| Inner ear decompression sickness | |
| Synonyms: | Audiovestibular decompression sickness |
| Field: | Diving and hyperbaric medicine |
| Symptoms: | Vertigo, nystagmus, nausea, ataxia, hearing loss |
| Causes: | Gas bubbles forming in inner ear and associated vascular system from supersaturation |
| Risks: | Deep diving, long decompressions, gas switching with helium mixtures, right-to-left shunt |
| Diagnosis: | By symptoms, inner ear involvement |
| Differential: | Decompression and dive history |
| Treatment: | Hyperbaric oxygen therapy |
| Frequency: | rare |
Inner ear decompression sickness, (IEDCS) or audiovestibular decompression sickness is a medical condition of the inner ear caused by the formation of gas bubbles in the tissues or blood vessels of the inner ear. Generally referred to as a form of decompression sickness, it can also occur at constant pressure due to inert gas counterdiffusion effects.
Usually only one side is affected, and the most common symptoms are vertigo with nystagmus, loss of balance, and nausea. The symptoms are similar to those caused by some other diving injuries and differential diagnosis can be complicated and uncertain if several possible causes for the symptoms coexist.
First aid is breathing the highest practicable concentration of normobaric oxygen. Definitive treatment is recompression with hyperbaric oxygen therapy. Anti-vertigo and anti-nausea drugs are usually effective at suppressing symptoms, but do not reduce the tissue damage. Hyperbaric oxygen may be effective for reducing oedema and ischaemia even after the most effective period for reducing the injury has passed.
IEDCS is often associated with relatively deep diving, relatively long periods of decompression obligation, and breathing gas switches involving changes in inert gas type and concentration. Onset may occur during the dive or afterwards. IEDCS is a relatively uncommon manifestation of decompression sickness, occurring in about 5 to 6% of cases. The most commonly used decompression models do not appear to accurately model IEDCS, and therefore dive computers based on those models alone are not particularly effective at predicting it, or avoiding it. There are a few rule of thumb methods which have been reasonably effective for avoidance, but they have not been tested under controlled conditions.
DCS is classified by symptoms. The earliest descriptions of DCS used the terms: "bends" for joint or skeletal pain; "chokes" for breathing problems; and "staggers" for neurological problems. In 1960, Golding et al. introduced a simpler classification using the term "Type I ('simple')" for symptoms involving only the skin, musculoskeletal system, or lymphatic system, and "Type II ('serious')" for symptoms where other organs (such as the central nervous system) are involved. Type II DCS is considered more serious and usually has worse outcomes. This system, with minor modifications, may still be used today. Following changes to treatment methods, this classification is now much less useful in diagnosis, since neurological symptoms may develop after the initial presentation, and both Type I and Type II DCS have the same initial management.
The term dysbarism encompasses decompression sickness, arterial gas embolism, and barotrauma, whereas decompression sickness and arterial gas embolism are commonly classified together as decompression illness when a precise diagnosis cannot be made. DCS and arterial gas embolism are treated very similarly because they are both the result of gas bubbles in the body. The U.S. Navy prescribes identical treatment for Type II DCS and arterial gas embolism. Their spectra of symptoms also overlap, although the symptoms from arterial gas embolism are generally more severe because they often arise from an infarction (blockage of blood supply and tissue death).
The usual symptoms are tinnitus, ataxia, difficulty with coordination, vertigo, nausea, vomiting, and hearing loss. It is not unusual for other symptoms of decompression sickness to be present simultaneously, which can make diagnosis easier, but sometimes only vestibular symptoms manifest.
Incompletely understood, but probably caused by nucleation and development of one or more inert gas bubbles which affect the function of the inner ear, either directly in the endolymphatic and perilymphatic spaces or by way of the perfusion or innervation of the inner ear.
It has been hypothesized that in divers with a right-to-left shunt shunt, gas embolism of the labyrinthine artery may be a cause.
Several factors are considered likely to increase the risk of IEDCS:
The inner ear, particularly the vestibule, is poorly perfused, and when saturated can take a relatively long tine to off-gas, which may be described as a slow tissue compartment. Supersaturated total inert gases loading may be due to decompression or to Isobaric counterdiffusion of gases after a switch in which the new gas mixture contains a relatively high partial pressure of a gas with higher diffusivity than the gas replaced, causing a net ingassing of the affected tissues and a consequently excessive combined inert gas supersaturation. The tissues may remain supersaturated for some time, which may trigger autochthonous bubble formation and growth from pre-existing bubble nuclei, and if venous gas bubbles concurrently pass through a shunt and reach the supersaturated area, the high local inert gas concentration may cause intravascular bubble growth.
The primary provoking agent in decompression sickness is bubble formation from excess dissolved gases. The earliest bubble formation detected is subclinical intravascular bubbles detectable by doppler ultrasound in the venous systemic circulation. The presence of these "silent" bubbles is no guarantee that they will persist and grow to be symptomatic. Gas bubble formation in blood vessels causes obstruction and inflammation, and platelet aggregation may occur. In more solid tissues there may be mechanical damage, and the presence of mobile bubbles in the fluids of the inner ear may cause abnormal stimuli. The pathogenesis remains elusive, and may have more than one mechanism. Development of the inner ear injury has been attributed to a vascular mechanism.
