Recurrent Acute Rhinosinusitis

Four or more episodes of acute rhinosinusitis per year, each meeting the diagnostic criteria for acute disease, with complete resolution of symptoms and, critically, absence of inflammation on endoscopy and imaging between episodes. The interval normality is what distinguishes this entity from chronic rhinosinusitis with acute exacerbations, and the distinction matters because the two have different underlying causes and different treatment.

Why episodes recur

The task is to identify why an ordinary viral upper respiratory infection converts to bacterial sinusitis repeatedly in this individual when it does not in most people. The causes fall into three groups.

Anatomical obstruction of the osteomeatal complex:

• Concha bullosa, an aerated middle turbinate, particularly when large or infected.
• Paradoxical middle turbinate.
• Marked septal deviation with contact against the lateral wall.
• Haller or infraorbital ethmoid cells narrowing the maxillary infundibulum.
• Agger nasi and frontal recess cells obstructing frontal drainage.
• Uncinate process variations, including medialisation or lateral attachment to the lamina papyracea.
• Post traumatic and post surgical scarring.

Host defence impairment:

• Common variable immunodeficiency, immunoglobulin A deficiency, immunoglobulin G subclass deficiency, and specific polysaccharide antibody deficiency, which is the commonest immune abnormality found in this group and is detected only by measuring vaccine responses.
• HIV infection.
• Diabetes mellitus.
• Immunosuppressive therapy and haematological malignancy.
• Primary ciliary dyskinesia and cystic fibrosis, which typically produce chronic rather than recurrent acute disease but should be considered.

Local and environmental drivers:

• Allergic rhinitis, which produces mucosal oedema at the osteomeatal complex with every allergen exposure.
• Odontogenic disease, which produces repeated unilateral maxillary infection until the tooth is treated.
• Gastro oesophageal and laryngopharyngeal reflux.
• Smoking, both active and passive.
• Occupational irritant exposure.
• Nasal foreign body in children.
• High exposure settings, such as young children in day care and teachers.

• Discrete, well demarcated episodes with the full symptom complex of acute rhinosinusitis: obstruction, purulent discharge, facial pain and reduced smell.
• Complete or near complete symptom freedom between episodes, which the patient can usually date precisely.
• Frequent antibiotic courses with prompt response and then recurrence weeks later.
• Consistent unilaterality of episodes, which points strongly to a local anatomical or dental cause.
• Clustering in winter, or with allergen season, which points to viral or allergic triggers respectively.
• Impact on work, school and quality of life, and cumulative antibiotic exposure with its consequences.

Features that indicate a different diagnosis

• Persistent symptoms between episodes, which means chronic rhinosinusitis with exacerbations, not recurrent acute disease.
• Facial pain as the sole recurrent symptom with no obstruction, discharge or objective findings, which is usually migraine or midfacial segment pain. This group is commonly and wrongly operated on.
• Unilateral bloody discharge, facial numbness or orbital signs, requiring exclusion of neoplasm.
• Recurrent infections at other sites, chronic wet cough, bronchiectasis, otitis media and skin infections, indicating immunodeficiency.

The essential principle is to investigate between episodes, not during them, since imaging and endoscopy during an acute episode cannot demonstrate the interval normality that defines the condition.

• Confirm the episodes objectively where possible. Documented episodes with recorded endoscopic findings or purulent discharge carry far more weight than patient report, since a substantial proportion of self reported recurrent sinusitis is recurrent viral illness or migraine.
• Nasal endoscopy between episodes, which should show a normal or near normal middle meatus. Persistent oedema or discharge redirects the diagnosis to chronic disease.
• Non contrast computed tomography of the sinuses performed between episodes, ideally at least 4 to 6 weeks after the last one. This is the key investigation. A normal scan between episodes confirms recurrent acute disease and simultaneously defines the anatomical variants that may be responsible.
• Endoscopically guided middle meatal culture during an episode, to document the organisms and guide targeted therapy.
• Allergy assessment with skin prick testing or specific immunoglobulin E.
• Immunological workup, which should be performed in essentially all adults with genuine recurrent acute rhinosinusitis: full blood count with differential, immunoglobulin G, A, M and E, immunoglobulin G subclasses, HIV testing, and specific antibody titres to pneumococcal polysaccharide and tetanus before and 4 weeks after booster immunisation. A failure to mount a fourfold rise or to achieve protective titres to the majority of pneumococcal serotypes indicates specific antibody deficiency.
• Dental assessment with panoramic radiography or cone beam computed tomography where episodes are unilateral and maxillary.
• Sweat chloride testing, cystic fibrosis genetics, nasal nitric oxide and ciliary studies where the history suggests these.
• Glucose and HbA1c.

