Blocked ears

Abstract

Blocked ears are a common presenting complaint in primary care, and although the cause is usually benign, a structured clinical approach and examination are essential to avoid missing more significant causes. In this article, we discuss the clinical approach, aetiology and management of the wide range of conditions that lead to the sensation of blocked ears, and provide guidance on referral to secondary care.

The RCGP curriculum and blocked ears

The role of the GP in the ear, nose and throat, speech and hearing clinical topic guide is to:

Identify symptoms that fall within the range of normal or are caused by self-limiting conditions

Ensure that a patient’s hearing impairment or deafness does not prejudice the information communicated or your attitude as a doctor towards the patient, and be able to communicate effectively

Perform effective assessment including conducting or interpreting more detailed tests and treatment including procedures where indicated

Demonstrate empathy and compassion towards patients with ear, nose and throat symptoms that may prove difficult to manage, e.g. tinnitus, facial pain, unsteadiness, hearing loss

The RCGP curriculum clinical topic guide details emerging issues and the knowledge and skills guide that may be relevant to the management of blocked ears in the community. This article will cover the following areas:

Typical and atypical presentations

Diagnostic features and differential diagnosis

Appropriate and relevant investigations

Management including self-care, initial, emergency and continuing care, chronic disease monitoring

Patient information and education including self-care

Prognosis

Clinical anatomy

The ear is divided into external, middle and inner parts. The external ear consists of the pinna, meatus and external auditory canal (one-third cartilaginous and two-thirds bony). The middle ear lies within the petrous temporal bone and is defined laterally by the tympanic membrane, medially by the lateral wall of the inner ear and contains the auditory ossicles (malleus, incus and stapes). The inner ear consists of cochlear and vestibular components (utricle, saccule and semi-circular canals) and is found in the temporal bone.

Sound is funnelled into the external auditory canal where it vibrates the tympanic membrane and, in turn the ossicular chain. The vibration experienced by the stapes footplate at the oval window of the cochlear results in movement of potassium-rich endolymph within the cochlear duct. The resultant displacement of hair cells within the Organ of Corti on the basilar membrane, in turn, generates an electrical impulse which is conducted along the vestibulocochlear nerve (CN VIII) to the auditory cortex in the superior temporal gyrus of the temporal lobe.

The Eustachian tube is a part bony, part cartilaginous structure that forms a conduit between the middle ear and nasopharynx. It is approximately 37 mm long and opens posteriorly at the level of the inferior turbinate (Bluestone, 2004). The tube has three key functions (Schilder et al., 2015):

The equalisation of pressure and ventilation of the middle ear

Clearance of secretions from the middle ear

Protection of the middle ear from infection that could be caused by nasopharyngeal secretions

Aetiology

Disruption or occlusion along any part of the conducting system can result in the sensation of blocked ears, as summarised in Table 1. In this article, we focus on pathology within the external and middle ear. It is unusual for disease of the inner ear or vestibulocochlear nerve to present with an isolated sensation of blockage. Instead, these conditions usually present with hearing loss, tinnitus, vertigo or cranial neuropathies.

Table 1.

Possible causes of ‘blocked ears’.

External ear	Middle ear	Other (incl. inner ear)
Congenital anomalies e.g. atresia, microtia	Cholesteatoma	Ménière’s disease
Cerumen impaction	Eustachian tube dysfunction	Temporomandibular joint dysfunction
Foreign body (organic, inorganic)	Otitis media with effusion	Adenoid hypertrophy
Malignancy (rare)Squamous cell carcinoma, Basal cell carcinoma, Melanoma	Acute otitis media	Nasopharyngeal carcinoma
Exostoses (surfer’s ear)	Glomus tympanicum	Sudden sensorineural hearing loss
Osteoma
Keratoses obturans

Clinical management approach

‘Blocked ears’ is a broad and largely non-specific term frequently used by patients. It is, therefore, important for the clinician to take both a detailed history and conduct a thorough examination to identify the possible causes.

History

When reviewing a patient with the blocked ears, as well as a routine history, it is important to ask specifically about other otological symptoms; see Box 1 for examples. A further assessment of risk factors should be undertaken, including past medical history (diabetes, immunosuppression, childhood meningitis), drug history (aminoglycoside antibiotics, loop diuretics, non-steroidal anti-inflammatories, social history (noise exposure, industrial chemicals) and family history. Other intracranial causes, e.g. trauma, infection, cerebrovascular accident should also be considered.

