The Journal of Laryngology and Otology July 1979. Vol. 93. pp. 659-678.

The Eustachian tube and its significance in flight* By AIR COMMODORE P. F. KING, O.B.E., F.R.C.S. THE Eustachian tube has long been an interest of mine, an interest which I am sure is shared by all otologists, as its anatomy and function are the key to many conditions of the middle ear. Apart from its eponymous description, it is also called the auditory, or pharyngo-tympanic, tube. All are synonymous, and I have used them in the text where each seems most appropriate. It is my aim to examine the anatomy and physiology of the tube, and to discuss its significance in flight in the light of present day practice and beliefs, with special reference to otic barotrauma. The auditory tube was known to the Ancient Greeks, and is mentioned by Aristotle, but it owes its name to Bartolomeus Eustachius (1520-74), who held the chair of Anatomy at Rome, and was one of the first to describe the auditory tube, adding that it acted like a janitor of the middle ear cleft (Tweedie, 1930). Much of his work was not published until 200 years after his death, but his book on the ear 'Epistola de Auditus Organis' was issued in 1562. Another early description came from Volcher Coiter (1534-1600) of Groningen in 1572. Perhaps the first to recognize the function of the tube was DuVerney (1648-1730) who, in 1683, stated that it was not an avenue for breathing nor of hearing, but one through which the air in the tympanum was renewed. In 1704 Antonio Valsalva (1665-1723) published his 'de Aure Humana Tractatus', and it was he who gave the tube its eponymous name, while his own name is associated with a now time-honoured technique of forcing air into the tympanum from the nasopharynx. Coming to more recent times, Adam Politzer (1883) first emphasized that the tube has a soft and a bony portion. Anatomy of the auditory tube

The auditory tube is some 36 mm long in the adult, and passes downwards, forwards and medially from the anterior wall of the tympanic cavity to the nasopharynx. The axis of the tube is fairly constant, and forms an angle of 30° with the horizontal plane, and of 45° with the median sagittal plane. * The Annual Address to the Institute of Laryngology and Otology, University of London, October 20th, 1978. 659

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The tympanic portion of the tube is bony and about 12 mm long. From a relatively wide opening in the tympanum it narrows down to an isthmus which is the point of attachment of the longer, cartilaginous portion. This bony portion is essentially an extension of the tympanic cavity, and takes little or no part in the mechanics of tubal opening. Schwartzbart (1944) emphasized this point by suggesting that the bony tube should be called the protympanum. The cartilaginous part of the tube is about 24 mm long, and composed of fibro-carfilage, broadly triangular in shape, whose narrow apex is attached to the narrow bony isthmus, and whose base bulges directly under the mucous membrane of the lateral wall of the nasopharynx, to form the torus tubarius, which is immediately behind the medial orifice of the tube. The upper part of the cartilage is bent laterally and downwards to produce a broad medial lamina and a narrow lateral lamina, so that on section the tube is hook-shaped, the apparent deficiency in the structure being completed by fibrous membrane, the fascia of Troltsch. The cartilage is fixed to the skull base in a groove between the petrous temporal and the greater sphenoid wing. Perhaps to provide greater protection for the middle ear the two parts of the tube are not in the same plane in the adult, the cartilaginous part inclining downwards more steeply. In the newborn infant the auditory tube is half as long as in the adult, the direction more horizontal, and the bony canal relatively wider than in the adult. The widest part of the tube is the pharyngeal orifice, the narrowest at the isthmus and the general shape well merits the French name of 'la trompe!' The tubal mucous membrane is of the ciliated columnar variety; it is rich in mucous glands in the cartilaginous portion, and as will be seen, these contribute to the difficulty in maintaining tubal patency. The physiology of the Eustachian tube

The primary role of the auditory tube is to maintain the equality of air pressure across the tympanic membrane, which is necessitated by the absorption of gas through the mucous membrane in the middle ear and by the variation in ambient atmospheric pressure. This is achieved by opening the tube to permit the passage of gas along it. In the resting phase, the tube is closed, and this comes about from the combination of several factors which include the elasticity of the cartilaginous support, the venous pressure, and the presence of a mucous blanket in the interior of the tube. Quantitative data relating to some of these factors have not been determined, but Perlman (1967) has shown that relatively small pressure differences across the tube are needed for separation of the mucosal sur-

