Acute Otitis Media

Also known as: AOM

Acute inflammation of the middle ear cleft with a middle ear effusion and rapid onset of signs and symptoms of middle ear infection. It is among the commonest reasons for antibiotic prescription in children, with a peak incidence between 6 and 18 months.

Pathogenesis

Viral upper respiratory infection causes nasopharyngeal and Eustachian tube inflammation with mucosal oedema and ciliary dysfunction. Tube obstruction produces negative middle ear pressure and effusion, which is then colonised by nasopharyngeal bacteria refluxed into the middle ear. In children the Eustachian tube is shorter, wider and more horizontal, roughly 10 degrees to the horizontal compared with 45 degrees in adults, and the tensor veli palatini has less effective opening action, which explains the age distribution and the marked risk in cleft palate and Down syndrome.

Microbiology in the conjugate vaccine era

Streptococcus pneumoniae, with non vaccine serotypes now predominating among pneumococcal isolates.
Non typeable Haemophilus influenzae, which in many settings has become the leading isolate and is strongly associated with concurrent purulent conjunctivitis and with recurrent disease.
Moraxella catarrhalis, almost universally beta lactamase producing but with a high spontaneous resolution rate.
Streptococcus pyogenes, associated with early perforation and mastoiditis.
Staphylococcus aureus and Gram negative organisms in neonates and in ears with grommets.
Viruses are detected in 40 to 70 percent, frequently in combination with bacteria.

Spontaneous resolution rates, which underpin observation strategies: approximately 80 percent for Moraxella, 50 percent for Haemophilus influenzae and 20 percent for Streptococcus pneumoniae.

Risk factors

Age under 2 years, day care attendance, absent or short breastfeeding, supine bottle feeding, pacifier use beyond 6 months, tobacco smoke exposure, siblings, cleft palate, Down syndrome, craniofacial anomalies, immunodeficiency, and allergic rhinitis.

Symptoms

Rapid onset otalgia, the cardinal symptom. In preverbal children, holding, tugging or rubbing the ear has poor specificity when it is the only sign.
Fever, present in about two thirds, usually below 39 degrees Celsius. Higher fever raises the possibility of pneumococcal disease or a complication.
Irritability, disturbed sleep, poor feeding, vomiting and diarrhoea in infants.
Sudden relief of pain accompanied by purulent otorrhoea indicates spontaneous perforation.
Conductive hearing loss and aural fullness.

Otoscopic findings, which are the basis of diagnosis

Moderate to severe bulging of the tympanic membrane is the most specific sign.
Opacification, loss of the light reflex and loss of visible landmarks.
Erythema alone is unreliable, since crying and fever produce vascular injection.
Reduced or absent mobility on pneumatic otoscopy.
Otorrhoea through a fresh perforation, not attributable to otitis externa.
Bullous myringitis with haemorrhagic blebs on the drum, most often associated with the same pathogens as ordinary acute otitis media.

Red flags for complications

Postauricular swelling, tenderness, fluctuance, loss of the postauricular sulcus and a pinna pushed forward and downward, indicating mastoiditis.
Facial nerve palsy.
Vertigo, spontaneous nystagmus or sensorineural loss, indicating labyrinthitis.
Neck stiffness, photophobia, seizure, drowsiness or focal neurology, indicating meningitis or intracranial abscess.
Persistent high fever, severe headache and swinging pyrexia, suggesting sigmoid sinus thrombosis.
Deterioration or failure to improve after 72 hours of appropriate antibiotics.

A clinical diagnosis requiring all three elements: acute onset, middle ear effusion, and signs of middle ear inflammation. Diagnosing acute otitis media on a red drum in a crying child is the commonest cause of unnecessary antibiotic prescription.

Pneumatic otoscopy is the reference bedside technique. Reduced mobility confirms effusion.
Tympanometry provides objective confirmation of effusion where otoscopy is difficult. A type B trace with normal canal volume indicates effusion.
Remove obstructing wax before pronouncing on the drum.
Tympanocentesis with culture is indicated in neonates under 6 weeks, immunocompromised children, severe systemic illness, failure of second line antibiotics, and suspected suppurative complication. It is both diagnostic and therapeutic.
Culture of fresh otorrhoea taken under direct vision when perforation has occurred.
Contrast enhanced computed tomography of the temporal bone with magnetic resonance imaging and venography when mastoiditis or intracranial complication is suspected. Do not delay antibiotics and neurosurgical involvement for imaging in a child with meningism.
Blood culture, full blood count and inflammatory markers only in systemically unwell or complicated cases.
Audiometry after 6 to 12 weeks when hearing loss persists.

