Middle Ear Barotrauma of Descent (Middle Ear Squeeze)

Middle ear barotrauma of descent is by far the most common organic medical disorder experienced by divers and patients undergoing hyperbaric medical treatment. It follows the failure to equilibrate middle ear and environmental pressures (autoinflation) via the Eustachian tubes during descent. An abnormal pressure difference (gradient) causes the tissue damage (Figure 7.3).

Middle ear barotrauma of descent. A diver moving from the surface (1 ATA) to 10-metre depth (2 ATA) with a blocked Eustachian tube, which causes failure to equalize the middle ear cavity and consequent middle ear barotrauma of descent.
Figure 7.3 Middle ear barotrauma of descent. A diver moving from the surface (1 ATA) to 10-metre depth (2 ATA) with a blocked Eustachian tube, which causes failure to equalize the middle ear cavity and consequent middle ear barotrauma of descent.

Any condition that blocks the Eustachian tube predisposes the diver to middle ear barotrauma. More commonly, it is caused by faulty technique during attempted voluntary middle ear autoinflation.

Diving marine animals avoid this disorder by having an arterio-venous plexus in the middle ear that responds to the pressure changes. It fills during descent and empties on ascent, accommodating the volume changes.


The Eustachian tubes may open when the pressure gradient between the pharynx and middle ear cavity reaches 10 to 30 mm Hg. These figures theoretically equate to an underwater depth of about 25 cm. Equalization of pressure occurs when the Eustachian tubes open. This can be achieved normally by yawning, moving the jaw or swallowing or by voluntarily inflating the middle ear cavity by the Valsalva manoeuvre. The procedure is termed ‘equalizing’ or ‘clearing the ears’ by divers and ‘middle ear autoinflation’ by otologists.

If the Eustachian tubes are closed during descent, a subjective sensation of pressure will develop when the environmental pressure (external to the tympanic membrane) exceeds that in the middle ear cavity by 20 mm Hg, or after about 25 to 30 cm descent in water (Figure 7.4).

Middle ear barotrauma of descent, showing greater anatomical detail.
Figure 7.4 Middle ear barotrauma of descent, showing greater anatomical detail.

Note: Extrapolations from physiological pressure gradients to sea water depths are not strictly appropriate because the tym-panic membrane is partly moveable and can offset some pressure change.

Discomfort or pain may be noted with a descent from the surface to 2 metres, a 150 mm Hg pressure change and causing a volume reduction of less than 20 per cent in the middle ear cavity. If the middle ear pressure is then equalized, for another 20 per cent middle ear volume reduction (and its associated ear pain to occur) the diver must descend to 4.4 metres, then to 7.3 metres, then to 10.8 metres, and so forth. Thus, the deeper the diver goes, the fewer autoinflation manoeuvres are required per unit depth to prevent symptoms. For this reason, barotrauma is more evident near the surface than at greater depths.

If equalization is delayed, a locking effect may develop on the Eustachian tube and prevent successful autoinflation. This effect results when the tubal mucosa is drawn into the middle ear, thereby becoming congested and obstructing the Eustachian tube.

If a diver continues descent without equalizing, mucosal congestion, oedema and haemorrhage within the middle ear cavity are associated with inward bulging of the tympanic membrane. This partly compensates for the contraction of air within the otherwise rigid cavity. The tympanic membrane will become haemorrhagic (the ‘traumatic tympanum’ of older texts). Eventually it may rupture.

It is commonly inferred that perforation is the ultimate damage from not equalizing the pressure in the middle ear cavity, and perforation follows the extreme degrees of haemorrhage described in gradings of middle ear barotrauma of descent. Many tympanic membrane perforations caused by diving are not associated with gross haemorrhages in the tympanic membrane. It is likely that perforation competes with middle ear effusion and haemorrhage as a pressure-equalizing process – the former demonstrating tympanic membrane fragility and the latter demonstrating vascular capillary fragility. Perforation is more likely with rapid descents or from old perforations and scarring.

There is a time factor in the development of middle ear congestion and haemorrhage, with greater degrees resulting from longer exposure to unequalized middle ear pressures.

