Middle Ear Barotrauma (2024)

Continuing Education Activity

Eustachian tube dysfunction (ETD) and middle ear barotrauma (MEBT) remain the two most common complications of SCUBA diving, commercial diving, and clinical hyperbaric oxygen treatment (HBO). Significant barotrauma (BT) may be associated with permanent complications such as hearing and balance deficits; thus prevention and recognition of ETD and BT remain important when evaluating for the hyperbaric environment and treating a pressure-related injury. This activity reviews the pathophysiology of ear barotrauma and highlights the role of the interprofessional team in its management.

Objectives:

• Describe the etiology of ear barotrauma.

• Review the pathophysiology of ear barotrauma.

• Summarize the management of ear barotrauma.

• Review the importance of improving care coordination amongst interprofessional team members to improve outcomes for patients affected by ear barotrauma.

Access free multiple choice questions on this topic.

Introduction

Otic Barotrauma (OBT) or ear barotrauma is a tissue injury to the ear secondary to inadequate pressure equalization between gas-filled body spaces and the external environment. Eustachian tube dysfunction (ETD) and middle ear barotrauma (MEBT) remain the most common complication of diving and clinical hyperbaric oxygen treatment (HBO).[1][2]

The outside portion of the ear, the pinna, is composed primarily of ridged cartilage covered by skin. Theexternal auditory meatus, or the opening to the external auditory canal (EAC),extends toward and ends at the tympanic membrane (TM).Posterior to the TM is the air-filled middle ear space containing three bony ossicles: the malleus, incus, and stapes. The umbo is the distal portion of the malleus and connects the bony ossicles to the TM. It is an expected anatomical finding on otoscopy and easily visualized. The other ossicles are visible when favorable anatomical conditions are present, such as a transparent TM. The third ossicle, the stapes, abuts the oval window, leading into the inner ear space. The inner ear space, containing the auditory (cochlea) and vestibular (semi-circular canals, utricle, and saccule) systems, is separated from the middle ear by the oval and round (labyrinthine) windows. The cochlea is responsible for sound transmission and is composed of threefluid-filled compartments: the scala vestibuli and scala tympani containing perilymph; and the scale media containing endolymph. The vestibular system, which is continuous with the cochlea, is responsible for spatial orientation and balance.

The middle ear space is covered by mucosa and is connected to the throat via the eustachian tube (ET), also referred to as the auditory tube. The ET opens just beyond the nasal openings in the posterior nasopharynx, allowing the drainage of fluid produced in the middle ear space. It is also responsible for the exchange of air between the nasopharynx and the middle ear space, maintaining equal pressure between the middle ear and the EAC. This is known as the equalization of the middle ear pressure. It is important to note that while equalization of the middle ear via the ET on ascent is passive, it requires an active maneuver on descent. Another less described air exchange takes place via the middle ear mucosa and mixed venous circulation. However, this transmucosal gas exchange is less important during rapid and large changes in ambient pressure occurring during diving, flying, or when being treated in a hyperbaric chamber.

Sound waves travel via the EAC producing TM vibration, which is then carried through, and amplified by, the bony ossicular chain. The stapes moves in and out against the thin membrane of the oval window, causing vibration and turbulence of the perilymph fluid within the cochlea, producing a wave of motion. The turbulence of the perilymph continues to the scala tympani and on to the round window where sound pressure is dissipated. This dissipation of pressure at the round window becomes an important factor in inner ear barotrauma (IEBT). Perilymph turbulence within thecochlea results in a shift of the basilar membrane, upon which sits theOrgan of Corti. Movement of the mechanosensory hair cells in the Organ of Corti results in sound transmission in the form of nerve impulses, which are received by the central nervous system via the eighth cranial nerve.

While most minor damage secondary to MEBT heals rapidly and uneventfully, major trauma, such as a perforation of the TM or IEBT may take weeks or months to heal.Significant barotrauma may be associated with permanent complications such as hearing and balance deficits. This is why it is important that divers, passengers of pressurized aircraft, and clinical hyperbaric patients be taught and understand how to equalize middle ear pressure often and early during the course of pressurization. Prevention and recognition of ETD and MEBT remain important when evaluating and treating a pressure-related injury.[3][4][5][6][7][8]

Etiology

The underlying etiology of MEBT is inadequate pressure equalization between the middle ear space and the external environment. As per Boyle’s law, an increase in ambient pressure results in a proportional decrease in the gas volume in air-containing body spaces. This increase in ambient pressure can occur when an individual moves down in a column of air (passenger in an aircraft, hyperbaric chamber), a column of water (diver), or due to blunt force trauma or blast injury to the EAC. As ambient pressure (atmospheric or hydrostatic) increases external to the body, it causes pressure to rise in the EAC, while the gas volume in the middle ear space decreases, creating a vacuum. In order to compensate for this decrease in gas volume, equalization of the middle ear space pressure is required. When the middle ear space is not filled sufficiently with air from the nasopharynx, MEBT occurs. As the largest gas volume changes underwater occur near the surface, restricting diving to shallow depths does not prevent MEBT.