Differential diagnosis

Otitis media with effusion: no acute inflammation, no significant pain or fever, retracted or neutral drum.
Acute otitis externa: pain on tragal pressure, canal oedema and debris, normal drum when visualised.
Referred otalgia from tonsillitis, dental disease or the temporomandibular joint, with a normal drum.
Bullous myringitis and herpes zoster oticus.
Mastoiditis, which should be considered whenever postauricular signs are present.

Analgesia first, in every child, from the outset

Paracetamol 15 mg/kg orally every 6 hours, maximum 60 mg/kg in 24 hours. Adults 1 g every 6 hours, maximum 4 g in 24 hours.
Ibuprofen 10 mg/kg orally every 8 hours with food, maximum 40 mg/kg in 24 hours. Adults 400 mg every 8 hours. Avoid in dehydration, significant renal impairment and varicella.
Alternating the two provides better coverage in severe pain.
Topical anaesthetic drops are not used where the drum may be perforated, and do not replace systemic analgesia.
Decongestants and antihistamines do not shorten illness or reduce complications and are not recommended.

Deciding on antibiotics

Observation with a safety net for 48 to 72 hours is appropriate for:

Children over 2 years with unilateral disease, mild pain, temperature below 39 degrees Celsius, no otorrhoea, reliable carers and access to review.
Provide a delayed prescription to be started if there is no improvement or if deterioration occurs.

Immediate antibiotics are indicated for:

Any infant under 6 months.
Children 6 to 24 months with bilateral disease.
Otorrhoea from perforation.
Severe symptoms: moderate to severe otalgia, otalgia for more than 48 hours, or temperature 39 degrees Celsius or above.
Systemic illness or suspected complication.
Immunodeficiency, cochlear implant, craniofacial anomaly, cleft palate, Down syndrome, or an only hearing ear.

First line antibiotic regimens

Amoxicillin 80 to 90 mg/kg per day orally divided into two or three doses, maximum 3 g per day. The high dose overcomes intermediate penicillin resistant pneumococci by exceeding the minimum inhibitory concentration in middle ear fluid.
Duration: 10 days for children under 2 years, for severe disease, for perforation and for recurrent disease. 5 to 7 days is adequate for uncomplicated disease in children over 2 years.
Adults: amoxicillin 500 mg to 1 g orally three times daily for 5 to 7 days.

When to use a beta lactamase stable agent from the outset

Amoxicillin within the preceding 30 days.
Concurrent purulent conjunctivitis, which predicts non typeable Haemophilus influenzae.
Recurrent acute otitis media unresponsive to amoxicillin.
Co amoxiclav dosed at 90 mg/kg per day of the amoxicillin component with 6.4 mg/kg per day of clavulanate, divided twice daily. Using a standard formulation to achieve high amoxicillin dosing delivers excessive clavulanate and causes diarrhoea, so use a high ratio preparation.
Adults: co amoxiclav 625 mg three times daily or 1 g twice daily for 5 to 7 days.

Penicillin allergy

Non severe, delayed rash: cefuroxime axetil 30 mg/kg per day divided twice daily, maximum 1 g per day; or cefdinir 14 mg/kg per day; or cefpodoxime 10 mg/kg per day divided twice daily.
Severe or immediate hypersensitivity: azithromycin 10 mg/kg on day 1 then 5 mg/kg daily for 4 days, accepting substantially inferior pneumococcal and Haemophilus activity; or clindamycin 30 to 40 mg/kg per day divided three times daily, which covers pneumococcus but not Haemophilus.
Ceftriaxone 50 mg/kg intramuscularly or intravenously once daily for 1 to 3 days when oral therapy is not tolerated or has failed. Three days is more effective than a single dose in treatment failure.

Acute otitis media with perforation and otorrhoea

Add ciprofloxacin 0.3 percent with dexamethasone 0.1 percent, 4 drops twice daily for 7 days. Topical therapy achieves far higher local concentrations than oral therapy.
Avoid aminoglycoside drops in a perforated ear.
Continue oral antibiotics as above in children under 2 years and in severe disease.

