In a presentation for AIRTIME, the ENT physician explored the clinical challenges of patients with upper airway conditions.
We’ve all seen these patients in our practice throughout the year – “Dr, I have sinusitis” , “Doc my nose starts to run and feels blocked every time I go for my early morning run”…
What is going on with these patients?
In a presentation patients with acute intermittent symptoms, Professor Richard Harvey established that the condition of rhinitis has a very different set of clinical characteristics from those of sinusitis.
Rhinitis is a condition of the nasal cavity and/or nasal airways that differs from sinus dysfunction. Features of rhinitis include reactive vascular congestion, glandular hypertrophy and mucosal oedema. The tell-tale signs of a jelly-like secretion in the nasal passages which bring about the patient’s symptoms clearly help support a diagnosis of rhinitis. On the other hand, sinus dysfunction is characterised by mucosal inflammation, mucosal dysfunction, and possible polyp formation. The nasal airways of sinus patients are not as congested compared to patients with rhinitis, but are inflamed and prone to secondary infection due to trapped mucus.
While the clinical characteristics of turbinate oedema and congestion as a result of long-term inhalant allergy are obvious from otolaryngeal images, Professor Harvey further considered clinical situations in patients with more subtle presentations of turbinate hypertrophy. Characteristics of middle turbinate (MT) oedema typically show the head of the middle turbinate taking on a jelly-like appearance, where the turbinate becomes swollen and polypoid like changes can be easily seen with an otoscope. In this situation the paradox for the patient is that while these changes can be present in the nasal passages, the patient invariably remains symptom-free.
A point highlighted by Professor Harvey is the strong predictive diagnostic measure of an underlying inhalant allergy in patients where these morphological and structural turbinate changes are present. In the presence of diffuse oedema there is a 91.7% chance that the patient has an underlying inhalant allergy and in the case of polypoid oedema a predictive value of 88.9%.
Further evidence of the predictive value of swollen middle and inferior turbinate (IT) structures in children was shared by Professor Harvey in the form of an Italian study. The study, conducted in 176 children with a mean age of 7.5±2.9 years, showed that with enlargement of the MT the subjects were 5x more likely to have an inhalant allergy compared to a turbinate with normal appearance. In the case of enlargement of the IT it was 3x more likely. Professor Harvey emphasised that this type of examination, with a simple, easy to use otoscope, should be routinely performed in cases where the index of suspicion of inhalant allergy is high.
How does a patient’s age influence the assessment of a patient with inhalant allergy? This question was addressed by Professor Harvey by showing Australian data, which clearly demonstrated an inverse relationship between the presence of allergic rhinitis (AR) and age i.e. the older the patient, the less common is AR. Similarly, in the case of chronic rhinosinusitis (CRS), the older the patient the more common is a diagnosis of CRS.
So, what are the signals we need to look out for to help detect and diagnose an inhalant allergy? In Professor Harvey’s view, any child visiting an ENT physician is, in itself, a signal of an underlying allergic condition. In another study, shared by Professor Harvey, more than 1000 subjects with MT swelling and inflammation (mean age of 5.8 years) showed a nine-fold increase for inhalant allergy.
An important distinction between AR and rhinitis, which is caused by non-allergic triggers, typically resulting from environmental stimuli, sheds light upon an important mechanism in non-allergic rhinitis (NAR) which involves neurogenic pathways. These differences have implications for treatment and this topic was explored by Professor Harvey in the course of the presentation.
NAR, also referred to as nasal hyperreactivity or nasal hyperresponsiveness (NHR), is triggered by a number of environmental factors such as smoke, perfume, paint fumes and weather changes. It is driven by a neural stimulus which is considered a protective response to environmental triggers. Afferent nerves pick up the sensory input from environmental changes such as smoke, while the symptoms of rhinorrhoea and congestion are a result of efferent nerve outputs. Hence, compared to simple AR, nasal hyperreactivity occurs through a very different pathway that is not IgE-mediated inflammation of the nose.
Professor Harvey said in reality, patients rarely fall into the discrete categories of AR or nasal hyperreactivity – there was a grey area in which untreated AR patients would also have a degree of nasal hyperreactivity.
A number of distinguishing clinical features help with the differential diagnosis of NAR, such as:
- Symptoms present later in life
- Absence of asthma, conjunctival or skin symptoms
- No seasonality or cat/animal induced symptoms
- No family history of allergies
- Symptoms are triggered by perfume or flagrances
In the current COVID-19 environment, and given that Australia is amid cold and flu season, the question of the role of viral infections and the impact on rhinitis becomes an important consideration. Professor Harvey reinforced the point that as in lower airway disease, viral infections in the upper airways creates an inflammatory response. In this situation, the rhinitis condition is exacerbated by the viral infection. As such, patients feel a lot worse and this has been characterised as “pouring petrol on the fire”. These infections are very rarely bacterial – 96% of RTIs in children are viral in origin. Professor Harvey said bacterial rhinosinusitis was almost always unilateral disease, yet patients with bilateral congestion continued to be prescribed antibiotics.
Professor Harvey touched upon the issue of smell loss in patients with influenza-like symptoms who were COVID-19 positive and the associated chemosensory dysfunction. In COVID-19 positive patients the loss of smell/taste was nearly 11 x greater compared with COVID-19 negative patients.
Professor Harvey said many patients sought advice from physicians regarding what might appear to be sinusitis, but often wasn’t. Otoscope examination can clearly show jelly-like oedema around the MT, the classic marker of inhalant allergy. In this situation radiologic examination shows that the sinuses are normal. So, what is going on in these patients?
Central compartment atopic disease or exuberant inhalant allergy has been recognised and commonly referred to as a “Black Halo” sign, which appears in radiologic images as central compartment thickening but where the sinuses appear normal. This condition has now been included in the recent EPOS 2020 guidelines as a very specific inhalant-driven phenotype.
As for treatment approaches to rhinitis, Professor Harvey cited the ASCIA guidelines noting the role of combination treatments as early as possible, adopting a step-up/step-down approach to calibrate dosing and frequency of administration. Professor Harvey also named a number of other therapeutic options including:
- Capsaicin for pain and sneezing
- Ipatropium and Botox for rhinorrhoea
- UV light therapy
- Cromoglycate
- Leukotriene antagonists
- Oral immunotherapy
Professor Harvey demonstrated the significant burden of disease that AR places upon patients and encouraged healthcare practitioners to look beyond the obvious causes and triggers of AR. Differentiating between AR and NAR has important ramifications for treatment selection and patient outcomes. While patients with AR are a common sight in primary care practices throughout the year, a diligent approach to look beyond the obvious symptoms is not to be sneezed at!
Professor Richard Harvey is a rhinologist (nose and sinus specialist) at Macquarie University and St Vincent’s Hospitals in Sydney. He is the program head of Rhinology & Skull Base Surgery at the Applied Medical Research Centre at the University of NSW and is a professor at both UNSW and Macquarie University. After several years of post-training fellowships, including formal fellowships in the US and UK, Professor Harvey practises in Sydney, one of only a few dedicated rhinologists in the country.