An individual may fail to equalize their middle ear space due to unforeseen requirement in the case of trauma, or improper technique and/or inability of the ET to open during activities involving increased ambient pressure. MEBT can occur at depths as shallow as 4 feet (1.2 meters) of seawater (fsw), and it only takes a pressure equivalent of 10 fsw(4.4 psi) to close the ET completely. This explains why it is one of the most common disorders observed in patients participating in these activities. Once complete closure of the ET occurs, it seldom reopens with the usual equalization techniques such as the Valsalva maneuver. At this point, decreasing the ambient pressure is required to reopen the ET.It is important to note that decreasing ambient pressure does not guarantee immediate reopening of the ET, and may not be feasible depending on the activity that caused the ETD. Divers may decrease their depth in the water by swimming toward the surface; hyperbaric chamber operators may decrease the depth of treatment by increasing the chamber exhaust until such time as the patient can clear their middle ear space. Unfortunately, pilots cannot necessarily stop landing the commercial pressurized aircraft and increase altitude when an occupant complains of ETD or MEBT.[9][10][11][12][13][14]

Epidemiology

Commonly, most people have experienced ambient pressure change when diving to the bottom of a deep pool, as an occupant of an aircraft, or as a passenger in a car when driving through various elevation changes. ETD and MEBTremain the two most common complications of SCUBA diving, commercial diving, and clinical hyperbaric oxygen treatment (HBOT). There is significant variability in the incidence and prevalence of ETD and MEBT reported in the literature, ranging from 4.1 – 82%.

Reports vary in terms of statistically significant differences regarding gender, age, allergies, type of diving, water temperature, season, smoking history, septal deviation, and previous history of otitis media. A history of head and neck cancers, as well as radiation treatment, have been associated with a higher incidence of ETD and MEBT, presumably secondary to radiation soft tissue damage of the ET or pharynx. Patients with an enlarged or shorter cochlear aqueduct, enlarged vestibular aqueducts, or an anatomical communication between the middle and inner ear may be at increased risk of IEBT.[4][14][15][16][17][18][19]

Pathophysiology

The pathophysiology of ETD and MEBT has been well described.

External Auditory Canal BT

External auditory canal (EAC) BT is less common as the canal typically communicates with the external environment. Barotrauma of the EAC canresult from cerumen impaction or a tight drysuit/wetsuit hood that inhibits this communication and results in an airspace vacuum on descent. Exostoses can lead to cerumen impaction which may increase the risk.

Middle Ear BT (MEBT)

The vacuum created in the middle ear-space causes an increase in blood flow through the subcutaneous vessels in the EAC, TM, ET, and middle ear space. This results in the vessels engorging with blood. As the pressure in the EAC rises and the vacuum in the middle ear space is further increased, blood vessels eventually extrude serum into the interstices and cause inflammation of the middle ear. This is otherwise known as a serous effusion or serous otitis. The effusion may contain small amounts of blood, converting it to a serosanguinous effusion, or trapped air bubbles. As pressure continues to increase without equalization of the middle ear space, blood vessels will eventually rupture, causing bleeding into or behind the TM. It will be appreciated as non-transparent frank blood. If allowed to continue, the increase in ambient pressure will eventually result in perforation of the TM and its associated complications. Theexact pressure required to rupture the TM remains unclear, but it is thought to be approximately 100 kPA. TM rupture while diving allows for the asymmetric entrance of water into the middle ear, resulting in caloric stimulation and vestibular symptoms.

Similarly, during periods of decreased pressurization, such as decompressing the hyperbaric chamber at the end of patient treatment, or ending a SCUBA dive by beginning the swim to the surface, a decompression injury from a condition known as a reverse block can occur. This signifies the inability of the increasing pressure within this space due to expanding gas volume to be released via the ET. Reverse blockage of the ET will result in MEBT if the pressure change is allowed to persist by ascending. This reverse blockage may also occur due to middle ear effusion and tubal ET edema caused on descent, which impairs the ability to ventilate the middle ear on ascent.

