Ear, nose and throat

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chapter 27 Ear, nose and throat

INTRODUCTION AND OVERVIEW

This chapter is a brief summation of commonly encountered otolaryngology, head and neck issues in general practice. It is not exhaustive but, rather, aims to give the reader an understanding of common problems and assist in management.

THE EAR

The ear is the organ of hearing. In medicine it is divided for descriptive and functional purposes into an outer, middle and inner ear (Fig 27.1). The ear amplifies sound, converting it from mechanical energy into an electrical impulse, which the individual translates. It is unusual for any disease process to affect more than one component at any one time.

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FIGURE 27.1 Anatomy of the ear

OUTER EAR

The outer ear acts as a funnel, collecting sound waves and concentrating them onto the tympanic membrane (eardrum). It includes the pinna (auricle) and external auditory canal (EAC), and it represents the part accessible to examination, and is not uncommonly an area of decoration by piercing. The EAC is cylindrical in shape, and approximately 2.5 cm long. The lateral EAC is composed of cartilage, and the medial part is bony. The cartilaginous aspect contains hair, and cerumen (earwax) is produced here. The canal is lined with very specialised squamous epithelium, which self-cleans in a migratory pattern from inside to out. It is important at this stage to understand the harm caused by cotton buds in inhibiting this process. Cotton buds tend to compress wax and can cause occlusion, deafness and infection.

Ear wax

Excess ear wax may present as loss of hearing acuity, tinnitus, a sense of fullness in the ear or dizziness.

The chemical basis of cerumen, or ear wax, is a fat. Like all body fats, the fluidity is affected by the ratio of omega-3 to omega-6 fatty acids and saturated fats.

Although genetic factors are thought to be involved, hard wax (inviting medical removal) may simply reflect a lack of omega-3s in the person’s diet. Hence, increasing omega-3 intake may help to prevent the problem. In the acute situation, treatment is with drops to soften the ear wax. This may need to be followed by syringing or suction aural toilet.

Trauma

‘Cauliflower ear’

‘Cauliflower ear’ is a commonly seen injury endured by rugby players caused by blunt trauma to the ear. The shearing forces cause a sub-perichondrial haematoma, (Fig 27.2) which compromises the diffusion nutrient supply to the cartilage. The haematoma is susceptible to infection, which can further deplete nutrient supply to the cartilage. The cartilage is replaced with fibrous scar tissue and deformity results. Therefore immediate haematoma evacuation is required in cases of acute trauma.

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FIGURE 27.2 Haematoma in cauliflower ear

Foreign body

Festive seasons and birthdays often herald the season of foreign bodies in the ears of children (Fig 27.3). Anything small enough, from beads to batteries, has been found there. The deeper the foreign body, the more difficult and painful it is to remove. In children a general anaesthetic may be required. In general, appropriate equipment allows easy removal with a compliant child. The hardest to remove is often the foreign body that others have attempted to remove. It may be associated with tympanic membrane perforation, although this is unlikely and depends largely on the mechanism of trauma. If associated with a perforated eardrum, it is reassuring to know that most heal spontaneously. Water precautions should be adhered to until the eardrum heals, and an audiogram is recommended (in a perforated tympanic membrane).

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FIGURE 27.3 Removal of foreign body from the ear

One unpleasant type of foreign body is an insect near or attached to the tympanic membrane. As first aid, instant pain relief and destruction of the creature, olive oil poured straight into the ear is safe and effective.

Otitis externa

Ear infections are particularly common in cultures where swimming is popular. Otitis externa (OE) refers to infection of the EAC (Fig 27.4). It is commonly caused by Pseudomonas, Staphylococcus aureus or fungal species. However, because the EAC is just like skin, other causes of OE include viral infection and allergy (seborrhoeic).

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FIGURE 27.4 Otitis extema

Otitis externa is often preceded by a combination of maceration (cotton buds) and water trapping. Dermatological conditions of the ear canal also predispose to OE. It is not uncommon to have exostoses, which can predispose to OE by water trapping. In OE the canal is typically oedematous and reddened. The diagnosis is made clinically with discharge, deafness and severe otalgia. In fungal infections, spores may be encountered. Compared with otitis media, otitis externa is exquisitely tender, esapecially with traction of the pinna, or there is pain with movement of the jaw, and the patient can therefore be difficult to examine.

A swab for culture and sensitivity of causative organisms can guide therapy decisions. The recalcitrant nature of OE is often due to inadequate use of ototopical medication. Oral antibiotics are rarely warranted for OE and reserved for systemic illness, severe surrounding cellulitis and recalcitrant infections. Topical preparations are far more effective in attaining higher antibiotic concentration at the infected site, and minimise the risk of antimicrobial resistance. It is important to perform a micro-ear toilet to clear the EAC of debris, to allow greater penetration of the antibiotics/antifungals. This is also possible with ‘tissue spears’—the corners of a tissue may be rolled and gently inserted into the ear in a twisting motion, to absorb moisture. This also allows better penetration of antibiotics and antifungals. A cotton bud has rigidity and therefore causes more trauma, whereas the tissue spear acts purely as absorbent. In severe cases of occlusion, an otowick is used. This is a cottonoid pledget that expands with ototopical antibiotic/antifungal preparations to allow delivery of the ototopical preparation to the area of inflammation/infection.