Failure at 48 to 72 hours

Re examine, confirm the diagnosis and exclude complications, then escalate:

Amoxicillin failure: switch to high dose co amoxiclav.
Co amoxiclav failure: ceftriaxone 50 mg/kg daily for 3 days.
Ceftriaxone failure: tympanocentesis for culture, with clindamycin plus a third generation cephalosporin considered pending results, and specialist involvement.
Reconsider mastoiditis, an alternative diagnosis, and adherence.

Myringotomy

Indications: severe unremitting pain, suppurative complication, failure of second line therapy, culture required in a neonate or immunocompromised child, and hyperpyrexia unresponsive to treatment. Perform in the anteroinferior quadrant to avoid the ossicles, jugular bulb and round window.

Complications and their management

Acute mastoiditis: admit, intravenous ceftriaxone 50 mg/kg twice daily plus consideration of anti staphylococcal cover, myringotomy with or without grommet, contrast computed tomography, and cortical mastoidectomy for subperiosteal abscess, failure to respond within 48 hours, or intracranial extension.
Facial nerve palsy: myringotomy and intravenous antibiotics, with high recovery rates. Decompression is rarely required.
Labyrinthitis: intravenous antibiotics, vestibular sedatives short term, and urgent assessment for meningitis.
Meningitis, extradural and subdural abscess, brain abscess, sigmoid sinus thrombosis and otitic hydrocephalus: intravenous ceftriaxone 2 g twice daily in adults or 50 mg/kg twice daily in children plus metronidazole, urgent imaging with venography, neurosurgical involvement and mastoid exploration.
Persistent effusion, present in 60 to 70 percent at 2 weeks, 40 percent at 1 month and 10 to 25 percent at 3 months. Arrange audiometry when it persists at 3 months.

Prevention

Complete pneumococcal conjugate vaccination and annual influenza vaccination.
Exclusive breastfeeding for at least 6 months.
Eliminate tobacco smoke exposure.
Avoid supine bottle feeding and discontinue the pacifier after 6 months.
Reduce day care exposure where feasible.

Clinical toolsCalculators

BMI GCS EDD Parkland Formula

Corrected Sodium Corrected Calcium Anion Gap Creatinine Clearance Insulin Calculations qSOFA Wells PE Wells DVT CHA₂DS₂-VASc HAS-BLED CURB-65 Centor/McIsaac

Vocal Cord Nodules

Also known as: Singer's nodules

Bilateral, symmetrical, benign lesions of the vocal fold epithelium and superficial lamina propria arising from repetitive phonotrauma. They are the archetypal benign phonotraumatic lesion and the clearest demonstration that voice disorders are often behavioural in origin and behavioural in treatment.

Why they occur where they do

Nodules form at the junction of the anterior and middle thirds of the membranous vocal fold. This is the point of maximum amplitude of vibration and therefore of maximum collision force during phonation. It is also the midpoint of the membranous fold, which extends from the anterior commissure to the vocal process, and it is a relative watershed for the vascular supply. The repeated impact at this point produces microtrauma, basement membrane injury, fibronectin deposition, oedema and eventually fibrosis and epithelial hyperplasia.

Pathophysiology and the vibratory consequence

Early lesions are oedematous and soft, with loose oedematous superficial lamina propria and an intact mucosal wave. With continued trauma they become firm and fibrotic, with thickened basement membrane, collagen deposition and epithelial hyperkeratosis. The lesion increases the mass of the vibrating cover and, once fibrotic, increases its stiffness, damping the mucosal wave. The bilateral lesions prevent complete glottic closure, producing a characteristic hourglass glottic configuration with an anterior and posterior gap, which causes air escape and breathiness. The patient compensates by increasing subglottic pressure and adductory force, which increases collision and perpetuates the lesion. Breaking this cycle is the treatment.

Epidemiology and risk

Commonest benign vocal fold lesion.
Adult women aged 20 to 50, and prepubertal boys, are the groups most affected. The female predominance in adults relates to a higher fundamental frequency with more vibratory cycles per unit time, a shorter membranous fold, a lower hyaluronic acid content in the superficial lamina propria which is less protective, and occupational factors.
Occupational groups: teachers, singers, actors, call centre workers, clergy, coaches, market traders, aerobics instructors and nursery staff.
Children: nodules occur in an estimated 15 to 20 percent of school aged children with dysphonia, associated with shouting and hard glottal attack. They frequently regress at puberty in boys as the larynx grows.

