Hyposmia

Reduced but not absent sense of smell. It is far more common than complete anosmia, affecting around 15 to 20 percent of adults and more than half of those over 65, and it is substantially underrecognised because patients adapt gradually and rarely present with it as a complaint.

Relationship to anosmia

Hyposmia and anosmia share the same causes and differ in degree. The practical distinctions are that hyposmia is more likely to be conductive and reversible, more likely to be detected only on objective testing, more likely to represent early or partial disease, and more likely to represent either the early stage of a progressive process or the recovering stage of an acute one.

Quantification

Objective testing grades severity, typically as normosmia, mild hyposmia, moderate hyposmia, severe hyposmia and anosmia, using threshold, discrimination and identification scores. Testing all three components is more informative than identification alone, since threshold reflects peripheral function and discrimination and identification reflect central processing, and the pattern helps localise the lesion.

Causes worth emphasising in the hyposmic patient

Chronic rhinosinusitis, with or without polyps, which is the commonest treatable cause and in which the fluctuating nature of the loss is a useful clue.
Allergic rhinitis, in which smell fluctuates with obstruction and season.
Post viral, particularly in the recovery phase of a previously complete loss.
Presbyosmia, which is progressive, bilateral and symmetrical, and which contributes to poor nutrition and reduced quality of life in the elderly.
Smoking, which causes a dose dependent reduction that partially recovers over years after cessation.
Neurodegenerative disease in its prodromal phase. Hyposmia is present in around 90 percent of patients with Parkinson disease and precedes motor symptoms by up to a decade. It is one of the strongest premotor markers.
Diabetes, chronic kidney disease, hypothyroidism and nutritional deficiency.
Medications, particularly in polypharmacy in the elderly.
Obstructive causes: septal deviation, turbinate hypertrophy, adenoid hypertrophy in children, and tumour.

Reduced intensity of smells rather than absence, often described as smells being faint or requiring effort.
Reduced flavour perception, with food described as bland.
Increased use of salt, sugar and strong seasoning, which has consequences for blood pressure and glycaemic control in patients with cardiovascular disease and diabetes.
Reduced appetite and unintended weight loss in the elderly, contributing to frailty and sarcopenia.
Difficulty detecting smoke, gas and spoiled food, though the risk is less absolute than in anosmia.
Fluctuation with nasal obstruction, allergen exposure, season and upper respiratory infection, which strongly indicates a conductive cause.
Frequently identified incidentally on testing rather than reported, particularly in older adults who attribute it to ageing and do not mention it.

Examination

Nasal endoscopy with specific attention to the olfactory cleft, which is where the relevant obstruction sits and which cannot be assessed with a speculum.
Assess for polyps, mucosal oedema, discharge, septal deviation, turbinate hypertrophy and masses.
Cranial nerve and neurological examination, including a screen for parkinsonian features: bradykinesia, rigidity, rest tremor, reduced arm swing and hypomimia. Given the strength of the association, a patient over 50 with unexplained progressive hyposmia deserves a deliberate look for these.
Cognitive screening where memory complaints coexist.
Nutritional assessment and weight in the elderly.

Objective psychophysical testing is essential, because self reported smell function correlates poorly with measured function and because grading severity guides both prognosis and management. Sniffin Sticks with threshold, discrimination and identification scoring, or the University of Pennsylvania Smell Identification Test, are the usual instruments.
Test each nostril separately.
Nasal endoscopy in every patient.
Computed tomography of the sinuses to assess the olfactory cleft and sinus disease, particularly where a conductive cause is suspected. Opacification of the olfactory cleft correlates with olfactory loss and predicts response to treatment.
Magnetic resonance imaging where the loss is unilateral, progressive without sinonasal disease, associated with neurological signs, or following trauma.
Blood tests: glucose and HbA1c, thyroid function, full blood count, vitamin B12, zinc, renal and liver function.
Medication review, which frequently identifies a contributory agent that can be substituted.
Neurology referral where parkinsonian or cognitive features are found, since olfactory testing contributes to early diagnosis.
A trial of oral corticosteroid, which distinguishes a conductive inflammatory component from a sensorineural loss and predicts the response to topical therapy and to surgery.