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faces and the breaking of the mucosal film. Rundcrantz (1969) has shown that compression of the neck veins reduced the air volumes passing along the tube, as did a horizontal position of the body compared to it being in a position of elevation of 20 per cent—and this is due to the increased hydrostatic venous pressure. The role of posture in this context has been confirmed by Ingelstedt et al. (1967)—and it would appear to constitute a strong argument against the adoption of the horizontal posture for pilots of high performance aircraft. The significance of this work by Rundcrantz can be carried into the care of the patient after intratympanic surgery—when there is a need to maintain equilibrium in middle ear pressures. There would be advantages in such cases sitting up at least at an angle of 30 degrees with the horizontal —but how many of us do this? Postural effects on tubal function may in reality be greater than those found at investigation because under ordinary conditions the tube has to equilibrate negative intratympanic pressures. Muscular opening of the tube

The auditory tube is opened by swallowing, yawning and gaping movements, which can be consciously employed to initiate tubal opening. The cartilaginous portion of the tube is cradled by muscles (Figs. 1, 2 and 3), and those concerned with the control of the patency of the tube fall into two groups: (a) Those muscles which by having an insertion into the walls of the tube exert a direct action. (b) Those muscles which by anatomical contiguity assist or influence tubal opening. In the first group we should consider tensor palati, levator palati, salpingo-pharyngeus, and lastly—the tensor tympani. The tensor palati muscle (tensor veli palatini) is the most important. It arises from the wall of the scaphoid fossa, the spine of the sphenoid and from the length of the anterolateral aspect of the tubal cartilage. Anatomists grace the fibres arising from the tube with the name dilator tubae (Gray, 1967). It passes round the pterygoid hamulus, joining the fibres of the same muscle from the opposite side in an aponeurosis forming part of the soft palate. Its nerve supply is from the 5th cranial nerve via the otic ganglion. McMyn (1940) believed that the tensor palati was the prime mover in opening the tube, with the other muscles in the group acting synergistically. Rich (1920) considered that the tensor palati is the only muscle involved in opening the tube—a view supported by Macbeth (1960) on phylogenetic evidence in whales and porpoises, which have a well developed tensor palati muscle that appears to be the sole mechanism of tubal opening in these animals. Holborow (1962), with an interest in the sequelae in the middle ear of cleft palate, came to the same conclusion, after experiments on dogs in

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FIG. 1 A diagram representing a dissection of the left tonsillar area and soft palate, to indicate the insertions of levator palati and tensor palati muscles.

Levator palati

Cartilaginous part of the Eustachian tube

Mucous membrane of the Fossa of Rosenmuller

Fibrous part of the Eustachian tube

Internal carotid artery

Superior constrictor

Tensor palati

FIG. 2 A diagram representing the major lateral relations of the Eustachian tube. (After Lederman).

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Eustachian tube

Levator palati Fossa of Rosenmuller

Superior constrictor

FIG. 3 A diagram representing a medial view of the Eustachian tube and its relationship to levator palati muscle. (After Lederman).

which the tendon of tensor palati was cut. Damage to the pterygoid hamulus, to the tensor palati tendon at operative repair, subsequent scarring, or poor development of the muscle go a long way to accounting for the relatively high incidence of ears with the sequel of conductive deafness or chronic middle ear disease associated with cleft palate. The role of the tensor tympani muscle in tubal opening is of relatively recent consideration. The muscle originates from the cartilaginous part of the tube and the adjoining part of the sphenoid bone, and from the walls of its own bony canal. Posteriorly it forms a tendon, which is angled at the processus cochleariformis to cross the tympanic cavity to the neck of the malleus. Its origin may well have an influence on the opening of the tube (Ingelstedt et ah, 1967), and this is supported by the fact that the soft part of the tube begins to open from the middle ear end (Holmquist, 1976) (in contradistinction to closure of the tube which starts at the nasopharyngeal end). Holmquist (1976) believes that both the tensor palati and the tensor tympani muscles act synergistically in relation to their action on the auditory tube—and, as they are known to have a common embryological origin and a common nerve supply deriving from the 5th cranial nerve, this would not be surprising. Recent work by Rood and Dorfe (1978) supports this view. They found that the tensor palati consists of two distinct groups of muscle fibres—a medial, described as dilator tubae, and a lateral group, the tensor palati.