Middle ear barotrauma of descent has two major causes:

  • Pathological processes of the upper respiratory tract obstructing the Eustachian tube.
  • Inadequate autoinflation techniques.

Blockage of the Eustachian tubes may be caused by mucosal congestion as a manifestation of upper respiratory tract infections, allergies, otitis media, effects of some drugs, respiratory irritants, venous congestion, mechanical obstructions such as mucosal polyps or individual variations in size, shape and patency of the tube.
Aviation exposure may also cause middle ear barotrauma of descent, and it is similar to diving exposure. It also may be countered by training the flier in the correct ‘equalizing ahead of the descent’ technique (see later).
For some divers, with very patent Eustachian tubes, attention to autoinflation is not of much import. For others, especially novice divers and those with less patent Eustachian tubes, early and positive middle ear autoinflation techniques are needed.
Opening of the Eustachian tubes is more difficult in the inverted position, when the diver swims downward. This has been attributed to increased venous pressure. It is easier if the diver descends feet first, when air flows more readily upward into the vertical tubes.

Factors leading to blockage of the Eustachian tube include the following:

  • Upper respiratory infections and allergies.
  • Premenstrual mucosal congestion.
  • Gross nasal disorders, septal deviation, mucosal polyps and so forth.
  • Delay in autoinflation during descent (flying or diving).
  • Descent to the point of ‘locking’.
  • Horizontal or head-down position.
  • Alcohol ingestion.
  • Cigarette or marijuana smoking, respira-tory irritants.
  • Drugs – cocaine, beta blockers, parasympathomimetics.

The incidence of middle ear barotrauma of descent varies with the foregoing factors as well as with the speed of descent and the adequacy of autoinflation techniques. Risk factors have been proposed, based on surveys of dive masters and instructors, indicating ear problems in 4.3 and 11.9 per 1000 dives for male and female divers, respectively. Higher numbers are reported in patients receiving hyperbaric medical treatment and in aviation exposures.


Symptoms consist initially of a sensation of pressure or discomfort in the ear, followed by increasing pain if descent continues. This pain may be sufficiently severe to prevent further descent.

Occasionally, a diver may have few or no symptoms despite significant barotrauma. This occurs in some divers who seem particularly insensitive to the barotrauma effects and also when a small pressure gradient is allowed to act over a prolonged time, e.g. when using scuba in a swimming pool or when not autoinflating the ears at maximum depth following the final metre or so of descent.

Some divers reduce the symptoms (but not the disorder) by slowing the descent or engaging in repeated short ascents after they notice discomfort (the ‘yo-yo’ descent).

CASE REPORT 7.1: JQ performed three scuba dives, to a depth of 5 metres. He was not able to equalize the pressure in his middle ears during descent, but in the first dive he did manage to achieve this after he had reached 5 metres. Following this first dive his ears felt ‘full’ or ‘blocked’. He then went down to 3 metres ‘to see if I could clear them’ for his second dive, with the same result. On the third dive he felt pressure in his ears during descent and again could equalize them only after he had reached the bottom; considerable pressure was used in attempted autoinflation. After ascent he again noted that his ears felt blocked and he again attempted to equalize them, this time using considerable pressure. Suddenly pain developed in the right ear, and it gave way with a ‘hissing out’. On otoscopic examination of the left ear there was a grade III aural barotrauma with a very dark tympanic membrane, haemorrhage over the handle of the malleus and the membrana flaccida and a small haemorrhage anterior to the handle of the malleus. The right ear had similar features, but with a large perforation (which caused the hissing sound as air escaped) posterior to the tip of the handle of the malleus. Daily audiograms revealed a 15-dB loss in this ear throughout the 150- to 4000-Hz range. This hearing loss disappeared after 2 weeks when the perforation had almost healed over.

The reason for the disorder in the middle ears was that they had ‘equalized’ by haemorrhaging and perforation.

Diagnosis: middle ear barotrauma of descent.

Difficulties are more frequently encountered within the first 10 metres because of the greater volume changes occurring down to this depth.

