Diffusion tensor MRI of spinal decompression sickness.

In order to develop more sensitive imaging tools for clinical use and basic research of spinal decompression sickness (DCS), we used diffusion tensor MRI (DTI) validated by histology to assess DCS-related tissue injury in sheep spinal cords. DTI is based on the measurement of water diffusion indices, including fractional anisotropy (FA) and mean diffusion (MD) to detect tissue microstructural abnormalities. In this study, we measured FA and MD in white and gray matter spinal cord regions in samples taken from sheep following hyperbaric exposure to 60-132 fsw and 0-180 minutes of oxygen pre-breathing treatment before rapid decompression. The main finding of the study was that decompression from >60 fsw resulted in reduced FA that was associated with cell death and disrupted tissue microstructure in spinal cord white matter tracts. Additionally, animals exposed to prolonged oxygen pre-breathing prior to decompression demonstrated reduced MD in spinal cord gray matter regions regardless of dive depth. To our knowledge, this is the first study to demonstrate the utility of DTI for the investigation of DCS-related injury and to define DTI biomarkers of spinal DCS.

Decompression illness: clinical aspects of 5278 consecutive cases treated in a single hyperbaric unit.

BACKGROUND: Decompression illness (DCI) is a major concern in pressure-related activities. Due to its specific prerequisite conditions, DCI is rare in comparison with other illnesses and most physicians are inexperienced in treatment. In a fishery area in northern China, during the past decade, tens of thousands of divers engaged in seafood harvesting and thousands suffered from DCI. We established a hyperbaric facility there and treated the majority of the cases. METHODS AND RESULTS: A total of 5,278 DCI cases were admitted in our facility from February 2000 through December 2010 and treated using our recompression schedules. Cutaneous abnormalities, joint and muscular pain and neurological manifestations were three most common symptoms. The initial symptom occurred within 6 h after surfacing in 98.9% of cases, with an overall median latency of 62 min. The shorter the latent time, the more serious the symptoms would be (P<0.0001). Nine cases died before recompression and 5,269 were treated using four recompression schedules, with an overall effectiveness rate of 99.3%. The full recovery rate decreased with the increase of the delay from the onset of symptoms to the treatment (P<0.0001). CONCLUSIONS: DCI presents specific occurrence rules. Recompression should be administered as soon as possible and should never be abandoned irrespective of the delay. The recompression schedules used were effective and flexible for variety conditions of DCI.

Combined effect of denucleation and denitrogenation on the risk of decompression sickness in rats.

We previously hypothesized that the number of bubbles emerging on decompression from a dive, and the resultant risk of decompression sickness (DCS), may be reduced by a process whereby effective gas micronuclei that might otherwise have formed bubbles on decompression are shrunk and eliminated. In a procedure defined by us as denucleation, exposure to hyperbaric oxygen (HBO) would result in oxygen replacing the resident gas in the micronuclei, to be subsequently consumed by the mitochondria when the oxygen pressure is reduced. Support for the validity of our hypothesis may be found in our previous studies on the transparent prawn and the reduction of DCS in the rat. In all of these studies, HBO pretreatment was given before supersaturation with inert gas at high pressure. The purpose of the present study was to compare DCS outcome in rats that underwent nitrogen washout (denitrogenation) alone (9 min O(2) at 507 kPa) after exposure to air at high pressure (33 min at 1,266 kPa), and rats treated by both procedures (denitrogenation + denucleation; 8 min of O(2) breathing followed by 5 min air breathing, both at 507 kPa) after high-pressure air exposure. This was done with the same nitrogen load in both groups before the final decompression (a nitrogen pressure of 467 kPa in fatty and 488 kPa in aqueous tissue). Six of 20 rats in the denitrogenation + denucleation group died, compared with 13 in the denitrogenation group (P < 0.03). Three rats in the denitrogenation + denucleation group suffered mild DCS, recovering completely within 2 h of decompression. The present study indicates an advantage in considering both denitrogenation and denucleation before decompression. This may have practical application before escape from a disabled submarine, when aborting a technical dive, or in the preparation of aviators for high altitude.

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.

Hyperbaric oxygen pretreatment reduces the incidence of decompression sickness in rats.

We have previously hypothesised that the number of bubbles evolving during decompression from a dive, and therefore the incidence of decompression sickness (DCS), might be reduced by pretreatment with hyperbaric oxygen (HBO). The inert gas in the gas micronuclei would be replaced by oxygen, which would subsequently be consumed by the mitochondria. This has been demonstrated in the transparent prawn. To investigate whether our hypothesis holds for mammals, we pretreated rats with HBO at 304, 405, or 507 kPa for 20 min, after which they were exposed to air at 1,013 kPa for 33 min and decompressed at 202 kPa/min. Twenty control rats were exposed to air at 1,013 kPa for 32 min, without HBO pretreatment. On reaching the surface, the rat was immediately placed in a rotating cage for 30 min. The animal's behaviour enabled us to make an early diagnosis of DCS according to accepted symptoms. Rats were examined again after 2 and 24 h. After 2 h, 65% of the control rats had suffered DCS (45% were dead), whereas 35% had no DCS. HBO pretreatment at 304, 405 and 507 kPa significantly reduced the incidence of DCS at 2 h to 40, 40 and 35%, respectively. Compared with the 45% mortality rate in the control group after 24 h, in all of the pretreated groups this was 15%. HBO pretreatment is equally effective at 304, 405 or 507 kPa, bringing about a significant reduction in the incidence of DCS in rats decompressed from 1,013 kPa.

Hyperbaric chamber nurse dies of decompression sickness; unit gets OK.

Experts in the field of hyperbaric medicine say the chambers used to treat dive accident victims and enhance the healing of problem wounds are safe despite the death last August of a nurse. Joyce Vause, 52, died of decompression sickness July 22, 1991 about an hour after she left work at Bay Medical Center, Panama City, FL. Shortly before her death, Vause has been in a hyperbaric chamber attending a patient who had been in a diving accident.