Disclaimer: The information contained within the Grand Rounds Archive is intended for use by doctors and other health care professionals. These documents were prepared by resident physicians for presentation and discussion at a conference held at Baylor College of Medicine in Houston, Texas. No guarantees are made with respect to accuracy or timeliness of this material. This material should not be used as a basis for treatment decisions, and is not a substitute for professional consultation and/or peer-reviewed medical literature. Barotrauma of the Middle and Inner Ear The most common causes of barotrauma today are from the use of the Self-Contained Underwater Breathing Apparatus (i.e. SCUBA gear), commercial air travel, and from hyperbaric oxygen chambers. In fact, hyperbaric oxygen therapy has been found to produce over a 50% incidence of barotrauma. Well over 50% of the medical problems that are related to barotrauma are referred to an Otolaryngologist. Over 90% of these complaints involve the ear. The noncompressible middle ear cavity makes the ear susceptible to damage from these ambient pressure changes. Middle ear pressure is governed by a law of physics known as Boyle's Law, which states that at a constant temperature, the volume of a body of gas is inversely related to the pressure to which it is subjected. Applying this law to diving, demonstrates that if a diver descends 33 feet (or the equivalent of 1 atmosphere of pressure), the ambient pressure will double from 1 atmosphere to 2 atmospheres. This will cause the volume of gas to be cut in half in the middle ear, resulting in a 50% increase in negative middle ear pressure if the eustachian tube is closed. The first 33 feet of descent represents the largest change in the volume of the middle ear while diving or during hyperbaric decompression. A diver must dive to greater than 150 feet in depth to equal the total volume change produced during the first 33 feet. This explains why the majority of otologic diving and hyperbaric injuries occur during shallow dives and not during deep water dives as one might expect. In fact, MEBT and IEBT have been reported to occur in as little as 8 ft of water. The pressure experienced during air travel is closely regulated by artificial means through the use of pressurized cabins. Commercial air lines maintain a constant pressure differential in the cabin of 8.5 psi above the changing ambient pressure outside the plane. At an altitude of 18,000 feet above sea level, a person in an unpressurized cabin would equilibrate the middle ear to an ambient pressure of 1/2 an atmosphere. Regulating cabin pressure at 8.5 psi above the changing ambient pressures, a passenger will experience a cabin pressure equal to that at sea level (i.e., 1 Atmosphere) while flying at an altitude of 16,000 feet and will require minimal middle ear equilibration. At 40,000 feet, the passenger will have a cabin pressure equal to 7000 feet above sea level. This pressurization is beneficial when a plane descends from a cruising altitude of 40,000 feet to land at sea level. The ambient pressure change experienced by the passenger is decreased by 2/3 since the passenger will be actually experiencing a descent equivalent to a 7000 foot descent. Although pressurized air travel has reduced the potential risks of barotrauma, it is important to keep in mind that only a pressure differential of 80mm Hg is required to close the eustachian tube in normal individuals. A descent from 37,000 ft to 27,000 feet cruising altitude will result in a cabin gauge pressure change equal to 80mm hg, resulting in difficulty with clearing the middle ear. In order to fully understand the effects that Boyle's Law has on Eustachian tube function, we will briefly review the normal anatomy and function of the eustachian tube. In the resting state, the eustachian tube is closed. A positive pressure within the nasopharynx, or a contraction of the tensor veli palatini, levator palatini, or the salpingopharyngeus is required to open the eustachian tube when middle ear pressure equalization is attempted. There are three common maneuvers which can be used to aid in middle ear pressure equalization. These are the Valsalva maneuver, the Frenzel maneuver, and the Toynbee maneuver. The Valsalva maneuver opens the eustachian tube by increasing the nasopharyngeal pressure above the middle ear pressure as a result of closing the naries and glottis while increasing intrathoracic and intra-abdominal pressure. This maneuver is the most common cause of barotrauma to the ear if performed too forcefully. The Frenzel maneuver is performed with a low pressure valsalva while contracting the muscles of the pharynx. This forces air into the eustachian tube without increasing the total intrathoracic pressure. Finally the Toynbee maneuver involves swallowing while pinching the nose, thus creating a negative nasopharyngeal pressure which can force the eustachian tube open. By far, the Frenzel and Toynbee maneuvers are the safest to perform during eustachian tube dysfunction as neither have been associated with barotrauma. . To date, there is no readily available test to identify patients with eustachian tube dysfunction other than a history of difficulty with clearing the middle ear. Factors which would lead to a decrease in eustachian tube function include recent upper respiratory infections, uncontrolled nasal allergy, nasal polyposis, and deviated nasal septum. The differential diagnosis of the disorders related to barotrauma are damage to the middle and inner ear, inner ear decompression sickness, and alternobaric vertigo. Middle ear barotrauma, also known as aerotitis media, is due to an inability to equilibrate to ambient pressure changes. The etiology can be located either in the middle ear or external ear. This process also occurs most commonly