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Peritonsillar Abscess

Also known as: Quinsy

A collection of pus in the potential space between the tonsillar capsule and the superior constrictor muscle. It is the commonest deep neck space infection, with an incidence of around 30 per 100000 in adults, peaking between 20 and 40 years.

Pathogenesis

Two mechanisms are recognised.

  • Progression from acute tonsillitis with spread of infection through the tonsillar capsule into the peritonsillar space, forming a cellulitis, that is peritonsillitis, which then suppurates.
  • Infection of the Weber glands, a group of 20 to 25 minor salivary glands in the supratonsillar space that drain through ducts into the tonsillar surface and clear debris from the crypts. Obstruction and infection of these glands produces an abscess in the supratonsillar position, which is why the great majority of abscesses are found superior and lateral to the tonsil. This mechanism explains why peritonsillar abscess occurs in patients who have had tonsillectomy and in those with no preceding tonsillitis.

Anatomy that determines drainage technique and its hazards

The abscess lies between the tonsillar capsule medially and the superior constrictor laterally, most often in the superior pole. Lateral to the superior constrictor lies the parapharyngeal space, which contains the carotid sheath. The internal carotid artery lies approximately 2 to 2.5 cm posterolateral and deep to the tonsil, and closer in children and in patients with a tortuous or medially displaced vessel. Needle aspiration and incision must therefore be directed in a strictly sagittal or slightly medial direction and must not be angled laterally, and depth must be controlled by using a needle guard or by exposing only 1 cm of the blade.

Microbiology

Polymicrobial, with a mixture of aerobes and anaerobes.

  • Streptococcus pyogenes, which is the most frequently isolated single aerobe.
  • Fusobacterium necrophorum, which is disproportionately common in adolescents and young adults and which carries the risk of Lemierre syndrome.
  • Streptococcus milleri group, Staphylococcus aureus, Haemophilus influenzae.
  • Anaerobes: Prevotella, Porphyromonas, Peptostreptococcus, Bacteroides.

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Nasal Septal Perforation

A full thickness defect of the septal cartilage or bone with loss of mucoperichondrium on both sides, creating a communication between the two nasal cavities.

Why perforations cause symptoms

Normal nasal airflow is laminar and follows a smooth path from the vestibule over the inferior turbinate to the choana. A perforation, particularly an anterior one, disrupts laminar flow and produces turbulence and crossflow between the cavities. Turbulent airflow dries the mucosa at the perforation edge, causing crusting, ulceration, bleeding and further enlargement. This is why anterior perforations are symptomatic and posterior perforations, sitting behind the region of maximal airflow, are often silent.

Causes

Iatrogenic and traumatic:

  • Septoplasty and submucous resection, the commonest single cause.
  • Nasal packing, cautery performed bilaterally at the same site, and cryotherapy.
  • Nasogastric and nasotracheal tubes.
  • Digital trauma, that is nose picking, which is a genuine and frequent cause.
  • Untreated septal haematoma and abscess.
  • Nasal piercing.

Inflammatory and granulomatous:

  • Granulomatosis with polyangiitis, which is the most important cause to exclude and which presents with crusting, granulation, a saddle nose, and systemic disease.
  • Sarcoidosis, with a strawberry mucosa appearance.
  • Eosinophilic granulomatosis with polyangiitis.
  • Systemic lupus erythematosus and other connective tissue disease.

Infective:

  • Tuberculosis, syphilis, which classically destroys bone and produces a saddle deformity, leprosy, rhinoscleroma, mucormycosis and other invasive fungal disease.

Drug related:

  • Intranasal cocaine, which causes vasoconstriction, ischaemia and direct toxicity, and produces large destructive perforations extending to the hard palate in severe cases.
  • Intranasal corticosteroid sprays directed at the septum, particularly with poor technique, which is a preventable cause.
  • Topical decongestant abuse.
  • Bevacizumab and other antiangiogenic agents.

Occupational and environmental:

  • Chromic acid, nickel, arsenic, cement dust, and other industrial exposures.

Neoplastic:

  • Squamous cell carcinoma, adenocarcinoma, natural killer T cell lymphoma of nasal type, and other malignancy. Any perforation with an atypical appearance, mass, bleeding or pain requires biopsy.