Posted by Jim Hoffmann on May 12, 2001 at 13:28:35:
In Reply to: Just a thought on Red Blood Cell rigidity posted by John Walker on May 12, 2001 at 10:52:21:
Dying by Pieces -Soft
Tissue
Damage in Divers
by Robert Monaghan, NAUI #8256
THE BEST OF SOURCES 189
MEDICAL ASPECTS
Hopefully, this advice will be in time, but we won’t know
for a while yet. Still, enough evidence is available to at
least provide this distant early warning. Those of you who
take my advice will be glad you did.
My basic argument is simple. Soft tissue damage afflicts
divers whose dive profiles give rise to bubbling. Isn’t it
unreasonable to believe that damage is confined to well-enervated
tissues? Some current research, based on the
sickle cell model, suggests that divers are especially prone
to damage in their brain, spinal tissues, retina, and bone.
The liver may also be damaged if dive profiles create
bubbling. Perhaps 5% to 30% of divers are also candidates
for shunting of bubbles into arterial circulation through
a hole in the heart.
It is suspected, based on the aseptic bone necrosis
studies, that a single incidence of DCS is enough to cause
damage. Worse, many tissues, such as the brain, don’t
provide a warning every time damage occurs. This
results in increasing levels of tissue damage, but without
the victim’s recognition that s/he is literally dying by
pieces. The solution I offer is to avoid dive profiles which
result in bubbling. Based on Spencer’s research, I believe
that use of the new NAUI dive tables will help achieve
this.
The general trend in these studies is twofold. First, the
exceptional exposure of professional or commercial divers
provides an advance warning of the problem areas for
sport divers. Second, some sport divers have diving
profiles and risks which parallel those of professional
divers. These risks may be ones you will face on your next
dive near or over the decompression limits. Many of these
problems, as with aseptic bone necrosis, take time to
develop and express themselves. You may have already
had one dive too many that has caused permanent damage
- or maybe that’s your next dive. If you avoid exceptional
exposures and use the NAUI dive tables (or
recommendations), I believe that you will also avoid most
of these problems. The arguments for use of no-bubbling
diving tables are compelling.
The Sickle Cell Model
The similarity between sickle cell anemia and decom-pression
injury was first noted 40 years ago and there is
now evidence that the similarity is no coincidence. The
mechanism by which the damage is caused could be
virtually identical in both conditions. This discovery has
led to increased concern that tunnel workers and divers
may be damaging other tissues besides bone. Cross and
a colleague, Jane Pimlott, wondered if exposure to pres-sure
might be producing a reaction analogous to a mild
sickle cell crisis. They measured the ability of human
blood cells to flow through a filter with a pore size equal
to the diameter of the capillaries in bone. At a pressure
of 2.5 atmospheres a suspension of human cells takes
about twice as long to flow through the filter as at normal
atmospheric pressure. And the blood cells of volunteers
who spent 48 hours at a pressure equivalent to diving at
a depth of 30 meters remained considerably less filterable
for at least a week.
“If the bone damage in tunnel workers and divers is due
to ‘log jamming’ of blood cells at the capillaries, it is very
likely that other tissues may also be damaged. Sickle cell
anemia damages tissues in the brain, spinal cord, and
retina, as well as in bone"
“Evidence of more widespread dam-age
in divers is, however, beginning
to mount.”
(“Diving Disease Linked to Brain
Damage” by Lesley Newson, New
Scientist, 8 October 1987, p. 26.)
Aseptic Bone Necrosis Model
Aseptic bone necrosis provides the
model for hard tissue damage which
we may find applicable to soft tissues
as well. About 5% of professional
divers develop bone necrosis (“Eye
Tests Reveal Dangers of Diving,” by
Lesley Newson, New Scientist, 21
January 1989, p. 33). The suggested
mechanism is nitrogen bubbles block-ing
circulation in the bones, resulting
in bone cell death. This tissue death
may not be a problem if it occurs in
the long shaft of the bones. But if the
death is at the cartilage surface of a
bone joint, which collapses, the joint
surface may become irregular on
healing. The result can be muscle
spasms around the joint, pain, and
poor joint function. The worst areas
are the shoulder and hip joints.
All it takes is just one bad bends
case. It is thought that the blockage
must be prolonged (e.g., six hours or
more). If one is bent, proper treat-ment
is a must to prevent this pos-sible
outcome. Alcoholics are espe-cially
susceptible. In D.A.N. figures,
(DAN Diving Accident Management
Seminar, Chris Wachholz 2/9/85),
based on a Royal Navy report, half of
the 350 men who had aseptic bone
necrosis (a 5% rate overall) had never
reported a bends case. The problem is
that blood flow is so sparse in the
joints that detection is quite difficult.
