed in a dry chamber that was pressurized with air to 70 m (8 ATA) for 25 min, followed by rapid (< 30 s) decompression under a series of temperature conditions (35 degrees, 27 degrees, or 10 degrees C during compression; 35 degrees, 20 degrees, or 10 degrees C post-decompression). Animals were observed for 30 min post-decompression for signs of DCS. DCS incidence in the 27 degrees C compression/20 degrees C post-decompression group was 50% by design. Data from all nine groups of paired temperature conditions were compared with each other using analysis of variance, Chi-square tests, and logistic regression. RESULTS: No significant differences in DCS incidence were found among the groups (30-52.5% DCS incidence per group, 42% DCS incidence overall). DISCUSSION AND CONCLUSIONS: This animal model emphasized potential temperature effects attributable to tissue N2 load acquired during compression; there was no evidence that environmental temperature from 10-35 degrees C during or post-dive modulated DCS incidence. It remains to be determined if temperature modulates DCS risk as a function of variable N2 elimination rates.

Probabilistic modelling for estimating gas kinetics and decompression sickness risk in pigs during H2 biochemical decompression.

We modelled the kinetics of H2 flux during gas uptake and elimination in conscious pigs exposed to hyperbaric H2. The model used a physiological description of gas flux fitted to the observed decompression sickness (DCS) incidence in two groups of pigs: untreated controls, and animals that had received intestinal injections of H2-metabolizing microbes that biochemically eliminated some of the H2 stored in the pigs' tissues. To analyse H2 flux during gas uptake, animals were compressed in a dry chamber to 24 atm (ca 88% H2, 9% He, 2% O2, 1% N2) for 30-1440 min and decompressed at 0.9 atm min(-1) (n = 70). To analyse H2 flux during gas elimination, animals were compressed to 24 atm for 3 h and decompressed at 0.45-1.8 atm min(-1) (n = 58). Animals were closely monitored for 1 h post-decompression for signs of DCS. Probabilistic modelling was used to estimate that the exponential time constant during H2 uptake (tau(in)) and H2 elimination (tau(out)) were 79 +/- 25 min and 0.76 +/- 0.14 min, respectively. Thus, the gas kinetics affecting DCS risk appeared to be substantially faster for elimination than uptake, which is contrary to customary assumptions of gas uptake and elimination kinetic symmetry. We discuss the possible reasons for this asymmetry, and why absolute values of H2 kinetics cannot be obtained with this approach.

Modulation of decompression sickness risk in pigs with caffeine during H(2) biochemical decompression.

In H(2) biochemical decompression, H(2)-metabolizing intestinal microbes remove gas stored in tissues of animals breathing hyperbaric H(2), thereby reducing decompression sickness (DCS) risk. We hypothesized that increasing intestinal perfusion in pigs would increase the activity of intestinal Methanobrevibacter smithii, lowering DCS incidence further. Pigs (Sus scrofa, 17-23 kg, n = 20) that ingested caffeine (5 mg/kg) increased O(2) consumption rate in 1 atm air by ~20% for at least 3 h. Pigs were given caffeine alone or caffeine plus injections of M. smithii. Animals were compressed to 24 atm (20.5-23.1 atm H(2), 0.3-0.5 atm O(2)) for 3 h, then decompressed and observed for signs of DCS. In previous studies, DCS incidence in animals without caffeine treatment was significantly (P < 0.05) lower with M. smithii injections (7/16) than in controls (9/10). However, contrary to our hypothesis, DCS incidence was marginally higher (P = 0.057) in animals that received caffeine and M. smithii (9/10) than in animals that received caffeine but no M. smithii (4/10). More information on gas kinetics is needed before extending H(2) biochemical decompression to humans.