Decompression sickness results from the formation of bubbles in the blood or
body tissues, and is caused by inadequate elimination of dissolved gas after a dive
or other exposure to high pressure. Decompression sickness may also occur with
exposure to subatmospheric pressures (altitude exposure), as in an altitude
chamber or sudden loss of cabin pressure in an aircraft. In certain individuals,
decompression sickness may occur from no-decompression dives, or decompression
dives even when decompression procedures are followed meticulously.
Various conditions in the diver or in the diver’s surroundings may cause absorption
of an excessive amount of inert gas or may inhibit the elimination of the
dissolved gas during normal controlled decompression. Any decompression sickness
that occurs must be treated by recompression. The following paragraphs
discuss the diagnosis of the various forms of decompression sickness. Once the
correct diagnosis is made, the appropriate treatment from Chapter 21 can be
chosen based on the initial evaluation.
A wide range of symptoms may
accompany the initial episode of decompression sickness. The diver may exhibit
certain signs that only trained observers will identify as decompression sickness.
Some of the symptoms or signs will be so pronounced that there will be little
doubt as to the cause. Others may be subtle and some of the more important signs
could be overlooked in a cursory examination.
For purposes of deciding the
appropriate treatment, symptoms of decompression sickness are generally divided
into two categories. Type I decompression sickness includes skin symptoms,
lymph node swelling and joint and/or muscle pain and is not life threatening. Type
II decompression sickness (also called serious decompression sickness) includes
symptoms involving the central nervous system, respiratory system, or circulatory
system. Type II decompression sickness may become life threatening. Because the
treatment of Type I and Type II symptoms may be different, it is important to
distinguish between these two types of decompression sicknesses. Type I and
Type II symptoms may or may not be present at the same time.
Type I decompression sickness includes joint
pain (musculoskeletal or pain-only symptoms) and symptoms involving the skin
(cutaneous symptoms), or swelling and pain in lymph nodes.
The most common symptom of decompression
sickness is joint pain. Other types of pain may occur which do not involve
joints. The pain may be mild or excruciating. The most common sites of joint pain
are the elbow, wrist, hand, knee, and ankle. The characteristic pain of Type I
decompression sickness usually begins gradually, is slight when first noticed and
may be difficult to localize. It may be located in a joint or muscle, may increase in
intensity, and is usually described as a deep, dull ache. The pain may or may not
be increased by movement of the affected joint, and the limb may be held preferentially
in certain positions to reduce the pain intensity (so-called guarding). The
hallmark of Type I pain is its dull, aching quality and confinement to particular
areas. It is always present at rest; it may or may not be made worse with
movement.
The most difficult differentiation
is between the pain of Type I decompression sickness and the pain resulting
from a muscle sprain or bruise. If there is any doubt as to the cause of the pain,
assume the diver is suffering from decompression sickness and treat accordingly.
Frequently, pain may mask other more significant symptoms. Pain should not be
treated with drugs in an effort to make the patient more comfortable. The pain may
be the only way to localize the problem and monitor the progress of treatment.
Pain in the abdominal and thoracic areas, including
the hips and shoulders, may:
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Be localized to joints between the ribs and spinal column or joints between the
ribs and sternum.
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Present a shooting-type pain that radiates from the back around the body
(radicular or girdle pain).
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Appear as a vague, aching (visceral) pain.
Any pain occurring in these regions should be considered as symptoms arising
from spinal cord involvement. Treat it as Type II decompression sickness.
The most common skin manifestation of diving is
itching. Itching by itself is generally transient and does not require recompression.
Faint skin rashes may be present in conjunction with itching. These rashes also are
transient and do not require recompression. Mottling or marbling of the skin,
known as cutis marmorata (marbling), may precede a symptom of serious decompression
sickness and shall be treated by recompression as Type II decompression
sickness. This condition starts as intense itching, progresses to redness, and then
gives way to a patchy, dark-bluish discoloration of the skin. The skin may feel
thickened. In some cases the rash may be raised.
Lymphatic obstruction may occur, creating localized pain
in involved lymph nodes and swelling of the tissues drained by these nodes.
Recompression may provide prompt relief from pain. The swelling, however, may
take longer to resolve completely and may still be present at the completion of
treatment.