The higher proportion of reversible causes makes hyposmia more rewarding to treat than complete anosmia, and this justifies a systematic search for a conductive component in every patient.

Treat conductive and inflammatory causes

Chronic rhinosinusitis with polyps: high dose intranasal corticosteroid, corticosteroid delivered by irrigation or in the head down forward position, a course of oral prednisolone 0.5 mg/kg for 5 to 10 days, escalation to endoscopic sinus surgery, and biologic therapy in severe type 2 disease. Dupilumab in particular produces substantial and sustained smell recovery.
Chronic rhinosinusitis without polyps: topical steroid, high volume saline irrigation, macrolide therapy where appropriate, and surgery for failure.
Allergic rhinitis: continuous intranasal corticosteroid, antihistamine, allergen avoidance and immunotherapy.
Anatomical obstruction of the olfactory cleft: septoplasty or turbinate reduction, with honest counselling that smell improvement is variable.
Steroid delivery technique matters. Standard sprays deposit almost nothing in the olfactory cleft. Use drops in the Mygind or Kaiteki position, or high volume irrigation, where smell is the target symptom.

Olfactory training

Indicated for post viral, post traumatic and idiopathic hyposmia, and as an adjunct after treatment of a conductive cause where recovery is incomplete.
The same protocol as for anosmia: four odorants, twice daily, 20 to 30 seconds each, for at least 12 weeks and preferably 6 to 12 months, with the odorant set changed every 12 weeks.
Outcomes are better in hyposmia than in anosmia, since more residual function remains to build on.

Address modifiable contributors

Smoking cessation, with counselling that recovery is gradual over years and is proportional to the duration of abstinence.
Optimise glycaemic control, treat hypothyroidism, and correct vitamin B12 and zinc deficiency where present. Do not give zinc without documented deficiency, and never intranasally.
Review and substitute medications where feasible.
Remove occupational toxin exposure.

Management in the elderly

Address the nutritional consequences directly. Refer to a dietitian where there is weight loss.
Enhance food using texture, temperature, colour, umami rich ingredients and trigeminal stimulants such as chilli, pepper and mint, which remain perceptible.
Discourage excessive salt and sugar addition, and offer alternative flavour strategies, since this is a real cardiovascular and metabolic risk in this group.
Safety measures: smoke alarms, gas detectors, date labelling of food, and consideration of induction or electric cooking.
Screen for depression and social isolation.

Follow up

Repeat objective testing at 6 and 12 months, and after any intervention, to document change objectively.
Progressive unexplained decline in an older adult warrants neurological review, since it may be the earliest manifestation of neurodegenerative disease.
Recovery of smell after treatment of sinus disease is often reported by patients as the single most valued outcome, which is a reason to measure and pursue it rather than treating it as a secondary endpoint.

Clinical toolsCalculators

BMI GCS EDD Parkland Formula

Corrected Sodium Corrected Calcium Anion Gap Creatinine Clearance Insulin Calculations qSOFA Wells PE Wells DVT CHA₂DS₂-VASc HAS-BLED CURB-65 Centor/McIsaac

Perilymphatic Fistula

An abnormal communication between the perilymphatic space of the inner ear and the middle ear, allowing perilymph leakage and transmission of pressure changes into the labyrinth. It remains a contested diagnosis because there is no reliable non invasive confirmatory test, and both overdiagnosis and underdiagnosis occur.

Sites of leak

Round window membrane, which is a three layered membrane approximately 70 micrometres thick and the commonest site.
Oval window at the annular ligament, particularly after stapes surgery.
Microfissures, including the fissula ante fenestram.
Bony defects from cholesteatoma erosion, temporal bone fracture, or congenital malformation, especially incomplete partition type III and enlarged vestibular aqueduct where a cerebrospinal fluid gusher may occur.
Surgical defects after stapedotomy or cochlear implantation.