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They found that this latter muscle has no origin on the Eustachian tube, and was continuous superiorly with the tensor tympani (the dilator tubae did have a tubal attachment), confirming the views of Politzer (1926), Proctor (1973) and Lupin (1969). The other two muscles in this primary group, levator palati and salpingopharyngeus, have been described fully by Proctor (1973). Salpingopharyngeus arises from the inferior part of the tubal cartilage near its pharyngeal end, and passes downwards to blend with palatopharyngeus. It is supplied by the pharyngeal plexus. The remaining muscle, levator palati, arises from the under surface of the petrous bone, and from the medial lamina of the auditory tube. It gradually comes to lie on the inferior surface of the tube, which it helps to support. Passing within the upper margin of the superior constrictor muscle, it spreads out into the soft palate—its fibres blending with those of its fellow of the other side. It is supplied by the accessory nerve through the pharyngeal plexus. It acts by elevating the soft palate at the beginning of swallowing, and if one considers this in association with the tensor palati muscle, it is likely that the levator palati will support and hold the tubal cartilage to permit the tensor palati to act on the curve of the tubal cartilage, and so open the lumen. The muscles in the second, supporting, group which assist in the opening of the tube are of less importance, and these are the upper parts of the superior constrictor of the pharynx, and the sphincter of the nasopharyngeal isthmus, of which the palatopharyngeus is the major contributor. Ambient atmospheric pressure

The role of the auditory tube in maintaining the equality of air pressure across the tympanic membrane has been mentioned. We should consider now the significance of altered or altering ambient atmospheric pressure, both on the tube and on the gas contained in the middle ear and nasopharynx. The behaviour of gases when subjected to pressure is exemplified by Boyle's Law (1662) which states that the pressure and the volume of an enclosed, fixed mass of gas are inversely proportional. From sea level, there is a progressive reduction in the atmospheric pressure as ascent continues, so that at 18,000 ft above sea level the pressure is half that at sea level— and this is halved again at about 34,000 feet. This will mean that in ascent, with diminution of atmospheric pressure, a given mass of gas contained within an elastic structure will expand. In the middle ear the expansion of gas will continue until it has pushed the tympanic membrane virtually to the natural limit of its excursion, an effect which can be seen with an otoscope in flight, or during simulated flight in a decompression chamber. As the tympanic membrane reaches its limit there is an involuntary escape of air along the auditory tube, as

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described by Hartmann in 1879, and confirmed by Armstrong and Heim (1937). During descent from altitude the same physical laws apply, but the sequence of events is reversed, so that as the descent continues the atmospheric pressure increases, and with it the volume of gas in the middle ear decreases. Air does not normally enter the middle ear automatically, so the auditory tube must be opened by swallowing movements, which are often involuntary, and occur every minute or so. If there is delay or failure in this opening mechanism an increasing differential pressure will act on the soft, nasopharyngeal end of the tube. If this pressure closing the tube exerts a force greater than that which can be developed by the muscles opening the tube, the tube will stay closed or 'locked'. Beyond this point the pathophysiological changes of barotrauma will occur. Armstrong and Heim (1937) showed that a positive extratympanic pressure of 90 mm Hg will lock the tube, but it is now known that this figure is variable, and will depend on the intrinsic strength of the tubal dilator muscles in any particular individual. Tumarkin (1957) has considered the possibility of barotrauma in those whose natural environment is the air—the birds. He remarks 'the Eustachian tubes in the bird run together and emerge in a common orifice, in the midline, and do not seem to provide any special protection against barotrauma!' He points out that some protection may be provided by the free communication with all other pneumatized spaces in the body. In the nature of bird flight, it is likely that only high flying predators would be exposed to risks of this sort. The passive state of the auditory tube

