Surfer's Ear

Etiology

Exostoses develop from prolonged irritation of the external auditory canal, typically with repeated cold seawater exposure.[1] This exposure stimulates new bone formation at the tympanic ring within the external auditory canal.[4] The prevalence and severity of (EAE) are directly proportional to the cumulative duration and frequency of cold water exposure.[5]

Epidemiology

Surfer’s ear dates back to prehistoric man. It has been utilized anthropologically to identify cultures with regular aquatic exposure.[6] In the general population, the prevalence of external auditory exostoses is 6.3 per 1000 people.[1] External auditory exostoses are more prevalent in coastal regions where water exposure is common, especially in those with a cooler climate and colder water temperatures. In more at-risk populations, such as surfers, the prevalence ranges between 26 and 73%.[5] Surfers have a proportionally higher risk of developing exostoses than participants in other cold-water sports.[7] The disease is more common in males than in females, most likely due to their higher involvement in cold water activities. Of note, males surfing regularly for 20 years or more have a one in two chance of developing significant exostoses (significant defined as more than two third ear canal obstruction), while there is a three in seven chance for females meeting the same criteria.[8] EAE may be seen in patients of all ages but most commonly presents in the third and fourth decade of life. The major risk factor is repeated and long-term exposure to cold water, with an odds ratio of 5.8.[1] In one study, winter water sport participants had significantly more exostoses than those who only practiced during the summer months.[9] No specific studies have compared the prevalence of exostoses between warm-water climates and cold-water climates. Each year of exposure to cold water increases the risk for the development of external auditory exostoses by about 12%.[1] There is a direct correlation between years of exposure to cold water and the severity of ear canal obstruction caused by EAE.[10] The colder the water, the more severe the disease can be.[2] Among surfers, there is a positive relationship between years of active surfing and the severity of exostoses.[11] Unless surfing more than 50 sessions per year, people who have surfed for less than 5 years are unlikely to develop exostoses.[12] Improvements in wetsuit technology have allowed water sport enthusiasts to expose themselves to colder water, which may lead to an increase in the prevalence and severity of EAE unless additional preventive measures are implemented.

Pathophysiology

Frequent cold water exposure over the course of years slowly induces bone growth.[1] While the exact mechanism is not confirmed, it is hypothesized and commonly accepted that cold water exposure induces vasodilation in the bony auditory meatus creating an increase in vascular tension.[13] This is associated with inflammation causing periostitis.[13] The inflammatory process stimulates osteoblast activity, followed by fibrosis and ossification, leading to new bone growth within the external auditory canal.[13] The area over the tympanic ring has a very thin layer (0.1mm) of stratified squamous epithelium covering the underlying temporal bone, making this the pathologic location for the formation of the bony exostoses.[4] The lack of insulating subcutaneous tissue between the epithelium and the underlying periosteum enables the bone growth to extend into the external auditory canal.[13] The process of EAE formation is considered to be a protective mechanism to shield the tympanic membrane from cold water and cold air.[5]

Studies demonstrate that exposure to water colder than 19° C  (66° F) leads to the more frequent development of exostoses.[5] The wind chill is also thought to contribute to bone formation when water is warmer than 19° C.[14] The bone growth typically occurs medially both posteriorly and anteriorly, leading to partial or full occlusion of the external auditory canal.[10] In the lateral auditory canal, the subepithelial layer is thicker in comparison to the medial side, and thus the effects of vasodilation and subsequent bone formation are less pronounced.[13] EAE may also be the result of pH, chemical, and physical irritants, although these causes are much less common than chronic cold water exposure. Although the growths are benign, occlusion can lead to conductive hearing loss and entrapment or buildup of debris, predisposing patients to recurrent otitis externa. Histologically, the exostoses consist of parallel, concentric layers of subperiosteal bone with numerous osteocytes.[15]

History and Physical

External auditory exostosis is usually an asymptomatic disease.[2] However, a patient with more progressed EAE may present with decreased hearing, ear fullness, chronic otitis externa, otorrhea, or a sensation of water trapped inside the ears. EAE is usually not the primary cause of a patient complaint but can be a risk factor for the underlying etiology of the patient’s presentation. For example, very rarely does this disease cause pain directly, but pain may be a secondary result of an otitis externa infection incited by external auditory exostoses. History is extremely important in making a diagnosis of this disease. The patient must have multiple years of repetitive exposure to cold water, usually through water activities such as surfing, kayaking, diving, or swimming.[1] The history should include the number of years of exposure to cold water. Some studies suggest a minimum of five years of cold water exposure before significant external auditory exostoses develop, while others suggest 10 years.[7]

