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Chronic Tonsillitis

Persistent low grade inflammation of the tonsils with continuous rather than episodic symptoms, distinguished from recurrent acute tonsillitis by the absence of symptom free intervals.

Pathophysiology

The tonsillar crypts, which number 10 to 30 per tonsil and which extend deep into the parenchyma, become chronically colonised. Three processes maintain the condition:

  • Crypt obstruction by debris, desquamated epithelium and bacteria, forming an anaerobic environment.
  • Biofilm formation on the crypt epithelium, in which organisms exist in a protected extracellular polymeric matrix that resists both antibiotic penetration and host immune clearance. Biofilms are demonstrable in the great majority of chronically inflamed tonsils and explain the failure of repeated antibiotic courses.
  • Fibrosis of the tonsillar capsule and parenchyma, with scarring that obliterates crypt drainage and perpetuates the cycle.

Tonsilloliths

Concretions formed within the crypts from trapped debris, food, desquamated epithelium and bacteria, which calcify over time with deposits of calcium, phosphorus, magnesium and ammonium. Anaerobic organisms within them produce volatile sulphur compounds, which are the cause of the characteristic halitosis. They are a specific and frequently underestimated cause of distress, since patients are commonly told nothing is wrong.

Microbiology

Polymicrobial, with anaerobes predominating: Fusobacterium, Prevotella, Porphyromonas, Peptostreptococcus and Actinomyces. Aerobes include Staphylococcus aureus, Haemophilus influenzae, Moraxella catarrhalis and streptococci. Beta lactamase production by these organisms inactivates penicillin within the crypt environment.

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Continue reading · Surgery

Tympanic Membrane Perforation

A defect in the tympanic membrane, classified by cause, site, size and duration. Each of these determines both the likelihood of spontaneous healing and the risk of long term sequelae.

Anatomy relevant to outcome

The pars tensa has three layers: outer squamous epithelium, middle fibrous lamina propria with radial and circular collagen, and inner mucosa. Healing depends on the fibrous layer and on migration of squamous epithelium across the defect. The pars flaccida lacks an organised fibrous layer and is where retraction and cholesteatoma originate. The blood supply runs along the malleus handle and the annulus, which is why anterior and marginal perforations, remote from this supply, heal less reliably.

Classification

  • By site: central perforations of the pars tensa leave a rim of drum around the defect and carry a low cholesteatoma risk. Marginal perforations reach the annulus and attic defects involve the pars flaccida; both allow squamous epithelial ingrowth and are associated with cholesteatoma.
  • By size: expressed as a percentage of the pars tensa. Small perforations under 25 percent produce a loss of 10 to 20 dB, subtotal perforations 30 to 40 dB.
  • By duration: acute until 3 months, chronic thereafter.

Aetiology

  • Infective: acute otitis media, chronic suppurative otitis media, necrotising otitis externa, myringitis.
  • Direct trauma: cotton buds, hairpins, hot slag or welding sparks, foreign bodies.
  • Barotrauma and blast injury: slap to the ear, explosion, diving, flying with Eustachian dysfunction.
  • Water: diving, water skiing, forceful irrigation.
  • Temporal bone fracture, particularly longitudinal fractures.
  • Iatrogenic: grommet extrusion, aural irrigation, surgical.

Mechanism of hearing loss

Conductive loss arises from reduced effective vibrating area and, when the perforation is large, from loss of the round window baffle so that sound reaches both windows in phase and cancels. Loss beyond 40 to 45 dB implies ossicular discontinuity or fixation rather than perforation alone, since a perforation alone rarely exceeds this.