Fig. 9.13 The nose and paranasal sinuses.
182 • The ear, nose and throat
• use of anticoagulants, including warfarin, apixaban or
• use of antiplatelet drugs (aspirin, clopidogrel).
Intranasal cocaine use can cause septal perforation, epistaxis,
A family history of atopy is relevant in rhinitis. In patients with
epistaxis it is important to establish a family history of hereditary
haemorrhagic telangiectasia or inherited bleeding disorders.
Occupation is relevant because exposure to inhaled allergens,
occupational dusts and chemicals may exacerbate rhinitis.
Exposure to hardwood dust is associated with an increased
risk of sinonasal cancers. Atopic patients should be asked
Heavy alcohol intake, leading to liver disease, can affect
coagulation and is relevant for epistaxis. Smoking impedes
mucociliary clearance and can contribute to nasal problems.
• Assess the external appearance of the nose, noting
swelling, bruising, skin changes and deformity.
• Stand above the seated patient to assess any external
• Ask the patient to look straight ahead. Elevate the tip of
their nose using your non-dominant thumb to align the
nostrils with the rest of the nasal cavity.
• Look into each nostril and assess the anterior nasal
septum (Fig. 9.16); note the mucosal covering, visible
vessels in Little’s area, crusting, ulceration and septal
perforation. In trauma, a septal haematoma should be
• Using an otoscope with a large speculum in an adult,
assess the inferior turbinates. Note any hypertrophy and
swelling of the turbinate mucosa.
• You may see large polyps on anterior rhinoscopy. To
distinguish between hypertrophied inferior turbinates and
nasal polyps, you can lightly touch the swelling with a
cotton bud (polyps lack sensation).
• Palpate the nasal bones to assess for bony or
• In trauma, palpate the infraorbital ridges to exclude a step
deformity and also to check infraorbital sensation. Eye
movements should be assessed to rule out restriction of
movement related to ‘orbital blowout’.
• Place a metal spatula under the nostrils and look for
condensation marks to assess airway patency.
• Palpate for cervical lymphadenopathy (p. 32).
• Note that rigid nasendoscopy and tests of olfaction are
confined to specialist clinics.
• quality of pain: for example, throbbing, aching, sharp,
• location of pain: unilateral or bilateral
• duration and frequency of pain
• associated nausea, photophobia or aura (migraine)
• relieving and exacerbating factors.
rhinosinusitis, trigeminal neuralgia (severe, sharp pain in a
trigeminal distribution), tension headache (band-like, tight pain)
and cluster headaches (unilateral nasal discharge, eye watering).
The most common cause of nasal deformity is trauma, resulting
in swelling, bruising and deviation of the nose. The swelling
following trauma will settle over a couple of weeks but residual
deviation may remain if the nasal bones were fractured and
displaced. It is important to establish the impact of the nasal
injury on function (nasal breathing, sense of smell) and cosmetic
Nasal septal destruction or perforation can result in ‘saddle
deformity’ of the nasal bridge. Causes include granulomatosis
with polyangiitis, trauma, cocaine abuse, congenital syphilis and
iatrogenic factors (septal surgery, Fig. 9.14B).
The nose can appear widened in acromegaly or with advanced
nasal polyposis (Fig. 9.14C). Rhinophyma can also result from
chronic acne rosacea of the nasal skin (Fig. 9.15).
• asthma (around one-third of patients with allergic rhinitis
• prior nasal trauma or surgery
• history of bronchial infection (cystic fibrosis or ciliary
disorders may affect the nose and lower airways).
For patients with epistaxis it is important to identify any history
of bleeding diathesis or hypertension.
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