Eventually, rupture of the ear drum may occur, usually after a descent of 1.5 to 10 metres (100 to 760 mm Hg pressure) from the surface. This causes instant equalization of pressures by allowing water entry into the middle ear cavity. After an initial shock, pain is automatically relieved; however, nausea and vertigo may follow the caloric stimulation by the cold water (depending on the spacial position of the head – see Chapter 38). Unless associated with vomiting or panic, this condition is seldom dangerous because it quickly settles when the water temperature within the middle ear cavity warms to that of the body.

Occasionally, there is a sensation of vertigo during the descent, but this is not as common as in middle ear barotrauma of ascent or inner ear barotrauma (see later), both of which can follow and be caused by middle ear barotrauma of descent. It may also result from the Valsalva manoeuvre.

Blood or blood-stained fluid may be expelled from the middle ear during ascent and run into the nasopharynx (to be spat out or swallowed) or appear from the nostril on the affected side (epistaxis). Blood is occasionally seen in the external ear, near a haemorrhagic tympanic membrane.

Following a dive that caused middle ear barotrauma of descent, there may be a mild residual pain in the affected ear. A full or blocked sensation may be felt. This is sometimes associated with a mild conductive deafness involving low frequencies and is the result of haemotympanum, fluid in the middle ear or some dampening effect on the ossicles. It is usually only temporary (hours or days). In severe cases, fluid may be felt in the middle ear for longer periods, possibly with crackling or bubbling sounds as it becomes aerated, before it resolves.

Tympanic membrane perforation, if it occurs, is usually either an oval or crescent-shaped opening below and behind the handle of the malleus or adjacent to previous scarring.

Middle ear barotrauma is classified into six grades based on the otoscopic appearance of the tympanic membrane. The grades are shown in Table 7.1.

Middle ear barotrauma of descent – tympanic membrane grading

The foregoing classification was based on Lieutenant Commander R. W. Teed’s observations on submariners, modified by Macfie and subsequently including a symptomatic grade 0 by Edmonds – where there is no obvious tympanic membrane disorder but a clear description of middle ear discomfort on descent and relief on ascent. The tympanic membrane appearance of the higher grades (1 to 5) is simple enough to be identifiable by diving paramedics. Nevertheless, more variable and complex pathologies may be observed, as are illustrated on the front of Plate 1.

A specialized otological classification was presented by O’Neill and is shown on the back of Plate 1. It is especially appropriate for hyperbaric units where specialist otologists are available and may eventually supersede traditional classifications (Table 7.2). The main difficulty with O’Neill’s classification is that tympanic membrane photography must precede diving, an impractical situation in the recreational setting at this stage.

O’Neill’s classification of middle ear barotrauma

Damage and disease involve the whole of the middle ear cleft (middle ear space and mastoid) and not just the tympanic membrane.

Recent overt or sub-clinical middle ear barotrauma of descent results in congestion of the middle ear spaces and subsequent Eustachian tube blocking. Autoinflation becomes progressively more difficult with repeated descents, possibly preventing further attempts. Alternately, if the middle ear is almost totally full of fluid, then there is little problem with further descents, but at the cost of middle or inner ear disease.

Sometimes the Eustachian tube may be narrowed and produce a ‘hissing’ sound during autoinflation, as opposed to the normal ‘popping’ sound of the Eustachian tube opening or the tympanic membrane movement.

A patulous Eustachian tube can also follow either descent barotrauma or forceful attempts at Valsalva techniques (see Chapter 37).


Clinical management consists of the following:

  • Avoiding all pressure changes such as diving, flying and forceful autoinflation techniques, until resolution.
  • Systemic or local decongestants occasionally (very rarely).
  • Systemic antibiotics, but only where there is evidence of a pre-existing or developing infection, gross haemorrhage or perforation, and possibly with culture and sensitivity tests.

In treating many thousands of middle ear barotrauma cases, the authors of this text rarely use decongestants or antibiotics. Investigations are of value (see Chapter 36).