On physical exam, the practitioner should be able to visualize multi-nodular masses at the tympanic ring with an otoscope. In general, the size of the masses is proportional to the degree of symptoms. The masses are firm, multiple, and often seen in the external auditory canal bilaterally. If the exostoses are large enough, they may obscure the sight of the tympanic membrane. It is not uncommon for cerumen to become impacted on the tympanic membrane as a result of entrapment behind or within the exostoses. If this is the case, carefully perform an ear lavage to better visualize the ear structures. Once removable debris or obstructions are resolved, consider assessing for hearing loss. If hearing loss is present, performing a Rhine and Weber test will demonstrate a conductive hearing loss as opposed to a sensorineural hearing loss.[16]

Evaluation

Patients will typically present with a secondary complaint, such as ear pain, hearing loss, or a sensation of fullness. These symptoms can be a result of otitis externa, cerumen impaction, tympanic membrane rupture, or a foreign body. All of these diagnoses have the potential to be a downstream effect of external auditory exostoses. The history and physical exam are typically all that is needed to diagnose external auditory exostoses. The most important component of the physical exam is otoscopy. External auditory exostoses have a firm, bony, and nodular appearance at the tympanic ring within the external auditory meatus. They are usually multiple and bilateral. While their position within the ear canal can vary, the first lesions most commonly are medial and anterosuperior.[10]

The degree of ear canal obstruction caused by the exostoses is usually proportional to the severity of symptoms.[17] The severity of exostoses is graded from 1 to 3 based on the percentage of occlusion of the canal as seen on the physical exam. Less than 33% occlusion is mild (grade 1), 33% to 66% occlusion is moderate (grade 2), and greater than 66% occlusion is considered severe (grade 3).[17] To further evaluate, a computed tomography (CT) scan of the external auditory canal with less than 1 mm thin slices may be performed. Imaging findings can be non-specific, and without history and physical exam clues, it can be challenging to differentiate exostoses from malignancies or infections.[16] On CT scan, the health care practitioner will note broad-based bony overgrowth in the external auditory canal. Usually, the CT scan is reserved for surgical planning and is not necessary for every patient with EAE [17]. Magnetic resonance imaging (MRI) is also occasionally utilized for surgical planning.

Treatment / Management

Early detection and prevention of progression of surfer’s ear are paramount once exostoses have been detected. Prevention involves patient education for the use of silicone earplugs and/or neoprene hoods to reduce auditory canal cold water exposure. EAE is a progressive disease; however, the risk of progression can be mitigated with consistent preventive measures. Treatment consists of medical management involving regular cleaning of the external auditory canal to remove any entrapped debris. This can help prevent the propagation of complications such as recurrent otitis externa, tympanic membrane rupture, and conductive hearing loss.

Once the exostoses are formed, they are irreversible unless surgical intervention is performed. If there is greater than 80% occlusion and symptoms are severe and persistent despite medical management, a canalplasty by an otolaryngologist may be considered.[17] The surgery typically involves general anesthesia with a post-auricular approach by elevating the skin overlying the exostoses and removing the bone with a drill.[17] Another technique is to approach directly from the external auditory canal and use chisels to remove the bony growth. Following surgery with the traditional approach, 68% of patients reported improved quality of life, while 14% had surgical complications.[17] Surgery complications include tympanic membrane rupture, delayed healing, canal stenosis, loss of high-frequency hearing, temporomandibular joint dysfunction, and facial nerve paralysis. Due to the rate of complication, surgery is reserved for those who are symptomatic and refractive to medical management. If the patient requires bilateral surgery, two canalplasties are performed about 6 weeks apart.[17](B2)

Differential Diagnosis

If masses are noted in the external auditory canal on the otoscopic exam, there are several differential diagnoses to consider. These include EAE, osteomas, cholesteatoma, keratosis obturans, aural polyps, and tumors.