Contributing factors: vocal misuse and abuse, hard glottal attack, speaking at an inappropriate pitch or volume, poor breath support, dehydration, laryngopharyngeal reflux, smoking, allergic rhinitis with throat clearing, and psychological stress with laryngeal muscle tension.

Hoarseness of gradual onset, typically described as rough and breathy.
Reduced vocal range with loss of the upper register and difficulty with soft high notes, which singers notice long before speakers do.
Vocal fatigue with the voice deteriorating through the day and through the week, and recovering with rest, which is a characteristic pattern.
Increased effort required to phonate.
Delayed voice onset and voice breaks.
Frequent throat clearing and a sensation of a lump.
Neck and laryngeal discomfort from compensatory muscle tension.
Symptoms present for months to years.
No pain, no dysphagia, no dyspnoea, no weight loss. Any of these should redirect the diagnosis.

Examination

Perceptual voice assessment using GRBAS or the Consensus Auditory Perceptual Evaluation of Voice, and a patient reported measure such as the Voice Handicap Index.
Reduced maximum phonation time.
Flexible nasolaryngoscopy showing bilateral, symmetrical, whitish or greyish elevations at the junction of the anterior and middle thirds, with an hourglass glottic closure pattern.
Signs of muscle tension dysphonia: supraglottic anteroposterior or lateral compression, which frequently coexists and which must be addressed.
Assessment of the whole larynx for reflux changes, other lesions and mobility.

Red flags indicating a different diagnosis

Unilateral lesion, which is not a nodule and requires a different differential including polyp, cyst, granuloma, papilloma and carcinoma.
Progressive rather than fluctuating hoarseness.
Sudden onset, suggesting haemorrhage or a polyp.
Pain, dysphagia, otalgia, haemoptysis or weight loss.
A neck mass.
Smoking history with a persistent white lesion, requiring biopsy for dysplasia and carcinoma.
Failure to improve with adequate voice therapy, which requires reassessment and often microlaryngoscopy.

Flexible nasolaryngoscopy, which identifies the lesions but which cannot reliably distinguish a nodule from a cyst or a small polyp.
Videostroboscopy, which is the key investigation and which should be regarded as necessary rather than optional in this condition. It assesses the mucosal wave, amplitude, symmetry, periodicity and glottic closure. A soft oedematous nodule preserves the mucosal wave; a fibrotic nodule reduces it; a subepithelial cyst produces a segmentally absent wave over the lesion with an associated contact reaction on the opposite fold which mimics a contralateral nodule. This distinction is central, because nodules respond to voice therapy while cysts do not, and operating on a nodule or persisting with therapy for a cyst are the two commonest errors in this area.
Acoustic analysis with jitter, shimmer and harmonic to noise ratio, and aerodynamic measures including maximum phonation time and phonation threshold pressure, which quantify the disorder and track response.
Direct microlaryngoscopy under general anaesthesia where the diagnosis is uncertain, where there is a suspicion of malignancy, and as part of planned surgery. Palpation of the lesion at microlaryngoscopy distinguishes a soft nodule from a firm cyst.
Assessment for reflux, allergy and nasal disease.

Differential diagnosis and the discriminating feature

Vocal fold polyp: usually unilateral, often pedunculated, frequently with a history of a single episode of vocal strain or of a haemorrhage.
Intracordal cyst: unilateral, subepithelial, with a segmentally absent mucosal wave and a contralateral reactive lesion. Does not respond to voice therapy and requires microsurgical excision.
Pseudocyst and fibrous mass.
Reinke oedema: diffuse bilateral polypoid swelling of the whole membranous fold in a smoker, with a very low pitched voice.
Sulcus vocalis and vocal fold scar: a linear depression with an adherent epithelium and an absent mucosal wave.
Contact granuloma: posterior, on the vocal process, associated with reflux and intubation.
Papillomatosis: exophytic verrucous lesions.
Dysplasia and carcinoma: usually unilateral, irregular, with leukoplakia and reduced mucosal wave in a smoker.
Muscle tension dysphonia without a lesion.

Voice therapy is the primary treatment, and surgery is reserved for failure. The order matters: operating first and offering therapy afterwards produces recurrence, because the behaviour that created the lesion is unchanged.