Finally, a condition known as alternobaric vertigo results from a discrepancy in equalization between ears due to the asymmetric stimulation of the vestibular system. This commonly occurs on ascent and results in transient vertigo that resolves with middle ear equalization.

Inner Ear BT (IEBT)

IEBT occurs when pressure changes are transmitted to the inner ear from the middle ear space or cerebral spinal fluid (CSF), resulting in inner ear hemorrhage, labyrinthine membrane tear, or perilymphatic fistula (PLF). IEBT may result from either an ‘explosive’ or ‘implosive’ force.

Theinner ear perilymph is connected to the CSF. Thus, any sudden increase in CSF pressures, such as Valsalva against a locked ET, can be transmitted through the perilymph to the labyrinthine windows, causing rupture of the round or oval windows into the middle ear space (explosive). Alternatively, sudden middle ear pressure increases transmitted via the labyrinthine windows to the perilymph fluid may result in an implosive force. As fluid is not compressible, this subjects the entire perilymph to higher pressures and turbulence, which are continuously transmitted to the round window. This may also cause disruptions of the basilar and Reissner’s membranes, as well as cochlear hemorrhage. A forceful Valsalva with eustachian tube dysfunction can both transmit pressure from the middle ear as well as increase CSF. The rupture or tear of either labyrinthine window results in the creation of a PLF and a steady flow of perilymph into the middle ear space.[4][7][11][12][13][20][21]

History and Physical

For MEBT to occur,there must be a history of exposure to a change in ambient pressure or trauma. Initially, the negative pressure gradient across the TM causes a sensation of fullness or dullness, which progresses to discomfort. This will advance to severe pain if the ambient pressure increase does not cease, or the pressure in the middle ear space is not equalized. Patients may report varying degrees of hearing loss secondary to serous or serosanguinous effusion within the middle ear space, or due to hemotympanum. In the event of TM rupture, patients will often report a history of increasing pain with an abrupt improvement, associated with varying degrees of hearing loss. A patient who develops IEBT or a PLF may also report hearing loss, tinnitus, hyperacusis, vertigo, nausea, and vomiting.[4][12][13][21]

It is important to note that some patients may suffer ETD and MEBT without experiencing symptoms. Jansen et al.[19]noted 74.4% of freshwater divers with ear barotrauma were asymptomatic. Mozdzanowski andPerdrizet[22] found an association between diabetic neuropathy and painless otic barotrauma. This highlights the importance of otoscopic evaluations on clinical hyperbaric patients before and after hyperbaric exposure, particularly in those with documented peripheral neuropathy.

Otoscopy directly and easily visualizes the EAC and TM, however, visualization of the TM may be obstructed due to impacted cerumen or exostoses. Cerumen should be disimpacted to facilitate visualization of the TM (and to facilitate middle ear equalization). A significant consideration is that all EACs are not anatomically identical and elicit slight variations.This is true when observing the appearance of superficial landmarks, including differences in skin color, vascular formations, vascular prominence, and different cartilaginous and bony configurations and shapes. Some patients may exhibit superficial changes related to prior trauma of the EAC and TM. The physiological and anatomical changes due to MEBT are readily and easily visualized via direct otoscopic examination. Physical examination may demonstrate varying degrees of erythema or bleeding into the tissues, middle ear space effusions, or TM perforation. In the event of IEBT, gait instability, nystagmus, and audiometric hearing loss may be revealed. For further information, please read below in the evaluation section.[13][14]

Evaluation

Once a patient has signs and symptoms of ETD and/or ear barotrauma, they should be evaluated via otoscopic examination to determine, and classify, the extent of the injury. This examination is important as it will help guide the diagnosis and treatment. Currently, there are three methods of evaluating and grading ETD and MEBT: the Teed, the Modified Teed, and the O’Neill grading systems. [13][14]It is important to note that while these classification systems are often used in the undersea and hyperbaric community, they are not often used by otolaryngologists.

Teed Classification

In 1944, Dr. Teed evaluated U.S. Navy diver trainees with otoscopic visualization following hyperbaric exposures in submarine escape training.TM pressure-related pathology became apparent during the course of those exercises and examinations, from which he developed the Teed classification.

