Approach to Hearing Loss
In this episode, kicking off a new series on otological and vestibular presentations, we walk through a clinical approach to hearing loss, covering the pathophysiology of sensorineural and conductive loss, a focused history and physical exam, key bedside tests, and a practical workup with imaging, labs, and audiometry, all built around a framework that can be carried into clinic.
Show Notes
Welcome to another episode of the Oto Approach, a podcast made by trainees for trainees to help you excel in ENT. My name is Kyrollos and I am a third year medical student. This episode is the first episode of a new series we’re starting on otological and vestibular presentations.
In this episode we’re gonna discuss an approach to hearing loss. Let’s imagine a patient presenting to your clinic complaining of only being able to hear every third word at a dinner party last night. They explain how disconnected they felt with the crowd as they had to continuously lean in, ask people to repeat themselves, and had to smile or nod to make conversation.
Hearing loss, as defined by the World Health Organization, is being unable to hear as well as someone with normal hearing or hearing thresholds of 20 dB or better in both ears (1). Hearing loss is one of the most common sensory impairments and has risen in incidence worldwide, which makes it an important presentation to be familiar with in otolaryngological and general practice (2).
Hearing loss can be grouped into two types - conductive hearing loss and sensorineural hearing loss. Sensorineural hearing loss is caused by damage that could be to the hair cells of the inner ear, the vestibulocochlear nerve, or processing centres in the brain such as the medial geniculate nucleus of the thalamus or the inferior colliculus (3).
So when we talk about what actually goes wrong in sensorineural hearing loss, there are five broad categories worth walking through.
The first is straightforward structural damage to the cochlea itself such as trauma to the inner ear, or congenital conditions where the architecture of the cochlea doesn’t develop normally. The second involves metabolism. The cochlea is exquisitely dependent on ion transport, essentially, the precise movement of charged particles to maintain the right chemical environment in the endolymph. When genetic mutations or acquired diseases disrupt that balance, hearing is affected. Third is vascular. The cochlea, and especially the stria vascularis which is the structure responsible for maintaining that ion-rich endolymph, relies on a very sensitive blood supply. Anything that compromises that supply, whether it's noise exposure, ototoxic medications, or a systemic vascular event, can knock out cochlear function. Fourth is a more mechanical one. In conditions like diabetes or autoimmune disease, changes in the cochlea can effectively crowd the basilar membrane, limiting the motility of the outer hair cells and the transduction capacity of the inner hair cells. And fifth is noise trauma specifically, which deserves its own mention. When the ear is exposed to intense sound, the vibrational interaction between the tectorial membrane and the basilar membrane becomes exaggerated, and that shearing force physically damages the stereocilia on the outer hair cells which reduces the stiffness and responsiveness of the whole organ of Corti. A similar end result happens with aminoglycoside antibiotics like gentamicin, which block potassium channels, prevent the hair cells from depolarizing, and can permanently disrupt the hair cell bundle (3).
When we think of conductive hearing loss, we can differentiate it from sensorineural hearing loss pretty easily. While sensorineural hearing loss results from inner ear pathology as we discussed, conductive hearing loss occurs as a result of the inability to CONDUCT sound waves from the outer ear into the inner ear.
So conductive hearing loss can arise anywhere along the sound delivery pathway, from the outer ear all the way into the footplate of the stapes. Let's work from the outside in.
Starting at the outer ear, you can get conductive loss from congenital abnormalities like aural atresia, where the external ear fails to form properly due to maldevelopment of the first and second branchial arches. But far more commonly, it's something much simpler, usually just a buildup of wax, debris, or a foreign body blocking the ear canal. The other big or common cause are tympanic membrane perforations, which could be caused by using a cotton swab too aggressively, by barotrauma from deep-water diving, or as a complication of otitis media (4).