Box 1.

Examples of specific questions when taking a history from a patient presenting with blocked ears.

• Is there any history of trauma/foreign body insertion? Blockage may be simply due to cerumen; the use of cotton buds is frequently associated with wax impaction and resultant hearing loss

• Is there associated hearing loss? Severity, onset and duration of hearing loss are important to establish. Patients presenting with sudden sensorineural hearing loss typically remember exactly what they were doing at the time of hearing loss. A fluctuating level of hearing loss should prompt clinicians to consider Ménière’s disease or Eustachian tube dysfunction.

• Is there associated otalgia? Otalgia is generally associated with infective/inflammatory processes e.g. otitis media. Severe pain in the presence of otitis externa is concerning for necrotising otitis externa (particularly in diabetic or immunocompromised patients) and may warrant specialist referral

• Is there associated otorrhoea? Persistent foul-smelling otorrhoea and hearing loss is concerning for cholesteatoma, necessitating adequate visualisation of the tympanic membrane and attic. If the tympanic membrane cannot be fully visualised the patient may need referral for microsuctioning and specialist opinion

• Are you experiencing episodes of disequilibrium/vertigo? Vestibular symptoms have a wide-ranging differential and workup should include a thorough neurological history and examination as well as ontological examination

• Is there associated tinnitus? Tinnitus has numerous causes and the history should be tailored appropriately to consider vascular (carotid artery stenosis) and neoplastic causes e.g. vestibular schwannoma

• Are the symptoms bilateral or unilateral? Unilateral symptoms and the presence of middle ear effusion raise suspicion for nasopharyngeal carcinoma and should prompt referral for nasoendocsopy and examination of the post-nasal space

• Is there any history or snoring/witnessed apnoeas? Adenoid hypertrophy is often noted is paediatric patients with mouth-breathing and snoring. It can also manifest with recurrent acute otitis media or otitis media with effusion due to obstruction of the Eustachian tube orifice.

Examination and investigation

There are a whole host of examination and investigation techniques for blocked ears. Here we focus on the assessment that can be performed in primary care or with referral to community services (e.g. audiology):

Otoscopy should be sufficient to reach the diagnosis in the vast majority of cases, allowing visualisation of external canal foreign bodies, cerumen, otitis externa, as well as middle ear pathology, e.g. otitis media with effusion, glomus tympanicum and cholesteatoma

Otoscopic examination should be complemented by a thorough examination of the head and neck, including cranial nerves. Evidence of cranial nerve involvement, for example, CVII (facial nerve) is concerning for a destructive middle ear pathology, e.g. cholesteatoma

Palpation of the neck may reveal cervical lymphadenopathy, which should raise suspicion of cutaneous, oral or nasopharyngeal malignancy

An effective assessment of hearing thresholds can be made in the consulting room with free field testing, and tuning fork tests to determine the nature of any hearing impairment (sensorineural vs conductive)

Further audiometric testing in the form of pure tone audiometry and tympanometry is available in the community and can be useful in quantifying hearing loss, determining its nature and confirming the presence of effusions or negative middle ear pressure

Nasoendoscopic examination is generally available only in secondary care and enables visualisation of the Eustachian tube orifice and post-nasal space, which may reveal inflammation or an obstructing mass (e.g. nasopharyngeal carcinoma). Computed tomography or magnetic resonance imaging is generally arranged by secondary care practitioners based on clinical findings or abnormal audiometry results (e.g. unilateral sensorineural hearing loss).

Disorder-specific features

We will now focus on some of the more common conditions to present in the community with blocked ears. We will review their presenting signs, symptoms and appropriate management.

Canal foreign bodies

A remarkable range of foreign bodies can be found lodged in external auditory canals of both paediatric and adult patients. Canal foreign bodies can be organic (flies, ants, cockroaches, etc.) or inorganic (beads, toy parts, stones, etc.). The type of foreign body determines the urgency of management, so it is important to take a full history from the patient (or parents).