Mechanisms of rupture

Explosive: raised cerebrospinal fluid pressure from straining, coughing, sneezing, lifting or a forceful Valsalva transmitted through the cochlear aqueduct and the internal auditory canal to the perilymphatic space, rupturing the membrane outward into the middle ear.
Implosive: raised middle ear pressure from barotrauma or Valsalva against a blocked Eustachian tube pushing the round window membrane inward.

Causes

Barotrauma from diving, flying and forceful Valsalva.
Head trauma and temporal bone fracture.
Penetrating middle ear injury, including cotton bud injury with stapes subluxation.
Acoustic trauma from blast.
Stapes surgery and other middle ear procedures.
Cholesteatoma with labyrinthine fistula.
Congenital inner ear malformation, presenting with recurrent meningitis or fluctuating hearing loss in a child.
Spontaneous, which is the most disputed category.

Sudden sensorineural hearing loss, or fluctuating and progressive hearing loss, temporally related to a straining, barotrauma or traumatic event.
Vertigo and disequilibrium, which may be episodic, positional or constant.
Tinnitus and aural fullness.
A popping sensation in the ear at the moment of the precipitating event, reported by a proportion of patients.
Symptoms provoked by straining, coughing, sneezing, nose blowing, lifting, and by loud sounds.
Postural aggravation, with symptoms often worse when lying on the affected side or with head position change.

The essential historical feature is the temporal relationship between a pressure event and the onset of audiovestibular symptoms. Without it, the diagnosis becomes very difficult to sustain.

Examination

Otoscopy is usually normal unless there is a traumatic perforation or middle ear pathology.
Fistula test: pressure applied to the external canal with a pneumatic otoscope or tragal compression produces vertigo and nystagmus. It has poor sensitivity, around 50 percent at best, and a negative test does not exclude a fistula.
Hennebert sign, that is nystagmus induced by pressure, and Tullio phenomenon, that is vertigo and eye movement induced by loud sound, may be present but are also features of superior semicircular canal dehiscence, which must be excluded.
Head impulse test, nystagmus assessment and test of skew.
Full neurological examination.

There is no reliable non invasive test, and the diagnosis is ultimately made at exploratory tympanotomy in equivocal cases.

Pure tone audiometry with masked bone conduction, repeated serially, which is the most important test. Progressive or fluctuating sensorineural loss supports the diagnosis and drives the decision to explore.
Tympanometry and acoustic reflexes.
Electronystagmography or videonystagmography with a fistula test using controlled pressure application.
Vestibular evoked myogenic potentials, principally to exclude superior canal dehiscence, where thresholds are lowered and amplitudes raised.
High resolution computed tomography of the temporal bone, seeking pneumolabyrinth, which is air within the vestibule or cochlea and is pathognomonic; a bony defect; middle ear fluid; and inner ear malformation. Reformats in the plane of the superior semicircular canal to exclude dehiscence.
Magnetic resonance imaging with high resolution T2 sequences to assess labyrinthine fluid signal and to exclude other causes.
Beta 2 transferrin and beta trace protein assay on middle ear fluid, which if positive confirms perilymph or cerebrospinal fluid. Sampling is technically difficult and false negatives are frequent because the volume obtained is tiny, but a positive result is highly specific. Cochlin tomoprotein assay is more specific for perilymph but is not widely available.
Exploratory tympanotomy remains the definitive diagnostic procedure. Intraoperative identification of a leak is itself unreliable, since local anaesthetic, blood and saline can be mistaken for perilymph, and the absence of a visible leak does not exclude an intermittent one.

