Lymphoid tissue found at the junction of the roof and posterior wall of the nasopharynx, thought to be involved in the development of humoral immunity as a component of the “gut associated lymphoid tissue” (GALT). Adenoid tissue is present at birth and during childhood, beginning to atrophy before puberty.
Adenoidal hypertrophy disturbs nasopharyngeal airflow and Eustachian tube function and can also act as a focus of infection for adjacent sites. Common clinical features are nasal obstruction and discharge, deafness due to middle ear effusion and otalgia due to recurrent otitis media.
Gross adenoidal enlargement, often associated with tonsillar hypertrophy, can cause sleep apnoea syndrome in which apneic episodes during sleep are associated with daytime somnolence and in severe cases pulmonary hypertension and cor pulmonale. Clinical suspicion of enlarged adenoid can be confirmed by lateral radiography.
Surgical removal (adenoidectomy) can be undertaken if enlarged adenoids are causing sleep apnoea, nasal obstruction or are a contributing factor to persistent middle ear effusions or recurrent otitis media.
Atrophic rhinitis (萎縮性鼻炎) Aetiology: A disease of unknown aetiology, occurring mainly in developing countries. It can occur following radical turbinectomy operations or radiotherapy to the nasal cavity. Clinical features: Nasal crusting, anosmia and fetor are present. Paradoxically, although the nasal cavity is widely patent, the sensation of nasal obstruction is common. Management: Treatment is by removal of crusts and nasal douches.
Hypersensitivity to inhaled or ingested allergens causes nasal mucosal oedema and exudation. Allergy may be seasonal (e.g. pollens) or perennial (e.g. dust). Allergies may be demonstrated by skin tests.
Presents as nasal obstruction, sneezing and rhinorrhea with mucosal oedema on examination.
Treat with steroid nasal spray and oral antihistamines. Avoid any known allergens.
Traumatic – after septal surgery, nose picking, cocaine sniffing and pressure from foreign bodies and nasal polyps.
Infective – due to syphilis and tuberculosis.
Chronic inflammatory – Wegener’s granulomatosis is a non-neoplastic upper airways granuloma associated with focal lung and kidney lesions. (Lethal) midline granuloma is thought to be an atypical lymphoma occurring in the midline of the face.
Asymptomatic, or nasal crusting and epistaxis are characteristic of septal perforation.
Treatment is by removal of crusts, nasal douches and treatment of underlying systemic conditions.
Septal abscesses usually result from secondary infection of a septal haematoma.
Manifests by the development of severe pain, nasal swelling and pyrexia following a septal haematoma. Cartilage necrosis often complicates septal haematoma and abscess with the production of a saddle-nose deformity.
Treatment is by incision and drainage with appropriate antibiotic therapy.
A collection of blood beneath the mucoperichondrium and posteriorly the mucoperiosteum of the nasal septum.
Usually complicates nasal trauma, either accidental or iatrogenic following septal surgery. Rarely a spontaneous haematoma can occur in a bleeding diathesis.
Presents as nasal obstruction with widening of the septum on inspection.
In the acute stage, treat by incision and drainage, however, after 48hrs, organization of haematoma occurs and evacuation of the clot is difficult. Antibiotics are given to prevent secondary infection.
Aetiology: Most cases of epistaxis are idiopathic, although bleeding can also result from a number of specific conditions.
Local conditions – include nasal trauma, nasal and paranasal sinus tumours and nasal septal perforations.
General conditions – include systemic bleeding diathesis such as leukemia, anticoagulant therapy and thrombocytopenia, and systemic vascular disorders. In hereditary hemorrhagic telangiectasia (Rendu-Oster-Weber syndrome), epistaxis is a prominent feature and usually arises from abnormal vessels on the nasal septum.
Systemic hypertension, although not a cause of epistaxis, is often associated with an increased severity of bleeding.
In most cases of epistaxis bleeding originates from the nasal septum, particularly Little’s area just behind the mucocutaneous junction where there is a rich anastomosis of vessels (Kiesselbach’s plexus). Bleeding from a posterosuperior site in the nasal cavity can occur, especially in the elderly.
Haemorrhage can present via the anterior nares or pass backwards via the nasopharynx where it is spat out or swallowed. In severe cases with profuse blood loss, hypotension and tachycardia may occur.
Initial measures to stop bleeding consist of exerting pressure on Little’s area by pinching the nose, with the patient leaning forward and spitting any blood into a bowl. If a bleeding vessel is seen, it may be coagulated with chemical or electric cautery following topical application of local anaesthetic, but this is rarely successful in the acute stage.
Epistaxis not responding to pressure necessitates nasal packing either with gauze impregnated with an antiseptic such as bismuth, iodoform and paraffin paste or with nasal balloons. Patients requiring nasal packing also require hospitalization.
In severe cases arterial ligation may be required. Endoscopic ligation or diathermy of the sphenopalatine artery in the nasal cavity is the commonest method. Other available arteries are the external carotid via the neck and the anterior ethmoidal via an inner canthal incision.
An alternative to arterial ligation in severe cases is arterial embolization performed with angiographic control by a radiologist. Intravenous resuscitation with blood or plasma substitute is necessary in cases where hypotension and tachycardia are present.
