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PubMed2003

Does repeated hyperbaric exposure to 4 atmosphere absolute cause hearing impairment? Study in Guinea pigs and clinical incidences.

HYPOTHESIS: Direct pressure applied on the inner ear cannot induce hearing loss. BACKGROUND: Three possible causes have been described in the literature for inner ear permanent lesions during scuba diving: pressure imbalance between the middle ear and the external ear, appearance of microbubbles in the internal ear, and direct effect of pressure on the inner ear. We seek to determine whether this last factor can be involved. METHODS: We submitted two groups of guinea pigs previously implanted with an electrode in the round window to a protocol of air diving in a hyperbaric chamber. Eardrums of animals in one of the two groups had been perforated beforehand. Twenty dives were practiced over 4 weeks. We chose dive parameters consistent with common sport diving: maximal pressure of 4 atmosphere absolute and duration of 30 minutes. Auditory threshold and cochlear spontaneous activity were recorded at regular intervals. Furthermore, we recorded spontaneous cochlear activity in Heliox 400-m and 600-m dives to determine whether our conclusions hold for "extreme" diving. RESULTS: In the group with perforated eardrums, no variation of those parameters were recorded, even in extreme diving. Important variations were noticed in the other group. CONCLUSIONS: Pressure applied directly on the inner ear during diving does not disturb cochlear activity.

Animals↗
PubMed2005

An adolescent scuba diver with 2 episodes of diving-related injuries requiring hyperbaric oxygen recompression therapy: a case report with medical considerations for child and adolescent scuba divers.

Worldwide, more than 1000 scuba (self-contained underwater breathing apparatus) diving injuries per year requiring hyperbaric recompression are documented. Approximately 80 to 90 fatalities per year are reported in North America. On average, there were 16 diving injuries requiring hyperbaric recompression therapy in scuba divers aged 19 years and younger in North America between 1988 and 2002. The youngest injured diver was 11 years old, and the youngest fatality was 14 years old during this time period. In the year 2000, certifying recreational scuba diving organizations lowered the minimum age to 8 from age 12 years for participation in the sport. We report a case of a highly trained adolescent scuba diver who, despite having advanced diving certifications, had 2 separate episodes of diving-related injuries requiring hyperbaric recompression therapy. A discussion of medical considerations in the care of the child and adolescent scuba diver is included.

Adolescent↗
PubMed1984

Bone necrosis due to decompression.

Death of areas of long bone has been known to be associated with work in compressed air and diving for many years. Detection and diagnosis require specialist knowledge, but familiarity with the condition has increased markedly over the last 20 years. Most of it is symptomless and causes no disability, but if areas adjacent to the joint surfaces of the upper end of the humerus and the upper end of the femur are affected, the joint may be seriously damaged and disability ensue. This problem has been defined by surveys of groups of workers using compressed air and divers in an attempt to establish prevalence. In general the more diving undertaken and the deeper the dives, the more probability there is of acquiring bone damage. The commonest area to be affected is the lower end of the femur, but the knee joint is never involved. The cause of bone damage is far from clear. None of the various explanations that have been offered are satisfactory, but research continues into the problem both in humans and in animals, particularly the miniature pig. At present it is difficult to quantify the risk taken by commercial divers in relation to changing technology either in terms of depth or duration of pressure.

Adult↗
PubMed1992

Cerebral vasculopathy in divers.

Brains from 12 amateur and 13 professional divers, all but one of whom died accidentally, were examined neuropathologically. Grossly distended, empty vessels (presumably caused by gas bubbles) were found in the brains of 15 out of 22 divers who died from diving accidents. Perivascular lacuna formation was found in cerebral and/or cerebellar white matter in three amateurs and in five professionals. In addition to lacuna formation, hyalinization of vessel walls was present in the brains of three amateurs and five professionals. Necrotic foci in grey matter occurred in seven cases and perivascular vacuolation of white matter occurred in seven cases. The vascular changes probably arose from intravascular gas bubble formation. In one professional diver, there was also unilateral necrosis of the head of the caudate nucleus.

Adult↗
PubMed2006

A case of type 3 DCS with a radiologically normal spinal cord.

A subtype of cerebral arterial gas embolism arising in divers, in which apparent spinal cord disease follows early cerebral manifestations, is well known and has been described as type 3 DCS. A case that clinically conformed to the pattern of type 3 DCS was examined radiologically. Despite clinical signs of spinal disease, magnetic resonance imaging scans of the spinal cord did not demonstrate pathology.

Adult↗
PubMed2001

Aerobic endurance training reduces bubble formation and increases survival in rats exposed to hyperbaric pressure.

1. The formation of bubbles is the basis for injury to divers after decompression, a condition known as decompression illness. In the present study we investigated the effect of endurance training in the rat on decompression-induced bubble formation. 2. A total of 52 adult female Sprague-Dawley rats (300-370 g) were randomly assigned to one of two experimental groups: training or sedentary control. Trained rats exercised on a treadmill for 1.5 h per day for 1 day, or for 2 or 6 weeks (5 days per week) at exercise intervals that alternated between 8 min at 85-90% of maximal oxygen uptake (VO2,max) and 2 min at 50-60% of VO2,max. Rats were compressed (simulated dive) in a decompression chamber in pairs, one sedentary and one trained, at a rate of 200 kPa x min(-1) to a pressure of 700 kPa, and maintained for 45 min breathing air. At the end of the exposure period, rats were decompressed linearly to the 'surface' (100 kPa) at a rate of 50 kPa x min(-1). Immediately after reaching the 'surface' (100 kPa) the animals were anaesthetized and the right ventricle was insonated using Doppler ultrasound. 3. Intensity-controlled interval training significantly increased VO2,max by 12 and 60% after 2 and 6 weeks, respectively. At 6 weeks, left and right ventricular weights were 14 and 17 % higher, respectively, in trained compared to control rats. No effect of training was observed on skeletal muscle weight. Bubble formation was significantly reduced in trained rats after both 2 and 6 weeks. However, the same effect was seen after a single bout of aerobic exercise lasting 1.5 h on the day prior to decompression. All of the rats that exercised for 1.5 h and 2 weeks, and most of those that trained for 6 weeks, survived the protocol, whereas most sedentary rats died within 60 min post-decompression. 4. This study shows that aerobic exercise protects rats from severe decompression and death. This may be a result of less bubbling in the trained animals. The data showed that the increase in aerobic capacity per se was not the main mechanism, but rather an acute effect that was most notable 20 h after a single, or the last, exercise bout, with less effect after 48 h.

Animals↗
PubMed1994

Diving physiology and pathophysiology.

Divers have worked at 500 m depth in the sea and have reached 700 m in simulated chamber dives. A prerequisite for this has been extensive physiological studies of the body's reactions to pressure and pressure changes. This paper reviews such physiological and pathophysiological studies with emphasis on recent developments.

Decompression Sickness↗