The seventh or facial cranial nerve may be affected, causing ‘facial baroparesis’. Recorded in both aviators and divers, this disorder sometimes follows middle ear barotrauma. It manifests as a unilateral facial weakness similar to Bell’s palsy, and it tends to recur in the same patient if the cause is not corrected.
The reason for this disorder is explained by the anatomy of the facial canal. This is open to the middle ear in some people and so shares its barotraumatic pathology. Also, middle ear air expands during ascent and could force its way into this seventh nerve canal.
Paralysis of the facial nerve makes frowning impossible, prevents the eye from closing on that side and causes drooping of the lower eyelid (which may result in tears running down the face because they do not drain into the nasolacrimal duct). The cheek is smooth, and the mouth is pulled to the normal side. Whistling becomes impossible, and food collects between the cheek and gum. A metallic taste may be noticed at the start of the illness, as may impaired taste in the anterior part of the tongue on the same side, from chorda tympani involvement. Hyperacusis may result from paralysis of the stapedius muscle.
Early treatment could include inhalation of 100 per cent oxygen for some hours, based on the theoretical pathophysiology involved, to remove air from the seventh nerve canal.
Both physicians and otologists frequently omit to interrogate patients with Bell’s palsy regarding their swimming, diving and aviation exposure.
CASE REPORT 7.2: This diver, who had been exposed to gunfire in the past, experienced considerable pain and difficulty in equalizing both middle ears during a dive to 10 metres. He continued to dive despite the pain and performed forceful autoinflations. He noted tinnitus, and he also experienced ear pain and vertigo during ascent. Otoscopic examination of the tympanic membrane revealed the effects of barotrauma. The diver became progressively more deaf, with a sensorineural pattern in both ears, over the next few days. Transient episodes of vertigo were noted. Exploratory surgery was performed. A fistula of the round window was observed, together with a frequent drip of perilymph fluid into the middle ear. The round window was packed. A similar procedure was performed 5 days later in the other ear, with the same result. Subsequent audiograms over the following month revealed a considerable improvement in hearing.
Diagnosis: inner ear barotrauma (with perilymph fistula of the round window) caused by middle ear barotrauma of descent and forceful autoinflation, resulting in sensorineural hearing loss.
Although not frequent, otitis media is an occasional complication of middle ear barotrauma, with the middle ear collecting fluid that forms a medium for growth of organisms (see Chapter 29). Thus, ear pain developing hours or days after middle ear barotrauma should be considered to indicate a middle ear infection. This not only is a serious illness in its own right, but is also a possible cause of narrowing of the Eustachian tube and further middle ear barotraumas.
The mastoid, being part of the middle ear cleft, responds in the same way as the middle ear to a negative pressure situation. Thus, the production of fluid and blood in the mastoid, especially during descent, can develop and produce the conditions conducive to bacterial growth.
Under these circumstances, the patient usually has pain and tenderness over the mastoid, and the pathological features can be demonstrated by CT scans of the temporal bone.
Although rare, meningitis is a possible extension of otitis media, mastoiditis, sinusitis and so forth and a complication of both labyrinthine fistula and pneumocephalus.
Another rare complication from the middle ear cleft and mastoid air cells is pneumocephalus, resulting from the expansion of gas in a space that is now occupied by blood and fluid from descent barotrauma. A rupture into the cranial cavity, with air and/or fluids, produces a sudden and excruciating headache, with the pathological features demonstrated by CT brain scans and magnetic resonance imaging (see Chapter 8). The bony roof over the middle ear–mastoid space, the tegmen tympani of the petrous temporal bone, is frequently very thin or incomplete, allowing for the contents of this space (air, blood) to rupture into the middle cranial fossa, into the epidural or sub-dural areas.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
This disorder is caused by distension of enclosed gases within the middle ear, expanding with ascent. Because it may prevent ascent, it is usually more serious than middle ear barotrauma of descent, which allows an uncomplicated return to safety.
During ascent, the middle ear opens passively, with a pressure gradient of less than 50 cm H2O. If the Eustachian tube restricts release, symptoms may include sensations of pressure or pain in the affected ear (reverse squeeze) or vertigo resulting from increased middle ear pressure difference (alternobaric vertigo). Occasionally, these conditions coexist.
Middle ear barotrauma of ascent usually follows recent, but sometimes mild, middle ear barotrauma of descent and/or the use of nasal decongestants. In each case the common factor is probably congestion and therefore blockage of the Eustachian tube.
