Ear Barotrauma

Article Author:
Owen ONeill
Article Editor:
Anthony Frank
3/15/2019 9:56:23 AM
PubMed Link:
Ear Barotrauma


Eustachian tube dysfunction (ETD) and middle ear barotrauma (MEB) remain the 2 most common complications of SCUBA diving, commercial diving, and clinical hyperbaric oxygen treatment (HBO). Reported incidence rates vary between 4.1% to 91%. In 1944, Dr. Teed studied the presence of MEB in US Navy divers during submarine escape training. Tympanic membrane (TM) pressure-related pathology became apparent during the course of those exercises and examinations. Dr. Teed evaluated the trainees with otoscopic visualization following hyperbaric exposures in the submarine escape tower.[1][2][3][1]

An increase in atmospheric or hydrostatic pressure effects only the air-containing spaces of the body. The middle ear space is most commonly affected. While most minor TM barotrauma heals rapidly and uneventfully, major trauma, such as a perforation of the TM, may take weeks or months to heal. Major TM barotrauma is likely associated with permanent complications such as hearing loss. This is why prevention and recognition of ETD and MEB remain important when evaluating and treating a pressure-related injury.

A complete discussion of inner ear anatomy is outside the scope of this topic, however, its relationship and connection to middle ear anatomy and MEB, as a cause of inner ear barotrauma, will be considered. This paper will focus on the anatomy of the external ear canal, TM, and middle ear space and how increased ambient pressure produces ETD and MEB. Inner ear barotrauma (IEB) and its complications will be discussed as relating to MEB.

The outside portion of the ear is called the pinna and composed primarily of ridged cartilage covered by skin, leading to the external auditory meatus, or the opening to the external auditory canal. The external ear canal is composed of two-thirds cartilage laterally and one-third bone medially, the entire circumference covered by skin. The external ear canal extends toward and ends at the TM. Otoscopy directly and easily visualizes the external ear canal and TM. Visualization of the TM may be obstructed if the canal holds impacted cerumen. Cerumen needs to be disimpacted to facilitate visualization of the TM (and to facilitate middle ear equalization).

A significant consideration is that all external auditory canals are not anatomically identical and elicit slight variations. This is true when observing the appearance of the 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 external ear canal and TM.

Behind the TM are 3 bony ossicles located in the middle ear space. They are known as the malleus, incus, and the 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. Other ossicles are visible when favorable anatomical conditions are present, such as a transparent TM. The stapes connects the ossicles to the oval window leading into the inner ear apparatus.

These bones are important in the manufacture of sound. Sound waves travel via the external auditory canal to the TM. TM vibrations are then carried through the bony ossicular chain and terminate at the oval window. The last and third bone is known as the stapes, and it abuts the oval window. The stapes moves in and out against the thin membrane of the oval window causing vibration and turbulence of the perilymph fluid 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.

Perilymph turbulence arrives at the inner ear apparatus, or cochlea, where it is recognized and interpreted. It is inside the cochlea and Organ of Corti, where sound is transmitted across tiny hair cells in the form of nerve impulses received by the central nervous system via the eighth cranial nerve.

The middle ear space is situated directly behind the TM and is covered by mucosa. It is connected to the throat via the Eustachian tube (ET), also referred to as the auditory tube. It is responsible for the drainage of fluid produced in the middle ear space, allowing it to enter the throat. The ET opens and drains just beyond the nasal openings in the posterior nasopharynx. This tube is also responsible for allowing the exchange of air between the external environment and the middle ear space, thereby maintaining an equal pressure between the middle ear space and the external auditory canal. This is known as the equalization of middle ear pressure. Another less described air exchange takes place via the middle ear mucosa and mixed venous circulation. This transmucosal gas exchange is less important during rapid and large changes in ambient pressure occurring during diving and flying or when being treated in a hyperbaric chamber.[4][5][6][7]


When the middle ear space cannot be filled sufficiently with air from the mouth and throat due to the failure of the ET to open, or when it is completely collapsed from increased external ambient pressure (atmospheric or hydrostatic), MEB will ensue. It only takes a pressure equivalent of 10 feet of seawater (4.4 psi) to close the ET completely. This explains why it is one of the most common disorders observed in patients participating in activities involving increased ambient pressure. Commonly, most people have experienced this ambient pressure change when diving to the bottom of a deep pool or as a passenger in a car when driving through various elevation changes. An increase in middle ear pressure is commonly observed when wet diving (SCUBA), dry diving (hyperbaric chamber treatment), or when landing as an occupant of a pressurized aircraft.

