66 Otitis Media with Effusion

Otitis media with effusion (OME) is the presence of fluid or an effusion in the middle ear space caused by inflammation of the middle ear cleft mucosa, but symptoms of infection are absent and there is no tympanic membrane perforation or otorrhoea.

66.1 Aetiology

The aetiology of OME (glue ear) is multifactorial, but there are two main theories regarding the same. These are the classic theory and the primary inflammation theory.

66.1.1 Classic Theory

The classic theory proposes that OME arises from Eustachian tube (ET) dysfunction. As a point of interest, the Eustachian tube is named after Bartholomeo Eustachi (1513–1574) who was the Professor of Anatomy in Rome and Physician to the Pope. He was one of the founders of the science of Human Anatomy and the first to describe the eustachian tube. Therefore, Eustachian has an upper case first letter.

Physiologically, between swallows, oxygen and nitrogen are absorbed/diffuse into the middle ear mucosa. A smaller volume of carbon dioxide is released from the mucosal cells into the middle ear cleft so that there is a net reduction in middle ear gas volume and therefore a negative middle ear pressure results. On swallowing or yawning, the Eustachian tube is pulled open so that air passes up the tube, equalising middle ear pressure to atmospheric pressure.

Eustachian tube dysfunction refers to the inadequate physiological opening of the tube. This can be caused by blockage of the mouth of the tube from enlarged adenoids, from swelling of the tube mucosa due to infection (perhaps from a upper respiratory tract infection [URTI] or from a source within the adenoids) or allergy, from weak palatal muscles that are unable to contract sufficiently strongly on swallowing to pull open the tube (the young and the elderly, and those with cleft palates) or from the angle of muscle pull being disadvantageous because the angle of the tube is more horizontally placed (young children).

When there is Eustachian tube dysfunction, middle ear pressure equalisation does not occur. If middle ear pressure becomes sufficiently negative, and for a long enough period, then a transudate from the middle ear mucosa will result, and a sterile middle ear effusion is therefore formed. This effusion is protein rich and attracts bacteria.

66.1.2 Inflammation Theory

This theory suggests that the middle ear mucosa becomes inflamed from bacteria already present in the middle ear or possibly from reflux of saliva containing URTI viruses or bacteria into the ET.

These microbes can then stimulate an immune response, with release of cytokines. Respiratory viruses may predispose to bacterial superinfection, or may stimulate an immune response themselves. Cytokines cause upregulation of mucin genes via a cyclic GMP-mediated pathway, leading to a secretion of mucin-rich fluid in the middle ear. The viscosity of the fluid impairs mucociliary clearance and the presence of subclinical bacterial infection causes prolonged stimulation of inflammation. The effusion persists, to be manifest clinically as OME.

Pepsin is found in the effusion of 60% of children with OME raising the possibility of a contribution to OME from gastro-oesophageal reflux too. Pepsin is thought to encourage mucin production.

It is likely that there is a contribution to OME from both models and neither is mutually exclusive. There is strong association of OME with recurrent URTIs, parental smoking, allergy and reduced overall nasopharyngeal dimensions. The adenoids are recognised as important contributors to OME, both as a source of pathological bacteria, but the contribution from obstruction of the orifice of the ET is probably less important. This is because we know that an adenoidectomy confers a significant reduction in the likelihood of recurrent OME when performed with grommet insertion regardless of the size of the adenoid pad.

66.2 Pathology

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