Closure of the tube is essentially a passive process, as in its natural state it is collapsed. When the associated muscles relax, or malfunction, or when a static pressure is no longer acting to maintain tubal patency, the tubal lumen collapses. Aschan (1954) has shown that this passive closure starts at the nasopharyngeal end. When an increasing pressure acts on the soft, nasopharyngeal end it compresses the collapsed tube, and this will lead to barotrauma if the tube is not opened; this site of the obstruction was shown by McGibbon (1942). It is also important that, following its opening, the tube should stay open long enough to permit the adequate passage of gas along its lumen. Different authorities have failed to agree regarding the length of time the tube stays open, and the figure varies between 0 • 1 and 0 • 9 seconds (Perlman, 1951; Aschan, 1955; Miller 1965). That this is of practical importance was shown by Dickson and King (1954) who found that the severity of barotrauma sustained in flight is related to the rate of descent from altitude, and hence to the rate of pressure change. It follows that a slow opening time of the tube—whatever the cause—will predispose to barotrauma. Other factors influencing the passage of gas along the tube

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will be the pressure difference across the tube, and the dimensions of the narrowest part (Elner et ah, 1971). Any condition which narrows the lumen of the tube by oedema, or which increases the amount or viscosity of the mucus coating the tubal membrane will predispose to barotrauma—either by reducing the rate of flow of gas along the tube, or by impairing the ability of the tube to open. Commonest amongst these are the effects of coryza, acute and chronic nasal infection, as well as allergic and vasomotor rhinitis. The long-term effects of congenital or traumatic malformation of the nasal skeleton, as well as gross malocclusion of the teeth and jaws should also be remembered. Overpressure in the nasopharynx

Overpressure of gas contained in the middle ear will passively open the auditory tube in ascent. In descent, the tube will open from some degree of overpressure applied at the nasal end of the tube as in Valsalva's manoeuvre. However, if the performance of this technique is delayed too long in descent it may become counter-productive by magnifying the already increasing overpressure in the nasopharynx. However, this technique and Frenzel's manoeuvre are commonly employed to clear the ears in flight— particularly by experienced aircrew, and a description of each of these methods is given. Valsalva's manoeuvre is carried out when the subject attempts forcible expiration with the lips tightly closed and the nostrils closed by compression of the nose. By doing this the air pressure in the nasopharynx is raised to force air along the auditory tube—a technique described by Antonio Valsalva in 1704 (Stevenson and Guthrie, 1949). While Valsalva's manoeuvre is employed commonly in flight to clear the ears, it can cause syncope on occasion. The manoeuvre produces a raised intra-thoracic pressure and this results in an increase in central venous pressure, and pooling of the blood in the venous system. In addition, pulmonary stretch reflexes have a well recognized potential for inducing cardiac arrythmia; it is the combination of these two factors which is believed to be responsible for the syncope which can occur (Duvoisin et ah, 1962)—and which could be disastrous if it occurred in the pilot of a high performance aircraft. Frenzel's manoeuvre

Hermann Frenzel (1938, 1950) developed a further mechanism for ventilating the middle ear. It consists of voluntarily closing the glottis, the mouth and the nose, while simultaneously contracting the muscles of the floor of the mouth and the superior pharyngeal constrictors. Not surprisingly it is a technique which has to be taught, and learnt. It has the advantage that it can be performed in any phase of respiration, and is independent of intrathoracic pressure. Chunn (1960) found that the mean

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total opening pressure when using the Frenzel technique was 6 mm Hg compared to a mean opening pressure of 33 mm Hg when using the Valsalva method. This is probably explicable by the contraction of tensor palati opening the tube in FrenzeFs manoeuvre, which does not occur in the Valsalva technique (Davison, 1962). Finally, mention should be made of the method described by Arnold Toynbee in 1853—which consists of swallowing with a closed nose; this opens the tube at ground level, and is useful in checking the patency of the tube. Initially, a small positive overpressure develops in the nasopharynx, but is soon replaced by negative pressure (Thomsen, 1958). Of these three methods of voluntarily opening the tube, the Frenzel method has the following advantages: (a) the auditory tube opens at a lower pressure; (b) equal or higher maximum pressures can be developed, giving an additional margin of safety; (c) the technique is independent of intrathoracic pressure and the phase of respiration, so that there is no tendency to syncope. Lastly, independence of the phase of respiration allows middle ear inflation at the end of expiration, which Poppen (1941) has suggested might be of value in reducing the incidence of delayed barotrauma. Despite the advantages of the Frenzel method, it is probably true to say that the Valsalva method is still that commonly employed, and the reason must lie in the comparative ease with which it is carried out. Otic barotrauma