Wachholz commented that perhaps
ten radiologists in the U.S. are ad-equately
experienced to detect such
problems. The possible cause may be
fat particles clotting circulation in
non-pressure cases.
From our viewpoint, some of the
more interesting aspects relate to the
fact that half the divers developed
aseptic bone necrosis without any
bends history. Detection is difficult
in these cases, especially while the
younger, more robust bodies can
accommodate or mask tissue losses.
With aging, the masking effect may
be lost. Much medical research was
required to prove the hazards of asep-tic
bone necrosis. For many, that
proof came too late. If you insist on
irrefutable proof of such damage, you
may wind up being the one who pro-vides
it for everyone. It is better to
dive conservatively and stay out of
the medical books.
The Retina
A recent study by Maurice Cross of
the Diving Diseases Research Centre
in Plymouth investigated blood
circulation using angiograms to de-tect
anomalies in blood circulation in
the diver’s retina. Damage to the
retina was found in over half the 80
divers studied. The retina was cho-sen
because of the ease of study.
Several photos demonstrate graphi-cally
how easy it is to spot aneurysms
on the retinal surface as part of the
study.
The study concluded:
“Tissue damage caused by diving is
more common and more severe than
had been previously thought.” Of 26
professional divers studied, all (100%)
had “abnormal retinas.
“The study is the first evidence of
damage to the eye tissue in amateur
(sport) divers and it suggests for the
first time that a career in diving almost
inevitably leads to damage.
“Evidence has mounted during re-cent
years to show that exposure to
pressure during diving subtly dam-ages
the central nervous system.
Doctors believe that the damage is
due to obstructions in the flow of
blood through the tissues.
“Their [doctors] concern increased
in the early 1980s when detailed neu-
rological examinations, and tests of
the memory and reactions of experi-enced
professional divers, suggested
that some of them might have slight
damage to the brain and spinal cord.
Then, in 1986, nuclear magnetic reso-nance
imaging revealed small areas
of damage in the brains of apparently
healthy North Sea divers.
“Minute areas of tissue had died,
probably because they had been
starved of blood, suggesting that cap-illaries
that supplied blood to the areas
had been blocked. The bone necrosis
of divers closely resembles that seen
in victims of sickle-cell anemia"
“The abnormalities they detected in
the angiograms of divers were very
similar to those seen in sickle cell
disease. There was clear evidence of
obstruction to the capillaries. The
researchers suggested three mecha-nisms
to explain how diving causes
this obstruction. When divers come
back to the surface, air bubbles some-times
form in their veins and their
lungs. If bubbles also form in the
arteries, they would block the capil-laries.
Bubbles forming in the lungs
trigger changes in the body’s clotting
mechanism which could result in
minute clots becoming trapped in the
capillaries. The third suggestions is
that the mechanism might also be
similar to that of sickle cell disease.
The pressure that divers experience
at 30 meters (99 feet) causes their
white blood cells to become rigid just
as red blood cells do during a sickle
cell crisis.
“Some of the divers studied had
relatively little damage even though
they had been diving for many years
and done a great deal of deep diving.
On the other hand, a few inexperi-enced
divers had quite extensive dam-age.”
(“Eye Tests Reveal Dangers of Div-ing”
by Lesley Newson in New Scien-tist
21 January 1989 P.33.)
There is some dispute about these
findings. (See “Ocular Fundus Le-sions
in Divers” by P. B. James in
Lancet, April 1, 1989 and reply by
Polkinghorne, et al. [p. 730-731 and
p. 731 respectively]). James notes
“The appearances are consistent
with occlusion at capillary level by
microbubbles. Isotope scans show
that divers with DCS and symptoms
apparently referable only to the spi-nal
cord have multiple areas of micro-circulatory
disturbance in the brain,
indicating the potential for
coincidental retinal and choroidal
effects.”
Although suggesting that ocular
changes may relate to CNS damage,
Polkinghorne, et al. do not indicate
the number of divers who had neuro-logical
DCS and who also had ocular
fundus changes.
The reply suggested that only one
patient had had neurological symp-toms.
Therefore, such CNS effects
don’t explain either their results or
those of other studies referenced.
Memory Defects in Divers?
The question of memory defects in
divers has been best discussed by a
series in Undercurrent, starting with
an article by Dr. William Shane of
N.O.A.A. The huge volume of re-sponses,
among the most to any Un-dercurrent
article to date, suggests
that the problems are more wide-spread
than many have previously
given credence. Now, other scientific
studies are beginning to supply fur-ther
anatomical and neurological
evidence of soft tissue damage.