Teed Grading involves a one-time evaluation by the same examiner, evaluating a person’s potential trauma to the TM. Teed’s original classification included 5 grades:

• Grade 0:Normal TM

• Grade 1:Retraction of TM with redness along the manubrium of the malleus

• Grade 2:Same as Grade 1 plus retraction of the TM with redness of the entire TM

• Grade 3:Same as grade 2 plus fluid in the tympanum or hemotympanum

• Grade 4:Perforation of the eardrum

Modified Teed Classification

The original Teed classification was modified to include another TM grade totaling 6 possible Teed results:

• Grade 0:Symptoms with no ontological signs of trauma

• Grade 1:diffuse redness and retraction of the TM

• Grade 2: Grade 1 plus slight hemorrhage within the tympanic membrane

• Grade 3:Grade 1 plus gross hemorrhage within the TM

• Grade 4:Dark and slightly bulging TM due to free blood in the middle ear (a fluid level may also be present)

• Grade 5:Free hemorrhage into the middle ear, TM perforation with blood visible in the external auditory canal.

A “normal” tympanic membrane exhibits many different anatomical variations, as discussed earlier. As video otoscopy is not necessarily built into these classification systems, it may be difficult to compare a patient’s current score to their baseline based on description alone, and interpersonal assessment may not be standardized.

O’Neill Grading System for ETD and MEBT

The O’Neill Grading System employs the use of a video otoscope to take a baseline photo of the TM before any hyperbaric exposure. The photo maintains a permanent record of what the initial physician visualized during the baseline exam that may be referenced with any episode of ETD or MEBT, and assists in reducing interpersonal grading variation. This baseline may be useful in the realm of clinical hyperbaric medicine, although baseline images would likely not be available for unforeseen MEBT due to diving, air travel, or trauma.

The O’Neill Grades are assigned as follows:

• Grade 0:Symptoms with no otologic signs of trauma

• Grade 1:Any increased redness of the TM when compared to baseline, serous or slightly serosanguinous fluid and/or trapped air behind the TM

• Grade 2:Frank bleeding in any location and/or perforation of the TM

The authors propose that the O’Neill system allows for a more consistent diagnosis between practitioners. In addition, the O’Neill grading system encompasses treatment guidelines, whereby the authors suggest that grades 0 and 1 are easily managed by the hyperbaric team with reinforced equalization education or physician-prescribed medical therapy, and Grade 2 requires referral to an otolaryngologist for further evaluation.

Differential Diagnosis

While MEBT may be easily visualized and diagnosed based on history or direct otoscopy, any patient experiencing sensorineural hearing loss or new-onset vertigo following exposure to a change in ambient pressure should be referred for further evaluation by otolaryngology to rule out IEBT and PLF. These conditions may be diagnosed using pneumatic otoscopy that results in the production of nystagmus and electronystagmography, however, due to lower sensitivity, there are cases in which PLF is only demonstrated with exploratory surgery.[7][14]

If IEBT is excluded, or in the event of a particularly provocative dive, inner ear decompression sickness (IEDCS) should be considered as it can occur with similar symptoms. While IEDCS is rare, it is important to consider it in the differential diagnosis as it requires recompression and hyperbaric oxygen therapy (HBOT). The HOOYAH criteria can assist in delineating IEBT versus IEDCS based on difficulty in equalization, the onset of symptoms, otoscopic examination, dive profile, additional symptoms, and hearing.[4][12][13]

Treatment / Management

Acute MEBT Management

Treatment of MEBT varies along a spectrum, from trigger management and enhanced equalization education to medical and/or surgical interventions. Most commonly, MEBT is managed by the hyperbaric team, emergency physician, or general practitioner. It is often treated conservatively and resolved without medical interventions.In dealing with MEBT due to ambient pressure changes, one needs to decide if the cause of the dysfunction is primary or secondary. Is the change in ambient pressure alone the cause of the dysfunction (primary ETD), or alternatively, does the patient have some underlying secondary issue or medical condition (secondary ETD)? This is important regarding the approach to treating the patient’s pathology and preventing further BT.

If MEBT occurs during pressurization, then further pressurization should be stopped in order to allow the ET and middle ear space to clear. Decompressing a few feet and reinforced equalization techniques may be beneficial to allow for equalization. In the event of underlying ETD, physician-prescribed medical therapy such as oral decongestants may be beneficial. Exposure to a hyperbaric environment should be aborted if equalization remains unsuccessful, with potential referral to otolaryngology for assessment and further management.

