Revise Notes Ent Flashcards by Sanjana Sathyan

Acute Otitis Media
Acute Otitis Media

Pathophysiology

Inflammation of the middle ear, of infectious aetiology

AOM most commonly affects young children (3-36 months peak incidence)

Causes
Bacterial - haemophilus, strep. pneumoniae, moraxella
Viral - RSV, adenovirus

Clinical features

Symptoms

Acute onset of unilateral ear pain
In children this may be suggested by ear tugging, rubbing or general symptoms such as irritability, poor feeding, crying

Examination Findings

Otoscopy: The tympanic membrane appears…
Erythematous, inflamed
Bulging

May have an air-fluid level (if effusion is present)
If there is perforation, there may be discharge in the canal

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AOM

Management

NICE advises admitting the following patients:

Severe systemic infection
Suspected complications of AOM (e.g. meningitis/mastoiditis)
Children < 3/12 with fever (T>38)

Consider admitting:
Any patient < 3/12 age
3-6 months with fever of 39 degrees or higher

Antibiotics

Most patients with AOM do not need antibiotics. There is no significant benefit in duration of illness/symptom severity.

Patients who should be considered for antibiotics include the following groups:
Patient is systemically very unwell - offer immediate ABx

Patient < 2 years with bilateral infection or otorrhoea - consider antibiotics (immediate or delayed script)

1st line: Amoxicillin for 5-7 days
Escalation: Co-amoxiclav - if worsening symptoms despite amox.
Pen all: Macrolide - clarithromycin/erythromycin

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Chronic suppurative otitis media

Pathophysiology

A complication of AOM in which there is chronic inflammation within the middle ear, resulting in recurrent otorrhoea through a perforated tympanic membrane.

Clinical Features

Symptoms

Otorrhoea for > 2 weeks, often white, yellow or green

Conductive hearing loss
Sometimes tinnitus, aural fullness
NO history of ear pain, fever, systemic illness
There is usually a history of acute otitis media

Otoscopy

Perforated tympanic membrane
Dried discharge or debris in ear canal

Management

Refer to ENT - management typically with aural toilet, topical antibiotics (quinolones - ciprofloxacin) and steroids.

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Acute mastoiditis

Pathophysiology

A complication of acute otitis media in which there is an extension of infection into the mastoid air cells.
Clinical Features

Symptoms

Ear pain
Otorrhoea
Worsening hearing loss

Examination Findings

Postauricular erythema, tenderness to palpation, boggy/fluctuance
Pinna can be displaced forward and downwards

Systemic upset - fever, sepsis
Otoscopy - erythematous, bulging tympanic membrane

Management

Emergency admission - IV ABx, may require surgery (e.g. cortical mastoidectomy)
Investigations - CT

References and Further Reading

NICE CKS. Otitis media - acute [May 2023]. Available at URL:

https://cks.nice.org.uk/topics/otitis-media-acute/

NICE CKS. Otitis media - chronic suppurative [July 2022]. Available at URL: https://cks.nice.org.uk/topics/otitis-media-chronic-suppurative/

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Labyrinthitis

Pathophysiology

Labyrinthitis describes the inflammation of the labyrinth.

It can be differentiated from vestibular neuronitis by the presence of hearing loss (which is NOT present in VN).
Clinical features

Clinical features

Symptoms:
Vertigo
Hearing loss
Tinnitus
But NOT aural fullness (suggests Meniere’s)

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Allergic Rhinitis
Pathophysiology

Exposure of the nasal mucosa to allergens results in IgE mediated inflammation of the nose

Causes
Seasonal allergic rhinitis - occuring at predictable times due to seasonal allergens (e.g. hay fever)

Perennial - seasons throughout the year due to persistent allergens (such as dust mites or animal allergies)

Clinical features

Sneezing
Nasal itching
Rhinorrhoea +/- congestion, post-nasal drip etc.

Frequently associated with allergic conjunctivitis - bilateral itchy eyes, hyperaemic/injected, tearing
History of atopy - asthma/allergies/atopic dermatitis, or FHx.

Management

Manage according to severity - symptoms are considered mild to moderate if they have minimal impact on QOL/ADLs/sleep, severe if they have more significant impact.