The mild vertigo is often rectified by further ascent, which may force open the less patent Eustachian tube. When the pressures in both middle ears are equalized with the ambient pressure, the stimulus to vertigo ceases. Also, subsequent opening of the tube is easier. Other divers may reach the surface while still having an asymmetry of pressure within the middle ear cavities, or residual damage from excessive middle ear pressure, and so experience vertigo following the ascent.
Most cases of vertigo from middle ear barotrauma of ascent are mild, lasting seconds or minutes. This is not always so, however, and there have been instances of temporary or permanent inner ear damage, seventh nerve palsy, severe pain during ascent and/or perforation of the tympanic membrane.
The vertigo is most pronounced when the diver assumes the vertical position and is least pronounced in the horizontal position. The spinning is toward the ear with the higher pressure. It tends to develop when the middle ear pressures differ by 60 cm H2O or more.
Otoscopic examination often reveals evidence of tympanic membrane injection or haemorrhage. Congestion of blood vessels is common but is less than with descent barotrauma. It is more pronounced around the circumference of the tympanic membrane than along the handle of the malleus. The tympanic membrane may appear to be bulging.
Hearing loss in the affected ear, if present, may be conductive and follow damage to the tympanic membrane or the middle ear structures. The tympanic membrane may rupture occasionally. Inner ear barotrauma with sensorineural hearing loss is a possible complication (see Chapter 37). Seventh nerve palsy is another possible complication.
For first aid, the diver may be able to take remedial action. A short descent may relieve symptoms and allow middle ear equalization. Occasionally, the Valsalva technique, jaw movements or performing a Toynbee manoeuvre (see earlier) will relieve the discomfort, as may sudden pressure applied to the external ear (by occluding the external ear with the tragus or middle lobe, then pushing on it and thus exerting external pressure on the water column in the external ear). Equalization may be easier if the affected ear is facing the sea bed, thereby using the pressure gradient along the now vertical Eustachian tube.
Fortunately, most effects are short-lived, and treatment should consist of prohibition of diving until clinical resolution has occurred, normal hearing and vestibular function are demonstrated and prevention of future episodes is addressed.
Rarely the diver is seen soon after the event, and if the middle ear is still distended, the first aid procedures described earlier may be satisfactory. Otherwise, the use of oxygen inhalation or minimal recompression is effective.
Antibiotics are used if there is evidence of infection, and decongestants are sometimes recommended to improve Eustachian tube patency. Usually, neither type of drugs is needed.
Decongestants, especially topical ones, are rarely of use in preventing this disorder, unless they prevent a causal middle ear barotrauma of descent. Usually, they have the opposite effect. Systemic decongestants are more effective, but they have other disadvantages, permitting the diver to descend with marginal improvement in Eustachian tube patency and inadequate autoinflation of middle ear.
Prevention is best achieved by avoiding nasal decongestants and by training the diver in correct middle ear equalization techniques during descent (see earlier). Unless descent barotrauma is prevented, ascent barotrauma is likely to recur.
Once middle ear barotrauma of ascent has been experienced, particular care should be taken to ensure that if it does recur the diver will always have adequate air to descend briefly, use the techniques described earlier and then gradually ascend. A low-on-air situation could cause extreme discomfort or danger if the diver’s ascent is restricted by symptoms.
Vestibular function has been tested experimentally during pressure changes in a recompression chamber, to replicate the sequence of events and verify the aetiology and diagnosis (see Chapter 38). This testing is not generally required.
Passive opening of the Eustachian tubes is the ideal and natural way to equalize pressure between the middle ear and the nasopharynx, although it is not always possible. Most amateur divers need to use an active technique, under their voluntary control, which will inflate the middle ears and prevent the pain and discomfort of barotrauma during descent. During ascent, passive equalization of ear pressures is more common, and active techniques are rarely needed.
Sometimes reluctant trainees use the failure to autoinflate ears as an acceptable excuse to avoid diving. Other times they are scared to use sufficient nasopharyngeal pressure for fear of causing damage.
It is part of the routine diving medical examination to ensure that the diving candidate can autoinflate the middle ear actively. This is achieved by using a positive pressure manoeuvre described to the diver while the examiner is observing the tympanic membrane and its movement with an otoscope. The latter is employed either by focusing on the light reflex or on another part of the tympanic membrane that reflects light (either the membrane flaccida or the circumference). As the candidate autoinflates the middle ear, the tympanic membrane moves outward.