If a patient cannot equalize during an urgent clinical hyperbaric treatment, an emergency needle myringotomy and/or urgent placement of tympanostomy ventilation tubes may be necessary. The procedure is classically performed in the anterior and inferior portion of the TM to avoid potential damage to middle ear structures, especially when performed emergently in extreme cases. This surgically created connection through the TM makes the need for equalization of middle ear pressure unnecessary and passive. Known complications associated with this procedure include infection, bleeding, migration of the tubes into the middle ear space, hearing loss, and chronic perforation requiring surgical repair.

Antibiotics are typically not indicated, unless signs or symptoms of infection develop, or in the case of exposure to contaminated water. It is important to avoid ototoxic antibiotics if concomitant TM perforation exists.[12][23]

Acute IEBT Management

Any patient suspected of IEBT should be assessed and managed by an otolaryngologist. While a small TM perforation may be managed by the team, a large TM perforation, a perforation that is not resolving, or a perforation associated with IEBT symptoms should be referred to otolaryngology as these cases may require advanced surgical correction. Continued middle-ear space bleeding, which is unusual, or middle ear space bleed that is not resolving should also be managed by otolaryngology. Conservative therapy may include bed rest and avoiding maneuvers that increase pressure transmission (coughing, straining with bowel movement, further changes in ambient pressure, Valsalva, loud noises, etc.) Steroids may be considered, although its effectiveness remains unclear in the literature. Surgical exploration and/or repair may be required if significant symptomatology exists, or if deterioration occurs despite conservative therapy.[4][12][13][21]

Predicting Otic BT

ETD and Otic BT cannot be 100% successfully predicted or prevented in any individual unless an anatomical connection between the external ear canal and middle ear space exists (such as myringotomy or ventilation tubes). The reason for interpersonal variation in their ability to equalize middle ear pressures during ambient pressure changes is unknown. Anatomic or physiologic differences have not explained the susceptibility of certain individuals to extreme ambient pressure changes and barotrauma.

Direct visualization of the TM to determine its mobility during equalization type maneuvers may play a role in the identification of individuals at risk for hyperbaric-associated ETD and MEBT, however, it does not successfully predict who will or will not have difficulty equalizing middle ear pressure during ambient pressure changes. While an abnormal nine-step ET function test may assist in identifying those at risk of otic BT, due to its low sensitivity it does not rule out the development of otic barotrauma in those with a normal test result. One study reports a positive predictive value of 86% with respect to predicting ETD if both the nine-step test and degree of mastoid pneumatization as identified by radiography is used, however, this is not practical as a screening tool.[18][24]

Prevention of further MEBT

There are no significant RCTs to evaluate ETD or MEBT prevention during clinical hyperbaric exposures. Further MEBT secondary to primary ETD may be prevented via increased patient education emphasizing equalization maneuvers and slowing the compression rate. There are multiple equalization techniques, such as Valsalva, béance tubaire volontaire (BTV), Toynbee, Frenzel, Edmonds, and Lowry. Equalizing early and often, and utilizing multiple techniques may assist patients having difficulties. A newer ear pressure release device, known as the Ear Popper, has been recently investigated. This device delivers a continuous flow of air into the nasal cavity based on the Politzer maneuver, which is delivered through the ET when swallowing occurs. The device has been used successfully inside a multiplace hyperbaric environment. In the literature, it has been documented as decreasing the need for myringotomy tubes in the pediatric population with chronic otitis media. At times, patients with primary ETD alone might require surgically placed myringotomy tubes to complete clinical hyperbaric treatment. When dealing with divers, the ability to equalize the middle ear space is optimized in the head-up position.

Alternately, if the patient has a secondary cause of ETD, that specific etiology needs to be treated. For example, if the patient is suffering from a URI with nasal and pharyngeal congestion, the congestion must be treated, and the patient should refrain from significant changes in ambient pressure until they can successfully equalize their ears. Radiation-induced damage causing ETD due to fibrosis and scarring may require medical therapy or myringotomy tubes. Endotracheal intubation may also serve as an obstruction to auto inflation of the ET that may require surgical myringotomy. Chronic otitis media is a chronic infectious and/or inflammatory condition that is not specific to the ET, but may prevent auto-inflation of the middle ear space via the ET. It is characterized more as an exudate than the transudate seen with ETD, and may be associated with a middle ear effusion.

