GENERAL
There
is a large amount of gas dissolved in the body fluids and tissues. Under static atmospheric conditions,
this gas is in equilibrium with that which is being breathed. The higher the pressure, the more gas
there is dissolved in the body. If
the atmospheric pressure is gradually reduced, the excess gas in the body
tissues is transported to the lungs dissolved in venous blood and is safely
exhaled. If, however, the atmospheric pressure is reduced too rapidly, the
capacity of the circulation to clear the excess gas in solution can be
exceeded. Under these conditions
gas may come out of solution and form bubbles. Decompression sickness results if more
bubbles are liberated than the body can tolerate, or if bubbles form within, or
are distributed to, particularly susceptible “target” organs.
There
are two situations where ambient atmospheric pressure may be reduced
sufficiently rapidly for DCS to occur.
Following each compression, divers and caisson workers are decompressed
from a higher (hyperbaric) pressure back to one atmosphere (normobaric
pressure). On the other hand,
aviators and astronauts may occasionally be decompressed from normobaric,
or near-normobaric pressure to low (hypobaric)
pressure. Nowadays this usually only happens during training or as a result of
an accident.
The
many symptoms and signs of DCS depend on which organs are involved. This section will discuss the diagnosis
of the more common presentations.
The treatment of the condition will be discussed later.
Depending
on the dive profile, different organs may be affected by DCS. For “bounce” dives, the more
common presentations are:
a. Cutaneous (of the Skin)
b. Musculo-skeletal
(the classic limb or pain-only) “bends”)
c. Lymphatic.
d. Central Nervous System (CNS)
disorders:
1. Spinal cord
2. Cerebral
e. Vestibular
(“staggers”)
f. Pulmonary
(“chokes”)
presentations have been arbitrarily divided
into two categories: 'Type I' disease principally consists of the less serious
conditions in group, a, b and c above.
'Type II' disease is comprised of the more serious conditions in groups
d, e and although these terms are still widely used, they are of limited value
since the two may co-exist. Treatment
must be direct at the most serious symptoms and signs.
Decompression
sickness usually presents within a short period of time following a dive. Symptoms may become apparent before
surfacing in saturation and occasionally in bounce dives, particularly where
decompression has been omitted. However, most symptoms occur after surfacing
and the majority of serious symptoms usually present within about 30 minutes. Most
musculo-skeletal symptoms also occur in this time
period, but it is not unusual for “limb-bends” to present many
hours after a dive. Decompression
sickness may be provoked or made worse many hours after a dive if the diver
takes a flight. If a diver has been asymptomatic for 48 or more hours after a
dive and has not flown, then symptoms which develop subsequently are probably
not dive-related.
The
dive profile is important when determining the diagnosis of decompression
sickness, but there are no absolute rules.
Sometimes decompression sickness is avoided despite the diver flouting
conventional practices. Conversely, decompression sickness may develop
following a non-stop dive or a dive where the decompression was performed
correctly.
CUTANEOUS SYMPTOMS FOLLOWING DECOMPRESSION
Symptoms and Signs
a. Itching of the skin, often accompanied by an
erythematous (red) rash is very common after diving
and frequently goes unreported. It is usually transient and does not normally
require recompression.
b. Occasionally, lymph nodes may become
enlarged and tender and this may be associated with oedema, (build up of fluid
in local area). ‘skin feels thickened and may
have the “pitted” appearance of orange peel. If pressure is applied
to the skin and then released, a visible indentation will remain. Although this condition will eventually
resolve spontaneously, it will be more rapidly relieved by treatment on Table
61. (See Treatment Tables).
c. True cutaneous
decompression sickness begins with one or more patches of intense itching. After a period of a few minutes and up
to an hour, the skin becomes reddened.
If left untreated, these patches assume a “marbled”
appearance consisting of cyanotic (blue) areas in generally pale skin. Although this condition will usually
resolve spontaneously over a period of a day or two, it is advisable to treat
the patient with recompression since it is occasionally a harbinger of more
serious symptoms of decompression sickness.
MUSCULO-SKELETAL OR PAIN-ONLY DECOMPRESSION SICKNESS
Symptoms and Signs
Limb pain,
particularly around joints, is a common manifestation of decompression
sickness. Following
“bounce” dives, the upper limbs tend to be involved more often than
the lower limbs and the shoulder is involved particularly frequently. Conversely, in saturation divers,
aviators and compressed-air (caisson) workers, it is the lower limbs and
particularly the knees which are involved most commonly.