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Vestibular Neuronitis

Pathophysiology

Inflammation of the vestibular nerve, most commonly occurs following a viral infection.
Clinical features

Vertigo
Vertigo is often severe, and begins suddenly

Vertigo is constant, even when head is still - but usually worsened by movement/changes in head position

This helps to differentiate from episodic vertigo such as BPPV (<1 min), MD (20mins+-24hrs)
Symptoms usually settle over a few days, and return to normal within 1-2 months

Other symptoms:
Imbalance, falls
Does NOT feature hearing loss ( labyrinthitis does - this is a key differentiating factor)

Does NOT cause tinnitus ( Meniere’s disease does)
There is often a history of a recent viral illness, e.g. URTI/flu-like illness

Examination findings
Fine horizontal nystagmus
Management

For rapid relief of severe vertigo/N&V - buccal/IM prochlorperazine (or cyclizine)
If symptoms less severe - short course (up to 3/7) of PO prochlorperazine/AH (cyclizine)

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Meniere’s Disease

Pathophysiology

Meniere’s disease is an inner ear disorder of uncertain aetiology
There is an association with endolymphatic hydrops (swelling of the membranous labyrinth),

which results from an imbalance in the production and reabsorption of endolymph within the inner ear.

Clinical features

Meniere’s is characterised by

Episodic vertigo
Spontaneous +/- N&V
Episodes last at least 20 minutes (and no longer than 24hs)

Fluctuating sensorineural hearing loss
Roaring tinnitus

A sensation of aural fullness - the feeling of ‘pressure’ within the affected ear - often precedes a vertigo attack
Symptoms are most commonly unilateral

Management

Patients with suspected MD should be referred to ENT for confirmation of diagnosis

For the relief of vertigo, nausea & vomiting:
Prochlorperazine or antihistamine (e.g. cyclizine) for up to 7 days

If rapid relief of symptoms is required (e.g. severe symptoms):
Buccal/IM prochlorperazine (or IM cyclizine)

Prophylaxis:
Consider a trial of betahistine to reduce frequency/severity of episodes

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Benign Paroxysmal Positional Vertigo

Pathophysiology

BPPV is caused by the movement of debris/crystals within the semicircular canals of the inner ear.

Movement of the head results in movement of the calcium carbonate crystals, which causes the endolymph to move and induces the spinning/rotational sensation of vertigo.

Clinical features

Most commonly presents between the ages of 50-70 yrs, women > men,

with recurrent episodes of transient vertigo - the room/surroundings spinning.

Vertigo is triggered by head movements/changes in position - classically when the person rolls over in bed or bends over.

Episodes of vertigo are usually short, lasting < 1-2 minutes
Hearing and tinnitus are NOT features of BPPV

Examination findings:
Dix-hallpike manoeuvre positive - provokes vertigo and nystagmus

Management

1st line: Epley manoeuvre
Suggest Brandt-Daroff rehabilitation exercises

NICE suggests that symptomatic drug treatment is of limited benefit for patients with BPPV

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Assessment of vertigo - Red flags

Red flag symptoms may suggest a central cause of vertigo (e.g. POCS) and require urgent brain imaging. They include:

An isolated episode of persistent vertigo (lasting > 24rs), with sudden onset.

Associated headache
Acute deafness (and not consistent with Meniere’s)

Not provoked/altered by change in position (e.g. normal head impulse test)
Abnormal gait/ataxia

Neurological signs identified o/e inc. CN abnormalities/sensory changes or weakness.

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Vertigo

Vertigo is a symptom which describes the sensation of the ‘room spinning’ or the (rotational) movement of one’s surroundings, in the absence of any true physical movement.

Causes of vertigo include

Central: Pathology within the brainstem/cerebellum
Posterior circulation stroke
Vestibular migraine
Intracranial tumours
MS

Peripheral: Typically an issue within the inner ear
ENT - BPPV, Meniere’s, vestibular neuronitis/labyrinthitis

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Sore Throat
Background

Sore throats are most commonly the result of an URTI with inflammation of the throat mucosa.
Presentations include:
Acute pharyngitis - inflammation of the mucosa of the oropharynx
Tonsillitis
Assessment

The FeverPAIN or Centor criteria are recommended to determine the risk of group A streptococcal infection, and therefore the requirement for antibiotics.

