2General and Otoscopic Examination

FThe general survey: clues outside the ear

A brief general examination frames the otologic one. Blood pressure, carotid palpation and a glance at the skin and craniofacial structures can each redirect the work-up: uncontrolled hypertension can intensify pulse-synchronous tinnitus, and neurocutaneous stigmata such as café-au-lait macules raise the possibility of neurofibromatosis with bilateral vestibular schwannomas [2013].

Craniofacial asymmetry, surgical scars or jaw misalignment hint at temporomandibular or somatosensory contributors that will be tested later. None of this is time-consuming, and it ensures that the ear is examined in the context of the whole patient rather than in isolation [2014].

FOtoscopy of the external canal

Otoscopy is the highest-yield single act in the bedside assessment because the commonest reversible causes live in the canal. Impacted cerumen and foreign bodies create a conductive barrier and often a low-pitched tinnitus that resolves the moment the obstruction is cleared, a result especially common in older patients and hearing-aid users [2014].

Otitis externa, with its oedematous, tender canal, can likewise be accompanied by tinnitus through altered conduction and local inflammation. The lesson of the canal is optimistic: a careful look, and where appropriate a simple removal, can abolish the symptom before any further test is contemplated.

TThe tympanic membrane and middle ear

The tympanic membrane is read like a window onto the middle ear. Central or marginal perforations and chronic suppurative changes signal conductive loss; retraction pockets and atelectasis betray eustachian-tube dysfunction; and air-fluid levels or bubbles indicate an effusion (otitis media with effusion) [2014]. Each of these is associated with a conductive hearing loss that is itself a common correlate of tinnitus, and many respond to medical or surgical treatment.

Pneumatic otoscopy adds the dimension of mobility: a drum that fails to move suggests effusion or ossicular fixation, refining the bedside impression before tympanometry confirms it. Reduced mobility with an intact drum and a conductive pattern points toward the middle ear rather than the canal [2013].

TOtosclerosis and the Schwartz sign

Otosclerosis classically produces a low-frequency conductive loss with a roaring or humming tinnitus from stapes-footplate fixation. The bedside clue is the Schwartz (or Schwartze) sign—a faint reddish-pink hue over the promontory seen through the drum, reflecting the increased vascularity of an active otospongiotic focus [2013].

It is an inconstant but useful sign that, when present, predicts the audiometric picture confirmed later: a low-frequency conductive notch and the characteristic Carhart notch at 2 kHz on bone conduction. Recognising it at the bedside lets the clinician anticipate a treatable, surgically correctable cause of tinnitus [2014].

CThe pulsatile red mass behind the drum

In a patient with pulsatile tinnitus, otoscopy becomes a search for a retrotympanic vascular lesion. A glomus tympanicum paraganglioma appears as a red pulsatile mass, typically in the anteroinferior quadrant, that may blanch on pneumatic pressure (the ‘rising-sun’ appearance and Brown sign) [2024]. An aberrant internal carotid artery or a high-riding, dehiscent jugular bulb can produce a similar retrotympanic colour through a thin drum.

The critical rule is restraint: a retrotympanic vascular mass must never be probed, biopsied or suctioned, because catastrophic bleeding can follow. Recognition mandates contrast-enhanced cross-sectional imaging and referral, not instrumentation [2008].