Once complete closure of the ET occurs, it seldom reopens with the usual performance of the Valsalva maneuver. At this point, decreasing the ambient pressure is required to reopen the ET.  Decreasing the ambient pressure does not guarantee immediate reopening of the ET.  Additionally, decreasing ambient pressure 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 which time the patient can clear the middle ear space. Performance of all these maneuvers does not guarantee the ET will be opened to equalize middle ear pressure. Unfortunately, pilots cannot stop landing the commercial pressurized aircraft and increase altitude when an occupant complains of ETD or MEB. 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.[8][9][10][11]


There is significant variability in the incidence and prevalence of ETD and MEB. There is no documented difference regarding gender, age, type of diving, cold versus hot water, or season, despite the notion of potential seasonal allergies causing Eustachian tube dysfunction. Head and neck radiation has been associated with a slightly higher incidence of ETD and MEB, presumably secondary to radiation soft tissue damage of the ET or pharynx.


As ambient pressure (atmospheric or hydrostatic) increases external to the body, it causes pressure to rise in the external auditory canal. This continuous increase in ambient pressure is eventually exerted on the tympanic membrane. If pressurization of the external environment is allowed to continue without proper equalization of pressure in the ET and middle ear space, this pressure will continue to be exerted through the canal and onto the surface of the TM. The pressure on the TM initially causes a sensation of fullness or dullness recognized by patients, divers, and plane passengers alike. This initial sensation will progress to the discomfort that often advances to severe pain if the ambient pressure increase does not cease or the pressure in the middle ear space is not equalized. If allowed to continue, the increase in ambient pressure will eventually result in perforation of the TM and its associated complications.

There is no agreed upon exact pressure required to rupture the TM. Many otolaryngologists and researchers observe that a middle ear pressure of 100 kPa, 14.7 psi, 1 ATM of hydrostatic pressure, or 2 ATA are required. Despite this observation, TM rupture has occurred at lower pressures.

On the infrequent end of the spectrum, some patients suffer ETD and MEB without experiencing symptoms. In 2014, Maodzanowski and Perdrizet reported an association between diabetic neuropathy and painless barotrauma. This suggests a potential association between diabetic peripheral neuropathy and neuropathic pathology of the external ear canal, TM, and middle ear space. This association also occurred in a small sub-group of clinical hyperbaric patients with diabetes who had asymptomatic barotrauma and associated peripheral neuropathy. This highlights the potential need to perform otoscopic evaluations on all clinical hyperbaric patients before and after each hyperbaric exposure. Minimally, otoscopic evaluation should be considered on all patients with diabetes after each clinical hyperbaric treatment even without symptoms, especially in those with documented peripheral neuropathy.

Pathophysiology of ETD and MEB have been well described. Prior to TM rupture, a number of physiologic and anatomic changes take place. These changes are readily identifiable by direct otoscopic examination and directly related to the negative pressure created in the middle ear space when equalization is prevented and does not occur. The vacuum created in the middle ear-space causes an increase in blood flow through the subcutaneous vessels in the external ear canal, TM, ET, and middle ear space. This results in the vessels engorging with blood. This physiological and anatomical change is readily and easily visualized via direct otoscopy and described as increased redness or erythema. As pressure in the external ear canal 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. Trapped air bubbles may also be visible through the TM during otoscopic evaluation. 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. Round window injury and fistula need to be considered in cases of TM rupture caused by increased ambient pressure.