IEDCS and inner ear barotrauma (IEBt) are the inner ear injuries associated with ambient pressure diving, both of which manifest as cochleovestibular symptoms. The similarity of symptoms makes differential diagnosis difficult, which can delay appropriate treatment or lead to inappropriate treatment.
Usually transient, but can persist. Has two versions, the usual block on descent, where ambient pressure is greater than pressure in the middle ear, and on ascent with middle ear pressure greater than ambient pressure, which may persist after surfacing. Reverse block can also occur on descent if the external auditory canal is blocked by an earplug, tightly fitting diving hood, severe exostoses or impacted cerumen. A blockage of the external auditory canal is also a common cause of inner ear barotrauma.
A normal response to a temperature difference reaching the semicircular canals, by way of ambient water flooding the external auditory canals unevenly. Also usually transient, but has rarely been known to persist for no obvious reason.
Transient, normally resolves shortly after getting onto solid land.
Distinguishing between IEDCS and IEBt can be difficult, and both can be present at the same time. While IEDCS is more likely to cause vertigo, and IEBt is more likely to cause hearing loss, these are not reliable distinguishing factors. Lindfors et al 2021 report that the most useful variables they found for distinguishing between IEBt and IEDCS are dive mode, (scuba versus freediving), breathing gas type (compressed air versus mixed gas), dive profile (deep or shallow), symptom onset (descending versus ascending or at surface), distribution of cochleovestibular symptoms (vestibular versus cochlear) and presence or absence of other DCS symptoms. It is considered appropriate in the presence of any symptom typical of DCS, to assume and treat for DCS with recompression.
| Barotrauma | Decompression sickness | |
|---|---|---|
| Conductive or mixed hearing loss | Sensorineural hearing loss | |
| Occurs during descent or ascent | Onset during ascent or after surfacing | |
| Cochlear symptoms (ie hearing loss) predominate | Vestibular symptoms (vertigo) predominant; right sided | |
| History of difficult ear clearing or forced Valsalva manoeuvre | No history of eustachian tube dysfunction | |
| Low-risk dive profile | Depth >15 m, helium mixtures, helium to nitrogen gas switches, repetitive dives | |
| Isolated inner ear symptoms, or inner and middle ear on the same sides | Other neurological or dermatological symptoms suggestive of DCS |
IEDCS caused by inert gas counterdiffusion can be avoided by avoiding gas switches where the relative concentration of inert gas diluents with dissimilar diffusivity is large.
Early recompression treatment with hyperbaric oxygen is more likely to prevent permanent inner ear damage. Recompression increases ambient pressure which returns gases into solution and hyperbaric oxygen improves oxygenation of ischaemic tissues while facilitating inert gas elimination. Slow decompression to normal atmospheric pressure allows controlled outgassing of residual inert gas to avoid re-formation of bubbles. U.S. Navy treatment table 6 has been successfully used, but multiple exposures of hyperbaric oxygen therapy may be necessary if symptoms are not resolved in the initial treatment or if symptoms return. Repeat treatments are focused on resolving sequelae as the initial bubbles will already have been resorbed during adequate initial treatment.
First aid treatment of 100% oxygen, or the highest available oxygen fraction is recommended for several hours or until recompression is available, as this establishes the highest possible ambient pressure oxygen window which induces a maximum inert gas gradient between the lungs and gases in the tissues, resulting in faster inert gas removal, while providing the greatest relief for ischaemic tissues. Rehydration is also indicated. Anti-inflammatory drugs may help, but could also increase leakage of fluids through damaged tissue.
The symptoms of IEDCS are not easily discriminated from symptoms of inner ear barotrauma, and a possible necessity for bilateral myringotomy should be assessed before hyperbaric oxygen therapy is started. In practice, if there is uncertainty about a diagnosis of barotrauma, recompression does not appear to cause harm.
Ameliorative: Anti-nausea drugs may be administered for short term relief. They should not mask vertigo, nystagmus, tinnitis or hearing deficits.
A minority of cases recover completely. About 90% of cases of diving-related vestibular dysfunction have mild to moderate long term residual symptoms. Vestibulocochlear assessment and exclusion of a right-to-left vascular shunt prior to continuing scuba diving is recommended. Recent experience in Finland reports a higher rate of complete recovery, of about 65 to 70% in technical and recreational divers respectively.
Otological injuries account for about 2/3 of all diving related injuries, but about 50% of all presentations are middle ear barotrauma. Decompression sickness is much less common, and IEDCS is rare, with an estimated incidence rate of 0.01–0.03% in recreational dives. It is becoming more frequently reported, bur epidemiological data remain limited to small case series. The condition is usually associated with deep diving on mixed gas, and is frequently accompanied by other central nervous system symptoms of decompression sickness. However it has also been known to occur as the only manifestation of decompression sickness following moderate or short and shallow scuba dives on air and nitrox.
In deep saturation diving, the greater frequency of inner ear DCS after upwards or downwards excursions compared with decompression to sea level may be explained by arterialisation of venous bubbles across pulmonary or intracardiac shunts, and subsequent growth if they reach the inner ear. Experimental work suggests that arterial bubbles last longer at hyperbaric pressures than at sea level.
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