Inner Ear Barotrauma


There is always the possibility of inner ear damage in divers who have any of the following:

  • A history of ear barotrauma of any type.
  • Previous difficulty in equalizing middle ear pressures.
  • Subsequent application of excessive force to achieve this equalization.
  • Structural abnormalities that make the divers susceptible to this damage.

In these cases, sensorineural hearing loss may immediately follow the dive, or it may develop over the next few hours or days. Tinnitus is a common association. Some patients may complain of vertigo, nausea and vomiting. Vertigo is often increased with exercise, altitude changes and head movements.

Combined cochlear and vestibular injury is experienced in 50 per cent.

Only cochlear injury occurs in 40 per cent.

Only vestibular injury occurs in 10 per cent.

There may be no otoscopic signs. This disorder has been reported from dives as shallow as 2 metres and has been observed in a surfer who dived under a wave. Animal experiments reproduce the pathological features with equivalent depths of 1 to 6 metres.

In the event of otological barotrauma, a sen-sorineural or combined hearing loss, tinnitus or demonstrable vestibular damage implies inner ear barotrauma.

In a series of 50 cases of inner ear barotrauma, most occurred in experienced divers, 10 per cent were in free divers, ear, nose and throat disease was present beforehand in 48 per cent, previous diving middle ear barotrauma occurred in 62 per cent, aviation middle ear barotrauma occurred in 24 per cent and inner ear barotrauma occurred in 12 per cent. In the eventful dive, 98 per cent experienced middle ear barotrauma (88 per cent descent, 10 per cent ascent). The incidence of symptoms was as follows: tinnitus, 86 per cent; hearing loss, 80 per cent; vertigo, 38 per cent; and dysacusis, 10 per cent. Sixty two per cent noted symptoms during the dive, and 38 per cent had symptoms within some hours. Both conservative and surgical treatments had a two thirds success rate, but most divers were treated conservatively. Tinnitus and vertigo often responded to early treatment.


Middle ear barotrauma is the most common cause of inner ear damage in diving. Various inner ear disorders have been demonstrated. For anatomical background, see Chapter 35 (Figure 7.5). Inner ear damage is also reported in aviators and flight attendants.

Diagrammatic representation of the ear anatomy.
Figure 7.5 Diagrammatic representation of the ear anatomy.

A perilymph fistula is a common pathological entity of inner ear disease. The perilymph leak is variable in volume and may come from the round window (most often), the oval window or a membrane rupture within the labyrinth.

Perilymph fistulae from the labyrinthine windows are now well recognized and result in a leakage of perilymph into the mastoid or middle ear space. In general medical practice, the disorder may be related to congenital syphilis, other infections, cholesteatoma or any sudden increase in intracranial or labyrinthine pressure. It can develop spontaneously or may be caused by trauma, especially with head injury, weight lifting and physical straining. The intracranial pressure wave so produced can be transmitted into the inner ear by the cochlea and possibly the vestibular aqueducts. An increased pressure of 120 mm H2O in the cerebrospinal fluid (CSF) is sufficient to induce this disorder in some patients.

Any procedure that involves manipulation of the ossicular chain can cause an oval window perilymphatic fistula, and this disorder occurs in up to 7 per cent of patients after stapedectomy.

The hearing may fluctuate, depending on the replacement of perilymph, or hearing loss may progress slowly or suddenly as the perilymph leaks out. The more quickly the ear replenishes its perilymph, the less likely it is to sustain permanent damage. The prognosis is better when only the low or middle frequencies are affected. The loss of pressure within the perilymphatic system, the relative endolymph hydrops (similar to Ménière’s disease) and the possible electrolyte imbalances affect the dynamics of the hearing and vestibular systems, and the damage may become permanent if it is not corrected.

The initial presentations with verified perilymph fistulae are sudden or fluctuating sensorineural hearing loss in 83 per cent, vertigo in 77 per cent, tinnitus in 63 per cent and aural fullness in 25 per cent.

Exposure to environmental pressure change is possibly one of the most common causes, and this includes ear barotrauma of diving or aviation exposure.