As the middle ear pressure increases, it subjects the entire perilymph to higher pressures and turbulence. This turbulence and pressure are continuously transmitted to the round window. If the pressure is not equalized and continues to rise, round window blowout may occur. Round window injury is frequently associated with MEB and TM rupture. The rupture or tear of the round window results in the creation of a perilymph fistula (PLF). This causes a steady flow of perilymph into the middle ear space. It may be associated with hearing loss, tinnitus, and vertigo, or initially, it may be asymptomatic. If these signs and symptoms are experienced following increases in ambient pressure associated with difficulty equalizing and ear pain, they should be immediately evaluated to rule out a perilymphatic fistula. It may be diagnosed using pneumatic otoscopy that results in the production of nystagmus (sensitivity 77%) or by electronystagmography (sensitivity 44%). Exploratory surgery is still needed to confirm the diagnosis and repair the defect. If the perilymphatic fistula is excluded, inner ear decompression sickness should be considered as it can occur with similar symptoms. Inner ear decompression sickness is reported in less than 1% of diving accidents. It was not initially reported or introduced as a significant diving pathology until 1972. It is important to recognize inner ear decompression sickness or consider it in the differential diagnosis, as it requires recompression and treatment in a hyperbaric oxygen chamber.

Less commonly, lacerations of the skin of the external ear may also occur. Skin lacerations will eventually culminate in a rupture of the TM if equalization of pressure in the middle ear space does not occur. These types of injuries require otolaryngology referral to assess for severe structural damage and complications.

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, reverse or depressurization occurs potentially causing a decompression injury from a condition known as a reverse block. This signifies the inability of the pressure to be released (decreased) from the ET and middle ear space. Reverse blockage of the ET will result in MEB if the pressure change is allowed to persist by ascending. Conversely, recompression may be necessary to allow the ET and middle ear space to clear. Once MEB has occurred, it may be visualized by direct otoscopy or otoscopic video. The anatomical changes associated with MEB have been historically classified by using various grading systems.

History and Physical

For MEB to occur, there must be a history of being exposed to increased atmospheric pressure with a dysfunction of the Eustachian tube. This could be in the form of wet scuba diving or dry hyperbaric exposure in a hyperbaric chamber. Most patients will complain of pain or pressure in the affected ear. It may also be associated with varying degrees of hearing loss. Physical examination may demonstrate blood in the external ear canal especially if the tympanic membrane has ruptured. Most commonly there will be varying degrees of erythema or bleeding into the tissues. For further information, please read below in the evaluation section.


Once a patient has signs and symptoms of ETD and/or MEB, they must be evaluated via otoscopic examination to determine and classify the extent of the injury. This examination is important as it will help decide the need for treatment based on the proper classification of injury. Treatment can take the form of enhanced equalization education, medical intervention or surgical intervention such as myringotomy and ventilation tube placement. Currently, there are 3 methods of evaluating and grading ETD and MEB: the Teed, the Modified Teed, and the O’Neill grading systems.

Teed Classification

The Teed classification was developed in 1944. It was composed of 5 levels of grading ear barotrauma and was not intended or developed for the evaluation of clinical hyperbaric patients. Despite this and other flaws, the Teed classification has been widely accepted as the hyperbaric grading system of choice due to a lack of an alternative system of grading. Teed Grading involves a 1-time evaluation by the same examiner, evaluating a person’s potential trauma to the TM, with no consideration for any additional examiners performing the exam at a later time with no baseline reference. 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.

These grades were applied without knowing what the patients original baseline exam revealed. The second exam was compared to a general description by the initial examiner such as a “normal TM.”

Modified Teed Classification

At some point in history, 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.

Both these Teed systems of classification are cumbersome and impractical, despite being utilized for many years by clinical hyperbaric physicians. It cannot be used easily by support staff such as nurses and technologists. The system provides no patient baseline exam that can be easily accessed by a different examining physician before the symptoms or barotrauma. Barotrauma may occur after multiple exposures to pressure weeks or months after the initial ear exam. This makes the original appearance of the TM difficult to remember, even for the original examining physician with a photographic memory. A “normal” tympanic membrane exhibits many different anatomical variations as discussed earlier. A modified Teed score of 0 to 3 for example, may be a patient’s normal baseline as described and demonstrated by O’Neill. Evaluation of post-hyperbaric ETD or MEB and potentially applying an overstated Teed score, may subject the patient to unnecessary medical or surgical treatment and an unnecessary interruption of hyperbaric therapy.