Ototopical medication has recently come under close scrutiny because of the potential toxic effect of the aminoglycosides in some ototopical medications. The Australasian Society of Otolaryngology, Head and Neck Surgeons recently published guidelines on their use.1

• When possible, topical antibiotic preparations that are free of potential ototoxicity are preferable to those that do have the potential for otologic injury in patients with an open middle ear or mastoid.
• When a potentially ototoxic antibiotic is chosen, it should be used only in infected ears and it should be discontinued shortly after the infection has resolved.
• When a potentially ototoxic antibiotic drop is prescribed for a patient with an open middle ear or mastoid, the patient or parent should be warned of the risk of ototoxicity.
• The patient or parent should be specifically instructed to call the physician or return to the office if the patient develops dizziness or vertigo, hearing loss or a worsening of hearing if such an impairment was already present, or tinnitus.
• If the tympanic membrane is known to be intact and the middle ear and mastoid are closed, then the use of potentially ototoxic preparations presents no risk of ototoxic injury.

Prevention: Keep the ear dry, especially with swimming and water sports. This can be achieved with fitted earplugs and a bathing cap. If the canal becomes wet, apply spirit drops to help dry the canal. Dry canal with a hair dryer held about 30 cm from the ear.

Malignant otitis externa

What may seem a simple ear infection in an immunocompromised patient (commonly the diabetic or elderly patient) can rapidly deteriorate into a life-threatening condition. A Pseudomonas infection can colonise and spread into the temporal bone and become very difficult to eradicate. The patient presents with severe otalgia, aural discharge and progressive cranial nerve neuropathies. These patients warrant urgent referral to otolaryngology services.

Tumours

Basal cell carcinoma and squamous cell carcinoma (melanoma is less likely) must not be forgotten in consideration of ongoing discharge and eczema of the pinna in elderly patients, especially as the area is prone to UV sun exposure. Initially superficial, these lesions tend to ulcerate and weep. They require definitive surgical management.

Prevention: Everyday sun protection with sunscreen, including the ears, and a hat with a broad brim.

Exostoses

Exostoses are a benign condition of the EAC seen frequently in avid swimmers, culminating over many years. They are more commonly associated with cold water exposure and are well represented in surfing communities. An osteoma is a single, solitary lump, whereas exostoses are multiple. They are smooth bony protuberances of the ear canal. Although benign in nature, they become problematic when they are large enough to inhibit the ear’s natural self-cleaning. Water trapping occurs on repeated swimming, and the ear canal becomes irritated, and macerated with attempted cleaning, and it is then only a matter of time before repeated infections occur. It is more a problem in this population as it limits the joy of the aetiology: swimming and water sports. Most are observed until they become problematic and then are surgically reduced.

Prevention: Fitted earplugs can be worn for swimming, and the ear canal should be dried with a hairdryer after swimming and hair washing.

TYMPANIC MEMBRANE

The tympanic membrane (eardrum) is the Rolf Harris of the ear. It is a thin membrane separating the external auditory canal from the middle ear, approximately 10 mm in diameter (Fig 27.5). It vibrates (wobbles) in response to mechanical energy from sound waves. It is attached to the ossicles (ear bones), which together amplify sound energy to the inner ear. The tympanic membrane is important not only in sound transmission but also in preventing water entering the middle ear cleft. The respiratory epithelium of the middle ear cleft differs from the squamous epithelium of the external auditory canal. Impaired function consequently has profound effects on the hearing ability of the affected ear. Various conditions can affect the tympanic membrane, and include:

• myringitis—infection of the tympanic membrane; may be viral or bacterial; treated with ototopical antibiotics
• bulla myringitis—an acutely painful condition characterised by bulla formation on the tympanic membrane; often caused by a virus and as such supportive therapy is required, although superimposed bacterial infection is not uncommon
• myringosclerosis—scarring of the tympanic membrane in the form of collagen deposits; appears as ‘clouds’ or ‘chalk marks’ on otoscopy and is often a result of trauma from infection or previous grommet insertion; intervention is rarely necessary unless the condition is causing conductive hearing loss.
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FIGURE 27.5 The tympanic membrane

Tympanic membrane perforation

Tympanic membrane perforation (Fig 27.6) may result from trauma (personal or surgical), infection or pressure changes. It may be marginal, involving part of the tympanic membrane annulus, or central, involving any other part. It needs to be distinguished from a retraction.

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FIGURE 27.6 Tympanic membrane perforation

Examine by removing the blood clot by suction or by gentle mopping. Exclude any foreign body and check the hearing, as perforation can cause hearing loss.

The mainstay of treatment is supportive, maintaining water precautions (to prevent infection) and obtaining an audiogram. Prescribe a broad-spectrum antibiotic and adequate analgesia. Review in two days, then weekly until healed. Perforations tend to heal spontaneously over days to months in a non-infected ear with good eustachian tube function. Hearing should be rechecked two months after the injury.