Management has two arms: correcting the underlying cause, and managing each episode appropriately while reducing unnecessary antibiotic exposure.

Treat the identified cause

• Allergic rhinitis: continuous intranasal corticosteroid such as mometasone furoate 100 micrograms per nostril once daily, an oral antihistamine such as cetirizine 10 mg daily during exposure, allergen avoidance, and allergen immunotherapy for confirmed single or dominant allergen sensitivity where symptoms persist despite pharmacotherapy. Immunotherapy is the only treatment that modifies the underlying allergic disease and can reduce recurrence substantially.
• Odontogenic source: dental extraction, endodontic treatment, or removal of a displaced root, implant or filling material. The sinus disease will recur indefinitely until this is done.
• Immunodeficiency: refer to immunology. Immunoglobulin replacement therapy for common variable immunodeficiency and for severe specific antibody deficiency with recurrent infection, and pneumococcal conjugate vaccination for specific antibody deficiency, which frequently produces a response where the polysaccharide vaccine did not.
• Smoking cessation and removal of occupational irritant exposure.
• Optimise glycaemic control.
• Treat reflux where present with a proton pump inhibitor such as omeprazole 20 mg twice daily for 8 to 12 weeks with lifestyle modification.

Managing the acute episodes

• Treat each episode as acute rhinosinusitis, using intranasal corticosteroid, saline irrigation and analgesia as the foundation.
• Reserve antibiotics for episodes meeting bacterial criteria, and use culture directed therapy where a previous culture is available.
• Given repeated antibiotic exposure, use co amoxiclav 625 mg three times daily for 7 days rather than plain amoxicillin, or a culture directed alternative.
• Avoid the pattern of a telephone prescription for every episode without assessment, which perpetuates unnecessary antibiotic use and delays diagnosis of the underlying cause.

Preventive medical therapy

• Continuous intranasal corticosteroid, which reduces episode frequency in patients with an allergic or inflammatory component.
• Daily saline irrigation year round.
• Influenza and pneumococcal vaccination.
• Prophylactic antibiotics are generally not recommended for recurrent acute rhinosinusitis given resistance and adverse effects. Where they are used in exceptional cases, such as during a winter season while awaiting surgery in a patient with very frequent episodes, this should be a specialist decision with a defined review point.

Surgery

Indications: documented recurrent acute rhinosinusitis, generally four or more objectively confirmed episodes per year, with a demonstrated anatomical abnormality obstructing the osteomeatal complex, after correction of medical and allergic factors, and with a normal interval scan confirming the diagnosis.

• Functional endoscopic sinus surgery targeted at the obstruction rather than a routine full clearance. This may consist of uncinectomy with maxillary antrostomy, resection of the lateral lamella of a concha bullosa, removal of a Haller cell, or anterior ethmoidectomy, tailored to the scan findings.
• Septoplasty where a deviation obstructs the middle meatus or prevents access.
• Balloon sinus dilation is an option in selected patients with limited disease and no polyps, dilating the maxillary, frontal or sphenoid ostium without tissue removal, and can be performed under local anaesthesia. Evidence for durable benefit in recurrent acute disease is less robust than for endoscopic surgery, and it does not address ethmoid disease.
• Outcomes are good in appropriately selected patients, with meaningful reductions in episode frequency and antibiotic use. Outcomes are poor in patients selected on symptoms alone with a normal interval scan, which is the most important selection principle in this condition.

Counselling and follow up

• Explain that surgery reduces but does not abolish episodes, and that it does nothing for an immune deficiency or an untreated allergy.
• Do not offer surgery to patients whose recurrent facial pain has no objective correlate. They will not improve, and pain frequently worsens.
• Review at 6 weeks and 3 months postoperatively with endoscopy, then annually, tracking episode frequency and antibiotic use as the outcome measures.
• Continue preventive medical therapy indefinitely after surgery.