“Tests carried out by the unit on
professional divers aged 24 to 39 have
revealed a marked deterioration in
the short-term memory and reason-ing
skills of the more experienced
divers. Divers with only one to four
years experience did significantly
better in the tests than those who had
been working for more than eight
years”
“Peter Morris, a senior lecturer in
psychology at the University of
Lancaster and director of the Diver
Performance Research unit, said that
the continual compression and de-compression
that divers are put
through could be the cause of the
apparent brain damage. Morris be-lieves
that small bubbles could still be
formed in the brain, causing tiny
lesions in the cortex. It is the cortex
which is responsible for memory and
mental ability. Initially, the effect of
this may not be significant, but over a
period of years it could lead to brain
damage”
(“Deep Sea Diving May Cause Loss
of Memory” by Emily Smyth, New
Scientist, 17 January 1985, p. 8,)
The underlying basis for perma-nent
neurological damage following
severe DCS may have come to light.
Light and electron microscopy have
revealed alterations in spinal cord
myelin sheaths after DCS. Myelin is
the vital insulator of larger nerve
fibers and, if damaged, can impair or
prevent transmission.The U.S. re-searchers
found that myelin taken
from the spinal cord after DCS is
distinctly widened with banded pat-terns
of disruption. These alterations
could be due to bubble formation de
novo or to the secondary effects if
ischemia. (Undersea Biomedical
Research, Vol 12, p. 251 reported in
“Bends Can Damage Nerves” New
Scientist 7 November 1985 p. 27.)
Why is it we seem to forget so
quickly? Remember the passage in
Human Performance and Scuba Div-ing
(The Athletic Institute, Chicago,
1970, p. 140) titled Neurological Dam-age
Following Decompression?
“Some findings reported by Dr. I.
Rozsahegyi of Hungary are of serious
concern (from ”Decompression of Com-pressed
Air Workers” in Civil Engi-neering,
ed. R. I. McCallum, Oriel
Press, Newcastle-Upon-Tyne).
“Among 179 persons who had suf-fered
DCS and who could be exam-ined
after four years, there could be
found sequelae of lesions caused by
decompression in 130 cases. In half of
these cases the sequelae were seri-ous.
The electroencephalographic
(EEG) records have revealed patho-
logical changes in two-thirds of 57
persons who had suffered DCS affect-ing
the central nervous system many
years ago.
A common experience is psychologi-cal
change in caisson workers follow-ing
the above-mentioned brain
involvement. Men previously calm
and self-controlled become impulsive
and easily fall into a rage.
Manifest or not, lesions of the cen-tral
nervous system tend to be perma-nent.”
Another cheery article ends
with.
“Although divers do not seem to
suffer from damage to the nervous
system now, symptoms could start
when they reach their fifties or six-ties.
(“Diving Disease Linked to Brain
Damage” by Lesley Newson, New
Scientist, 8 October 1987, p. 26.) Do
we have something to look forward
to?
The 20/20 Show referenced work by
Dr. Ian Calder, a London Pathologist,
who examined spinal columns from
eight professional and three sport
divers. His goal was:
“To ascertain whether some active
divers have unrecognized cord de-generation,
perhaps as a result of
decompression exposures. Cords from
three of the professional divers showed
damage using the more sensitive
Marchi tests. Our results document
important tract degeneration in the
spinal cord of some professional divers;
the cords from three amateur divers
were unaffected.The tract
degeneration may have been
detectable had a full neurological
examination been carried out before
their final dives. Our results also
indicate that some professional divers
appear to be unwittingly working with
tract degeneration in the spinal cord.”
(“Preliminary Communication:
Spinal Cord Degeneration in Divers,”
A. C. Palmer, I. M. Calder, J. T.
Hughes, The Lancet, December 12,
1987 p. 1365.)
How’s Your Liver?
Been hitting the bottle lately? Too
bad!
“High pressure appears to interfere
with the function of the liver among
divers, according to Geoff Doran of
Charing Cross Hospital, London.
Doran analyzed the blood and urine
of people taking part in dives to more
than 300 meters and those who were
diving regularly to depths of between
30 and 50 meters. He detected
abnormally high levels of a number of
proteins in the blood of all the divers.
The levels were far higher in the
groups that dives to the greater
depths.
Some of the proteins Doran detected
in the blood are enzymes normally
found inside liver cells, which sug-gests
that the divers had damaged
liver cells. Doran also found abnor-mally
high concentrations of toxins.
“The divers’ urine also contained
abnormally high concentrations of
histamine, indicating abnormal blood
biochemistry. Doran detected high
levels of toxic substances in the blood
known as endotoxins.