The
pain usually begins gradually and is poorly localised; it may slowly resolve
spontaneously and is then known as a “niggle”. Niggles may flit from joint to
joint. If the pain gets worse, it
becomes more readily localised and is described as a dull, boring ache, akin to
tooth ache. Sometimes the joint is
held in a particular position that is least painful, but pain is seldom made
worse by movement. If the pain is
in the lower limb, weight bearing may be poorly tolerated on that limb.
Examination
a. There are often no objective
signs. Occasionally, there is a
rash over the affected joint.
Notably, the “classical” signs of inflammation: redness,
swelling, warmth to the touch and tenderness are missing.
b. Until recently, the overwhelming
proportion of cases of decompression sickness in amateur divers which presented
for treatment were pain-only bends. This no longer appears to be true. The reasons for this are unclear. It may be that diving practices have
changed with more deep dives being conducted. Alternatively, it may be that a smaller
proportion of limb bends are occurring or being reported or, possibly, that
careful examination of diving casualties is resulting in the detection of
serious symptoms more frequently than before.
c. Even cases of apparently
straight-forward limb bends must be fully examined. A patient with a painful limb bend may
not notice a mild paraesthesia or a small area of
numbness. Ensure no neurological
symptoms can be detected before the choice of a therapeutic table is made. The diagnosis of Type 1 decompression sickness
can only be made when careful examination has failed to elicit signs of more
serious disease.
Progress
Pain-only
bends usually resolve completely without treatment over a period of 12-72
hours. However, rapid relief is
usually obtained from therapeutic recompression. In cases where the onset of pain has been
rapid, early recompression may prevent the onset of subsequent neurological
symptoms.
CENTRAL NERVOUS SYSTEM (SPINAL CORD) DECOMPRESSION SICKNESS
a. The spinal cord is frequently
involved in serious decompression sickness. It may be involved alone or with other
parts of the nervous system. Dives
which readily appear to provoke spinal cord disease
are: short, deep dives with a rapid ascent to the surface.
b. Onset
The onset of symptoms commonly occurs
rapidly after reaching the surface, with about half serious cases becoming
symptomatic within 10 minutes. Less
than 10% of serious cases present more than 4 hours after completing the dive.
c. Symptoms
and Signs
In severe cases, the condition is
heralded on the onset of a constricting, aching pain in the lower abdomen or
pelvis - so called “girdle pain”. Occasionally, the site of such pain is
the upper abdomen or chest. Shortly
afterwards, the patient may notice pins and needles, numbness and muscular
weakness in the legs which rapidly progresses to paraplegia. It is possible for all four limbs to be
involved and, in severe cases, shock may complicate
the clinical picture. In less
severe cases, the onset is not so dramatic and progress to paraplegia may be
delayed and incomplete. There may
be little in the way of girdle pain in such cases. On examination, it is often possible to
determine a “level” above which spinal cord function is
normal. This level is often in the
lower thoracic or upper lumber segments.
It is occasionally possible to determine different levels for motor innervation and the various sensory modalities. The bladder is frequently involved in
spinal decompression sickness. The
patient may report difficulty initiating urination, but often, this will be
detected by the absence of urinary output and the presence of a distended
bladder on examination of the abdomen.
d. Progress
Unless severe spinal cord
decompression sickness is rapidly treated with recompression, a complete
recovery is unlikely. The prognosis
for cases with a less dramatic onset is better; even without recompression the
condition often shows some spontaneous improvement. Nonetheless, improvement will be more
complete and rapid with recompression.
CEREBRAL DECOMPRESSION SICKNESS
The brain is increasingly
recognised as a target for decompression sickness and because of its complex
structure and function, many varied manifestations of
the disease are possible.
The onset of cerebral
decompression sickness is frequently rapid: over 50% of serious cases present
within 10 minutes of reaching the surface.
Symptoms and Signs
Progress
VESTIBULAR DECOMEPRESSION SICKNESS (STAGGERS)
a. While otitic barotrauma may result from quite shallow dives, especially
those in which there may have been difficulty in clearing the ears, inner ear decompression sickness
is quite rare and is only a likely diagnosis following deep oxy-helium (and
occasionally air) dives.
b. Onset
The onset of vestibular
sickness is usually a few minutes after surfacing from a bounce dive. In saturation dives, the syndrome may occur
during decompression or a depth after a switch in the inert gas component of the mixture
which can result in isobaric counterfusion. There may be signs of decompression
sickness in other organs.
C. Symptoms
and Signs
The syndrome consists of vertigo,
nausea, and vomiting and, less commonly, deafness and tinnitus.
d. Progress
Unless treated promptly, the
recovery of inner ear function may be incomplete. It is important however, that the
diagnosis is made accurately since round window fistulae should not be
recompressed unless the patient displays evidence of other dysbaric
disease which would benefit from recompression.