Organic matter is more likely to result in canal infection and should be removed as soon as possible, whereas inert matter, e.g. beads, gravel, may be safely left for a couple of days ahead of an ear, nose and throat (ENT) Emergency Clinic appointment. Alkaline button batteries require immediate referral for removal, as prolonged contact with the canal can cause rapid ulceration and tissue necrosis (Capo and Lucente, 1986).

Techniques for removal depend on the nature of the foreign body and include irrigation (contraindicated in tympanic membrane perforation) and instrument removal (wax hook, crocodile forceps). Instrumentation should only be attempted under direct vision by a trained practitioner, due to the risk of tympanic membrane perforation or canal laceration. Live insects can cause significant pain and distress to the patient and should be killed before attempted removal, by drowning in olive oil or lignocaine (Davies and Benger, 2000). Drowning in water should be avoided, due to swelling of organic matter by osmosis.

If the foreign body is not easily removed in the primary care setting, referral to an otolaryngologist should be made. Multiple attempts are likely to result in canal lacerations, tympanic membrane perforation and increasing levels of patient distress and non-compliance.

Impacted cerumen

Cerumen, or ear wax, consists of the glandular secretions from modified apocrine sweat glands and sloughed epithelial cells. Cerumen production forms part of the self-cleaning mechanism of the external auditory canal which protects and lubricates the canal. The lateral migration of cerumen is assisted by jaw movement (Roland et al., 2008) and can become disrupted by infection (otitis externa), dermatological conditions (eczema, seborrheic dermatitis), anatomical factors (exostoses, narrow canal) or foreign bodies (cotton buds, hearing aids). Cerumen impaction is defined as the symptomatic accumulation of cerumen, and it affects 6% of the population (Jabor and Amedee, 1997). Symptoms may include deafness, tinnitus, pressure, otalgia, cough or itching.

Treatment is indicated if symptomatic, or in asymptomatic patients to enable visualisation of the tympanic membrane or perform audio-vestibular assessments (Schwartz et al., 2017). Removal may also be indicated in hearing aid users to allow moulds to be taken or prevent whistling. Treatment includes cerumenolytic agents (see Box 2), electronic irrigation, manual removal under direct vision and micro-suction by community services or secondary care. Manual syringing is not recommended (National Institute for Health and Care Excellence (NICE), 2018a).

Box 2.

Ear drops for cerumen impaction.

High-level evidence is sparse as to which topical cerumenolytic agents are the most effective, but the following are generally well tolerated and safe:

• Olive oil drops

• Almond oil drops

• Sodium bicarbonate 5% solution drops

Many branded preparations contain organic solvents that can cause irritation of the external auditory canal and are generally no more effective than these simple remedies.

A universal dosing regimen of two drops twice daily for several days can be adopted. Patients should be advised to allow the drops to warm to room temperature before use and following administration lie with the affected ear upward for at least 10 minutes to ensure adequate delivery. (BNF, 2019)

Future management is focussed on patient education emphasising that cerumen is involved in a normal physiological process and essential for cleaning and protecting the ear. Patients should be advised against over-cleaning or canal instrumentation (cotton buds, hair clips, etc.). Patients should also be advised against using ear candles. Tympanometric measurements in the ear canal have shown that ear candles do not produce the negative pressure that was postulated to assist wax removal. They can, in fact, result in wax deposition. In a survey of 122 otolaryngologists, there were 21 ear injuries identified as resulting from the use of ear candles; their use should therefore be strongly discouraged (Seely et al., 1996).

Otitis externa

Colloquially known as ‘swimmer’s ear’, otitis externa is inflammation of the external auditory canal that can be caused by a range of factors. The condition is common, affecting 10% of the population at least once in their lifetime and typically presents with otalgia, itching and otorrhoea. Due to the accumulation of debris and canal oedema, it can also result in the sensation of blockage and hearing loss.

Risk factors for the development of otitis externa include repeated water exposure, high humidity, canal trauma (cotton buds), prolonged use of topical steroids or topical antibiotics and underlying medical or dermatological conditions such as diabetes, immunosuppression, or eczema.

The majority of acute cases of otitis externa are infective and most commonly bacterial (Rosenfield et al., 2014). Infective causes can be bacterial (Pseudomonas aeruginosa, Staphylococcus aureus), fungal (Candida albicans, Aspergillus niger) and viral (herpes simplex, herpes zoster). Chronic, or resistant treatment cases are often non-infective, and due to an underlying dermatological condition, such as seborrheic dermatitis or eczema.