Investigations using otoscopy and modified diving tympanometry (see Chapter 36) are reasonably reliable in predicting which candidates will have trouble resulting from Eustachian tube disorders. However, many divers fail because of an inadequate autoinflation and diving technique.
The following techniques for autoinflation are recommended. Different candidates perform them with varied ease. In each case, practice of the technique is recommended on land, before subjecting the novice to hyperbaric and aquatic conditions that interfere with the application of this new skill.
The Valsalva manoeuvre is probably the most easily understood. It involves occluding the nostrils, closing the mouth and exhaling so that the pressure in the nasopharynx is increased. This separates the cushions of the Eustachian tube and forces air up this tube into the middle ear. The pressure required to achieve this is usually 20 to 100 cm H2O.
Middle ear equalization answers to clients’ problems
I descend a bit slower than my buddies. Or,
If there is any pressure, I halt my descent and wait a bit. Or,
I may ascend until the ear clears (yo-yo technique).
Answer: Why? If you are not equalizing the middle ear promptly or sufficiently, then these procedures merely allow the middle ear to fill with blood or tissue fluids and thus allow further descent with less pain or discomfort. This is not a sensible way to equalize the middle ear. It results in middle ear congestion, Eustachian tube obstruction and other disorders that may be temporary or permanent.
Client: I am trying to use swallowing to equalize the middle ear.
Answer: If you have any difficulty with middle ear equalization, then employing techniques that result in relatively negative middle ear pressures, cause middle ear congestion and Eustachian tube blockage. Use the positive pressure Valsalva technique (or Lowry or Edmonds techniques) before and during descents.
Client: I have middle ear equalization problems when I swim down the shot line.
Answer: This requires greater force to autoinflate the middle ear because you are trying to force air down the Eustachian tube. Descend feet first and you can blow air up the Eustachian tube. Air travels more easily up than down in the water. Remember bubbles? They rise.
Client: If there is any water in my ears (fullness, crackling) after the dive, I use alcohol ear drops to dry them out.
Answer: It is likely that the ‘water’ is really fluid in your middle ear from barotrauma. See earlier.
Client: I sometimes have a bit of blood from my nostril (or in my throat).
Answer: Although the blood may be from your sinus, following expansion of air with ascent, it is more likely from the middle ear on that side. In either case, correct middle ear equalization (‘ahead of the dive’) may well fix both. See earlier.
Client: When I dive and equalize the middle ear, I hear a squeaking sound in my ear.
Answer: This suggests a narrowed Eustachian tube, possibly from inadequate middle ear equalization and barotrauma. The sound you should hear when you equalize the middle ear and the ear drum moves outward is a click or pop. It takes a split second to achieve. It is not a long, drawn-out sound.
Client: I can often dive once, without problems, but cannot equalize the middle ear on other dives.
Answer: You have probably produced some middle ear congestion (barotrauma) in the first dive but continued the dive. By the second dive, you start off with significant middle ear congestion, and so middle ear equalization is more difficult.
Client: One ear equalizes before the other.
Answer: Not a problem. It is normal. You may wish to assist the slow ear by pointing it toward the surface as you equalize the middle ear.
The force necessary for successful autoinflation will vary with the diver’s body position. Using the Valsalva technique, novice divers average 40 cm H2O in the head-up, vertical position and in the horizontal ‘ear-up’ position. In the horizontal ‘ear-down’ position they need 50 cm H2O. In the vertical, swimming-down position they average about 60 cm H2O.
The Valsalva manoeuvre used by divers is modified from that employed originally by Antonio Valsalva to increase intrathoracic pressure. Trials performed on divers indicate that they do not produce the prolonged high thoracic pressures often encouraged by cardio-thoracic physiologists. With the latter, the problems induced by prolonged high Valsalva pressures include cardiac arrhythmias, hypertension and hypotension, arterial and venous haemorrhages, pulmonary and otological barotrauma, gastric reflux, stress incontinence and the possible shunting of blood through right-to-left vascular shunts (atrial septal defects and patent foramen ovale) thus increasing the possibility of paradoxical gas embolism with diving.
The Frenzel manoeuvre involves closing the mouth and nose, both externally and internally (this is achieved by closing of the glottis), and then contracting the muscles of the mouth and pharynx upward (‘lifting the Adam’s apple’). Thus, the nose, mouth and glottis are closed, and the elevated tongue can be used as a piston to compress the air trapped in the nasopharynx and force it up the Eustachian tube. Pressure of less than 10 cm H2O may accompany this manoeuvre.