Symptoms suggestive of strep: Scarlet fever rash, T>38.5, exudate, LN, no cough

FeverPain - 1 for each of the following:

Fever
P - Purulence (exudate on tonsils/pharynx)
A - Attend within 3/7 of symptom onset
I - Inflamed tonsils
N - No cough/coryzal symptoms

Centor criteria - 1 for each of:

C - cervical LN
E - exudate on tonsils
N - no cough
T - temperature >38

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Sore throat
Urti
Mng

Management

Withhold DMARDs and carbimazole whilst awaiting result of a FBC
Antibiotics:

FeverPAIN score of 4 or 5, or Centor score of 3 or 4 - antibiotics

1st line: Phenoxymethylpenicillin
Pen all: Clarithromycin (erythromycin if pregnant)

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Peritonsillar Abscess (Quinsy)

Most common in children aged 2-5yrs
Often occurs as a complication of streptococcal tonsillitis

Clinical features

Systemic upset - fever, SIRS
Sore throat, neck pain

Trismus, muffed ‘hot potato voice’
Uvular deviation away from the quinsy
Hallitosis

Management

Admit - IV antibiotics
Needle aspiration/incision & drainage

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Glandular fever (Infectious mononucleosis)

Pathophysiology

Cause: Ebstein-Barr virus (EBV) 90% (others - CMV/HIV/toxoplasmosis)
Spread: Salivary - kissing/sharing food/drink

Following acute infection, EBV persists lifelong in a low-grade replicative, carrier state.
Most common in patients aged 15-24 yrs

Clinical features

Symptoms

Prodromal symptoms - myalgia, malaise, fatigue, sweats

Non-specific rash (classically triggered after treatment of sore throat with amoxicillin)
Pyrexia
Severely sore throat
Examination findings

Lymphadenopathy - classically bilateral posterior cervical LN

Enlarged tonsils - may come together in the midline, covered in white exudate “whitewash”

Palpable splenomegaly
RUQ tenderness or sometimes hepatomegaly

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Mild-moderate symptoms, or mild persistent symptoms:

1st Line - Either:
PRN intranasal antihistamine (azelastine) OR
PRN non-sedating oral antihistamine (cetirizine/loratadine)

Moderate-severe symptoms, or failure of 1st line treatments

Regular intranasal coricosteroid during period of allergen exposure (e.g. spring/summer for hayfever) - mometasone furoate, fluticasone propionate

Further management

Persistent symptoms despite IN steroid..

Nasal congestion - short-term nasal decongestant - xylometazoline for 1 week
Watery rhinorrhoea - IN anticholinergic (ipratropium bromide)

Nasal itching/sneezing - REGULAR PO antihistamine, or combination intranasal steroid/antihistamine

For very severe symptoms, significantly affecting QOL - low dose prednisolone for 3-10 days.

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Bell’s Palsy & Ramsay Hunt
Bell’s Palsy

Pathophysiology

An acute, unilateral lower motor neurone facial nerve palsy resulting in facial weakness/paralysis.
Aetiology unclear, possibly viral
Clinical features

Rapid onset of facial muscle weakness
Unilateral and involves upper and lower parts of the face, with resultant facial droop

50% of patients complain of pain in the ear and postauricular region

LMN pathology – facial paralysis with forehead involvement (LMN).

Other symptoms include postauricular pain, dry eyes, reduced taste

Management

1st Line: Prednisolone 50-60mg OD for 10 days
Eye care - lubricating eye drops and tape eye close at bedtime if required.

Antivirals alone are not recommended. There may be ‘a small benefit’ when used in combination with steroids - NICE advises specialist advice.

References and Further Reading

NICE CKS: Management of Bell’s Palsy [2019]. Available at URL: https://cks.nice.org.uk/topics/bells-palsy/

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Ramsay Hunt Syndrome

Pathophysiology

Infection of the geniculate ganglion by varicella zoster virus resulting in a lower motor neuron facial nerve palsy, with accompanying zoster oticus (vesicular ear rash).

Clinical features

Symptoms

Facial droop - acute LMN facial nerve palsy - involves muscles of the forehead
Ear pain

A painful, erythematous vesicular rash (zoster oticus) within the ear canal and mucuous membrane of the oropharnyx

SNHL, tinnitus, vertigo, hyperacusis - if vestibulocochlear nerve involvement
Preceding flu-like illness
Loss of taste on anterior 2/3rds tongue

Management

1st line: Antivirals (aciclovir, valaciclovir, famciclovir) AND steroids (prednisolone 60 mg OD 5/7)

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Cerumen
Background

Cerumen (earwax) is produced in the external auditory canal. Accumulated cerumen within the canal can become impacted and lead to conductive hearing loss.