In the middle ear, the two big ones are acute otitis media and otitis media with effusion. Otitis media with effusion is actually the most common cause of acquired hearing loss in children. The good news is that it's usually transient and often resolves on its own. The concern, though, is when it persists because even a moderate degree of hearing loss during critical developmental years can have real consequences for speech and language (5). To prevent this, tympanostomy tubes can be inserted which help with prevention of recurrent ear infections and the downstream consequence of speech and language delay. The criteria for tube insertion for children includes persistent otitis media with effusion for 3 months with documented hearing loss, >3 documented ear infections over 6 months or greater than 4 infections within the past year with at least 1 of the episodes being in the past 6 months or children at risk for developmental delay, including those with autism spectrum disorders, craniofacial syndromes or down syndrome.
Interestingly, for adults, a non resolving middle ear effusion should raise suspicion for a nasopharyngeal tumor until proven otherwise. Another serious middle ear cause is cholesteatoma, a benign lesion where squamous epithelium aggregates within the auditory canal causing local erosion of surrounding bony surfaces. Surgical removal is the treatment, and the primary goal there is getting a safe, dry ear and restoring hearing is actually the secondary objective.
Finally, the ossicles themselves can be the culprit to hearing loss. Head trauma can disrupt the ossicular chain entirely. Or you can have a disease process like otosclerosis, where spongy bone from the otic capsule is gradually replaced by dense sclerotic bone. This predominantly affects the anterior oval window, leading to fixation of the stapes. Otosclerosis is twice as common in women, tends to present in early adulthood, and produces a slowly progressive conductive hearing loss which makes it one of those diagnoses that can go unrecognized for years (4).
So, how do we approach a patient presenting with hearing loss? As always, a history and physical. You want to characterize the hearing loss itself first. When did it start, how long has it been going on, is it constant or does it fluctuate,was the onset sudden or gradual, is it getting worse, and is it unilateral or bilateral? What are the functional impairments that have occurred?
Is it more of a high-tone loss such as trouble hearing consonants and speech clarity or a low-tone loss in which sounds are more muffled? And critically, how much is it affecting speech intelligibility? Then you want to build out the context. Has there been a recent infection, fever, or upper respiratory illness? Any loud noise exposure? Any recent trauma? And that includes things people don't always think of as trauma, like barotrauma from diving, straining, weightlifting, or a head injury.You also want to ask about previous ear surgeries or infections, and go through medications carefully. There's a fairly long list of ototoxic drugs that can quietly damage hearing, including certain aminoglycosides, loop diuretics, and platinum-based chemotherapy agents. On the systemic side, autoimmune disease, hypertension, diabetes, vascular disorders, TMJ disease, stroke, and even depression all have documented associations with hearing loss and should be on your radar. And don't forget family history as genetic hearing loss is more common than most people realize. Finally, ask about associated symptoms. Aural fullness, vertigo, tinnitus, otalgia, otorrhea, autophony, hyperacusis , unexplained weight loss. A useful mnemonic for building your differential is KITTENS - which stands for Kongenital, Infectious, Traumatic, Toxic, Endocrine and metabolic, Neoplastic, and Systemic and vascular. Running through that framework stops you from missing categories.
On exam, start with otoscopy. You're looking at the ear canal for cerumen impaction, stenosis, or any lesions, and then at the tympanic membrane: its color, thickness, whether there's fluid behind it, any perforations, retractions, or scarring. While you're there, you can do a Valsalva test to check eustachian tube patency by asking the patient to perform a Valsalva and watch the drum for movement.
Pneumatic otoscopy lets you actively test tympanic membrane mobility by applying positive and negative pressure. You can also use this to test for a perilymph fistula or superior semicircular canal dehiscence. If applying positive pressure triggers nystagmus that reverses with negative pressure, that's Hennebert's sign, and it's a meaningful finding.
On external inspection, you're looking for malformations, auricular pits, scars, swelling, and checking for mastoid and tragal tenderness. Round this out with a complete head and neck exam looking for cervical lymphadenopathy, a full neurological and vestibular assessment, and listening for bruits.
You can also do two bedside tests that cost nothing and tell you a lot. Let me give you a hint - both are done at 512 Hz. If you’re thinking of the Rhinne and Weber test, you’re absolutely right!
