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Dysbarism is the term given to medical complications of exposure to gases at higher than normal atmospheric pressure. It includes barotrauma and decompression illness.
An understanding of the pathophysiology of dysbarism requires an understanding of the gas laws.
Barotrauma occurs as a consequence of excessive expansion or contraction of gas within enclosed body cavities. It principally affects the middle ear, the sinuses and the lungs. Lung barotrauma may result in gas embolism, pneumomediastinum or pneumothorax. Inner-ear barotrauma is rare but serious and may mimic vestibular decompression illness.
Decompression illness occurs when gas bubbles develop within the body. This may occur as a complication of pulmonary barotrauma or when a diver whose tissues are supersaturated with nitrogen (or other breathing gas such as helium), ascends too rapidly.
The clinical manifestations of decompression illness may affect many body systems and are extremely variable in nature and severity. Loss of consciousness or neurological symptoms and signs (including cognitive dysfunction) indicate serious decompression illness.
If a diver becomes unwell during or after diving, then diving is the likely cause of the illness, until proven otherwise. Early consultation with a diving medicine specialist is mandatory, especially where retrieval to a recompression facility may be necessary.
The seriously injured diver should be managed lying flat and urgently referred for recompression treatment. The diver should not exceed 300 m altitude during retrieval for recompression treatment.
Nondiving causes of dysbarism include caisson work, altitude decompression, recreational use of compressed gases (nitrous oxide and helium) causing pulmonary barotrauma and gas embolism and medical adverse events where gas enters the circulation. These cases are likely to benefit from early recompression with hyperbaric oxygen.
This chapter focuses on medical problems that develop secondary to breathing gases at higher than normal atmospheric pressure (dysbarism). This usually occurs in the context of scuba (self-contained underwater breathing apparatus) diving, a popular recreational activity in Australasia. Diving is generally very safe and serious decompression incidents occur approximately 1:10,000 dives. However, because of a high participation rate, between 200 and 300 cases of decompression illness are treated in Australia each year. It is estimated that 10 times that number of divers experience less serious health problems after diving. Emergency physicians are often the first medical staff to assess the diver after a diving accident and it is essential they understand the risks and potential injuries.
An understanding of pressure and some gas laws is essential to understand the pathophysiology of diving injuries. The air pressure at sea level is 1 atmosphere absolute (ATA). Multiple units are used to measure pressure ( Box 24.3.1 ). For every 10 m a diver descends in seawater, the pressure increases by 1 ATA. This pressure change impacts on gas spaces within the body according to Boyle’s law.
Atmosphere absolute (ATA)
kPa (SI units)
Bar
m of sea water (MSW)
mm of mercury (mm Hg)
pounds per square inch (PSI)
Boyle’s law states that, at a constant temperature, the volume of a gas varies inversely to the pressure acting on it:
where P = pressure, V = volume and k = constant.
The proportionate change in volume is greatest near the surface ( Table 24.3.1 ).
Depth (m) | Absolute pressure (ATA) | Gas volume (%) |
---|---|---|
0 | 1 | 100 |
10 | 2 | 50 |
20 | 3 | 33 |
30 | 4 | 25 |
40 | 5 | 20 |
Dalton’s law states that the total pressure ( P t ) exerted by a mixture of gases is equal to the sum of the pressures of the constituent gases ( P x , P y , P z ):
Therefore as divers breathe air at increasing atmospheric pressure, the partial pressures of nitrogen and oxygen increase:
A diver breathing air at 40 m is inhaling a gas with a partial pressure of oxygen equivalent to breathing 100% oxygen at the surface. At partial pressures above 3 ATA, the P N 2 affects coordination and judgement (‘nitrogen narcosis’). Oxygen may also become toxic at partial pressures greater than 1 ATA. Recreational scuba diving generally has a limit of 40 m because of these effects.
Henry’s law states that at a constant temperature the amount of a gas that will dissolve in a liquid is proportional to the partial pressure of the gas in contact with the liquid:
where Q = volume of gas dissolved in a liquid, k = constant and P gas = partial pressure of the gas.
Henry’s law is relevant in diving illness because it is the basis of decompression illness (DCI). As the ambient pressure increases, the diver is exposed to increasing partial pressures of nitrogen (or other gas such as helium), which dissolves in bodily fluids. The amount of nitrogen absorbed depends on both the depth (which determines the partial pressure of nitrogen) and the duration of the dive. Tissues also take up nitrogen at different rates depending on their blood supply and permeability. Eventually, the tissues become saturated with nitrogen and no further absorption occurs. As the diver ascends and ambient pressure decreases, the partial pressure of nitrogen in some tissues will exceed ambient pressure, resulting in tissue supersaturation. If the diver ascends slowly enough, nitrogen diffuses out of the tissues and is transported, safely dissolved in the blood, to the lungs for elimination. This is known as ‘off-gassing’.