As divers become more experienced, they tend to use such techniques as jaw movements, commencing a yawn, swallowing, lifting the soft palate and so forth, which allow for equalization of the middle ear without pressurizing the nasopharynx.
The Toynbee manoeuvre involves swallowing with the mouth and nose closed, and it is of value in relieving the overpressure in the middle ear during ascent. It is also of value during descent when movement of the Eustachian cushions produces a nasopharyngeal opening of the Eustachian tube, with an equalization of pressures between the nasopharynx and the middle ear. Thus, the final pressure in the middle ear with the Toynbee manoeuvre may be negative (less than environmental).
A combination of techniques has also been proposed. A very successful one is the combination of the Toynbee and Valsalva techniques, known as the Lowry technique. This involves occlusion of the nostrils, then a swallowing movement that is made continuous with a Valsalva manoeuvre. The diver is thus advised to ‘hold your nose, swallow and blow at the same time’. Despite the rather confusing (and impossible to achieve) instruction, the technique is extremely valuable in resistant cases. It is easily learned with practice, on land.
The Edmonds technique is rather similar and involves the opening of the Eustachian cushions by rocking the lower jaw forward and downward (similar to the start of a yawn) so that the lower teeth project well in advance of the upper teeth and performing the Valsalva manoeuvre at the same time.
The Edmonds number 2 technique is to advise the diver to ‘block your nose, close your mouth then suck your cheeks in, then puff them out – quickly’.
Soft palate contraction is a technique whereby the diver contracts and raises the soft palate, thereby moving the Eustachian cushions, occluding the nasopharynx and causing minimal elevation of the pressure within this space, opening the Eustachian tube and forcing air up the tube. It is sometimes called the béance tubaire voluntaire or BTV, and it is usually employed by experienced divers who have relatively patent Eustachian tubes and who, over the years, have developed this muscular skill. An interesting variation of the BTV is the Roydhouse technique. Here the diver is asked to identify the uvula hanging down from the posterior of the hard palate, then raising it as he or she moves the back of the tongue downward. This opens the Eustachian tubes, and the diver can verify it by hearing his or her own humming sounds reverberate in the ears.
When examining potential divers, attempts to demonstrate either the Frenzel technique or the BTV are not usually successful. In the author’s practice, during otoscopy, the Valsalva manoeuvre is tried first, followed by the Toynbee, the Lowry and then the Edmonds techniques. If there is any difficulty remaining with equalization, then the candidate is advised to repeat the most effective procedure a few times a day and achieve success, determined by hearing both ears click, before commencing diving.
Academic arguments abound as to which is the best technique. Whichever works is the best. The major problem is not the danger of middle ear autoinflation, but the dangers of not autoinflating.
Some techniques (Valsalva, Lowry, Edmonds) have the disadvantage of a transitory pressure that may extend into the thorax, but this is not usual with divers. These techniques have the advantage of distending the middle ear and thus allow further descent without the problems of a negative middle ear pressure developing and producing middle ear congestion and Eustachian tube obstruction. These techniques are therefore better for novice divers and for those who have trouble with middle ear autoinflation. They also assist in equalizing sinus pressures and avoiding sinus barotraumas.
Other techniques (Toynbee, BTV) are effective if there is easy and frequent middle ear autoinflation. They either equalize the pressures passively or produce negative middle ear pressures. Wave action or descent can also cause a negative middle ear pressure with resultant congestion and Eustachian tube obstruction, and these techniques may aggravate this condition.
Experienced divers, who have mobile tympanic membranes, resembling small spinnakers, can often descend to great depths before they need to equalize their middle ear pressures. They also autoinflate their ears by using less pressure.
Most patients with an inability to autoinflate their middle ears who have been referred to the authors of this text have suffered more from inadequate diver instruction than from Eustachian tube obstruction. To ascertain the extent of this problem, 200 consecutive otoscopic examinations were recorded on potential diving candidates. Autoinflation was successful using the Valsalva, Toynbee, Lowry or Edmonds technique in 96 per cent of subjects, with 4 per cent unsuccessful in one or both ears.
Decongestants probably do work on the mucosal membranes and do improve nasal air flow, but their effect on the Eustachian tube is greater at the nasopharyngeal orifice. Thus, these drugs may be more effective in reducing descent than ascent middle ear barotrauma.