Serial audiometric examination should be undertaken to exclude any hearing loss and to assist in other diagnoses (especially inner ear barotrauma) and management if such a hearing loss is present.

Impedance audiometry (tympanometry) may be used to follow the middle ear pathological changes. If there is a perforation, this investigation can aggravate it. Occasionally, this test is needed to verify a tympanic membrane perforation that is difficult to visualize.

Serial audiograms should be performed on all but the most minor cases of middle ear barotrauma.

Diving can be resumed when resolution is complete and voluntary autoinflation of the middle ear has been demonstrated during otoscopy. If there is no perforation (grades 0 to 4), recovery may take from 1 day up to 2 weeks.

With perforation (grade 5), recovery may take 1 to 2 months, if the condition is uncomplicated and managed conservatively. Although the tympanic membrane may appear normal much earlier, recurrent perforation frequently results from premature return to diving. There is rarely an indication for such surgical procedures as tympanoplasty, unless healing is incomplete or if the lesion recurs with minimal provocation.

It is important to clearly identify and correct the contributing factors (pathological processes and autoinflation technique) in each case before diving or flying is resumed.


Prevention of this disorder consists of ensuring patency of the Eustachian tubes before diving and appropriate training in autoinflation techniques to be used while diving.

Autoinflation is best checked by otoscopic examination of the tympanic membrane during a Valsalva manoeuvre, when the tympanic membrane will be seen to move outward. The degree of force needed to autoinflate, and the degree of movement of the ear drum, will provide an estimation of the probable ease of pressure equalization when diving.

If either tympanic membrane appears to move sluggishly or if much force is necessary, then decongestant nasal drops or sprays may marginally improve the patency of the Eustachian tubes. These agents are of value to trainees who can use them to facilitate middle ear autoinflation techniques and improve this skill on land before diving. Pseudoephedrine may reduce aviation-induced barotrauma problems to some degree, more so than nasopharyngeal sprays.

The use of decongestants to improve Eustachian tube patency while diving is to be discouraged. In a prospective comparison of topical decongestants, these drugs did not seem to be of value in preventing middle ear barotrauma.

The rebound congestion of the mucosa is cited by otologists as a reason for avoidance of decongestants, but the diving clinician is also concerned with the systemic problems of sympathomimetic agents and the increased incidence of middle ear barotrauma of ascent encountered with these medications. The reason for this may be that decongestants are more effective in improving nasal airflow and thereby affecting the pharyngeal cushions of the Eustachian tube than in influencing the tubal mucosa or middle ear orifice, which may be affected by the same pathological process. Decongestants, both local and general, are effective only in the marginally obstructed tube, thus permitting a slow descent and some descent barotrauma with resultant congestion of the middle ear orifices of the tube – which then block on ascent and cause middle ear distension and ascent barotrauma (see later).

From the safety aspect, difficulties with descent are less dangerous than with ascent.

In most cases, and especially in the novice diver, practice and instruction in middle ear autoinflation and the use of correct diving techniques are much more effective than drugs in ensuring Eustachian tube patency and reducing barotrauma.

It is possible to measure the force or pressure necessary to open the Eustachian tubes. Eustachian tube patency and middle ear pressure changes can be measured if specialized impedance audiometers are employed clinically. See Chapter 36 for more information.

When dealing with divers who have not adequately autoinflated their middle ears during descent – despite the ability to perform this in the clinic – the following errors are commonly encountered.