during the descent as a forced valsalva is attempted, increasing the middle ear pressure and allowing for damage of the tympanic membrane to occur. This process can also occur during ascent if eustachian tube dysfunction causes air trapping, otherwise known as "reverse Squeeze." The external ear canal can also be a source of middle ear barotrauma if a closed space is created between the outer rim of the concha bowl and the tympanic membrane. The closed space may be due to either a cerumen impaction, ear plugs, or external otitis. As a diver descends, ambient pressure will increase, causing a net negative pressure gradient between the external ear canal obstruction and the tympanic membrane. The obstructing plug is then forced deeper into the external ear, resulting in a tympanic hemorrhage or perforation. The patient typically experiences extreme pain as the descent phase of the dive begins, despite an ability to clear the middle ear. Edmonds et al from the Australian Diving Medical Center, devised a grading system for middle ear barotrauma. The grading scale is from zero to five. Grade 0 is when a patient experiences symptoms of middle ear barotrauma and no physical findings are present. Grade I is when the presence of tympanic membrane injection can be seen. Grade II has injection as well as hemorrhage within the tympanic membrane. Grade III includes gross hemorrhage and Grade IV includes gross hemotympanum. Grade V includes the presence of a tympanic perforation. There are three common forms of IEBT: Cochlear Damage resulting in intracochlear and intralabyrinthine hemorrhage, perilymphatic fistula formation, and IEDS secondary to the formation of gas bubbles beneath the round window. IEBT usually occurs with MEBT, although the absence of MEBT cannot exclude the presence of IEBT. The symptoms of sensory neural hearing loss, vertigo, and or tinnitus should indicate the presence of possible IEBT. The etiology of IEBT has been proposed by Goodhill et al to be secondary to implosive or explosive forces within the cochlea. Goodhill proposed that forces exerted on the cochlea during a forced Valsalva have different effects depending on the patency of the eustachian tube. When the eustachian tube is forced open suddenly, an acute rise in middle ear pressure will result causing an inward bulge of the round window and an outward bulge of the stapes foot plate. If the force is strong enough, implosion of the round window and a secondary outward pull on the stapes footplate may occur. If the eustachian tube is blocked, a valsalva maneuver will cause an elevation of CSF pressure which will be transmitted through a patent cochlear aqueduct or internal auditory canal causing a rise in the intracochlear pressure. If the difference between the perilymphatic space is sufficiently greater than the middle ear pressure, an explosive rupture of the round or oval window ligament will occur. Both the implosive and explosive forces generated by a force valsalva are theorized to cause a perilymphatic fistulae or dislocation and rupture of Reissner's membrane, as well as the basilar membrane, the saccule, the utricle, or the semicircular canals. Antonelli and Paparella have studied the temporal bone pathology in scuba diving deaths and confirmed the presence of these pathologic findings. Simmons et al have demonstrated through experimental models that pressure differentials of less than 2 cm of water can cause labyrinthine ruptures. IEBT secondary to cochlear damage will present with nonfluctuating high frequency sensorineural or mixed hearing loss with or without tinnitus or vertigo. There is typically no progression of symptoms. The treatment of IEBT secondary to damage to the membranous labyrinth and cochlea includes bed rest with head elevation, the use of vasodilators, steroids, histamine, and carbogen, in an effort to decrease inflammatory changes and increase the delivery of oxygen. Parell et al have shown that if proper precautions are taken to maintain proper eustachian tube function, no further deterioration takes place in hearing if a patient returns to diving after experiencing cochlear IEBT. IEBT secondary to a perilymphatic fistulae typically presents with fluctuating sensorineural or mixed hearing loss, as well as vertigo exacerbated with positional changes, and a sense of constant disequilibrium. On physical exam, a positive Hennebert's sign (the presence of nystagmus when positive and negative pressure is applied to the EAC in the presence of an intact tympanic membrane) has been cited by Thompson and Kohut as a strong positive indicator of a perilymphatic fistula in patients with or without the presence of hearing loss. Healy et al have indicated that a positive Romberg sign and the presence of positional nystagmus are consistent with the presence of a perilymphatic fistula. When present, the most common location of the perilymphatic fistula has been demonstrated by Goodhill et al to be at the anterior rim of the oval window in the area of the fistula ante fenestram, which is one of the weakest areas of the otic capsule. The management of patients suspected of having a perilymphatic fistula includes bed rest with head elevation and avoidance of increased intracranial pressure for a variable period of days, with intermittent regular audiograms. The length of time a patient should be observed before an exploratory tympanotomy is performed is very controversial. In a study by Paparella et al, it was shown that in chinchillas suffering a traumatic round window perforation, all perforations had partially healed after 3 days, and all were completely healed after 9 days. The results of this study form the basis for conservative management of perilymphatic fistulas. Simmons et al recommend that if hearing loss or vestibular symptoms are progressive, or if after 10 days