On examination, the canal is typically erythematous, oedematous and contains varying degrees of debris. In fungal cases (otomycosis) white threadlike hyphae and black spores may be visible. In severe cases, there may be inflammatory polyps, abscesses, granulation tissue or even exposed bone. Attention should also be made to the pinna and face, looking for signs of spreading cellulitis or perichondritis.

Treatment involves topical antibiotic/antifungal agents with or without a topical steroid which has been shown to reduce pain. There is strong evidence that topical therapy is effective in otitis externa, but no clear evidence to support recommending a particular preparation. Rosenfeld et al. (2014) showed higher rates of bacteriological cure with the use of quinolone-based agents. However, the clinical significance of this is unclear, as the presence of bacteria does not necessarily imply active disease.

When deciding on which topical preparation to use several factors should be considered, including patient allergies, previous treatments, tympanic membrane integrity, cost and local prescribing guidelines. In recurrent or resistant cases, an ear swab is useful for directing antimicrobial therapy. The author’s preference is to use acetic acid 2% solution in mild cases for its antimycotic and antibiotic properties, and in moderate-to-severe cases, a quinolone–steroid combination preparation (Cilodex®). Quinolones give a broad spectrum of cover and unlike aminoglycoside-based drops are suitable for use in the presence of tympanic membrane perforation. Table 2 describes several other topical agents appropriate for use in otitis externa.

Table 2.

Topical ear preparations for use in otitis externa.

Type	Example
Astringent/acidic preparations	Acetic acid 2% spray (Earcalm®)
Corticosteroid preparations	Betamethasone sodium phosphate 0.1% drops (Betnesol®, Vista-methasone®)
Antibiotic preparations	Aminoglycoside: Gentamicin 0.3% drops (Genticin®) Non-aminoglycoside: Chloramphenicol 5% drops
Antifungal preparations	Clotrimazole 1% solution (Canesten®)
Combination preparations	Quinolone with corticosteroid: Dexamethasone 0.1%, ciprofloxacin 0.3% (Cilodex®) Aminoglycoside with corticosteroid: • Dexamethasone 0.1%, neomycin sulphate 3250 units/mL, glacial acetic acid 2% (spray: Otomize®) • Dexamethasone 0.05%, framycetin sulphate 0.5%, gramicidin 0.005% (drops: Sofradex®) • Hydrocortisone acetate 1%, gentamicin 0.3% (drops: Gentisone HC®)
Combined corticosteroid and antibiotic/antifungal preparations	Clioquinol with corticosteroid: Flumetasone pivalate 0.02%, clioquinol 1%

Source: NICE (2018b).

Where the canal is too oedematous or occluded by debris to allow for drug delivery, the patient may require referral to an ENT clinic for microsuction or wick insertion. During treatment, patients should be advised to keep their ears dry, avoid trauma to the canal and use earplugs or Vaseline®-coated cotton wool to occlude the canal when showering.

A majority of cases respond to topical treatment within 7–10 days and require no further follow up, however, resistant cases may take months to resolve and require protracted courses of topical therapy or referral to an ENT specialist.

Oral antibiotics have a limited role in uncomplicated otitis externa, but are indicated in systemically unwell patients, those with underlying risk factors (diabetes, immunocompromise) and where there is evidence of pinna or facial cellulitis. Topical therapy is generally superior to oral therapy, as it allows for much higher antimicrobial concentrations to be delivered to the canal (100 to 1000 times higher), which avoids prolonged courses of sub-therapeutic antibiotic and the resultant development of resistant organisms (Rosenfield et al., 2014). Systemic antibiotics should be selected based on local antimicrobial guidelines and should provide cover against common causes of otitis externa such as P.aeruginosa and S.aureus.

Necrotising otitis externa (formally known as malignant otitis externa) is a complication of otitis externa where infection progresses into osteomyelitis of the temporal bone. The condition is more common in diabetic or immunosuppressed patients and should be suspected in cases with severe otalgia, granulation tissue at the bony-cartilaginous junction of the external auditory canal or those with cranial neuropathies.