O’Neill Grading System for ETD and MEB

The O’Neill Grading System employs the use of a video otoscope to take a baseline photo of the TM, before hyperbaric exposure. The photo maintains a permanent record of what the initial physician visualized during the baseline exam. It is quite useful in the realm of clinical hyperbaric medicine and is easily used by physicians, nurses, and technologists alike. It creates a lasting baseline picture of the patient’s TM that may be referenced with every episode of ETD or MEB at the time of follow up. 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

These 3 grades are simple to recognize by any member of the hyperbaric team, whether the physician, nurse, or technologist. Results are seamlessly communicated with increased accuracy, even when the current examiners are different from the original assessors. Diagnosis is significantly more consistent than with other grading systems.

This O’Neill grading system also suggests and simplifies the treatment decision for any member of the team based on its consistency. Grades 0 and 1 are easily managed and treated by the hyperbaric team with reinforced equalization education or physician prescribed medical therapy. Grade 2 requires referral to the otolaryngologist for further evaluation before the continuation of hyperbaric exposures.

Treatment / Management

As mentioned above in the evaluation section, the O’Neill grading system suggests and simplifies the treatment decision for any member of the team based on its consistency. Grades 0 and 1 are easily managed and treated by the hyperbaric team with reinforced equalization education or physician prescribed medical therapy such as oral decongestants like pseudoephedrine despite only being studied in the wet scuba diving population. Nasal decongestants have not been shown to be beneficial unless treating secondary ETD as mentioned above. The O'Neill Grade 2 requires referral to the otolaryngologist for further evaluation prior to the continuation of hyperbaric exposures. Continued bleeding, which is unusual, may need to be controlled by the otorhinolaryngology (ENT) surgeon. ENT can also manage perforated TMs. At times, certain cases may require surgery to repair a ruptured TM.Most commonly, MEB is treated conservatively and resolves without any necessary medical therapy. ET dysfunction and MEB during an urgent clinical hyperbaric treatment may require an emergency needle myringotomy or urgent placement of myringotomy tubes. Lastly, and currently under investigation, is a device known as the Ear Popper. This device delivers a steady and constant flow of air into the nasal cavity based on the Politzer maneuver. The safe but forceful stream of air is delivered in the ET when swallowing. The device has been used successfully and safe 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.[12][13][14][15]


Complications associated with MEB have been discussed but can be summarized as perforation of the TM with associated hearing loss, vertigo, middle and external auditory canal infection especially post perforation and disruption of the skin of the external ear canal. Recurring chronic pain has been reported. 

Pearls and Other Issues

Prevention of ETD and MEB

The reason that some people and not others can equilibrate ET and middle ear high-pressure changes is unknown. Anatomic or physiologic differences have not explained the susceptibility of certain individuals to extreme ambient pressure changes and barotrauma. Hence, ETD and MEB cannot be successfully predicted or prevented in any individual, unless an anatomical opening and connection between the external ear canal and middle ear space is created. This is accomplished by performing a myringotomy with or without placement of ventilation tubes. 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. However, placing these tubes increases the likelihood of well-known complications associated with the procedure such as infection, bleeding, migration of the tubes into the middle ear space, hearing loss, and chronic perforation requiring surgical repair.

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 hyperbaric oxygen treatment, tunneling work, and flying in a pressurized aircraft, but should not be considered or used routinely as a prophylactic modality in asymptomatic patients.

Direct visualization of the TM to determine its mobility during Valsalva type maneuvers may only play a role in the identification of individuals at risk for hyperbaric-associated ET and MEB. Despite identifying those at risk, (no TM motion on Valsalva maneuvers), does not successfully predict who will or will not have difficulty equalizing middle ear pressure during actual hyperbaric exposure. There are no significant RCTs to evaluate ETD or MEB prevention during clinical hyperbaric exposures. Wet scuba divers may have some benefit when pre-treated with pseudoephedrine. The aviation literature reports a decrease in barotrauma associated with 120 mg of pseudoephedrine, taken 30 minutes before flights in a pressurized aircraft.

