DECOMPRESSION ILLNESS - a patient's guide
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 IT 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.
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.
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.
THE HYPERBARIC CHAMBER