The condition is potentially life-threatening and can be further complicated by sigmoid sinus thrombosis, meningitis and intracranial abscesses. Suspicion should prompt same-day referral to an ENT clinic for review and consideration of computerised tomography or magnetic resonance imaging and parenteral antibiotics.

Acute otitis media

Acute otitis media (AOM) is a common inflammatory condition of the middle ear of both viral and bacterial aetiology. Patients are typically paediatric and present with otalgia, vomiting, ear tugging, and fever. Older patients may also report hearing loss. Diagnosis is evident at otoscopy with an inflamed bulging tympanic membrane +/- and infected effusion.

In most cases, the condition is self-limiting (3 to 7-day duration) and management is with simple analgesia and antipyretics (paracetamol, ibuprofen). If the patient is systemically unwell, has signs of complications or is at high risk of complications, then immediate antibiotics and referral to hospital may be indicated. Patients with a history of cochlear implant warrant earlier treatment with antibiotics, and discussion with ENT.

Otitis media with effusion (Glue ear)

Otitis media with effusion (OME) is the accumulation of fluid in the middle ear without signs of acute infection. It primarily affects the paediatric population, with 90% of children experiencing an episode before school age (Rosenfeldet al., 2016).

OME may occur due to mucosal inflammation following an episode of AOM, or be due to Eustachian tube dysfunction without AOM. Effusions are generally self-limiting and resolve after 4 to 6 weeks, but in some cases become recurrent and chronic. In persistent cases, paediatric patients may present with hearing loss, delayed language development and behavioural problems.

OME is less common in the adult population, but similarly can occur following an episode of AOM, upper respiratory tract infection, secondary to allergy, or following barotrauma. Adult patients generally present with reduced hearing and a sense of aural fullness. Persistent effusions for over 12 weeks or recurrent unilateral acute otitis media (more than two episodes in 6 months) should be referred to an ENT clinic for further assessment.

If there is no clear precipitant for a unilateral effusion or if there are other signs or symptoms of malignancy (e.g. weight loss, nasal obstruction, epistaxis, cervical lymphadenopathy) the patient should be referred urgently (2-week-wait pathway) to an ENT clinic to exclude a nasopharyngeal tumour. Patients of Southeast Asian origin are at an increased risk of developing this malignancy, as are smokers, patients with previous Epstein–Barr virus infection and a history of exposure to formaldehyde.

Effusions are evident on otoscopy with a straw-coloured, retracted drum and fluid levels visible behind the tympanic membrane. Tympanometry will show reduced tympanic membrane compliance and audiometry will describe a conductive hearing loss.

Following a diagnosis of OME, a period of active observation should follow in combination with advice and support to minimise the impact of the hearing loss. Auto inflation (e.g. Otovent nasal balloon) may be trialled in co-operative patients (NICE, 2008).

In children with persistent, documented OME for over 3 months and a hearing level of 25–30 dBHL or worse, surgical intervention should be considered in the form of grommets. Non-surgical management is in the form of hearing aids.

Eustachian tube dysfunction

Patients typically present with symptoms of pressure or blocked ears and may report popping sounds, crackling, autophony and muffled hearing. A 2015 Consensus statement defined Eustachian tube dysfunction as a problem with the ventilatory function of the Eustachian tube (Schilder et al., 2015) and defined three subtypes (see Table 3):

Dilatory/obstructive dysfunction

Baro-challenge induced dysfunction

Patulous dysfunction

Table 3.

Subtypes of Eustachian tube dysfunction.

Type	Comments
Dilatory/Obstructive	Also termed obstructive dysfunction. Usually due to an upper respiratory tract infective or inflammatory process e.g. allergic rhinitis. May be as a result of acquired anatomical abnormalities e.g. trauma, nasopharyngeal mass.
Baro-challenge induced	Symptoms manifest following a change in ambient pressure e.g. altitude change or scuba-diving
Patulous	Due to an abnormally patent Eustachian tube, whose classic attribution is to weight loss, pregnancy or chronic disease (O’Connor and Shea, 1981) Patient typically complain of voice autophony and aural fullness(Hussein and Adams, 2015)

Otoscopy may be normal or reveal a retracted tympanic membrane or effusion. In patulous dysfunction, the tympanic membrane may be seen to move with breathing; this typically resolves on lying flat which occludes the patent Eustachian tube. If the patient reports hearing loss, the clinician should conduct tuning fork tests to determine if it is conductive and refer on for formal audiometry and tympanometry.

