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.




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.





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.




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.




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.





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.




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








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.




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.





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.




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.





Bubbles of gas may enter a diver's arterial blood by a number of routes:


a.       As described in Para 2-5, alveolar gas may enter the venous drainage of the lungs as a result of pulmonary over-inflation.  Once in the pulmonary veins the gas bubbles enter the left side of the heart and are then distributed around the body in arterial blood.


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 (Para 2-5), or rarely, refer to cardiac ischemia which results from gas embolism of the coronary arteries.  In this event, the pain may be severe, is classically described as “constricting” and may extend down the left arm.  This pain may be accompanied by fatigue, breathlessness and shock.  Involvement of the spinal cord in arterial gas embolism is very rare.  If there are such signs, the diagnosis is probably decompression sickness.


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.





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.







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.