PULMONARY DECOMPRESSION SICKNESS (STAGGERS)
a. Fortunately, this is a rare manifestation of
decompression sickness. It is
thought to occur when there is sufficient intravenous bubbling to obstruct a
large proportion of the vessels of the pulmonary circulation.
b. Onset, Symptoms and Signs
The onset of pulmonary DCS is
rapid. Patients become symptomatic
within about half an hour of reaching the surface. The condition commences with central
chest pain and cough, which may be aggravated by taking deep breaths or
inhaling cigarette smoke.
Breathlessness and central cyanosis follow and, shortly thereafter,
signs of shock. Unlike mediastinal emphysema, which is a differential diagnosis,
pulmonary DCS is progressive and the patient may deteriorate rapidly.
c. Progress
Although rare, this is potentially the most dangerous
form of decompression sickness since, if the patient is not rapidly treated
with recompression cardiovascular collapse, loss of consciousness and death may
follow.
PULMONARY OVER-INFLATION SYNDROME (DECOMPRESSION PULMONARY
BAROTRAUMA) (BURST LUNG)
The
pulmonary over-inflation syndrome is caused by rupture of alveolar air sacs
during over pressurisation of the lung.
In diving, this may be caused when gas, which is trapped in the lung for
any reason, expands during ascent.
The conditions may be asymptomatic or give rise to one or more of the
following symptoms and signs:
a. A sharp
chest pain, usually behind the breast bone.
b. Shortness of breath.
c. Difficult or painful
.
d. A cough which may be productive
or slightly blood-stained sputum.
There are three possible routes
for the gas which escapes from a ruptured lung to take. It may enter the
interstitial tissue space of the lung and migrate into the middle of the chest
(the mediastinum). From there, the gas may spread up into
the subcutaneous tissues of the neck and head.
Alternatively,
the lung may rupture into the pleural space and thereby give rise to a pneumothorax.
Finally, alveolar gas may escape into the pulmonary circulation. Following transit through the heart, the
gas is then distributed to the body as arterial gas emboli.
PREVENTION OF PULMONARY OVER-INFLATION SYNDROME
Careful
consideration must be given to the following:
a. The Careful Selection of Divers
People
who are know to have lung disease and have a past
history of serious respiratory disorders, including spontaneous pneumothorax, should not dive.
b. Assessment
Immediately Before a Dive
A diver with a cold or hay fever which is causing
respiratory symptoms such as a cough or wheeze should be considered temporarily
unfit to dive.
c. Training and the correct use of
equipment.
d. When making an emergency ascent, the diver
must exhale adequately. The rate of
exhalation should match the rate of ascent. For a free ascent, where the diver uses
natural buoyancy to travel towards the surface, the rate of exhalation must be
great enough to avoid embolism, but not so great as to reduce buoyancy. With a buoyant ascent, where the diver
is assisted by an external source of buoyancy such as a B.C (Buoyancy
compensator), the rate of ascent may far exceed that of a free ascent. Under these circumstances, exhalation
should commence before ascent, and should be a steady, forceful blow.
e. Other factors in the prevention of gas
embolism include the planning of the dive and adherence to that plan. The avoidance of emergencies such as
running out of air, will promote safe ascents.
ARTERIAL GAS EMBOLISM (AGE)
Bubbles
of gas may enter a diver's arterial blood by a number of routes:
a. As described in
b. Following decompression, bubbles
of gas may be released into the veins. Although the lungs are normally capable
of filtering considerable quantities of gas, this capacity may be overwhelmed
when large amounts of gas are present.
Bubbles may then be free to traverse the pulmonary circulation and enter
the left side of the heart.
c. In a small proportion of the
normal, adult population there is a communication between the two upper
chambers of the heart, the left and the right atria. This is necessary during foetal life,
but in some people it fails to close completely after birth. While people normally experience no
problems with this condition, this so-called “Patent Foramen Ovale” may provide a route in adult life for bubbles
to pass from the right to the left side of the heart.
Once gas bubbles have entered
the arterial circulation, they are distributed to the whole body. These bubbles cause tissue injury by
obstructing small blood vessels and
by damaging their delicate lining.
The brain and heart are particularly susceptible to bubble embolism,
since they both require a continuous supply of blood.