There are two postulated mechanisms for this disorder in diving. If the middle ear pressure is not equalized during descent, the tympanic membrane moves inward because of the pressure gradient; as a result, the foot plate of the stapes is pushed inward. This causes a displacement of perilymph through the helicotrema, so that the round window membrane bulges outward. If at this stage a forceful Valsalva manoeuvre is performed, there is a sudden increase in the pressure within the middle ear cleft that causes the tympanic membrane to be very rapidly returned to its normal position, the stapes to move outward and the round window to be pushed inward. The reversed flow of perilymph may not be sufficiently rapid to avoid damage to the inner ear structures that results in haemorrhages or rupture of the round window membrane.

The other explanation involves a pressure wave transmitted from the CSF through a patent cochlear aqueduct during the Valsalva manoeuvre and ‘blowing out’ the round window into the middle ear. This has been demonstrated in animal experiments, with a rise of CSF pressure. The aqueduct constricts with age, and this may explain why children are more susceptible.

Inner ear barotrauma has occurred in unconscious patients and guinea pigs, thus indicating that a forceful Valsalva manoeuvre is not a necessary prerequisite.

Animal experiments suggest multiple pathological processes for the inner ear damage, mainly labyrinthine window ruptures, intralabyrinthine membrane ruptures, haemorrhage and acoustic trauma. Stretching of the round window, thus permitting the entry of air into the cochlea and causing sensorineural hearing loss, has been demonstrated. Increasing the CSF pressures by 120 to 300 mm Hg can also transmit pressure through the cochlear aqueduct and increase the perilymph pressure in the inner ear, thereby rupturing the round window. Rupture of the round window membrane can develop in water as shallow as 1.3 metres.

It is likely that cochlear and vestibular haemorrhages and internal inner ear membrane ruptures are common, but they are not so amenable to treatment.

End artery spasm, thrombosis and gas or lipid embolism are aetiological proposals that have little experimental or clinical support.

Post-mortem histological examination of temporal bones after inner ear barotrauma, or at autopsy, may indicate an occasional association with enlarged vestibular and/or cochlear aqueducts that allows for a greater CSF-perilymph communication. These anomalies may be detected on high-resolution computed tomography (CT) scans. Other anomalies or malformations are sometimes detected that may indicate a predilection for inner ear barotrauma. These anomalies may be detected by high-resolution CT scans.

A tear of Reissner’s membrane results in an isolated loss in one or two frequencies (tested In 100-Hz increments between 400 and 1300 Hz).

A progressive sensorineural loss or vertigo that develops hours or days after a barotrauma incident is most likely the result of a fistula of the round window with leakage of the perilymph into the middle ear and/or air into the perilymph. This can develop at any stage of the dive or afterward.


Many of these divers develop the first symptoms after the completion of the dive while performing energetic tasks, e.g. pulling up the anchor. This may be because the middle ear (including the round window) has been damaged by the earlier barotrauma. The subsequent fistula follows a rise of pressure in the CSF, the cochlear aqueduct and the perilymph, as a result of exertion.

Sudden tinnitus and hearing loss may be more frequent in patients with inner ear haemorrhages.

Progressive deterioration of sensorineural hearing, over hours or days, fluctuating hearing loss and position-induced hearing loss indicate a perilymph fistula. Persistence of vestibular symptoms may indicate perilymph fistula.

Deafness is of the sensorineural type, either a total loss (all frequencies) or a selectively high-frequency loss (4000 to 8000 Hz). It also may be variable and altered by changing head positions, possibly because of the buoyancy of air in the perilymph or increased leakage into the middle ear. If left untreated, the sensorineural hearing loss may become total and/or permanent.

Tinnitus, with a roaring, popping or running water sound, is frequent. Aural fullness and hyperacusis are described.

Impairment of speech discrimination may precede or overshadow the delayed and progressive hearing loss.

There is often an associated conductive or lower-frequency hearing loss that resolves over the subsequent 1 to 3 weeks and may be mistakenly interpreted as a therapeutic success. Bone conduction audiograms are indicated to identify this condition.

Oval window fistulae, probably caused by damage from the stapes foot plate, have been observed, often with a severe vestibular lesion that may persist until surgical repair. This fistula is more likely in divers who have had surgical treatment of otosclerosis.

The symptoms of inner ear barotrauma may include those of vestibular origin such as vertigo, nausea, vomiting and ataxia. Vestibular symptoms vary from almost unnoticeable to incapacitating.

In the cases that initially, predominantly or solely involve vestibular function, the symptoms may progressively diminish as adaptation occurs. Even though the symptoms may diminish, the disorder may progress to destruction of the vestibular system. In other cases, vertigo may persist or recur while the fistula persists or recurs.