Having discussed the functional anatomy and physiology of the auditory tube we are now in a position to relate this to the syndrome of otic barotrauma and the pathophysiological changes which occur. In this paper we are concerned with the clinical entity which occurs during flight, but otic barotrauma will occur whenever there is a sufficient change of ambient atmospheric pressure, coupled with an inability to equalize the pressure in the middle ear with the surrounding atmosphere. What was originally of importance and concern to professional aviators and their advisers has now been made commonplace by the enormous growth of aviation as a mode of transport, and a glance at the number of passengers passing annually through the major airports (Tables I and II) will underline this, and give some idea of the number of people potentially at risk. Despite relatively recent interest in barotrauma, that physical changes occur in the ears with changes of altitude, and hence of atmospheric pressure, has been known since man first flew. The early balloonist J. A. C. Charles complained of pain in the right ear during his first flight in a hydrogen balloon in December 1783. Nor is flight, actual or simulated in the decompression chamber, the

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P. F. KING TABLE I PASSENGERS THROUGH UK AIRPORTS 1 9 7 7

All UK Airports

440 m

Heathrow Gatwick Manchester Luton

23-4 m 6-6 m 2-8 m 2-0 m

Table I. Showing the number of air passengers passing through airports in the United Kingdom, 1977. (The numbers are expressed in millions). TABLE II PASSENGERS THROUGH MAJOR US AIRPORTS 1 9 7 7

Chicago New York Atlanta

42 m 27 m 25 m

Table II. Showing the number of air passengers passing through some of the major United States airports, 1977. (The numbers are expressed in millions).

only environment in which barotrauma occurs; it is common in underwater divers, can occur in miners (de Vos, 1966), and in those undergoing treatment in hyperbaric oxygen chambers (Morrison, 1972). As early as 1920 Wollaston had described the effect of diving on the ear, and recognized the need for divers to open the auditory tube. As in so many countries, the development of aviation has been stimulated by war—and the military arm has been dominant in the search for solutions to problems which have arisen from men entering a new environment. Despite the scale of aircraft production and usage, and flying manpower in the Great War there was little interest in the effects of pressure change on the ears. This may well have been due to the relatively slow rates of descent then current, so that symptoms were not disabling. However, Sidney Scott (1919) recorded typical cases. Armstrong and Heim gave a clear description of the sequence of events in barotrauma in 1937, but the stimulus of World War 2 led Dickson and his colleagues in the Royal Air Force to complete the ground work, and to give an overall picture of barotrauma. A study of the situation will show a continuing interest in tubal function and barotrauma, particularly in Sweden and the United States, and the clinical entity still remains a problem. Definition

'Today, we have naming of parts...' Henry Read, 1914— By definition, otic barotrauma is damage to the ears resulting from pressure. It will occur in any situation where a change of pressure is

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acting on the middle ear and tubal system: and the tube which becomes obstructed in these circumstances will produce characteristic physiological changes in the ear(s), with signs and symptoms—and a possible chain of complications. The syndrome is probably best described as otic barotrauma, but has been known in the past as aerotitis media (Armstrong and Heim, 1937), aviation pressure deafness (McGibbon, 1942) and otitic barotrauma (Dickson et ah, 1947). Collectively, the syndromes related to pressure changes are termed dysbarism (Hinchcliffe, 1972). Patho-physiology

Our knowledge of the patho-physiology of otic barotrauma owes much to Dickson, McGibbon and Campbell (1947), whose experimental work on cats related so closely to the clinical findings seen in man. A series of cats were decompressed to a pressure corresponding to an altitude of 20,000 ft, and then recompressed. The histological changes noted in the ears of these experimental animals were all of vascular origin, and ranged from congestion of the mucous membrane to oedema, bleeding into the mucosa of the middle ear space, seromucinous effusion, and polymorph infiltration. The negative pressure differential across the tympanic membrane is shown by the invaginated appearance of the drumhead on otoscopy, and the varied signs of vascular disturbance—congestion, single or multiple haemorrhagic bullae, and fluid or blood in the middle ear are all in accord with what is believed to be the patho-physiological mechanism. Such signs will be accompanied by a feeling of tightness in the ear(s), pain, some hearing loss (which is conductive in nature), and occasionally by vertigo. . The range of middle ear pressures