Those diving to the greatest depths
may have had levels of endotoxins
high enough to produce symptoms of
toxicity.
“Most divers never go to depths
great enough to produce symptoms of
HPNS or liver damage, but even the
relatively shallow depths that
amateurs reach do produce biochemi-cal
changes. (“Deep Diving Puts Pres-sure
on Livers” by Lesley Newson in
New Scientist 12 November 1988 p.
32).
Patent Foramen Ovale
The report in Lancet by DAN physi-cians
Drs. Richard Moon, Enrico
Camporesi, and Joseph Kisslo stirred
a great deal of controversy thanks to
the airing of the 20/20 segment on
sport diving.
Dumford et al. reported that 17% of
173 dives by sport scuba divers to
depths of 6-39 msw resulted in ve-nous
gas emboli.
“We postulate that patent foramen
ovale may be a risk factor for the
development of neurological DCS by
allowing the passage of venous gas
emboli into the systemic circulation.
“All 11 had shunting during breath-ing
at rest, and all were in the group
with serious signs and symptoms.
Eleven of 18 patients with serious
DCS had shunting (Chi-square =
49.49, p=0.0001 compared with con-trols).
None of the patients with mild
symptoms had shunting.
In contrast, only 9 (5%) of the 176
controls had shunting detectable
during breathing at rest.
“We propose that in a susceptible
individual, venous gas emboli may
enter the systemic circulation and
cause arterial embolization. Besides
direct arterial occlusion, these gas
bubbles could also °seed’ susceptible
tissues (e.g., spinal cord) and precipi-tate
symptoms of DCS by adding to
an already high endogenous inert gas
load. Immersion in water could also
increase the shunt.” (“Patent
Foramen Ovale and Decompression
Sickness in Divers,” Richard E. Moon,
Enrico M. Camporesi, Joseph A.
Kisslo, The Lancet, 11 March 1989
pp. 513-14.)
An even more significant report,
from our viewpoint, was contained in
the follow-up report titled “Neuro-logical
Decompression Sickness” by
P. T. Wilmshurst, J. C. Byrne, and M.
M. Webb-Peploe in the following April
1, 1989, Lancet.
“We have described neurological
symptoms due to paradoxical gas
embolism after decompression in a
diver with an atrial septal defect. We
would add that intracardiac shunts
are associated with neurological
symptoms occurring soon after a dive,
but late symptoms are caused by a
different mechanism.”
One diver did 75 dives without inci-dent
before running into trouble.
Then he made seven more dives, but
ran into trouble again two months
later.
“We then did contrast echo-cardiog-raphy
on five more patients who had
had neurological DCS; four had a
patent foramen ovale.” The five divers
with a patent foramen ovale had had
acute and severe neurological
symptoms within 15 minutes of
surfacing from a dive in which de-compression
procedures were cor-rectly
followed. All were experienced
(average 314 dives). The previous
dives were uneventful.
“Thus, acute neurological symptoms
can occur in anyone with a patent
foramen ovale which shunts right to
left, provided the dive has produced
venous bubbles. Safe decompression
procedures are no guarantee that an
individual with a patent foramen ovale
will escape neurological DCS, because
many decompression tables allow
venous bubble nucleation.”
Since a patent foramen ovale has
been shown to be a feature of up to
30% of postmortem studies, the po-tential
problem for divers is enor-mous.
“The patent foramen ovale has its
origin in the development of the em-bryo:
before the lungs become func-tional,
there is no difference between
the venous and the arterial circula-tion,
and the upper chambers of the
heart are not separate. The wall
separating them begins to grow as
birth approaches. Because pressures
in the upper chambers of the heart
are usually very low, an incomplete
closure of the wall between them does
not significantly impair cardiac
function and cardiac shunting occurs
only rarely. But even an occasional
flow of bubble laden blood into the
arteries would be dangerous for a
diver.
“Divers have known for a long time
that the safety measures practiced to
prevent bends do not work for every-one.
Some divers have developed
serious DCS after carrying out a dive
with a depth and duration that should
have been safe. The presence of a
cardiac shunt could explain why this
occurs.” (“Hole in the Heart Brings
on the Bends” by Lesley Newson,
New Scientist 20 may 1989 p. 30.)
Conclusion
Perhaps none of this is enough to
convince you - but I think you’ll have
to agree that research is beginning to
reveal some very different views of
soft tissue damage than we have
traditionally seen suggested. The
obvious point is that we need to change
how we dive to reflect these new
understandings. Isn’t a no-bubbling
schedule superior, given the 5-30%
patent foramen ovale prevalence
among divers? Should we attend
those great drinking parties,