Clinical Features

History of use of cotton buds, hearing aids, earplugs
Hearing loss is the most common complaint

Feeling of fullness in ears, earache, tinnitus
Otoscopy: Accumulation of earwax, can be adherent to tympanic membrane, occlusion of canal by cerumen

Management

Softening of wax to aid removal
Ear drops - sodium bicarbonate 5%, olive oil QDS for 5 days

If continued symptoms - consider ear irrigation or microsuction

Cholesteatoma
Pathophysiology

An abnormal collection of keratinocytes, and squamous epithelium in the middle ear.

Cholesteatomas are expanding and invasive, and cause damage to structures within the middle ear.
If untreated, this can lead to problems with hearing/balance.

They can also become infected.
Can be congenital (epidermal cysts) but usually develop later in life (acquired) due to eustachian tube dysfunction.

Clinical features

Symptoms

Recurrent foul-smelling, purulent discharge (which doesn’t respond to treatment with ABx)
Hearing loss

Tinnitus
Dizziness, loss of balance if left untreated
Otoscopy

Discharge within canal, crust in upper TM, perforation.

Management

Refer all cases of suspected cholesteatoma to ENT - require CT imaging and audiology assessment

Management - surgical removal
Admit if vertigo or CN7 palsy, complications such as meningitis/IC abscess.

Imn Investigation Management Supportive management - simple analgesia, symptoms usually last 2-4 weeks Avoid contact sport/heavy lifting for 4 weeks (risk of splenic rupture)

Investigations If < 12 yrs or immunocompromised Bloods - check EBV serology after > 1 week If > 12 yrs and no history of immunocompromise FBC with differential wcc and monospot test (heterophile antibodies) - perform in 2nd week of illness. FBC with > 20% atypical/reactive lymphocytes OR if lymphocyte count is > 1/2 of WCC then 10% atypical lymphocytes - suggests EBV If monospot negative - repeat in 5-7 days Transaminitis - AST/ALT are usually deranged (>2-3x ULN)

Chondrodermatitis Nodularis Helicis Pathophysiology Chondrodermatitis Nodularis Helicis (CNH) is a common inflammatory condition affecting the cartilage and skin of the helix or antihelix of the ear, sometimes referred to as Winkler's disease. Causes: The exact cause is unknown, but contributing factors include: Chronic pressure - e.g. sleeping on one side, trauma, underlying connective tissue disease. Poor blood supply to the thin cartilage of the ear leads to ischemia, inflammation, and eventual nodule formation.

Clinical Features CNH typically presents as a painful, firm nodule on the helix (in men) or antihelix (in women), often measuring 4–6 mm. The lesion is typically painful, aggravated by pressure (e.g., lying on the affected side). The nodule is oval-shaped with a central crust and surrounding erythema. In some cases, it may bleed or discharge a small amount of scaly material. Demographics: More common in fair-skinned, middle-aged, and older men, though 10–35% of cases occur in women. Due to its appearance, CNH can mimic other conditions like SCC.

Chondrodermatitis Nodularis Helicis

Management Conservative measures: Relieve pressure: Use protective padding at night, modify sleeping position Pharmacological management: Topical potent steroids Intralesional steroid injections (e.g., triamcinolone) to reduce local inflammation. Topical nitroglycerin: Improves blood flow by vasodilating the arterioles. Surgical Options: Excision, curettage Recurrence rates: Surgical treatments have a 10–30% recurrence rate, making non-surgical management preferable in some cases

Croup (acute layngotracheobronchitis) Pathophysiology A viral URTI resulting in inflammation ( +/-obstruction) and subglottic oedema of the larynx, trachea and bronchi Cause: Parainfluenza virus (Alt: RSV) Incidence: Children usually between 6 months and 6 yrs old. Clinical features Prodromal URTI - coryzal Harsh, barking cough (seal-like) which is worse at night Hoarse voice Stridor Respiratory distress

Classification Mild – Seal-like barking cough with stridor Moderate – sternal recession Severe - intercostal recession + agitation/ lethargy Management All children - single dose of oral dexamethasone (0.15mg/kg) (alt: IM dex, or inhaled budesonide) Admit any child with moderate or severe croup as above In addition to dex, nebulised adrenaline may be beneficial

Epiglottitis Pathophysiology Infection with resultant inflammation of the epiglottis, which can result in airway obstruction Causes: HIb (now rare due to vaccination), now most commonly streptococcus (S.pneumoniae or pyogenes)