The changes described above are easily understandable if we consider the effect of a loss of altitude through a known range. If the middle ear remains unventilated in a descent from, for example, 10,000 feet above sea level, when the ground (sea-level) is reached where the ambient pressure is 760 mm Hg, the middle ear will contain air at a theoretical pressure of 522-6 mm Hg. This is the ambient pressure at 10,000 ft, so there will be a pressure difference of 237 mm Hg. Now, the absolute pressure within the blood vessels in the tympanic membrane is the sum of the ambient pressure (atmospheric pressure) plus the present blood pressure. If we regard the capillary pressure as being 20 mm Hg then the absolute pressure in the capillaries will be 780 (760+20) mm Hg. But, the pressure of the tissue fluid surrounding the capillaries is only 522-6 mm Hg, and because of this the vessels become engorged. Depending on the rate of pressure change, and the fragility of the capillary vessels, the sequence of changes noted above will occur.

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P. F. KING Rupture of the tympanic membrane

As one would anticipate, the differential pressure across the drumhead occurring in descents can rupture the membrane. The precise incidence of rupture is difficult to determine, but in one series I reported this type of damage occurred in 38 of 897 ears with barotrauma (King, 1975a) an incidence of 4-2 per cent. Similarly, in 1357 patients who were seen with a view to tympanoplasty, in 14 the cause of the tympanic defect was barotrauma (King, 1975b). In essence, rupture of the membrane from this cause is not common, but it is by no means a rarity. The commonest site for a tear is the antero-inferior quadrant—that part situated close to the tympanic orifice of the auditory tube—but tears will occur at the site of previous scars. If there is a rapid onset of barotrauma, as will occur with a fast rate of pressure change, the drumhead may be avulsed from the tympanic ring, and be wrapped around the handle of the malleus, leaving a wide open middle ear. Rupture of the tympanic membrane is often accompanied by bleeding from the ear, though this will not occur with the tearing of avascular or atrophic scars, and with the occurrence of rupture the acute pain will go. The problem of rupture lies not in its occurrence, but in its management. Many tears will heal spontaneously provided there is no interference or untimely removal of blood clot. Relatively small unhealed tears of the pars tensa will mend well with autogenous grafts used as inlays, or onlays, or placed between the layers of the drumhead. Gross ruptures are not difficult to mend surgically, but the functional results may not be adequate to permit trouble-free flight, particularly for the military pilot, and every care should be taken to avoid excessive scarring, middle ear adhesions or anterior angle blunting—all of which may be prejudicial to easy movement of the drumhead. In this connection it may be timely to add a note of warning with regard to the desirability of flight shortly after tympanoplasty. If possible, these operations should be carried out in a period when the patient is unlikely to need to fly within 6-8 weeks of the operation, so that risk to the newly bedded graft is minimized. It would be wise to insist on a similar period elapsing after operation in those who come from abroad, before a return home by air, to avoid disappointment for the patient and the surgeon. Rupture of inner ear windows

Rupture of the oval or round window membrane during barotraumatic change is a relatively new concept, though as long ago as 1933 Hughson and Crowe showed that the round window membrane bulged into the tympanic cavity during a rise in pressure of the cerebrospinal fluid. It was not until 1971 that Goodhill drew attention to spontaneous rupture of the round window membrane, following a rise in intracranial pressure associated with coughing, sneezing or straining—and he believed that a