Since two of the most important
organs of the body may be involved in gas embolism, it must be diagnosed
quickly and accurately. The usual
features of the disease are as follows:
a. Dive Profile
Gas
embolism is possible following any dive during which a breath is taken from a source
of compressed gas, even at depths as shallow as 1 metre.
b. Presentation
The onset is sudden and occurs
on reaching the surface or shortly thereafter. It is most unlikely that the
onset of gas embolism caused by pulmonary over-inflation will occur after more
than 10 minutes have elapsed on the surface.
c. Symptoms
and Signs
The number of possible symptoms
and signs is enormous. The most
dramatic presentation is a sudden loss of consciousness. The least obvious may be a subtle change
of mood or a loss of short-term memory.
Common manifestations include: visual symptoms, sensory or motor
deficits with a cortical distribution (which generally affect one side of the
body more than the other), a disturbance of balance, fatigue, disorientation
and convulsions. Chest symptoms may
also be apparent. These relate
either to pulmonary over-inflation as described above (
d. Progress
This
condition usually improves spontaneously.
However, particularly in cases with cerebral involvement, this
improvement may only be temporary and within a few hours the symptoms and signs
can return. Whereas improvements of
the initial symptoms are normally rapid and complete with recompression, this
secondary deterioration is much less responsive to treatment. For this reason, the treatment of choice
for AGE is EARLY RECOMPRESSION. Treatment on a therapeutic table should
be undertaken even if spontaneous improvement has occurred to the point of
apparent recovery. This is to reduce the risk of secondary deterioration.
Patients
with arterial gas embolism should be transported to a recompression chamber as
a matter of urgency. First aid
should be administered. Patients
should be transported lying flat. A
supine position is suitable for conscious patients and the recovery position
should be used for those with a reduced level of consciousness.
PNEUMOTHORAX
A pneumothorax occurs when alveolar gas escapes into the
pleural space. This is often
painless, but may cause a sharp pain which is made worse by taking a deep
breath. Depending upon how much gas
leaks into the pleural space, there may be shortness of breath
and possibly, slight blueing of the lips and finger nail beds (cyanosis). Normally there are few physical signs,
so this condition may not be recognised except by medical staff. This is not a life-threatening condition
because it is possible to survive with the one intact lung. Occasionally, however, the leak is such
that gas escapes into the pleural space with each breath, but is unable to
return to the lung. Under these
circumstances the volume of the pneumothorax
gradually increases. This is known
as Tension Pneumothorax. It is dangerous because if gas continues
to escape from the perforated lung, the pressure generated within the chest may
eventually cause both lungs to collapse.
Cyanosis will become pronounced and shock, unconsciousness and death
will ensue unless the patient is treated appropriately.
A
tension pneumothorax is rare under normal conditions
at the surface. However, a simple pneumothorax which occurs at depth may increase in size
during decompression and effectively become a tension pneumothorax. If a diver's condition deteriorates
during ascent, especially if the symptoms are respiratory,
a pneumothorax should always be suspected.
A
small pneumothorax can be treated by 100% O2 on
the surface, large pneumothoraces and ALL tension pneumothoraces
require draining. A chest drain,
large bore I.V. cannula, or some other device with a
one-way value (such as a Heimlich valve), should be inserted by an
appropriately trained individual.
If pneumothorax occurs coincidentally with arterial gas
embolism or decompression sickness, it should not prevent the immediate
commencement of recompression therapy.
Divers who are recompressed in this condition will experience relief of
their pneumothorax. However, a chest drain, as described
above, with a one-way valve must be inserted before decompression commences, to
prevent expansion of the trapped gas during the ascent.
MEDIASTINAL AND SUBCUTANEOUS EMPHYSEMA
If gas
escapes into the interstitial tissue space, it may track along the outside of
the airways and blood vessels to the hila of the
lungs and from there into the mediastinum. This is the space between the lungs
which contains the heart, large blood vessels and major airways.
The
presence of a little gas in the mediastinum is often symptomless. If tissues are stretched, mild to moderate retrosternal pain may be felt. Other possible symptoms include a
sensation of fullness in the chest or throat and a change in the tone of voice
or hoarseness.
Gas in
the mediastinum may migrate up into the subcutaneous
tissues of the neck, occasionally, the head. It is not usually painful and may only
be detected by noticing swelling or crepitation (the
skin "cracks”) when doing up a collar.
Subcutaneous
emphysema usually resolves gradually without treatment. Asymptomatic mediastinal
emphysema also requires no treatment.
If there are troublesome symptoms, resolution will be accelerated by breadiing 100% O2 on the surface. In the very
rare instances where there are serious symptoms, recompression may be
necessary. If there is no
associated pneumothorax, it is safe to recompress to
10m for an hour 100% O2.