Medical prophylaxis is controversial. Pre-treatment with pseudoephedrine may decrease the risk of barotrauma during air travel in adults, however, its efficacy in children remains unclear. The effectiveness of topical decongestants to reduce barotrauma remains unclear. There is significant variation in the use of topical decongestants, oral decongestants, topical nasal steroids, and oral antihistamines to prevent barotrauma in hyperbaric centers. Clinical hyperbaric patients may have multiple medical/surgical health issues controlled with polypharmacy regimens, and may be more prone to contraindications to decongestant use. Pre-treatment with pseudoephedrine prior to diving may decrease the incidence and severity of middle ear barotrauma in divers. However, the use of medication prior to diving remains controversial due to concerns regarding side effects, and the potential for the medication to wear off prior to the end of diving.[25][26][27][27][28][11][29]

Compression Rates and Slope and Their Influence on ETD and MEBT

Attempts of preventing or decreasing episodic ETD or MEBT have been attempted by altering the compression rate (time) and slope (linear versus non-linear) during hyperbaric chamber compression. A slower rate of compression has been shown to reduce the incidence of MEBT during hyperbaric treatments, however many of the studies were underpowered and did not always reach statistical significance. A more recent prospective study by Varughese et al.[30]demonstrated that a linear slower rate of compression of 3 fsw/minute in a multiplace chamber statistically reduced the incidence of MEBT compared to non-linear as well as a faster rate of compression of 4.5 fsw. Comparison of compression rates and slopes to reduce ETD and MEBT remains an interesting and ongoing topic of clinical hyperbaric research.[30][31][32]

Surgical Intervention

ETD preventing equalization and/or MEBT may require elective myringotomy with placement of tympanostomy ventilation tubes. Myringotomy in any form is not an acceptable option for those taking part in wet diving activities with the risk of water entry into the middle ear space and its potential complications. Myringotomy can be considered in those taking part in dry hyperbaric activities such as HBOT, tunneling work, and flying in a pressurized aircraft.Myringotomy should not be considered or used routinely as a prophylactic modality in asymptomatic adult patients. Some hospitals may utilize prophylactic myringotomy in infants and intubated patients, however, this is not standard treatment[21][12][13][20][28]

Regardless of the underlying cause, a patient having experienced otic barotrauma should not be exposed to a hyperbaric environment until symptoms have resolved and otoscopic exam has normalized.

Differential Diagnosis

Any condition that results in aural fullness, hearing loss, tinnitus, and/or vertiginous symptoms should be considered in the differential diagnosis. This may include, but not limited to, cerumen impaction, otitis media, otitis externa, IEDCS, caloric stimulation, Menieres, Benign Paroxysmal Positional Vertigo (BPPV), vestibular neuronitis,acoustic neuroma, etc.

Complications

Complications associated with otic barotrauma have been discussed but can be summarized as serous effusion, serosanguinous effusion, frank bleeding into the middle ear, perforation of the TM, and IEBT. These may be associated with transient and/or chronic hearing loss, vertigo, and gait instability. External auditory canal, middle ear infections, chronic pain, as well as transient facial nerve palsy have also been reported.[4][12][33][34]

Deterrence and Patient Education

Avoiding known risk factors, utilization of equalization techniques early and often, and the treatment of any underlying secondary ETD causes areparamount with respect to the prevention of ear barotrauma. Patients and divers must be educated on the complications of ear barotrauma and prevention techniques.

Pearls and Other Issues

• Ear BT occurs due to inadequate pressure equalization between the middle ear spaceand the external environment.

• ETD and MEBT are the most common complication of diving and clinical HBOT.

• MEBT is commonly treated conservatively by the hyperbaric, emergency, or family practice team and often resolves without the requirement of further interventions.

• Any patient suspected of IEBT should be assessed and managed by otolaryngology.

• Significant BT may be associated with permanent complications such as hearing and balance deficits; thus it is important that clinicians, divers, and patients understand how to prevent BT.

• A patient with ear BT should not be exposed to a hyperbaric environment until symptoms have resolved and the otoscopic exam has normalized.

• There is no reliable tool to predict the development of ear BT.

Enhancing Healthcare Team Outcomes

The management of MEBT and ETD is best done with an interprofessional team that may include an emergency department physician, otolaryngologist, hyperbaric medicine consultant, primary care provider, a physician trained in diving medicine, hyperbaric nurses, and certified hyperbaric technologists. Prevention of ear barotrauma, as well as prompt recognition of the condition, referral, and management by the most appropriate provider is paramount to improving patient outcomes.

Review Questions

• Access free multiple choice questions on this topic.

• Comment on this article.

References

1.

Bove AA. Diving medicine. Am J Respir Crit Care Med. 2014 Jun 15;189(12):1479-86. [PubMed: 24869752]

2.