Symptoms associated with inner ear baro-trauma may include the following:

  • Sensation of blockage or fluid in the affected ear.
  • Tinnitus of variable duration.
  • High-frequency or total hearing loss, hyperacusis.
  • Vestibular disturbances such as nausea, vomiting, vertigo, disorientation and ataxia.
  • Clinical features of an associated middle ear barotrauma (with or without conduc-tive hearing loss).

Unfortunately, the clinical differential diagnosis of cochlear or vestibular trauma, haemorrhage and perilymph fistula, based on the foregoing criteria, is by no means certain.

Once inner ear barotrauma has been experienced, the diver is more predisposed to similar incidents, which further aggravate both the tinnitus and the hearing loss.
Cochlear injury is permanent in more than half the cases, whereas vestibular symptoms are usually temporary.

Meningitis is a possible complication of perilymph fistulae.

Inner ear barotrauma is suspected in the pres-ence of hearing loss, tinnitus, vertigo or ataxia.


To demonstrate inner ear barotrauma, serial investigations may be necessary. Any combination of middle ear barotrauma symptoms, nausea, vertigo, tinnitus and hearing loss should be immediately and fully investigated by serial measurements of clinical function, daily audiometry up to 8000 Hz (with bone conduction if the loss is in the <4000 Hz range) and positional electronystagmography. Caloric testing is indicated only if the tympanic membrane is intact or if the technique guards against pressure or fluid transmission into the middle ear.

A test proposed to support the diagnosis of perilymphatic fistula, as opposed to other causes of inner ear damage, is positional pure tone audiometry. The patient lies horizontal with the affected ear uppermost, for 30 minutes, and the hearing improves more than 10 dB in at least two frequencies when the patient lies supine. The theoretical explanation for this improvement is that air is displaced from the perilymph-leaking windows.

Hennebert showed that an increase in pressure in the ear canal could produce nystagmus in patients who were known to have perilymph leakage. Tullio described a similar response with loud sounds. In patients with perilymph fistula, the vertigo is induced by any activity that increases the pressure in the ear canal (ascent and/or descent, loud sounds of low frequency, the Valsalva manoeuvre, tragus pressure, pneumatic otoscopy or tympanometry).

Other investigations are sometimes thought to be even more sensitive than the basic electronystagmogram. In diagnosing perilymph fistulas, Kohut suggested that the presence of Hennebert’s sign, or its equivalent the Tullio phenomenon, is required before vestibular symptoms are attributed to a perilymph fistula. Other tests being investigated to verify this disorder include dynamic posturography, vestibulo-spinal response (body sway) reactions to stress (Hennebert’s or the Tullio phenomenon) and electrocochleography.

Investigations that may be of value include temporal bone polytomography and high-resolution and contrast imaging techniques. Until now they have not been particularly helpful in diagnosis or treatment of diving induced perilymph fistulae, but their discrimination is improving. Objective testing becomes especially important when the history of antecedent trauma is vague or remote. A perilymphatic fistula test or elevated SP/AP ratio (cochlear summating potential and auditory nerve action potential) on electrocochleography significantly raises the likelihood of perilymphatic fistula.

There is no agreed upon diagnostic test with enough sensitivity and specificity to identify the presence or absence of perilymph fistula reliably.


Treatment should be initiated promptly.