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sudden change of middle ear pressure in flight might produce the same result. That this belief was correct has been shown by an increasing number of reports of cases of this nature, occurring either in flight (Fraser, 1975; Morrison, 1975; Tingley and MacDougall, 1977) or in diving, and work by Farmer (1977) would suggest that such an injury is more common in divers than aviators. This is not surprising when one remembers that the ambient environmental pressure at a depth of 17 ft below sea level is 1160 mm Hg, and with the tube blocked from the surface downwards there will be a pressure differential of 400 mm Hg on the tympanic and window membranes. A further factor with regard to rupture of the oval window is that increasing pressure acting on the drumhead and pushing it inwards, will cause inward movement of the stapes at the oval window, with tearing of the annular ligament. While this is rare, I have recently seen 3 cases of this sort, all occurring in middle aged aircrew who had gone back to flying after staff appointments. The fistula in each was proved by tympanotomy, each was successfully closed by means of a fat graft, and all have gone back to flying. Typical examples are given: A 41-year-old Wing Commander was returning to active flying after a period at Staff College, and was flying in a Shackleton aircraft on a conversion course. He knew he was nearly over a cold, and on attempting to clear the ears on descent he experienced pain in the right ear, rushing tinnitus and deafness on that side. On leaving the aircraft he was giddy and stumbling to the right. When seen, the history and the presence of a right sensorineural deafness suggested a fistula, and this was confirmed at right tympanotomy, when a perilymph leak was seen at the upper limit of the oval window. This was successfully plugged (Fig. 4)—and he has since gone back to flying. In another case, arising in a 50-year-old pilot (Figs. 5 and 6), flying as a passenger in a Jaguar T2, vomiting and disorientation were so severe that at the dispersal the patient had to be removed from the cockpit of the aircraft. This is a good illustration of the hazard which would befall a pilot if he suffered such a lesion while in control of the aircraft. Two other features deserve mention, having a possible relation to membranous window rupture. The first of these is a consideration of alterno-baric vertigo, so named by Lundgren (1965), though it was termed pressure vertigo by Melvill Jones in 1957. This is a sudden onset of vertigo which coincides with passive equalization of middle ear pressure during a rapid ascent, or by the production of an overpressure in the middle ear by Valsalva's method during descent, or on the ground. There are now several case histories in the literature (Melvill Jones, 1957; Lundgren and Malm, 1966; Brown, 1971; Tingley and MacDougall, 1977), and in many the symptoms occur when

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FIG. 4 Pure tone air and bone conduction audiogram in a Navigator suffering from a barotraumatic oval window fistula, after the incident, and after operative repair of the fistula.

there is some difficulty in ventilating the middle ear. The following is a case which is of interest. A 33-year-old Victor captain experienced vertigo during passive pressure change on ascent from ground level to 20,000 ft. Tubal function was good and there was no clinical abnormality. A run in a decompression chamber duplicated his symptoms in a fast ascent to 8,000 ft over 1 minute, when he complained of a sensation of pitching forward, and complex nystagmus was recorded. A Shephard grommet was fitted to each ear, but failed to relieve his symptoms. The grommets were checked repeatedly to exclude blockage. Finally, he was given a DCT with the grommets in situ; this reproduced the symptoms and the nystagmus. This suggested that the gaseous transfer through the lumen of the grommet was not adequate. The only other abnormality was an excessive sensitivity to pitch motion stimuli when tested on the turn table. He is flying now in a restricted flying category. The mechanism by which the sensory receptors of the vestibular system are stimulated is still the subject of conjecture and Tingley and MacDougall (1977) suggest that rupture of the round window may be a cause, though Tjernstrom (1974) has suggested that vertigo may result from transmission to the labyrinthine fluids of changes in the middle ear pressure via the round window membrane, possibly in association with poor patency of the cochlear aqueduct (Tjernstrom, 1977). We are likely to learn more of

673

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p

6 The tympanogram obtained preoperatively in the case of oval window tear shown in Fig. 5. FIG.

this condition if, in such cases, tympanotomy is carried out to determine the integrity of the windows. Though disabling vertigo of this nature is uncommon, Melvill Jones (1957) reported that some 10 per cent of pilots whom he interviewed had suffered from this condition. The second feature is to note the special risk in flight to those who have had the operation of stapedectomy, when sudden change in the ambient pressure may result in a window tear. The possible fate of the stapedectomized ear in these circumstances has been investigated by Rayman (1973). Tearing of one or both windows will be accompanied by severe sensorineural hearing loss, which may fluctuate—and untreated is likely to be permanent. Vertigo may also occur. The possibility of this occurrence places a grave responsibility on surgeons when considering the operation of stapedectomy, and in the after-care of such patients, who should be advised of the potential hazard to the hearing from this cause. There is likewise a responsibility on airlines who undertake the carriage of passengers either to warn intending passengers, or to safeguard them against sudden pressure change in the operation of the aircraft, or both. Delayed otic barotrauma

While we are concerned today primarily with the role of the auditory tube in flight, delayed otic barotrauma is a good illustration of the consequences arising from a passive closure of the tube after flight.