Management is generally directed at identifying and treating the underlying cause. Isolated Eustachian tube dysfunction treatment remains controversial. Trials have been conducted in the use of surfactants, decongestants, steroids, ventilation tubes, laser Eustachian tuboplasty, adenoidectomy and balloon dilation of the Eustachian tube, but there is generally a lack of high-quality evidence and no consensus (Van Heerbeek et al., 2002).

Referral to an ENT clinic is indicated if there is suspicion of nasopharyngeal carcinoma (unilateral effusion with no clear precipitant, systemic features of malignancy) or if symptoms fail to resolve with conservative or medical management after 12 weeks.

Ménière's disease

Its classic diagnosis is as a triad of hearing loss, tinnitus and vertigo, Ménière's disease (endolymphatic hydrops) is a disease of the membranous labyrinthine system of the inner ear.

Early Ménière's disease may present with isolated symptoms of ear blockage without hearing loss or tinnitus. Otoscopy and tympanometry will be unremarkable, and symptoms may be episodic and fluctuating in severity. In contrast to Eustachian tube dysfunction, patients will typically go on to develop a low-frequency sensorineural hearing loss.

A diagnosis of Ménière's disease is made based on the 2015 AAO-HS criteria (Goebel, 2016), as shown in Box 3. Confirmation of the diagnosis requires referral to an ENT consultant (NICE, 2017).

Box 3.

2015 AAO-HS diagnostic criteria for Ménière's disease.

• Two or more spontaneous episodes of vertigo, each lasting between 20 minutes and 12 hours

• Low- to mid-frequency sensorineural hearing loss confirmed on audiometry in affected ear

• Fluctuating aural symptoms (hearing, tinnitus, or fullness)

• Not better accounted for by another vestibular diagnosis

Acute attacks can be managed with anti-emetics or antihistamines, e.g. prochlorperazine, promethazine, and in severe cases may require hospital admission for intravenous fluids (NICE, 2017).

Long term management includes lifestyle modifications such as reducing salt intake, caffeine and alcohol and trials of pharmacotherapy with diuretics or betahistine; although there is insufficient data to confirm the efficacy of either (James and Burton, 2001; Thirwall and Kundu, 2006). Refractory disease is managed in secondary care with systemic steroids, intratympanic steroids or surgical procedures such as grommet insertion, endolymphatic sac decompression, vestibular neurectomy and labyrinthectomy.

Disorders of the temporomandibular joint

Temporomandibular joint (TMJ) disorders may produce symptoms that mimic ear pathology, due to its proximity to the middle ear and its innervation. The auriculotemporal nerve (mandibular division of trigeminal) provides sensation to anterior pinna, canal and lateral tympanic membrane and provides a mechanism for referred otalgia in TMJ disease (Jaber et al., 2008).

Patients may report aural pressure, otalgia, pre-auricular tenderness, tinnitus or hearing clicking or popping sounds. Otoscopic and tympanometry will be normal, and examination of the TMJ will reveal tenderness over the muscles of mastication (masseter, temporalis, medial and lateral pterygoid muscles). Treatment is focussed on patient education, analgesia and jaw rest in the majority of cases but may require referral to oral and maxillofacial surgery if particularly severe or any history of trauma (NICE, 2016).

KEY POINTS

‘Blocked ears’ is a broad and largely non-specific term frequently used by patients and a common presenting complaint in primary care caused by a wide range of usually benign conditions that can most often be managed in primary care

Accurate diagnosis is possible with a detailed history and thorough examination

Alkaline button batteries require immediate referral, as prolonged contact with the canal can cause rapid ulceration and tissue necrosis

Unprovoked unilateral otitis media with effusion in an adult is a red flag sign and should be urgently referred to ENT to exclude a nasopharyngeal tumour

Early Ménière's disease may present with isolated symptoms of ear blockage without hearing loss or tinnitus

In ear pain without otological signs consider TMJ disorders

Footnotes

ORCID iD

Oliver J Wright

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