Intern@tion@l Dre@m.net |
Open a
bottle of carbonated soda and bubbles fizz to the top as pressure is released,
an apt analogy for what happens when a diver ascends too rapidly. The nitrogen
that is dissolved in the bloodstream under the increased partial pressures
experienced at depth come out of solution as bubbles during a too-rapid ascent.
These bubbles can then block blood vessels, resulting in pain and neurological
symptoms: decompression sickness (DCS).
Until recently, there was
no way to determine whether or not there were nitrogen bubbles in the
bloodstream in the absence of clinical symptoms. But within the last several
years, Doppler ultrasound machines have been used to prove the presence of
clinically silent bubbles in the bloodstreams of divers after completing dives
that were within no-decompression limits. The medical significance of these
silent bubbles is a subject of debate. Some say they serve as seeds for larger
bubbles that may produce clinically apparent DCS. Others contend the bubbles
are a warning of impending DCS, but little else. There are several studies
under way , most notably a large-scale effort by DAN, to determine the importance of
these bubbles.
A twist on the role that
silent bubbles may play caused quite a stir in the diving community last year
when the medical journal The Lancet suggested these bubbles may be responsible
for structural changes identified in the brains and spinal cords of divers. The
Lancet study was among the first to look at whether or not there are MRI
differences that can be identified between recreational divers and age-matched
nondiving controls. The study found two areas of significant difference between
the two groups: an increase in the number of unidentified bright objects (UBOs)
in the brain and spinal cord of the divers as compared to the nondivers; and a
significantly higher number of abnormalities in the intervertebral disks of the
divers. UBOs are abnormalities that are thought to represent small areas of
damage in the brain, but no one knows with certainty whether or not they
correlate to any neurological deficits. The study suggested that both
differences may be due to the silent microbubbles formed during ascent, leading
to small, silent lesions that do not immediately manifest themselves as DCS,
but cause damage as more lesions accumulate over time.
What does this finding mean
to the recreational diver? There are several weaknesses in the Lancet article
that render its conclusions, if not invalid, at least indeterminate. The study
recruited amateur divers who had made at least 40 dives a year for at least
four years. While there are certainly many divers who dive this much or more,
this is not necessarily a population that is representative of the sport diving
community. There are a vast number of recreational divers who make only a few
dives a year, and it is hard to say if these findings would apply to these
divers.
Also, the study found no
correlation between the number of abnormalities found on MRI, and the number of
dives or years of diving experience. If these lesions are caused by tiny
bubbles in the microvasculature of the brain and spinal cord, then one would
expect to find an increased number of lesions in those with more dives. This is
especially true of those who have been diving for a greater number of years.
Therefore, the study's conclusion--that long-term amateur diving can cause
brain and vertebral disk damage in the absence of identifiable episodes of
DCS--is weakened because a linear relationship between the amount of diving and
number of lesions found was not established.
Perhaps the most important
question concerns the significance of the UBOs found on MRI. The Lancet study
does not say that the lesions found on MRI are responsible for any neurological
changes, merely that they exist. Whether or not divers are at increased risk of
long-term neurological damage from these changes is an area that requires more
investigation.
In the meantime, there are
a few things that divers can do to minimize the potential risk from
microbubbles (see "Compression Obsessions"). These include a slow ascent
rate, ideally no more than 30 feet per minute once above 60 feet, and a safety
stop of at least three minutes at 15 feet, minimizing any potential long-term
damage that microbubbles might cause.