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Acute Laryngitis

Acute inflammation of the laryngeal mucosa lasting less than 3 weeks, producing hoarseness through disruption of the vibratory properties of the vocal folds.

Why inflammation produces hoarseness

The vocal fold has a layered structure: squamous epithelium, the superficial lamina propria known as Reinke space, which is a loose gelatinous layer with few fibroblasts and permits the mucosal wave, the intermediate and deep lamina propria forming the vocal ligament, and the thyroarytenoid muscle. Inflammation causes oedema and cellular infiltration of Reinke space, increasing the mass and stiffness of the cover and impairing the mucosal wave. This raises phonation threshold pressure, lowers fundamental frequency, and produces the characteristic rough, breathy, low pitched voice.

The critical clinical consequence is that phonation against an inflamed, stiff fold requires greater subglottic pressure and greater adductory force, which causes further trauma. This is the mechanism by which vocal use during acute laryngitis produces vocal fold haemorrhage, mucosal tear and, in the longer term, benign lesions. Voice rest is therefore not a comfort measure but a treatment to prevent structural injury.

Aetiology

Infective, the great majority:

  • Viral, in 90 percent or more: rhinovirus, influenza, parainfluenza, adenovirus, respiratory syncytial virus, coronavirus, SARS-CoV-2.
  • Bacterial superinfection or primary bacterial laryngitis with Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis and Streptococcus pyogenes, which is uncommon.
  • Fungal laryngitis with Candida, in inhaled corticosteroid users, the immunocompromised, and after antibiotics.

Non infective:

  • Vocal misuse and abuse: shouting, screaming, prolonged loud speaking, singing without training, cheering at events.
  • Laryngopharyngeal reflux.
  • Inhalational injury: smoke, chemicals, thermal injury, chlorine.
  • Allergic and irritant exposure.
  • Inhaled corticosteroids, both directly and through candidal infection.
  • Radiotherapy.
  • Trauma, including intubation.

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Acute Rhinosinusitis

Also known as: Acute sinusitis

Inflammation of the nasal and paranasal sinus mucosa of less than 12 weeks duration, with complete resolution of symptoms. The nose and sinuses share a continuous mucosa, which is why rhinosinusitis rather than sinusitis is the accurate term.

Pathophysiology

Viral upper respiratory infection produces mucosal oedema at the osteomeatal complex, the narrow common drainage pathway for the maxillary, anterior ethmoid and frontal sinuses. Obstruction of the ostium impairs ciliary clearance, lowers intrasinus oxygen tension and raises carbon dioxide, and produces a stagnant secretion pool that favours bacterial proliferation. Ciliary beat frequency falls, mucus becomes more viscous, and the cycle perpetuates.

Anatomical drainage, which determines symptom localisation and complication risk

  • Maxillary, anterior ethmoid and frontal sinuses drain into the middle meatus through the osteomeatal complex.
  • Posterior ethmoid and sphenoid sinuses drain into the sphenoethmoidal recess and superior meatus.
  • The nasolacrimal duct drains into the inferior meatus.
  • The lamina papyracea separating the ethmoid from the orbit is paper thin and dehiscent in a proportion of people, which is why the ethmoid is the source of most orbital complications, particularly in children.
  • The frontal sinus posterior table abuts dura, and its diploic veins communicate with the dural venous sinuses, explaining intracranial complications and Pott puffy tumour.

Classification by duration and course

  • Acute viral rhinosinusitis, or common cold: symptoms less than 10 days.
  • Acute post viral rhinosinusitis: symptoms increasing after 5 days or persisting beyond 10 days, with less than 12 weeks total.
  • Acute bacterial rhinosinusitis: a subset of post viral disease, occurring in only 0.5 to 2 percent of viral upper respiratory infections in adults and 5 to 10 percent in children.
  • Recurrent acute rhinosinusitis: four or more episodes per year with complete resolution between.

Microbiology of bacterial disease

Streptococcus pneumoniae, non typeable Haemophilus influenzae, Moraxella catarrhalis, Streptococcus pyogenes, Staphylococcus aureus, and anaerobes in odontogenic disease. Nosocomial sinusitis in intubated and nasogastric tube fed intensive care patients involves Pseudomonas, Klebsiella and Staphylococcus aureus.

Predisposing factors

Viral infection, allergic rhinitis, anatomical variants including concha bullosa, a deviated septum, Haller cells and a large agger nasi cell, nasal polyps, dental disease and dental procedures, immunodeficiency, ciliary dyskinesia, cystic fibrosis, smoking, swimming and diving, nasal foreign body in children, and nasogastric or nasotracheal intubation.