  1. Not autoinflating early enough, i.e. waiting until the sensation of pressure is felt. This indicates a negative middle ear pressure. Commonly the novice diver, instead of performing a Valsalva manoeuvre before descent, will concentrate on his or her struggle to descend and will often be 2 to 3 metres underwater before remembering to clear the ears. This situation is referred to as ‘equalizing behind the dive (exposure)’ and is overcome by autoinflating on the surface before descent and with each metre of descent. Alternately, the diver may employ autoinflation after each breath during descent. Open water diving, without use of a descent line or anchor line, disrupts control of the descent and thus contributes to this barotrauma.
  2. Attempting to autoinflate while in the horizontal or, even worse, head-down position. If only one ear causes difficulty, it is advisable to tilt that ear toward the surface while attempting autoinflation. This manoeuvre stretches the pharyngeal muscles and puts the offending tube in a more vertical position, thus capitalizing on the pressure gradient of the water.
  3. Diving with problems that cause Eustachian tube obstruction, such as mucosal congestion from such factors as infections, irritants such as cigarette smoke, drugs or allergies. After an upper respiratory tract infection has cleared, another week or two is necessary before diving is resumed safely. Divers who have an allergic diathesis should avoid the allergens (e.g. avoid dairy products for 12 to 24 hours before diving). Divers should be advised of the dangers of delaying middle ear autoinflation and of using excessive force in achieving it.

Correct middle ear autoinflation for divers: ‘equalizing ahead of the dive’

  • Practice and ensure reliable middle ear autoinflation on land. Only then, consider diving.
  • Autoinflate the middle ear on the surface immediately before descent.
  • Autoinflate every 1 metre of descent. Use a descent line.
  • Autoinflate with the head upright.
  • Do not descend if pressure is felt on the ears. Abort the dive.
  • Do not use multiple ascents (yo-yo) or waiting at depth, to equalize.
  • Do not dive if you have upper respiratory disorders.

Some physicians have claimed the use of local proteolytic or allegedly mucus-softening enzymes to be of value. Even if they did work, they would have the same complications as decongestants.


There are repeated promotions of ear plugs to reduce the symptoms of middle ear barotrauma in both divers and aviators. The principle on which these ear plugs are employed is as follows: A small malleable, plastic, compressible and porous plug is fitted with an airtight seal into the external ear. This allows for air to move more slowly into the external ear space during pressurization (descent) in a chamber.

The use of these ‘hyperbaric plugs’ will delay the inward distortion of the tympanic membrane (being pulled into the middle ear) given that the membrane tends to move in the opposite direction, i.e. outward, because of the external ear obstruction. Thus, the discomfort and pain of the ‘negative’ pressure in the middle ear are less, and the barotrauma may be slower in developing.

Nevertheless, use of these ear plugs does not change the pathological features of middle ear barotrauma, other than the effect on the tympanic membrane. Thus, the damage to the middle ear mucosa, the oval and round windows and the inner ear all remain (being dependent on the pressure gradient between the middle ear space and its surrounding body tissues). The only thing that has really changed is that the symptom of pain with middle ear barotrauma has been lessened.

The potential costs of reducing the symptoms of middle ear barotrauma are as follows: the production of mild external ear barotrauma of descent; the persistence of pathological features of ear barotrauma affecting the middle ear mucosa and inner ear; possible aggravation of ascent barotraumas affecting the ear because of the disorder induced in the middle ear during descent; and vertigo from unequal middle ear pressures when the plugs are not inserted equally into both sides.

It is doubtful that the masking of middle ear disease by reducing the symptoms is a wise move.

An alternative to the hyperbaric ear plugs is to pressurize more slowly (i.e. the same effect on the middle ear without inducing external ear barotrauma to achieve it).
‘Diving’ ear plugs, in which a restricted opening replaces the ceramic filter, slow the barotrauma disorder as described earlier and increase the possibility of ascent barotrauma.

Gadgets that connect the oral cavity with the external ear have been used in the false belief that they overcome the effect of impaired middle ear autoinflation. This could happen only if there is a tympanic membrane perforation, in which case the diver should not be diving.

In patients who are unconscious and need hyperbaric treatment (in a recompression chamber), middle ear barotrauma is particularly frequent, and myringotomy is often required.

Professor Joe Farmer stated that myringotomies are required for hyperbaric exposure in patients who are comatose or who have a tracheostomy or orotracheal or nasotracheal tubes. If repeated treatments are considered likely, tympanostomy tubes can be inserted.

As an alternative for divers in recompression chambers, who should need only one such treatment, an alternative to myringotomy in conscious patients is to have repeated pauses or a very slow descent, accepting slower barotrauma and giving more opportunity for autoinflation.