  1. Avoid any increase in CSF pressure, such as from the Valsalva manoeuvre, sneezing, nose blowing, straining with defecation, sexual activity, coughing, lifting weights, fast movement or physical exertion. Loud noises should be avoided; some clinicians recommend ear plugs or other devices to reduce the external ear pressure changes. Divers very commonly perform middle ear autoinflation, almost as a matter of habit. Advise the patient that under no circumstances should autoinflation be attempted. Otherwise, the already damaged round window may not withstand the pressure wave.
  2. Almost total bed rest with the head elevated to 30 degrees and careful monitoring of otological changes are indicated. This instruction is given irrespective of which of the other treatment procedures are followed.
  3. Bed rest should continue until all improvement has ceased and for a week or more, to allow the inner ear membranes to heal and the haemorrhages to resolve.
  4. If there is no improvement within 24 to 48 hours in cases of severe hearing loss, or if there is progressive deterioration in hearing, operative intervention should be considered. It may be delayed for 1 to 2 weeks in less severe cases, to allow the associated middle ear disorder to heal, but this may be at the expense of more permanent sensorineural hearing loss. This is a judgement call without a great deal of experimental evidence to assist.
  5. Reconstructive micro-aural surgery is indicated when there is deterioration or no improvement with bed rest, with severe hearing loss or incapacitating vertigo. In patients with developing hearing loss, repair to the round or oval window will prevent the further leakage of perilymph and has proved curative in some cases, sometimes restoring hearing acuity. It may stop vertigo and may reduce tinnitus, both of which may be disabling. In a survey of 197 cases of presumed perilymphatic fistula (not necessarily related to diving), Fitzgerald reported that 87 per cent of patients with vestibular symptoms had complete or nearly complete relief. With hearing loss, 40 per cent had improvement. If a fistula is not visualized during middle ear exploration, a graft should still be applied to the window because sometimes the fistula is intermittent. Some surgeons use colour dyes to make the leakage more obvious. Others employ techniques to increase the CSF pressure. Surgery, which was employed in most cases in earlier years, is rarely needed now if conservative treatment is given conscientiously. After 2 weeks’ delay, it will rarely improve hearing. Middle ear surgical exploration is not indicated in cases of inner ear haemorrhage because it is not a harmless procedure, and in rare cases it can induce further or complete hearing loss.
  6. Prohibition of diving and flying is essential for the first few weeks following a perilymph fistula. If medical evacuation by air is required, an aircraft with the cabin pressurized to ground level is necessary. For most cases, but especially those precipitated by minimal provocation and in patients who have poor Eustachian tube function or nasal disease, it is prudent to advise against any further hyperbaric (scuba or free diving) exposure. The same applies if permanent hearing loss, tinnitus or vestibular asymmetry persists.
  7. Treatment of vertigo is based on routine medical principles. Vertigo is usually suppressed by cerebral inhibition within a few weeks, but may be precipitated by sudden movement or other vestibular stimulation (caloric or alternobaric). It may persist if the fistula remains patent.
  8. Other regimens. Vasodilators (e.g. nicotinic acid, carbogen) have been recommended by some investigators, but little evidence exists to show any favourable effect. Aspirin is to be avoided because of its anticoagulant effects. Steroids have no verified place in treatment of this type of hearing loss.
  9.  Air entry into the perilymph, as a cause of the disorder, has yet to be quantified. As a relatively harmless procedure, the authors sometimes add 100 per cent oxygen breathing to the conservative treatment regimen for 4 to 6 hours a day for 3 days.
  10. Hyperbaric oxygen therapy has been used and recommended by some experienced hyperbaric therapists, and so it warrants further consideration and investigation. There is no reason to believe that recompression therapy per se, employing air or normoxic gases, is of value. Hyperbaric oxygen therapy may be of value in other forms of sudden hearing loss, with or without steroids. The authors of this text have tried it in patients with inner ear barotrauma, but had to proceed to surgery subsequently. Hyperbaric oxygen therapy has the potential to aggravate the fistula and increase the perilymph flow into the middle ear during descent – both from the relatively negative middle ear pressures and the need for the Valsalva manoeuvre. It has been responsible for apparent ‘cures’ in some cases of middle ear barotrauma with conductive generalized hearing loss, misdiagnosed and reported as inner ear barotrauma. In these cases, if the middle ear is autoinflated with descent, the gas expansion removes middle ear fluid on ascent.

An excellent review of the various approaches to this disorder in divers is given by Elliott and Smart.


After inner ear barotrauma there may be an apparent complete cure or persisting residue. The cochlear acuity (especially lower-frequency hearing) may improve for a few weeks, and then the remaining high-frequency loss is usually permanent, to be aggravated by the influence of ageing.

Tinnitus often improves over the next 6 to 12 months, possibly the effect of repair or death of damaged sensory endings.

If the vestibular system is damaged and asymmetry persists, the patient will never be able to dive or fly safely, because of alternobaric vertigo. He or she may continue to have occasional vertigo, aggravated by sudden head movement, which is then a hazard in all occupations that involve balance, exposure to heights or driving.

The authors of this text would advise against piloting aircraft because of the danger of alternobaric vertigo, which has followed some cases of unilateral inner ear damage.

Too many cases of inner ear barotrauma have recurred for these authors to propose a resumption of diving – either free or with equipment – once permanent inner ear damage has been demonstrated.