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DECOMPRESSION ILLNESS - a patient's guide
Dr Stephen Adams - Visiting Doctor to the Royal NZ Navy
WHAT IS IT?
The effect on the body of bubbles forming from sudden
decreases in pressure. This is similar to bubbles formed
when a container of carbonated beverage is opened. It is
not quite so vigorous as seen in a bottle as the pressure
change is not usually so sudden and also because the body
is inherently unsaturated with gas due to biological processes
in the tissues. These bubbles are usually nitrogen (rather
than the carbon dioxide in a soft drink) as this is the
predominant component of air but may also occur with other
non-metabolised gases such as helium if a mixture including
large proportions of these are breathed.
WHEN DOES IT OCCUR?
During almost any significant decompression (sudden decrease
in pressure) bubbles are formed in the tissues (solid components
of the body). The tissues can cope with a certain amount
of bubbles before injury becomes apparent. The bubbles in
the veins are filtered out harmlessly in the lungs until
the lungs are no longer able to cope. If this capacity to
filter the bubbles out is exceeded or the bubbles find a
way around the lungs e.g. via a small hole in the heart,
they can reach the arteries and block the smaller ones (especially
in the brain and spinal cord).
A second way for bubbles to occur inside the body is if
pressure in the lung alveoli (air sacs) or the airways significantly
exceeds the pressure in the tissue e.g. during breath holding
while ascending from a dive. In this case air may enter
the tissue (surgical emphysema) or the circulation (gas
embolism). This also occasionally occurs during medical
procedures involving compressed gases.
Tissue bubbles may cause injury through direct disruption
of tissues e.g. nerves, by compressing blood vessels and
reducing blood flow or by toxic chemical changes the bubbles
precipitate. The injury may continue to evolve due to the
last mechanism.
HOW WILL I KNOW IF I HAVE DCI?
The effects may be very local e.g. pain in a tendon, distant
from the site of injury e.g. numbness or weakness in a hand
from a bubble in the spine, generalised e.g. lethargy from
bubbles in the brain or even catastrophic e.g. coma from
bubbles in the brain. Symptoms may include pain, rash, with
or without itchiness, numbness, tingling, weakness, paralysis,
impaired thinking or consciousness, shortness of breath
or cough, dizziness or loss of balance, or loss of bowel
or bladder control. The onset of symptoms is likely to be
within 24 hours ascent from a dive but may continue to evolve
for much longer.
There is no single diagnostic test for decompression illness.
The diagnosis may be arrived at from an analysis of the
symptoms, physical findings, and response to recompression.
Although the diving profile may support the diagnosis, adherence
to any table or computer cannot exclude DCI.
Other acute illnesses that may mimic decompression illnesses
include hyperventilation, hysteria, side effects of drugs
especially mefloquine (Lariam), and acute cerebrovascular
event (stroke) while some incipient illnesses e.g. spinal
or brain tumours occasionally become symptomatic following
a dive. Injuries during diving e.g. shoulder sprain from
putting on a cylinder may be difficult to differentiate
from musculoskeletal DCI.
Examination of a suspected DCI case will usually include
a review of recent and past diving history and illnesses,
then a general physical examination of the patient with
a focus on areas where symptoms have been noted. A thorough
neurological examination with a short mental status examination
will usually be made in all cases as subtle abnormalities
may be uncovered. Special attention will be paid to the
ears, hearing and balance as they are the most common sites
of injury in both diving and recompression therapy.
Special tests that may be indicated include chest x-ray,
ECG, spirometry and audiometry to exclude other injuries
and also assess safety of recompression therapy. MRI scanning
is a very useful investigation for the presence or extent
of neurological DCI but its availability may be limited
at recompression chambers and urgency of treatment often
makes an early MRI impossible.
WHAT CAN BE DONE?
First aid is to lie the patient down, arrange transfer,
preferably by ambulance, to an emergency department or hyperbaric
facility. High flow oxygen and an intravenous infusion should
be started as soon as possible.
Other resuscitation and supportive measures may be necessary
during transfer.
The definitive treatment for DCI is recompression. This
uses pressure to shrink the bubbles with oxygen at high
levels to increase reabsorption of nitrogen and reverse
chemical changes caused by the bubbles. The importance of
high oxygen levels is one reason why returning to the water
for "in-water" recompression is not recommended, the others
being safety and the difficulty of completing recompression
times in the order of five hours plus.
The exact regime used varies from centre to centre and
is often referred to as a "table" which specifies pressure
or depth (equivalent depth in water), duration, gas mix(es)
and ascent profile. Initial recompression is directed primarily
at shrinking and removing bubbles, is usually longer (taking
many hours or even days in the case of "saturation" tables)
and may be deeper than follow-up treatments which are directed
at achieving high levels of oxygen in the tissues. During
this first treatment response treatment is followed and
the diagnosis may be reevaluated in light of this.
The treatment is carried out in a Recompression Chamber,
which is a pressure chamber that range from a small cylinder
2m long and 1m diameter of perspex or steel up to a large
rectangular room or even complex of rooms. There will be
some form of communication to the outside and a source of
gas for breathing via mask or hood. There may be an air
lock for transfer of personnel or supplies to and from the
outside.
HAZARDS OF RECOMPRESSION THERAPY INCLUDE:
DCI - although the tables are designed to ascend very
slowly there is a small risk of DCI from Recompression Chamber
Therapy. This occurs mostly in deep (>30m) treatments and
appears to be more of a hazard to staff in the chamber than
to patients being treated.
Oxygen toxicity - in order to reach high levels of oxygen
in the tissues the toxic limits for oxygen are approached
more closely than in scuba diving. The most common acute
problem is convulsions. By and large these are frightening
for the observer but do little harm to the victim who recovers
when brain tissue oxygen levels fall during the convulsion.
Chronic toxicity affects mostly the lungs with a measurable
but reversible loss in lung function with time in a high
oxygen environment and occasionally a burning pain on taking
deep breaths.
Barotrauma (pressure injury) of the ears, sinuses and
teeth and lungs. This is common but easily dealt with by
slow pressure changes and frequent manoeuvres to clear.
Sudden loss of chamber pressure could be disastrous but
is very unlikely.
Fire hazard - increased levels of oxygen and no quick
escape make fire in a chamber catastrophic. Chambers are
carefully designed to minimise fire risk and chamber disasters
in recent decades have mostly been due to materials brought
in by patients.
FUTURE TRENDS
Although there are some promising drug treatments e.g.
intravenous lignocaine being evaluated, none are yet proven
and are likely to be an addition to hyperbaric therapy,
or perhaps to buy time while hyperbaric therapy is arranged.
PROGNOSIS:
Untreated mild DCI often appears to clear up by itself
but there is a concern that nerve cells in particular are
lost and the body's reserves of these become depleted, so
that in another episode the effect is much worse and may
be irrevocable. This "worse second episode" effect also
occurs with treated DCI where the injury was major or recovery
was incomplete and diving should be stopped.
In the event of a full recovery a diving physician should
still be consulted as a time off diving is usually recommended.
Where injury out of proportion to the apparent hazard occurs
diving should be stopped as it becomes impossible to set
safety limits for future diving. In the case of obvious
arterial gas embolism it is recommended to stop diving as
the site of gas entry is likely to be weaker after recovery
than at the time of the initial injury. Cardiac Ultrasound
"Echo" is sometimes used to look for a predisposing heart
abnormality in these cases in case it is repairable, but
will not result in a clearance to dive.
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