Scientific papers 2000 - 2003
The risk of decompression sickness is a safety problem
related to offshore diving operations. Modem safety
management defines a systematic approach to such a
problem based on policy edition, support from an
organisation, planning and implementing, monitoring,
reviewing, and auditing. These activities are analysed in
light of the experience of a large diving company,
achievements are listed, and areas of improvement are
identfied. It is shown that the next edition of
decompression procedures will require hundreds of
thousands of dive records to identify the critical factors,
define models, and validate new procedures. This exceeds
the experience of a single diving company or even a
single nation, and it is believed that efforts of
decompression sickness management should be
coordinated at a European level.
R.G. Dunford, R.D. Vann , W.A. Gerth, C.F. Pieper, K.
Huggins, C. Wacholtz, and P.B. Bennett.
Decompression sickness (DCS) is a pathological event
thought caused by intravascular and extravascular gas
bubbles. The bubble theory of DCS is supported by
empirical evidence, and venous gas emboli (VGE) can be
detected after diving using non-invasive Doppler
ultrasonic methods, but the etiology of DCS is complex,
and VGE are frequent after symptom-free dives. High VGE
levels, however, are associated statistically with increased
DCS incidence suggesting that VGE and DCS may share a
common origin. Further, VGE might initiate DCS should
they cross or bypass the pulmonary capillary filter and be
transported by the arterial circulation to organs such as
the brain or spinal cord.
Authors: Jay B. Dean, Daniel K. Mulkey, Alfredo J. Garcia,
Robert W. Putnam, and Richard A. Henderson
As ambient pressure increases, hydrostatic compression of
the central nervous system, combined with increasing
levels of inspired PO2, PCO2, and N2 partial pressure, has
deleterious effects on neuronal function, resulting in O2
toxicity, CO2 toxicity, N2 narcosis, and high-pressure
nervous syndrome. The cellular mechanisms responsible
for each disorder have been difficult to study by using
classic in vitro electrophysiological methods, due to the
physical barrier imposed by the sealed pressure chamber
and mechanical disturbances during tissue compression.
The documents are classified chronologically from 2000 to 2003.
Click on their descriptions to open and download them.
Authors: Carturan, D., A. Boussuges, P. Vanuxem, A. Bar-
Hen, H. Burnet, and B. Gardette.
This study aimed to assess the effects of ascent rate, age,
maximal oxygen uptake (VO2 max), and percent body fat
on the production of bubbles after diving. Fifty male
recreational divers performed two dives at 35 m during 25
min and then ascended in one case at 9 m/min and in
the other case at 17 m/min.
They performed the same decompression stops in the two
cases. Twenty-eight divers were Doppler monitored at 10-
min intervals until 60 min after surfacing, and the data
were analyzed by Wilcoxonsigned-rank test to compare
the effect of ascent rate on the kinetics of bubbles.
Twenty-two divers were monitored 60 min after surfacing.
Authors: Z. Nachum, A. Shupak, O. Spitzer, Z. Sharoni, Y.
Ramon, A. Abramovich, I. Doweck, C.R. Gordon
Inner ear decompression sickness (IEDCS) may result in
permanent, severe cochleo-vestibular deficits, unless
immediate diagnosis is reached and the correct treatment
is commenced early. Previously reported IEDCS cases
were mostly associated with deep mixed helium diving,
whereas after sport air diving this entity is considered to