any vestibular symptoms remain, an exploratory tympanotomy should be performed. Parell and Becker also advocate this 10 day observation period. Singleton and Kohut are proponents of a 5 day observation period. Goodhill et al suggest a 48 hour observation period. Pullen et al suggest that the shape of the audiogram should indicate if an exploratory tympanotomy should be performed. He advocates immediate surgery if an audiogram demonstrates a flat shaped total or near total SNHL in the presence of a history of diving or air travel within the past 72 hours. However, he states that if the hearing loss is limited to only the high frequencies, a down-sloping audiogram, a closure of a perilymphatic fistula has not been shown to improve hearing and, thus, surgery is contraindicated unless vertigo is present. Inner ear decompression sickness (IEDS) is a form of nontraumatic cochlear damage and is the result of gas bubble formations within the inner ear. It is commonly seen after dives to extreme depths using a Helium oxygen mixture as a substitute for nitrogen oxygen mixture, in order to minimize the narcotic effects of nitrogen. IEDS occurs as a diver returns to the surface and, in an attempt to accelerate helium elimination from the tissues, changes from an oxygen-helium mixture to an air mixture. McCormick et al demonstrated that if rapid decompression occurs, inert gas bubbles of helium will form within the microvessels and otic fluids, causing a blockage of the microcirculation and resulting ischemia of the stria vascularis, spiral ligament and semicircular canals. A hypercoagulable state is produced secondary to the activation of factor XII, resulting in further vascular occlusion. As previously stated, the treatment of this disorder is immediate recompression to approximately three atmospheres deeper than the depth at which the symptoms began to occur. Farmer et al have demonstrated a near total return to baseline hearing if recompression is initiated immediately. Proper diagnosis is crucial, as the hyperbaric chamber recompression will aggravate inner ear damage due to perilymphatic fistulas and cochlear barotrauma. The differentiation between IEDS and IEBT can be made based on the following criteria.
The last disorder related to barotrauma is the phenomenon known as alternobaric vertigo. This is a syndrome first described by Lundgren in 1965 as vertigo occurring during ascent due to unequal pressure in the right and left middle ear. The duration of the vertigo is usually from a few seconds to minutes and is not associated with hearing loss. In his review of 2053 Swedish divers, Lundgren found a 16.7% incidence of alternobaric vertigo. A review of 526 Australian naval divers by Bayliss cited a 0.4% incidence. Although this process is self-limiting, a diver experiencing alternobaric vertigo while attempting a valsalva maneuver at the surface, should not undergo a dive or air travel. As people become more active in both air travel and recreational water sports, education regarding the hazards of extreme middle ear pressure changes should be expanded. Patients who are more susceptible to aural barotrauma, either due to lifestyle, upper respiratory infections, or after ear surgery, should take extra precautions to guard against eustachian tube function during air travel or underwater sports or simply avoid these activities when the risks of barotrauma are the greatest. Case Presentation A 36-year-old man experienced difficulty clearing his left ear while snorkeling to a depth of 35 feet in Cozumel, Mexico. After attempting a forced valsalva maneuver, the patient reported sudden hearing loss and tinnitus in his left ear that continued to persist. He denied any sensation of dysequilibrium or vertigo. A history of a previous high frequency SNHL was noted before the diving incident. No other past history of middle or inner ear disorders was noted. No history of a recent URI, nasal obstruction, or recent eustachian tube dysfunction was reported. Physical exam demonstrated a Grade III tympanic membrane hemorrhage with an intact drum. The right ear canal, tympanic membrane, and middle ear appeared normal. The Weber exam lateralized to the right ear and ear conduction was greater than bone conduction in the left ear. No evidence of spontaneous nystagmus was noted. Hennebert's sign and Rhomberg sign were negative. Fistula test was negative. An audiogram was obtained demonstrating an 80 dB SNHL on the left and no change in the high frequency loss on the right. An MRI scan demonstrated no abnormalities. The patient was placed on steroids and antibiotics. Carbogen therapy was initiated and two stellate ganglion blocks were performed. A repeat audiogram was obtained one week later that demonstrated improvement in the left SNHL. The patient continued to report no dizziness. The patient was advised to refrain from exertion for 1 month and schedule a follow-up audiogram in six months. Bibliography Anson B, Caldwell DW, Bast TH. The fissula ante fenestram of the human otic capsule. Ann Otol Rhinol Laryngol 1948;57:103-128. 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Arch Otolaryngol 1968;88:41-48. Singleton GT, Karlan MS, Posh KN, Bock DG. Perilymph fistulas: diagnostic criteria and therapy. Ann Otol Rhinol Laryngol 1978;87:797-803. Talmi YP, Finkelstein Y, Zohar Y. Barotrauma-induced hearing loss. Scand Audiol 1991;20:1-9. Talmi YP, Finkelstein Y, Zohar Y. Decompression sickness induced hearing loss. A review. audiol 1991;20:25-28. Thompson JN, Kohut RI. Perilymph fistulae: variability of symptoms and results of surgery. Otolaryngol Head Neck Surg 1979;87:898-903. Grand Rounds Archive | Department Home page BCM Public | BCM Intranet | Privacy Notices | Contact BCM | BCM Site Map | ©2001-2006 Baylor College of Medicine
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