Clinical and hospital hyperbaric patients are not always young and have multiple medical/surgical health issues controlled with polypharmacy regimens. They are also more prone to contraindications to decongestants. Decongestants may enhance urinary obstruction in older men with benign prostatic hypertrophy or induce cardiac arrhythmias in patients with a prior history of or are prone to the same.  Oxymetazoline, a topical nasal spray is of no benefit preventing ETD and MEB when studied in a small prospective trial comparing its use to a placebo

Compression Rates and Slope and Their Influence on ETD and MEB

Attempts of preventing or decreasing episodic ETD or MEB have been attempted by altering the compression rate (time) and slope (linear versus non-linear) during hyperbaric chamber compression. In a quasi-experimental prospective trial presented at the Undersea and Hyperbaric Medical Society (UHMS) Annual Meeting in June 2017, Varughese and O’Neill demonstrated that a linear compression rate of 45 feet of seawater over 15 minutes in a multiplace chamber practically and statistically reduced the incidence of ETD and MEB when compared to 3 other rates of compression: 10 minutes linear, 10 minutes non-linear, and 15-minute non-linear rates. This is the only prospective clinical trial of its design for demonstrating a potential prevention strategy for decreasing the incidence of ETD and MEB. A regression analysis of this data is in progress to evaluate the potential confounding effects of ETD and MEB when evaluating compression rate and slope. Vahidova et al. performed a prospective clinical audit demonstrating that a slower compression rate yielded less ETD and MEB than standard rates of compression. Comparison of compression rates and slopes to reduce ETD and MEB remains an interesting and ongoing topic of clinical hyperbaric research. This topic remains the most common secondary effect of clinical hyperbaric oxygen therapy, diving and flying in a pressurized aircraft.

Enhancing Healthcare Team Outcomes

The management of MEB and ETD is best done with a multidisciplinary team that includes an emergency department physician, ENT surgeon, hyperbaric medicine consultant, primary care provider and a physician trained in diving medicine.

There is a wide variation in diagnostic criteria for ETD. Pressure disequilibrium causes the primary symptoms in the affected ears. In dealing with cases caused by increasing ambient pressure, 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). On the other hand, does the patient have some concomitant secondary issue or medical condition resulting in the ETD and MEB (secondary ETD). This is important regarding the approach to treating the patient’s pathology.

Primary ETD may be treated via increased patient education, emphasizing equalization maneuvers, slowing compression rate, or using an ear pressure release device that continuously blows air into the ET via the nose (Politzer maneuver). These maneuvers have significantly proven successful in treating aerotitis/barotitis and decreasing the need for myringotomy in the pediatric population. In an ongoing study by the author, one such device is proving to be a positive tool for achieving compression in the dry hyperbaric environment and as a rescue method of equalization. At times, patients with primary ETD alone might require surgically placed myringotomy tubes to complete clinical hyperbaric treatment.

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, we aim at treating the congestion and perhaps have the patient refrain from significant changes in ambient pressure until the congestion is resolved. Endotracheal intubation may also serve as an obstruction to auto inflation of the ET that may require surgical myringotomy. Radiation damage causing ETD due to fibrosis and scarring may require medical therapy or myringotomy tubes in those partaking in dry diving or hyperbaric pressurization as a patient or employee of a clinical hyperbaric center or commercial airline. Certain patients, divers, or hyperbaric employees may never be cleared to dive or undergo hyperbaric exposure with a non-remitting condition causing chronic ETD and MEB. It remains important to recognize that chronic otitis media is not the same as ETD, but rather a chronic infectious and/or inflammatory condition that is not specific to the ET and is characterized more an exudate than the transudate seen with ETD. The condition prevents auto inflation of the ET and middle ear space. It may also be associated with a middle ear exudative effusion. Causes of secondary ETD and the inability to equalize must be looked at independently and treated accordingly for successful compression in the hyperbaric environment.


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