Some otologists have recommended the use of the pneumatic otoscope to demonstrate passive tympanic membrane movement. This instrument is certainly of value in assessing middle ear disease, but it is inadequate for diving assessment because it fails to demonstrate the procedure that is required, i.e. voluntary autoinflation of the middle ear.
Other investigations of more value in assessing middle ear autoinflation include the modified tympanogram (see Chapter 36) and examination of the Eustachian cushions with a fibre optic nasopharyngoscope.
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).
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).
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.
Cigarette or marijuana smoking, respira-tory irritants.
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.
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.
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.
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.
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.
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.
HYPERBARIC EAR PLUGS
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.
Because the external auditory canal is usually open to the environment, water enters and replaces the air in the canal during descent, equalizing the pressures.
If the external ear is occluded, water entry is prevented. Contraction of the contained gas is then compensated by tissue collapse, outward bulging of the tympanic membrane, local congestion and haemorrhage. This is observed when a pressure gradient between the environment and the blocked external auditory canal is +150 mm Hg or more, i.e. 2 metres descent in water (Figure 7.2).
The common causes of blockage of the external auditory canal include wax or cerumen, large exostoses, foreign bodies such as mask straps, tight-fitting hoods and mechanical ear plugs.
Clinical symptoms are usually mild. Occasionally, a slight difficulty in equalizing the middle ear is experienced. Following ascent there may be an ache in the affected ear and/or a bloody discharge.
Examination of the external auditory canal may reveal petechial haemorrhages and blood-filled cutaneous blebs that may extend onto the tympanic membrane. Perforation of this membrane is uncommon.
Treatment for this condition includes maintenance of a dry canal, removal of any occlusion, possibly cleansing of the canal with an antiseptic solution warmed to body temperature and prohibition of diving until all epithelial surfaces appear normal. Secondary infection may result in a recurrence of the pain and may require antibiotics and local treatment (see Chapter 29).
This condition is easily prevented by ensuring patency of external auditory canals and avoiding ear plugs or tight-fitting hoods that do not have apertures over the ear to permit water entry.
External ear barotrauma of ascent is theoretically possible.
Barotrauma is defined as the tissue damage caused by expansion or contraction of enclosed gas spaces, according to Boyle’s Law and its pressure-volume changes.
The volume change in gas spaces with depth is proportionally greatest near the surface, and so it is in this zone that ear barotrauma is more frequently experienced. It is probably the most common occupational disease of divers, experienced to some degree by most.
Ear (also called otological or aural) barotrauma may affect any of the following:
External ear (when a sealed gas space exists).
Middle ear (which incorporates an enclosed gas space).
Inner ear (which adjoins a gas space) (Figure 7.1).
Middle ear barotrauma is the most common form. Barotrauma problems may contribute to panic and diving deaths in novice divers or to permanent disability – tinnitus, balance and hearing loss.
In the earlier literature on caisson workers’ and divers’ disorders, otological barotrauma symptoms were hopelessly confused with decompression sickness symptoms. This confusion still exists in many clinical reports today.
Barotrauma refers to damage to tissues resulting from changes in volume of gas spaces, which in turn are caused by the changes in environmental pressure with descent and ascent (Boyle’s Law).
Barotrauma of descent is a result of a failure or an inability to equalize pressures within the ear cavities as the volume of contained gas decreases. Because enclosed cavities are surrounded by cartilage and bone, tissue distortion is limited, and the contracting space may be taken up by engorgement of the mucous membrane, oedema and haemorrhage. This, together with the enclosed compressed gas, assists in equalizing the pressure imbalance. It is commonly called a ‘squeeze’ by divers.
Barotrauma of ascent is the result of the distension of tissues around the expanding gas within the ear, when environmental pressures are reduced, i.e. on ascent. Divers use the misnomer ‘reverse squeeze’ to describe it.
Middle ear barotrauma of descent is the most common disorder encountered by divers.
Similar problems are encountered with aviation and space exposure, in hypobaric or hyperbaric chambers and by caisson workers (who work under increased pressure).
Barotrauma is classified according to its anatomical sites and whether it is caused by ascent or descent. It may occur in any combination in the external, middle, or inner ear.
Breathing helium-oxygen gases when diving makes equalization of pressures (‘autoinflation’) in middle ear and sinus cavities easier, and so barotrauma is less.
General information on the ear in diving, including many references to barotrauma, is included in Chapters 35 to 38.