Clinical features Usually effects children 2-7yrs Abrupt onset of sore throat, odynophagia Continuous stridor with drooling of salvia/secretions Muffled voice Fever Tripod position to ease breathing Management May require ET intubation if severe obstruction IV Cefotaxime/cefuroxime

Suspected cancer - 2WW Referral Criteria Ear Bloody otorrhoea - external ear ca. Laryngeal cancer Age > 45 years with either: Persistent unexplained hoarseness Unexplained neck lump Nasopharyngeal cancer Persistent bleeding/crusting with unilateral nasal obstruction Unilateral middle ear effusion and hearing loss (which is not associated with infection) Oral cancer Unexplained oral ulceration/lesion (>3 weeks) Unexplained neck lymp Lump in the lip/oral cavity Red/white patch in the oral cavity (erythroleukoplakia) Thyroid cancer Unexplained thyroid lump Others red flags Unexplained, persistent (>4 weeks) sore/painful throat (esp. if otlagia present) Unilateral polyp - malignant until proven otherwise Unexplained, persistent unilateral earache (>4 weeks, normal otoscopy) Can reflect referred otalgia

Nasopharyngeal carcinoma Risk factors Southeast Asian or Chinese ancestry (esp. cantonese), salty diet, EBV Pathology Carcinoma of the nasopharyngeal epithelium Clinical features Epistaxis Nasal or hoarse voice Unilateral nasal obstruction Lymphadenopathy Persistent lump in neck > 3 wks Unilateral hearing loss or tinnitus Diagnosis MRI, nasoendoscopy Management Radiotherapy and chemotherapy, often in combination

Laryngeal cancer Pathophysiology Squamous cell carcinoma most common. RFs: Smoking Clinical features Hoarseness or altered voice Stridor Odynophagia or dysphagia Haemoptysis Unexplained neck lump

Diagnosis MRI, nasoendoscopy/laryngoscopy Management Transorla resection if early, radiotherapy, chemo-radiotherapy

Acoustic neuroma (vestibular schwannoma) Pathophysiology Benign tumours arising from the Schwann cells which form the myelin sheath surrounding the vestibulocochlear nerve (CN8) Most ANs occur at the cerebellopontine angle Association: Bilateral ANs - Neurofibromatosis T2 Clinical features Triad: Progressive, unilateral hearing loss is the most common symptom Unilateral tinnitus Vertigo

Investigations Gold standard - MRI of internal auditory meatus Management Most cases are managed conservatively with observation/interval MRI monitoring (due to very slow growth), radiosurgery, surgical excision

Other ENT Disorders Presbycusis Age-related hearing loss which results from the degeneration of the cochlea and associated inner ear structures. Clinical features A progressive, irreversible, bilateral SNHL Usually begins in adults > 50-60 yrs HL is most marked with high frequency sounds Examination NAD

Otosclerosis Abnormal bone remodelling within the middle ear, which results in the resorption and subsequent sclerosis of the stapes bone. Aetiology Possibly viral. Sometimes hereditary, suggested by family history. Clinical features Insidious, gradually worsening conductive hearing loss, typically bilateral Usually presents in young adults 30-40 yrs May be associated tinnitus No pain

Glomus jugulare A rare, slow-growing paraganglioma that develops within the jugular foramen Clinical features Pulsatile tinnitus Aural fullness Hearing loss Otoscopy: A “red/blue coloured mass” may be seen behind the TM

Epistaxis Background 90% of cases of epistaxis originate from the Kiesselbach plexus within Little’s area on the anterior nasal septum. Posterior bleeds are less common, and suggested by profuse bleeding often from both nares, inability to identify bleeding point, bleeding down throat/swallowed. Management Admit if profuse/posterior bleed/hemodynamically unstable etc. First aid measures If ongoing bleeding after 10 minutes, options include: Nasal cautery with silver nitrate stick to bleeding point for 5-10 seconds Nasal packing with nasal tampons (merocel), inflatable packs (rapid-rhino), ribbon gauze (only in secondary care) If ongoing bleeding/unstable, secondary care measures may include: Electrocautery Formal packing Arterial embolization