Buzzacott P, Denoble PJ, editors. DAN Annual Diving Report 2018 Edition: A Report on 2016 Diving Fatalities, Injuries, and Incidents [Internet]. Divers Alert Network; Durham (NC): 2018. [PubMed: 31021587]

3.

Sadé J, Ar A. Middle ear and auditory tube: middle ear clearance, gas exchange, and pressure regulation. Otolaryngol Head Neck Surg. 1997 Apr;116(4):499-524. [PubMed: 9141402]

4.

Rozycki SW, Brown MJ, Camacho M. Inner ear barotrauma in divers: an evidence-based tool for evaluation and treatment. Diving Hyperb Med. 2018 Sep 30;48(3):186-193. [PMC free article: PMC6205852] [PubMed: 30199891]

5.

Fuchs JC, Tucker AS. Development and Integration of the Ear. Curr Top Dev Biol. 2015;115:213-32. [PubMed: 26589927]

6.

Alvord LS, Farmer BL. Anatomy and orientation of the human external ear. J Am Acad Audiol. 1997 Dec;8(6):383-90. [PubMed: 9433684]

7.

Elliott EJ, Smart DR. The assessment and management of inner ear barotrauma in divers and recommendations for returning to diving. Diving Hyperb Med. 2014 Dec;44(4):208-22. [PubMed: 25596834]

8.

Bruss DM, Shohet JA. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Apr 3, 2023. Neuroanatomy, Ear. [PMC free article: PMC551658] [PubMed: 31869122]

9.

Kim CH, Shin JE. Hemorrhage within the tympanic membrane without perforation. J Otolaryngol Head Neck Surg. 2018 Nov 06;47(1):66. [PMC free article: PMC6218969] [PubMed: 30400952]

10.

Ritenour AE, Wickley A, Ritenour JS, Kriete BR, Blackbourne LH, Holcomb JB, Wade CE. Tympanic membrane perforation and hearing loss from blast overpressure in Operation Enduring Freedom and Operation Iraqi Freedom wounded. J Trauma. 2008 Feb;64(2 Suppl):S174-8; discussion S178. [PubMed: 18376162]

11.

Mallen JR, Roberts DS. SCUBA Medicine for otolaryngologists: Part I. Diving into SCUBA physiology and injury prevention. Laryngoscope. 2020 Jan;130(1):52-58. [PubMed: 30776099]

12.

Lechner M, Sutton L, Fishman JM, Kaylie DM, Moon RE, Masterson L, Klingmann C, Birchall MA, Lund VJ, Rubin JS. Otorhinolaryngology and Diving-Part 1: Otorhinolaryngological Hazards Related to Compressed Gas Scuba Diving: A Review. JAMA Otolaryngol Head Neck Surg. 2018 Mar 01;144(3):252-258. [PubMed: 29450472]

13.

Neblett LM. Otolaryngology and sport scuba diving. Update and guidelines. Ann Otol Rhinol Laryngol Suppl. 1985 Jan-Feb;115:1-12. [PubMed: 2857546]

14.

O'Neill OJ, Weitzner ED. The O'Neill grading system for evaluation of the tympanic membrane: A practical approach for clinical hyperbaric patients. Undersea Hyperb Med. 2015 May-Jun;42(3):265-71. [PubMed: 26152108]

15.

Brett KD, Meintjes W. Incidence of otic barotrauma in Canadian Armed Forces shallow-water diver candidate students 2011-2015. Undersea Hyperb Med. 2018 May-Jun;45(3):249-255. [PubMed: 30028912]

16.

Cyran AM, Kosla A, Kantor I, Szczepanski MJ. Tympanometric evaluation of Eustachian tube function in Polish scuba divers. Undersea Hyperb Med. 2018 Jul-Aug;45(4):437-443. [PubMed: 30241123]

17.

Cohn JE, Pfeiffer M, Patel N, Sataloff RT, McKinnon BJ. Identifying eustachian tube dysfunction prior to hyperbaric oxygen therapy: Who is at risk for intolerance? Am J Otolaryngol. 2018 Jan-Feb;39(1):14-19. [PubMed: 29054767]

18.

Uzun C. Evaluation of predive parameters related to eustachian tube dysfunction for symptomatic middle ear barotrauma in divers. Otol Neurotol. 2005 Jan;26(1):59-64. [PubMed: 15699720]

19.