The Rinne test compares air conduction to bone conduction. You strike the fork, hold it near the ear canal, then move it to the mastoid. In a normal ear or in most sensorineural hearing loss, air conduction is better, that's a positive Rinne. If bone conduction is louder, the Rinne is negative, meaning the fork "flips," which suggests a conductive hearing loss of at least 15 to 30 dB, or occasionally a severe-to-profound SNHL with crossover to the other cochlea.
The Weber test is even simpler. Strike the tuning fork and place it on the center of the forehead or the vertex. Normally it should be heard equally in both ears. If it lateralizes, that's informative. In a unilateral conductive loss, the sound goes toward the affected ear; in a unilateral sensorineural loss, it goes toward the better ear. A handy mnemonic: "We Create Best Students": Weber lateralizes to the Worse ear in Conductive loss, and to the Better ear in Sensorineural loss.
When investigating hearing loss, audiometry is the cornerstone as it formally characterizes the type, degree, and configuration of the hearing loss and separates conductive from sensorineural from mixed. More on this later!
For imaging, a CT of the temporal bone without contrast is your go-to for structural questions — complications of ear infections, cholesteatoma, mastoiditis, temporal bone fractures, congenital malformations, or aberrant anatomy. If you're worried about a cerebellopontine angle lesion like a vestibular schwannoma or meningioma or demyelinating disease like MS, then you want an MRI of the brain and brainstem with and without gadolinium. Thin-slice heavily T2-weighted sequences can also pick up labyrinthine malformations and cochlear nerve abnormalities.
Labs are ordered selectively based on clinical suspicion. For example, for infectious etiologies, such as lyme disease or syphilis, treponemal studies can be ordered.
Management naturally splits along the SNHL versus CHL divide. For sensorineural hearing loss, hearing aids are the standard treatment for mild to moderately severe loss. Once you get into the moderately severe to profound range, cochlear implantation becomes the conversation. For single-sided deafness specifically, options include a Contralateral Routing Of Signal (CROS) hearing aid, a bone conduction device, or cochlear implantation.
For conductive hearing loss, management varies widely depending on what's causing it, from something as simple as clearing a wax plug to surgical repair of the ossicular chain or tympanic membrane.
And on the horizon are biologic therapies. As our understanding of the molecular basis of hearing loss has grown, so has translational research. Free radical scavengers, growth factors, apoptosis inhibitors, monoclonal antibodies, gene therapy, and cell-based therapies are all active areas of investigation, with several currently in clinical trials. It's not standard practice yet, but it's where the field is heading.
So that brings us to the end of our approach to hearing loss. We covered a lot of ground today. From the pathophysiology of sensorineural and conductive hearing loss, to taking a focused history, working through the exam, and building out a workup with imaging, labs, and audiometry. Hopefully next time a patient describes that dinner party moment, you'll have a clear framework for working through it.
Now, you'll remember we called audiometry the cornerstone of investigating hearing loss. So in our next episode, we'll pick up right there and walk through how to actually read an audiogram: what those lines and symbols are telling you, how to separate conductive from sensorineural from mixed, and the classic patterns you'll want to recognize on sight.
As always, all the references for this episode are listed in the show notes, so if you want to go deeper on any of the topics we covered today, everything is linked there.
This is the first episode of our new otology and vestibular series, so if you enjoyed it, stay tuned, we have a lot more coming. I also wanted to thank Dr. Rashi Ramchandani for her support on this episode. If you found this helpful, please share it with a fellow student, leave us a review, and let us know what topics you'd like us to cover next. Thanks for listening to the Oto Approach. Until next time!
References
1. Deafness and hearing loss [Internet]. [cited 2026 May 6]. Available from: https://www.who.int/news-room/fact-sheets/detail/deafness-and-hearing-loss
3. Tanna RJ, Lin JW, De Jesus O. Sensorineural Hearing Loss. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2026 [cited 2026 May 11]. Available from: http://www.ncbi.nlm.nih.gov/books/NBK565860/ PubMed PMID: 33351419.
4. Sooriyamoorthy T, De Jesus O. Conductive Hearing Loss. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2026 [cited 2026 May 11]. Available from: http://www.ncbi.nlm.nih.gov/books/NBK563267/ PubMed PMID: 33085414.