Early diagnosis of the deafness is the key to successful auditory rehabilitation, particularly in children with congenital deafness. With early intensive auditory training most children will develop the ability to communicate orally. Lip reading is an adjunct to oral communication. Manual communication, as in sign language, may be applicable for severely deaf people. Hearing aids Hearing aids amplify and modify incoming sound. The most modern aids use digital technology to tailor the performance of the aid to individual patterns of hearing loss. The postaural aid is mostly widely used, although body-worn and in the ear alternatives exist. Aids to communication such as electromagnetic loop systems can enable hearing aids in function in a group environment such as a theatre or lecture hall. Cochlear implants Direct electrical stimulation of the cochlear portion of the inner ear in response to incoming sound waves has been investigated in the development of cochlear implants. Electrodes are either placed on the surface of the cochlear(extracochlear) or inserted into the lumen of the cochlear(intracochlear). The use of cochlear implantation is now established in patients with both acquired and congenital severe sensorineural hearing loss. Profoundly deaf children ideally have implants fitted before primary school age.
Bullous myringitis Aetiology: An influenza virus infection of the tympanic membrane and deep external meatus, often associated with an acute otitis media. Clinical features: Presents as otalgia, deafness and serosanguinous otorrhoea. Haemorrhagic bullae are seen on otoscopy. Secondary bacterial infection can occur with purulent otorrhoea leading to otitis externa. Management: Treat with analgesics; local and systemic antibiotics for secondary bacterial infection. Tympanosclerosis Aetiology: Deposits of collagen beneath the mucosa of the tympanic membrane and middle ear following otitis media or middle ear surgery, particularly grommet insertion. Clinical features: Tympanosclerosis is mostly asymptomatic. Deposits are visible as white chalk patches in the tympanic membrane. Middle ear deposits may cause conductive deafness by ossicular fixation. Management: None if asymptomatic. Ossiculoplasty may be required for conductive deafness.
Intracranial spread of organism may occur via the middle ear by thrombophlebitis or by penetration of the dura of the middle or posterior cranial fossae. Meningitis Clinical features: Presents as headache, neck stiffness and photophobia. Lumbar puncture confirms the diagnosis. Pneumococcus and Haemophilus influenzae are common pathogens. Management: Treatment is by intravenous antibiotics followed by mastoidectomy once the meningitis has revolved. Venous sinus thrombosis Follows spread of middle ear and mastoid infection through the bone over the sigmoid sinus. Clinical features: Presents as headache, pyrexia and rigors. Extension of thrombus to the superior sagittal sinus leads to CSF outflow obstruction: otitic hydrocephalus. Management: Treatment is by intravenous antibiotics and mastoidectomy, during which infected thrombus may need to be removed from the sinus lumen. Intracranial abscess Extradural, subdural and cerebral abscesses occur. Infection spreads into the middle and posterior cranial fossae leading to temporal lobe and cerebellar abscesses respectively. Diagnosis by CT scan and treatment by neurosurgical drainage.
Pressure by cholesteatoma on the facial nerve in the middle ear or mastoid.
Presents as partial or complete lower motor neurone facial paralysis with evidence of chronic middle ear disease on otoscopy.
Treatment is by immediate surgical decompression of the facial nerve via a mastoidectomy operation.
Follows erosion of the bony labyrinth most commonly over the lateral semicircular canal. In the early stages compression of the air in the external meatus causes vertigo from mechanism stimulation of the labyrinth (fistula test). Later purulent infection in the inner ear causes severe vertigo and sensorineural deafness.
Treatment is by intravenous antibiotics and eradication of cholesteatoma via mastoidectomy.
Otorrhoea is associated with pain behind the eye and diplopia, caused by fifth and sixth nerve irritation resulting from air cell infection at the petrous apex.
Chronic otitis media (慢性中耳炎) Aetiology: Chronic inflammation of the middle ear cleft is usually associated with a perforation of the tympanic membrane. Perforation usually result from previous episodes of acute otitis media when the membrane fails to heal following rupture, but can be due to direct or indirect trauma. In children, perforations can persist following extrusion of ventilation tubes from the tympanic membrane. Organism can reach the middle ear from the Eustachian tube or from the external meatus. Chronic middle ear infection is also associated with ossicular damage, with the incudostapedial joint being the most commonly affected linkage. Clinical features: A central perforation in the pars tensa part of the membrane is associated with recurrent otorrhoea and conductive deafness. This type of perforation is regarded as safe as neurological complications are rare. An attic or marginal perforation can be associated with the development of a cholesteatoma and is regarded as unsafe. Management: Cases of central perforation should be kept dry. If recurrent otorrhoea occurs, ear drops containing a mixture of steroid and antibiotic are used and attention should be paid to possible source of infection in the nasopharynx, nose and paranasal sinuses. A dry perforation can be repaired by myringoplasty. Traumatic central perforations usually heal spontaneously.
Acute mastoiditis (急性乳突炎) Aetiology: Acute mastoiditis may complicate acute otitis media. Infection of the mastoid air cell system occurs. Clinical features: Presents as worsening of otalgia with tenderness over the mastoid antrum. The external meatus may be narrowed by oedema of the posterior-superior wall. In advanced cases a subperiosteal abscess may push the ear forward. Diagnosis is confirmed by opacity of the mastoid cells on CT scan. Management: Initially high-dose parenteral antibiotic therapy is required, although in cases that fail to respond to antibiotics, or in which a subperiosteal abscess has formed, surgical drainage via a cortical mastoidectomy is required.