Jansen S, Meyer MF, Boor M, Volland R, Pracht ED, Klünter HD, Hüttenbrink KB, Beutner D, Grosheva M. Repetitive freshwater diving: risk factors and prevalence of barotrauma. Undersea Hyperb Med. 2017 Sept-Oct;44(5):407-414. [PubMed: 29116695]

20.

Klingmann C, Praetorius M, Böhm F, Tetzlaff K, Plinkert PK. [Fitness to dive in the otorhinolaryngological field]. HNO. 2008 May;56(5):509-18. [PubMed: 18415065]

21.

Livingstone DM, Smith KA, Lange B. Scuba diving and otology: a systematic review with recommendations on diagnosis, treatment and post-operative care. Diving Hyperb Med. 2017 Jun;47(2):97-109. [PMC free article: PMC6147252] [PubMed: 28641322]

22.

Mozdzanowski C, Perdrizet GA. Peripheral neuropathy may increase the risk for asymptomatic otic barotrauma during hyperbaric oxygen therapy: research report. Undersea Hyperb Med. 2014 Jul-Aug;41(4):267-72. [PubMed: 25109078]

23.

Vrabec JT, Clements KS, Mader JT. Short-term tympanostomy in conjunction with hyperbaric oxygen therapy. Laryngoscope. 1998 Aug;108(8 Pt 1):1124-8. [PubMed: 9707229]

24.

Fernau JL, Hirsch BE, Derkay C, Ramasastry S, Schaefer SE. Hyperbaric oxygen therapy: effect on middle ear and eustachian tube function. Laryngoscope. 1992 Jan;102(1):48-52. [PubMed: 1731157]

25.

Ryan P, Treble A, Patel N, Jufas N. Prevention of Otic Barotrauma in Aviation: A Systematic Review. Otol Neurotol. 2018 Jun;39(5):539-549. [PubMed: 29595579]

26.

Jones JS, Sheffield W, White LJ, Bloom MA. A double-blind comparison between oral pseudoephedrine and topical oxymetazoline in the prevention of barotrauma during air travel. Am J Emerg Med. 1998 May;16(3):262-4. [PubMed: 9596428]

27.

Wright T. Middle-ear pain and trauma during air travel. BMJ Clin Evid. 2015 Jan 19;2015 [PMC free article: PMC4298289] [PubMed: 25599243]

28.

Capes JP, Tomaszewski C. Prophylaxis against middle ear barotrauma in US hyperbaric oxygen therapy centers. Am J Emerg Med. 1996 Nov;14(7):645-8. [PubMed: 8906761]

29.

Brown M, Jones J, Krohmer J. Pseudoephedrine for the prevention of barotitis media: a controlled clinical trial in underwater divers. Ann Emerg Med. 1992 Jul;21(7):849-52. [PubMed: 1610044]

30.

Varughese L, O'Neill OJ, Marker J, Smykowski E, Dayya D. The effect of compression rate and slope on the incidence of symptomatic Eustachian tube dysfunction leading to middle ear barotrauma: a Phase I prospective study. 2019 Mar-Apr-MayUndersea Hyperb Med. 46(2):95-100. [PubMed: 31051053]

31.

Heyboer M, Wojcik SM, Grant WD, Chambers P, Jennings S, Adco*ck P. Middle ear barotrauma in hyperbaric oxygen therapy. Undersea Hyperb Med. 2014 Sep-Oct;41(5):393-7. [PubMed: 25558548]

32.

Vahidova D, Sen P, Papesch M, Zein-Sanchez MP, Mueller PH. Does the slow compression technique of hyperbaric oxygen therapy decrease the incidence of middle-ear barotrauma? J Laryngol Otol. 2006 Jun;120(6):446-9. [PubMed: 16772053]

33.

Grossman A, Ulanovski D, Barenboim E, Azaria B, Goldstein L. Facial nerve palsy aboard a commercial aircraft. Aviat Space Environ Med. 2004 Dec;75(12):1075-6. [PubMed: 15619863]

34.

Hyams AF, Toynton SC, Jaramillo M, Stone LR, Bryson PJ. Facial baroparesis secondary to middle-ear over-pressure: a rare complication of scuba diving. J Laryngol Otol. 2004 Sep;118(9):721-3. [PubMed: 15509373]

Disclosure: Owen ONeill declares no relevant financial relationships with ineligible companies.

Disclosure: Kaighley Brett declares no relevant financial relationships with ineligible companies.

Disclosure: Anthony Frank declares no relevant financial relationships with ineligible companies.