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Delayed otic barotrauma occurs after long flights, and gives rise to aural discomfort and deafness which may develop during sleep. It results from the breathing of 100 per cent oxygen, so that the middle ear contains a much raised tension of that gas. With the subsequent passive closure of the tube, and with no active ventilation of the middle ear (to be expected in sleep) the absorption of oxygen through the middle ear mucosa will result in the development of a significant pressure differential. Comroe et al. (1945) reported this phenomenon originally, which was later investigated by Melvill Jones (1958, 1959), who found that with the tube unopened, the rate of pressure change is doubled when the middle ear is filled with oxygen as opposed to being filled with air. Neither the severity of the symptoms, nor the appearances, are so marked as one sees in acute barotrauma. Apart from some invagination of the drumhead, and perhaps some fluid in the middle ear, there is little to see. While the condition is more than a clinical curiosity, it is not common, and not disabling—but should be borne in mind when one is confronted by a patient with hearing loss coming on after flight. Chronic otic barotrauma

While chronic otic barotrauma results from disordered function of the auditory tube—it is a clinical condition in which one episode of barotrauma predisposes to another. It arises because the original factor predisposing to barotrauma may itself be chronic, and sometimes undetected; or because the oedema and interstitial bleeding in the tubal mucosa may be unresolved, and so further decrease the size of the tubal lumen, thus predisposing to further attacks. Perhaps the commonest single cause of chronicity is to return an individual to flying too soon. In terms of Service flying it may well be false economy to be precipitate in returning aircrew to flying, as repeated barotrauma can produce a situation where the ultimate period away from flying is far in excess of a reasonable period for recovery from the primary lesion. Pressurization and the pressure cabin

Before discussing the management of barotrauma we should consider the role of pressurization and the pressure cabin in relation to tubal function in flight. It is the reduction of barometric pressure which is the largest factor in the production of the adverse physiological effects of flight at high altitudes. The logical way to secure satisfactory conditions for the occupants of high flying aircraft is to provide within the aircraft, an atmosphere at a pressure appropriate to bodily needs. As the cabin pressure has to be greater than that of the surrounding atmosphere, the difference between the two pressures will be represented

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by a differential pressure which tends to force the cabin walls outwards. It follows that the absolute pressure within the pressure cabin will be equal to the barometric pressure existing at a level at which the aircraft is flying. For convenience, we consider conditions inside the aircraft in terms of the altitude which is being simulated by pressurization, so that in aircraft with pressure cabins we have 'aircraft altitude' and 'cabin altitude'. The use of a pressure cabin will effectively reduce the range over which barometric pressure is acting, but below 15,000 ft the rate of pressure increase will predispose to barotrauma. This is an important factor in deciding the rate at which pressurization should diminish during descent of the aircraft. The roles of aircraft in the civil and military sphere have resulted in the concept of a high differential cabin and a low differential cabin. In Transport aircraft conveying passengers, the high differential cabin is employed to maintain a cabin altitude of 8,000 ft, even when the aircraft is flying at 60,000 ft. The maximum pressure differential is 430 mm Hg. This is a practical application of the doctrine of the greatest good for the greatest number. In military aircraft, on the other hand, a low differential cabin is employed. In this context failure of the pressure cabin during combat must be accepted as an operational hazard, and the risks of too great a pressure change are minimized by employing a relatively low cabin differential pressure. The management of barotrauma

The management of barotrauma is outside the context of this paper, though the principles of treatment bear repetition. Treatment in general is directed to the relief of pain and the reventilation of the middle ear, and this will frequently involve the treatment of attendant and provocative lesions in the nose. The use of grommets in some cases, particularly those which tend to be chronic and for which no obvious cause can be found, has been advocated by me (King, 1975), and until recently I have assumed that this will suffice. However, increasing experience suggests that not every case will benefit from a grommet, even when the lumen is of proved patency, and this would suggest that, in such cases, the rate of exchange of gas through the lumen is not sufficient to prevent symptoms and signs. Perhaps the answer lies in fitting shorter grommets with a larger lumen. Conclusion

The function of the Eustachian tube impinges on every aspect of the mechanism of the middle ear in health and disease; and this importance grows if man is placed in an abnormal atmospheric environment, whether it be in the air or under water. The sequelae of maladjusted pressure within the middle ear were once

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