Abstract
Anosmia, or loss of smell, is a frequently reported symptom following viral upper respiratory tract infections. While many patients recover spontaneously, a proportion develop persistent post-viral olfactory dysfunction, which can significantly affect quality of life, nutrition, safety, and psychological wellbeing. This case describes an adult patient presenting with persistent smell loss following a viral illness, initially reassured as having a selflimiting condition. Ongoing symptoms, including parosmia and reduced enjoyment of food, prompted ENT assessment. The case highlights the importance of recognising post-viral smell loss as a genuine and potentially disabling condition, excluding alternative causes, providing safety advice, and initiating evidence-based supportive management such as olfactory training. Current evidence suggests that treatment options remain limited, but olfactory training is widely recommended as a low-risk intervention, while steroids and other therapies require careful patient selection and counselling.
Introduction
Smell disorders are commonly encountered in ENT practice and may present as complete smell loss, reduced smell, distorted smell perception, or phantom smells. Post-viral olfactory dysfunction is one of the recognised causes of acquired smell loss and has received increased attention since the COVID-19 pandemic. Viral injury may affect the olfactory epithelium, supporting cells, inflammatory pathways, and olfactory sensory neurones, contributing to persistent smell disturbance in some patients.
Although anosmia may appear minor compared with other ENT complaints, its impact can be substantial. Patients may report reduced appetite, weight change, impaired enjoyment of food, anxiety about personal hygiene, reduced ability to detect smoke or gas, and emotional distress. Parosmia, where familiar smells become unpleasant or distorted, may be particularly distressing and can occur during recovery. (Figure 1 on olfactory epithelium)
This case illustrates the assessment and management of persistent post-viral smell loss, with emphasis on excluding red-flag pathology, counselling patients realistically, and supporting recovery through structured smell rehabilitation.
Figure 1
Case Presentation
Clinical History
A 42-year-old patient presented to ENT clinic with a 5-month history of reduced sense of smell following a viral upper respiratory tract infection. The initial illness involved nasal congestion, sore throat, fatigue, and mild fever, which resolved within one week. However, the patient noticed that they could no longer smell coffee, perfume, or food cooking.
Over the following months, there was partial improvement, but the patient developed parosmia. Familiar smells such as onions, toothpaste, and meat became unpleasant and distorted. The patient reported reduced enjoyment of meals, anxiety about detecting smoke at home, and concern that the symptom had not resolved despite recovery from the original infection.
There was no unilateral nasal obstruction, epistaxis, facial swelling, visual disturbance, neurological deficit, head trauma, or previous sinonasal surgery. The patient had no known history of chronic rhinosinusitis or nasal polyposis.
Examination
Anterior rhinoscopy showed mild nasal mucosal congestion but novisible mass, purulence, crusting, or unilateral abnormality. Flexible nasendoscopy demonstrated a patent nasal airway
bilaterally, healthy middle meatus appearances, and no evidence of nasal polyps, tumour, or significant inflammatory disease. Cranial nerve examination was otherwise normal. There was no
cervical lymphadenopathy. The absence of unilateral nasal signs, epistaxis, neurological symptoms, or progressive obstruction supported a likely diagnosis of post-viral olfactory dysfunction.
Investigation findings
Objective smell testing was arranged to document baseline olfactory function and monitor recovery. Testing demonstrated significantly reduced odour identification,
consistent with hyposmia approaching anosmia. Given the clear post-viral onset, normal endoscopic examination, and absence of red-flag symptoms, imaging was not initially required. The patient was advised that CT or MRI may be considered if symptoms became unilateral, were associated with nasal bleeding or obstruction, or if neurological symptoms developed.
Figure 2: — anatomy of the olfactory nerve pathway.
Management
The patient was counselled that recovery after post-viral smell loss can be gradual and unpredictable. They were advised that some patients improve over weeks to months, while others experience longer-term symptoms. The emotional and practical impact of smell loss was acknowledged.
A structured olfactory training programme was recommended (Figure 3 Smell retraining kit). The patient was advised to smell a set of familiar odours twice daily, focusing attention on each
smell for approximately 20 seconds. Common odours used include rose, lemon, clove, and eucalyptus, although household scents may also be used if safe and consistent. Evidence
reviews support olfactory training as a low-risk intervention for post-viral olfactory dysfunction, though outcomes vary between patients.
Figure 3
Safety advice was provided, including checking that smoke alarms were functional, considering gas detectors if relevant, checking food expiry dates carefully, and asking household members to assist with detecting spoiled food or environmental hazards.
Topical nasal steroid treatment was discussed but not started immediately because there was no endoscopic evidence of significant inflammatory sinonasal disease. The patient was
advised that steroids may be considered in selected cases, particularly where rhinitis or chronic rhinosinusitis is present, but current evidence does not support strong universal recommendations for steroids in all cases of post-viral smell loss. A follow-up appointment was arranged after 3 months to reassess symptoms, repeat smell testing if required, and review response to olfactory training.
Discussion
This case highlights several important features of post-viral smell loss. Firstly, anosmia should not be dismissed as a minor symptom. Smell contributes to flavour perception, appetite, environmental safety, emotional memory, and social confidence. Patients with persistent olfactory dysfunction may experience isolation, frustration, anxiety, and reduced quality of life.
Secondly, careful history and examination are essential. A clear viral trigger, bilateral smell disturbance, and normal nasal endoscopy support a post-viral cause. However, clinicians must
remain alert to red flags. Unilateral nasal obstruction, epistaxis, facial pain, orbital symptoms, neurological signs, or visible unilateral nasal pathology should prompt further investigation and imaging, as these may indicate structural, inflammatory, or neoplastic disease.
Thirdly, parosmia should be recognised as part of the post-viral olfactory recovery spectrum. Patients may describe distorted smells as burnt, chemical, rotten, metallic, or sewage-like. This can be more distressing than complete smell loss because it interferes with eating and daily routines. Reassurance that parosmia is a recognised phenomenon can be helpful, but patients also require practical coping strategies.
Management remains challenging because there are limited proven treatments. Olfactory training is commonly recommended because it is safe, inexpensive, and supported by evidence for potential benefit. Steroids, supplements, platelet-rich plasma, and other emerging therapies remain areas of ongoing research, and patients should be counselled carefully about uncertainty of benefit.
The role of the ENT clinician is therefore to confirm the likely diagnosis, exclude concerning pathology, validate the patient’s symptoms, offer realistic expectations, and provide structured rehabilitation and safety advice.
Conclusion
Post-viral smell loss is a common but often under-recognised condition with significant functional and psychological consequences. Persistent anosmia or hyposmia following a viral illness should be assessed carefully, particularly when symptoms do not improve or when associated with red-flag features.
This case demonstrates the importance of ENT assessment, nasal endoscopy, objective smell testing where available, and patient-centred counselling. Olfactory training should be offered as a low-risk supportive intervention, while medical therapies should be considered selectively and discussed in the context of limited evidence.
For clinicians in primary care and ENT practice, the key learning point is that smell loss deserves active assessment and support. Timely recognition, appropriate referral, safety counselling, and structured follow-up can significantly improve patient confidence and quality of care.