Differential diagnosis and the discriminating feature

Superior semicircular canal dehiscence: autophony, air bone gap with present acoustic reflexes, lowered vestibular evoked myogenic potential thresholds, and a visible dehiscence on reformatted computed tomography. This is the most important condition to exclude, since the symptoms overlap almost completely and the treatment differs entirely.
Ménière disease: episodic vertigo of characteristic duration with fluctuating low frequency loss and no precipitating pressure event.
Sudden idiopathic sensorineural hearing loss: no precipitating event and no pressure sensitivity.
Labyrinthine concussion after head trauma, without a fistula.
Inner ear decompression sickness in a diver, distinguished by the dive profile and timing.
Enlarged vestibular aqueduct, which produces fluctuating loss after minor head trauma and is seen on imaging.

Conservative management, which is the first line in most cases

Strict bed rest with the head elevated 30 to 45 degrees for 5 to 10 days.
Absolute avoidance of straining: stool softeners such as lactulose 15 mL twice daily or a macrogol preparation, avoidance of heavy lifting, no nose blowing, no Valsalva, and instruction to sneeze with the mouth open.
Avoidance of coughing where possible, with antitussives if needed.
No flying, diving or exertion.
Corticosteroids are frequently given, using prednisolone 1 mg/kg orally daily to a maximum of 60 to 80 mg for 7 to 14 days with a taper, on the same basis as for sudden sensorineural hearing loss, though evidence specific to fistula is limited.
Serial audiometry, at least twice weekly initially, since the trajectory of hearing determines whether to explore.
Many fistulae seal spontaneously within 1 to 2 weeks with these measures.

Indications for exploratory tympanotomy

Progressive sensorineural hearing loss despite 5 to 10 days of strict conservative management.
Persistent or disabling vertigo.
Pneumolabyrinth on imaging, which is a definite fistula.
Known penetrating middle ear trauma with stapes subluxation.
Post stapedectomy patients with vertigo and hearing deterioration, where a fistula or an overlong prosthesis is likely and where early exploration is indicated.
Recurrent meningitis in a child with an inner ear malformation, where the leak is a route for infection.
Deteriorating hearing in an only hearing ear, where the threshold for exploration is lower.

Operative approach

Transcanal tympanotomy under local or general anaesthesia, elevating a tympanomeatal flap.
Careful inspection of the round and oval window niches under high magnification after removing mucosa and any obscuring tissue. Use a Valsalva or jugular compression manoeuvre with the head down to provoke a visible leak.
Seal both round and oval windows regardless of whether a leak is identified, using autologous soft tissue: perichondrium, temporalis fascia, fat or areolar tissue, placed after abrading the mucosal surfaces to promote adhesion.
In post stapedectomy cases, assess the prosthesis length and position and replace it if it is too long or displaced.
Endoscopic approaches offer superior visualisation of the round window niche.
Where there is a bony defect from trauma or malformation, a formal repair with fascia, cartilage and bone pate is required, and in a cerebrospinal fluid leak with recurrent meningitis, obliteration of the middle ear with blind sac closure of the canal may be necessary.

Postoperative care

Continue head elevation, avoidance of straining and stool softeners for 1 to 2 weeks.
No flying, diving or heavy exertion for at least 6 weeks.
Serial audiometry at 2 weeks, 6 weeks and 3 months.
Vestibular rehabilitation once the acute phase has passed.

Outcomes and counselling

Vertigo improves in the majority after repair, in the region of 70 to 90 percent.
Hearing recovery is far less predictable and often does not occur, particularly where the loss has been present for weeks. Counsel patients that the primary aim of surgery is to stop further deterioration and to control vertigo rather than to restore hearing.
Recurrence occurs and re exploration is sometimes needed.
Permanent avoidance of diving is advised after a confirmed fistula.
Where hearing is not recovered, proceed to hearing rehabilitation with an aid, a contralateral routing device or cochlear implantation as appropriate.

Hyposmia

Overview

Clinical Features

Diagnosis

Management

Overview

Clinical Features

Diagnosis

Management