In the early stages, symptoms of Type II
decompression sickness may not be obvious and the stricken diver may consider
them inconsequential. The diver may feel fatigued or weak, and attribute the
condition to overexertion. Even as weakness becomes more severe, the diver may
not seek treatment until walking, hearing, or urinating becomes difficult. For this
reason, symptoms must be anticipated during the postdive period and treated
before they become too severe.
Many of the symptoms of Type II
decompression sickness are the same as those of arterial gas embolism, although
the time course is generally different. (AGE usually occurs within 10 minutes of
surfacing.) Since the initial treatment of these two conditions is the same and since
subsequent treatment conditions are based on the response of the patient to treatment,
treatment should not be delayed unnecessarily in order to make the
diagnosis in severely ill patients.
Type II, or serious symptoms, are divided into
three categories: neurological, inner ear (staggers), and cardiopulmonary (chokes)
symptoms. Type I symptoms may or may not be present at the same time.
These symptoms may be the result of involvement of
any level of the nervous system. Numbness, paresthesias (a tingling, pricking,
creeping, “pins and needles,” or “electric” sensation on the skin), decreased sensation
to touch, muscle weakness, paralysis, mental status changes, or motor
performance alterations are the most common symptoms. Disturbances of higher
brain function may result in personality changes, amnesia, bizarre behavior, lightheadedness,
incoordination, and tremors. Lower spinal cord involvement can
cause disruption of urinary function. Some of these signs may be subtle and can be
overlooked or dismissed by the stricken diver as being of no consequence.
The occurrence of any neurological symptom is abnormal after a dive and should
be considered a symptom of Type II decompression sickness or arterial gas embolism,
unless another specific cause can be found. Normal fatigue is not uncommon after long dives and, by itself, is not usually treated as decompression sickness. If
the fatigue is unusually severe, a complete neurological examination is indicated
to ensure there is no other neurological involvement.
If profuse intravascular bubbling
occurs, symptoms of chokes may develop due to congestion of the lung circulation.
Chokes may start as chest pain aggravated by inspiration and/or as an
irritating cough. Increased breathing rate is usually observed. Symptoms of
increasing lung congestion may progress to complete circulatory collapse, loss of
consciousness, and death if recompression is not instituted immediately.
Decompression sickness symptoms usually occur
shortly following the dive or other pressure exposure. If the controlled decompression
during ascent has been shortened or omitted, the diver could be suffering
from decompression sickness before reaching the surface.
In analyzing several thousand air dives in a database set up
by the U.S. Navy for developing decompression models, the time of onset of
symptoms after surfacing was as follows:
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42 percent occurred within 1 hour.
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60 percent occurred within 3 hours.
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83 percent occurred within 8 hours.
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98 percent occurred within 24 hours.
While a history of diving (or altitude exposure) is necessary for the
diagnosis of decompression sickness to be made, the depth and duration of the
dive are useful only in establishing if required decompression was missed.
If the reason for postdive symptoms is firmly
established to be due to causes other than decompression sickness or arterial gas
embolism (e.g., injury, sprain, poorly fitting equipment), then recompression is not necessary. If the diving supervisor cannot rule out the need for recompression,
then commence treatment.
Aviators exposed to altitude may experience
symptoms of decompression sickness similar to those experienced by divers. The
only major difference is that symptoms of spinal cord involvement are less
common and symptoms of brain involvement are more frequent in altitude decompression
sickness than hyperbaric decompression sickness. Simple pain, however,
still accounts for the majority of symptoms.
If only joint pain was present but resolved before reaching
one ata from altitude, then the individual may be treated with two hours of 100
percent oxygen breathing at one atmosphere followed by 24 hours of observation.
If symptoms persist after return to one ata from altitude, the stricken individual
should be transferred to a recompression facility for treatment.
Individuals should be kept on 100 percent oxygen
during transfer to the recompression facility. If symptoms have resolved by the
time the individual has reached a recompression facility, they should be examined
for any residual symptoms. If any decompression symptom had been present at
any time or if even the most minor symptom is present they should be treated with
the appropriate treatment table as if the original symptoms were still present.