On exam alone, it can be challenging to distinguish EAE from osteomas. The patient history helps to make this clinical distinction. Clinicians should have a high index of suspicion for EAE if the patient has a history of repeated cold water emersion. External auditory exostoses are generally bilateral and multinodular. Osteomas are most commonly pedunculated, singular, unilateral, and positioned laterally in the ear canal.[18] While osteomas are most commonly found in the external auditory canal, they can also be found in the mastoid cortex, facial bones, and mandible.[15] Histologically, exostoses and osteomas are different, and a definitive diagnosis can be confirmed following surgical excision. Osteomas consist of lamellated bone with a small quantity of osteocytes surrounding fibrovascular channels.[15] Exostoses consist of parallel, concentric layers of subperiosteal bone and have an abundance of osteocytes.[15] 

A cholesteatoma is a cystic mass of keratinized squamous epithelium located in the middle ear.[19] They are sometimes congenital, however, are most commonly a result of chronic otitis.[19] They are formed from abnormal negative pressure within the ear canal, leading to a pocket or cyst that fills with old skin cells and debris. Cholesteatomas grow and change more rapidly than exostoses. Keratosis obturans is the buildup of keratin in the external auditory canal.[20] It is hypothesized that this is a result of either overstimulation of cerumen-producing glands or due to epithelial cell dysregulation.[20] They are usually unilateral and most commonly seen in younger persons.[20]

Aural polyps are benign fleshy growths in the external auditory meatus or inner ear.[19] They are caused by irritation, which can be a result of cholesteatomas, foreign objects, or inflammation from chronic otitis externa.[19] These are different from EAE as they have a fleshy appearance instead of a bony appearance. Less common are malignant tumors in the ear canal. These can include squamous cell carcinomas, carcinoid tumors, and embryonal rhabdomyosarcomas.[19] Squamous cell carcinomas are more common in the elderly. Carcinoid tumors in the ear canal are exceedingly rare but have been found.[19] Embryonal rhabdomyosarcomas are highly malignant and are generally seen in children.[19]

Prognosis

External auditory exostoses are benign and usually asymptomatic.[2] Generally, they can be medically managed with frequent ear cleaning to improve symptoms and prevent complications. EAE is a progressive disease, and without appropriate preventive measures, it can lead to complications such as conductive hearing loss, recurrent otitis externa, otalgia, otorrhea, cerumen impaction, and water trapping.[2] If the exostoses occlude more than 80% of the auditory canal and symptoms persist and despite medical management, surgical excision may be required.[17] The outcomes in most patients are good, but the rates of surgical complications to relieve the disorder are somewhat high.[7][17]

Complications

The severity of complications from external auditory exostoses is proportional to the size of the exostoses. The size of the exostoses is proportional to the duration and frequency of exposure to cold water.[1] Complications can be a progressive problem as more time elapses, especially with recurrent exposure. EAE complications include hearing loss, otalgia, otorrhea, cerumen impaction, water trapping, recurrent otitis externa, and in severe circumstances, mastoiditis and tympanic membrane rupture.

Conductive hearing loss is a common complication of EAE. The degree of hearing loss is relative to the degree of ear canal occlusion, which is predominantly determined by the size of exostoses. The associated hearing loss is generally due to cerumen impaction on the tympanic membrane caused by blockage from the exostoses.[4] This can be improved with ear lavage. The process of the buildup of cerumen or other debris is what leads to symptoms of otalgia, otorrhea, and water trapping. While often associated with debris or cerumen, these symptoms can be caused by the exostoses themselves if they are occluding a significant portion of the auditory canal. If the level of entrapment is severe and untreated, this can put excessive pressure on the tympanic membrane and cause it to perforate or rupture. Patients who engage in high-impact water activities such as surfing are at higher risk for this.

The ear canal occlusion that can occur due to large exostoses may also propagate an inflammatory process leading to acute external otitis.[4] This can become a chronic, recurrent problem. Otitis externa is best treated via antimicrobial otic drops. Oral agents are less successful in penetrating the tissue of the external auditory canal and are best reserved for otitis media.[21] The most common pathogens of otitis externa are Staphylococcus aureus and Pseudomonas aeruginosa.[21] Ofloxacin is a fluoroquinolone that will cover both microbes. While neomycin is a reasonable treatment option for otitis externa, it only covers S. aureus. It is particularly important to cover for P. aeruginosa in patients with diabetes.

In severe cases when otitis externa is recurrent or left untreated, patients can be at risk for developing mastoiditis. Patients are particularly prone to this if they develop a perforation in their tympanic membrane. Seawater can then enter the middle ear and stimulate a more serious infection. Mastoiditis requires prompt treatment with IV antibiotics that cover S. aureus, Pseudomonas, Streptococcus pneumoniae, Haemophilus influenzae, and enteric gram-negative rods. Unasyn is an ideal antimicrobial agent.[22] A head CT should always be performed when mastoiditis is suspected. This is done to evaluate for intracranial spread. Treatment should not be delayed as the diagnosis can be made clinically, and if untreated, mastoiditis can cause permanent hearing loss.[22]