Otitis Externa Otitis Externa Pathophysiology Inflammation of the external auditory canal Causes Acute OE (< 6/52) - typically caused by bacterial infection (most commonly Pseudomonas aerg. or staph aureus) Chronic OE (>3/12) - commonly caused by fungal infection (aspergillus/candidiasis) Other causes include: Complication of AOM Seborrhoeic dermatitis Contact dermatitis

Clinical features Symptoms Acute onset of ear pain or pruritus Ear discharge Chronic OE is suggested by persistent pruritus of the ear canal for > 3 months. Examination findings Pain on palpation of the pinna or tragus/ tragal tug Otoscopy: erythema of the external auditory canal +/- oedema, discharge or debris

Otitis Externa Pathophysiology Inflammation of the external auditory canal

Management Acute OE Aural toilet - swabbing/irrigation to remove debris and facilitate topical treatment 1st line: Topical antibiotics +/- topical corticosteroid for 1-2 weeks Consider PO antibiotics (ciprofloxacin) if immunocompromised, severe OE or spreading infection (e.g. cellulitis) Chronic OE Fungal infection - topical antifungal (e.g. clotrimazole) +/- steroid If no infective cause - topical corticosteroid (e.g. seborrhoeic dermatitis)

Malignant Otitis Externa Background MOE is a severe complication of OE, where infection spreads into the temporal bone causing acute osteomyelitis. Risk factors include any cause of immunocompromise, most commonly poorly controlled diabetes Clinical features Symptoms Severe pain in the affected ear Smelly, purulent discharge Systemic upset - fever, tachycardia

Examination findings Conductive hearing loss Facial nerve palsy on affected side Otoscopy: Granulation tissue within the external auditory meatus, exposed bone Management Arrange emergency hospital admission, usually IV antibiotics (ciprofloxacin), for 6 weeks.

Otitis Media with Effusion Pathophysiology The accumulation of fluid (effusion) within the middle ear Causes: Most cases occur following an episode of AOM (or viral URTI) RFs: Association with cleft palate, Down's syndrome, allergic rhinitis Age: Bimodal peak - 2 years, 5 years.

Clinical features Symptoms Hearing loss - the most common symptom In young children/infants it may present as delays in speech or language development, poor concentration/ progress at school, asking for things to be repeated, or watching TV with high volume. There may be mild earache or recurrent URTI/ear infection Otoscopy Tympanic membrane discolouration - e.g. yellowing Air/fluid level, or bubbles behind the TM Retracted TM (indrawn due to pressure) Blunting of light reflex

Otitis Media with Effusion

Investigations Pneumatic otoscopy Tympanometry Audiometry should be performed Management 1st Line: Watchful waiting for 3 months Spontaneous resolution is common, so observation is appropriate for most children Monitoring involves 2 x hearing tests (audiometry), 3 months apart Exceptions: Patients with Down’s syndrome or cleft palate should be referred to ENT Secondary care treatments include Autoinflation during active observation, to facilitate drainage of the middle ear Surgical Mx: Myringotomy/grommet insertion

Rhinosinusitis Background Inflammation of the nasal cavities and paranasal sinuses Acute rhinosinusitis - resolution within 12 weeks Usually triggered by a viral URTI (rhinovirus/RSV/parainfluenza) results in inflammatory changes within the sinuses. Rarely followed by a bacterial infection (2% cases) , which thrive in the altered/inflamed sinuses (most commonly strep pneumoniae or haemophilus influenzae b) Chronic - symptoms > 12 weeks Inflammatory rather than infective

Clinical features Most commonly follows a cold - history of viral/coryzal illness Specific symptoms include: Nasal congestion or nasal drip, speech may sound nasal Frontal headache/facial pain, worse on leaning forward Anosmia Bacterial sinusitis is suggested by purulent nasal discharge, fever, elevated CRP Examination findings: Pain on palpation over the sinuses

Management Symptoms < 10 days Conservative Mx for most patients - usually resolves spontaneously within 2-3 weeks Symptoms > 10 days without improvement Consider a high-dose nasal corticosteroid (mometasone) Bacterial rhinosinusitis If bacterial rhinosinusitis is suspected (non-resolving symptoms, fever >38, severe facial pain, elevated inflammatory markers), or the patient is systemically very unwell, or at risk of complications - prescribe antibiotics: No life-threatening features - Phenoxymethylpenicillin Systemically very unwell, or no improvement with PenV - co-amoxiclav Chronic sinusitis (>12 weeks) Intranasal corticosteroids for up to 3/12 (mometasone/fluticasone)