If the diver ascends too rapidly, sufficient nitrogen bubbles will form in their body to cause decompression illness. Oxygen does not cause problems because it is rapidly metabolized by the tissues.
Barotrauma occurs when changes in ambient pressure lead to expansion or contraction of gas within enclosed body cavities. The change in gas volume distorts or tears adjacent tissue. Injury by this mechanism may occur to the middle ear, inner ear, sinuses, lungs, eyes (via the diver’s mask) and rarely, the gut. Different injury patterns occur in breath-hold divers (snorkellers) compared to those breathing compressed air. Both breath-hold and scuba divers may experience injury of the middle and inner ear, sinuses and eyes if they do not equalize pressures in the gas spaces as they descend. Breath-hold divers are unlikely to injure their lungs as their lung volumes reduce as they descend and return to their original volume as they ascend to the surface by the increasing ambient pressure.
Middle-ear barotrauma (MEBT), the most common medical disorder of diving, usually occurs during descent. Increased ambient pressure results in a reduction of middle-ear volume. If equalization of the volume via the eustachian tube is inadequate, a series of pathological changes results. The tympanic membrane (TM) is deformed inwards, causing inflammation and haemorrhage. Middle-ear mucosal oedema is followed by vascular engorgement, effusion, haemorrhage and, rarely, TM rupture.
Symptoms of middle-ear barotraumas include ear pain, tinnitus and conductive hearing loss. Mild vertigo may also be experienced. More severe vertigo and pain occur if water passes through a perforated TM. Severe vertigo and significant sensorineural hearing loss should alert the emergency physician to possible inner-ear barotrauma (IEBT) (see below). MEBT severity is graded by visual inspection of the TM ( Table 24.3.2 ). An audiogram is useful to document any hearing loss.
Grade 0 | Symptoms without signs |
Grade 1 | Injection of TM along handle of malleus |
Grade 2 | Slight haemorrhage within the TM |
Grade 3 | Gross haemorrhage within the TM |
Grade 4 | Free blood in middle ear |
Grade 5 | Perforation of TM |
Treatment of MEBT consists of analgesia, decongestants and ear, nose and throat (ENT) referral if there is TM perforation or suspected IEBT. Antibiotics are indicated for TM rupture because of potential contamination with water. The patient should not dive again until symptoms and signs have resolved, any TM perforation has healed, and the eustachian tube is patent.
Sudden pressure changes between the middle and inner ears can cause rupture of the round or oval windows or a tear of Reissner’s membrane. This usually occurs during rapid descent without equalizing or forceful Valsalva manoeuvres.
Symptoms include sudden onset of tinnitus, vertigo, nausea and vomiting, vestibular symptoms and profound sensorineural hearing loss, which may not be apparent until the diver has left the water. Onset of symptoms after the dive while performing an activity that increases intracranial pressure (e.g. heavy lifting) suggests IEBT. Coexistent middle-ear barotrauma is absent in about one-third of cases.
The main differential diagnosis is DCI involving the inner ear or vestibular apparatus. Frequently it is difficult to distinguish between IEBT and vestibular DCI, although the latter is frequently accompanied by other symptoms or signs of DCI. Because of this overlap in clinical syndromes, early specialist advice should be sought.
Treatment of IEBT consists of avoidance of activities that increase intracranial pressure and urgent (same day) ENT referral for more detailed assessment and audiometry. Surgical repair may be undertaken when vertiginous symptoms are severe. Vomiting should be treated with antiemetics and the diver kept supine with their head on a pillow. If DCI is excluded, then a 45° semirecumbent position is preferred. If DCI cannot be excluded the diver should have a trial of recompression. In one series, exposure to pressure did not worsen IEBT. The benefit of steroids in IEBT has not been confirmed.
It was thought that further diving was contraindicated after IEBT, but recent case data suggest that diving might be possible following full recovery of hearing.
Ear-canal barotrauma is very rare and only occurs if there is a complete obstruction of the canal (usually by wax or ear plugs), creating a noncommunicating gas cavity between the obstruction and the TM. Treatment is symptomatic. ENT specialist referral may be necessary if the TM cannot be visualized.
Mucosal swelling and haemorrhage occur if the communication of the sinuses with the nasopharynx is blocked and equalization of sinus pressure is not possible during descent. The frontal sinuses are most commonly involved.
Sinus pain usually develops during descent. Maxillary sinus involvement can refer pain to the upper teeth or cheek. There may be resolution of the pain at depth, due to mucosal oedema and blood filling the volume deficit left by gas compression. Pain and epistaxis may occur as the diver ascends. The pain usually persists after diving. Tenderness will be noted over the affected sinus. In doubtful cases, a sinus computed tomography (CT) scan will assist the diagnosis.
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