Voice therapy, which is first line in essentially every case

Referral to a speech and language therapist with experience in voice disorders.
Vocal hygiene: adequate hydration with the aim of pale urine, avoidance of throat clearing with substitution of a hard swallow or a sip of water, avoidance of whispering, avoidance of shouting and of speaking over background noise, avoidance of caffeine, alcohol and smoking, and adequate sleep.
Direct therapy techniques: resonant voice therapy, semi occluded vocal tract exercises including straw phonation, lip trills and humming, which reduce vocal fold collision force while maintaining vibration; confidential voice; and the Lessac Madsen resonant voice therapy or vocal function exercise programmes.
Elimination of hard glottal attack, using easy onset and breathy onset techniques.
Optimisation of breath support and reduction of laryngeal muscle tension, with manual circumlaryngeal therapy where there is palpable tension.
Adjustment of habitual pitch and loudness.
Occupational modification: amplification for teachers, scheduled voice rest periods, reduced speaking hours, and workplace acoustic improvements.
A course of therapy is typically 6 to 12 sessions over 3 to 6 months, and adherence determines outcome. Explain at the outset that this is a behavioural treatment requiring sustained practice, not a passive intervention.
Around 70 to 90 percent of true nodules resolve or improve sufficiently with adequate therapy, which is why surgery should not be offered first.

Treat coexisting conditions

Laryngopharyngeal reflux with lifestyle modification and a proton pump inhibitor taken 30 to 60 minutes before meals for 8 to 12 weeks.
Allergic rhinitis and chronic rhinosinusitis, which drive throat clearing and cough.
Chronic cough.
Smoking cessation.
Psychological factors and stress, with referral where anxiety is driving muscle tension.

Surgery

Indications:

Failure of an adequate trial of voice therapy, meaning a properly delivered course with documented adherence over at least 3 to 6 months.
Fibrotic, mature nodules that are unlikely to resolve with therapy alone, though these should still have therapy first and afterwards.
Diagnostic uncertainty requiring tissue.
Suspicion of malignancy.
A professional voice user whose livelihood is at stake and in whom therapy has failed, after full discussion of the risks.

Technique:

Microlaryngoscopy under general anaesthesia with suspension, using microlaryngeal instruments and an operating microscope.
Microflap technique with a cordotomy incision lateral to the lesion and elevation of the epithelium, allowing removal of the lesion from within the superficial lamina propria with preservation of the overlying epithelium and the deeper layers.
Preserve the superficial lamina propria absolutely. This layer cannot be reconstructed, and its loss produces permanent scarring with an absent mucosal wave and a voice that is worse than before surgery. Overzealous excision is the principal complication and it is irreversible.
Avoid stripping the vocal fold, which is an obsolete technique that produces scarring.
Cold steel instruments are preferred to laser for these lesions, given the thermal injury to adjacent lamina propria with laser.
Address both folds where both are involved, but avoid dissecting both anterior commissure regions in the same operation where the lesions are close to the commissure, given the risk of anterior glottic web formation.

Perioperative and postoperative care

Absolute voice rest for 3 to 7 days, followed by graduated return to voice use under therapist supervision over 2 to 4 weeks.
Hydration and humidification.
Antireflux therapy.
Avoid nonsteroidal anti inflammatory drugs and aspirin perioperatively given bleeding into the fold.
Mandatory postoperative voice therapy. Surgery without behavioural change guarantees recurrence, and this must be stated before the patient consents.
Return to professional voice use at around 4 to 6 weeks, guided by stroboscopy.

Children

Voice therapy is the treatment. Surgery is very rarely indicated in a child with nodules.
Many resolve spontaneously at puberty, particularly in boys, as the larynx enlarges.
Therapy must be age appropriate and involve parents and teachers, addressing shouting behaviour and the environment. In a child who shouts because of a hearing loss, treat the hearing loss.
Assess for adenotonsillar obstruction, allergy and reflux, which contribute.

Follow up

Review with videostroboscopy at 3 and 6 months, and again after any surgery. Continue therapy support for professional voice users indefinitely. Recurrence indicates that the phonotraumatic behaviour has resumed and calls for renewed behavioural intervention rather than repeat surgery.

Acute Otitis Media

Overview

Clinical Features

Diagnosis

Management

Overview

Clinical Features

Diagnosis

Management