Non-healing perforations may require surgical repair with a myringoplasty. Referral is warranted earlier if suspicious of complications such as inner ear involvement expressed as tinnitus, vertigo, sensorineural hearing loss, bleeding, otalgia or facial nerve paralysis.

Prevention: Discourage any objects being inserted into the ear canal except by trained professionals.

MIDDLE EAR

The middle ear is a collective term describing the space bounded by the tympanic membrane laterally and the inner ear medially. It houses the ossicles, the bones of sound conduction. It is lined by respiratory mucosa and has a connection to the posteriorly based mastoid air cells, and is drained by the eustachian tube antero-inferiorly. The external ear collects the sound waves, while the middle ear amplifies the sound transmission to the inner ear. The eustachian tube’s primary function is to allow equalisation of pressure, to maximise sound transmission.

Middle ear effusion

Failure of adequate drainage is not uncommon in children, as the eustachian tube is shorter, the diameter is thinner and it lies in a more horizontal plane than the adult eustachian tube (Table 27.1). The narrow lumen is easily obstructed in upper respiratory tract infections, there is less capacity for natural drainage, and its length is thought to allow more exposure to reflux and, hence, inflammation. Adenoidal hypertrophy may predispose to lower eustachian tube obstruction. (In the adult population, one must be wary of neoplastic postnasal obstruction.)

TABLE 27.1 Issue in a child’s eustachian tube, compared with an adult

Anatomy Consequence
More horizontal lie Less capacity to drain
Smaller diameter More easily occluded
Shorter
Easier to reflux
More prone to inflammation

Failure of drainage leads to accumulation of fluid, as water is absorbed through the middle ear mucosa, the tympanic membrane is retracted or the fluid thickens. Consequently, the ossicles fail to vibrate, and lack of aeration of the middle ear cleft leads to dampening of the sound waves and conductive hearing loss.

Surgical treatment (grommets ± adenoidectomy) is usually reserved for non-resolving effusions causing developmental delay such as speech and learning. Most will, spontaneously, resorb or drain within 4–6 weeks. Referral is indicated if there is persistent middle ear effusion three months after an attack of acute otitis media, or if there are signs of hearing loss, frequent recurrences or severe complications (e.g. mastoiditis).

Acute otitis media

Accumulation and contamination of middle ear fluid, which is normally sterile, leads to infection, otitis media. It is a common disease of the paediatric population. The patient typically presents as a febrile, runny-nose mouth breather. Again, this is because of the special relationship of the eustachian tube with the post-nasal space. Because of this relationship it may also be associated with rhinitis, sinusitis, snoring, obstructive sleep apnoea and asthma-like associations. It has an increased incidence in lower socioeconomic groups, and an alarmingly high prevalence in the Australian Indigenous population.

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FIGURE 27.7 Middle ear with Eustachian tube

The common organisms found in infection of the middle ear include Streptococcus pneumoniae, Haemophilus influenzae and Moraxella catarrhalis. A less likely cause of infection is gram-negative bacteria or a viral aetiology.

The controversy surrounding the use of oral antibiotics in acute otitis media has been noted. In a meta-analysis it was found that the NNT (number needed to treat to benefit one patient) was 17. The benefit was small—a reduction in pain by 12 hours. In this study, the likelihood of complications was not increased in the non-treated group.2,3 Against this, the cost of increasing antibiotic resistance, and the disruption to the ecosystem of the gut flora, have to be counted.

Pain relief in otitis media can be as simple as showing the parent how to use a 2 mL syringe to put olive oil into the child’s ear.

Complicated otitis media (see below) requires full medical treatment.

Recurrent otitis media has been considered a response to food allergy. The theory is that cytokines released when problem foods are eaten results in oedema of membranes in the respiratory tract. Easy blockage of small passages, such as the eustachian tube, ensues.

It can be a useful trial of therapy to put all children on a strict one-month dairy-free diet before sending them for tonsillectomy, grommets or other surgical interventions. Many respond to this diet, and a few respond once gluten/wheat, citrus and other food allergens are also withdrawn. It should be noted that such ‘allergic’ responses are not usually mediated through the immunoglobin E (IgE) arm of the immune system and as such should not, strictly speaking, be called allergies.

The immune mechanisms involved may be IgG or IgA mediated, or a direct cytokine response not involving any immune globulin. Inhalant allergens must also be considered; and, of course, a marked and statistically significant association has been found between the incidence of otitis media and tonsillectomy in children and parental smoking in the home environment.

Otitis media, along with chronic sinusitis, recurrent tonsillitis and migraine, all tend to cluster within individuals and families. Understanding the biochemistry helps us see them as systemic problems, and rationalises the approach.

In babies and children, a red tympanic membrane does not necessarily mean otitis media. The tympanic membrane can appear red if the child is crying.

Complications of otitis media

Acute otitis media generally responds well to adequate analgesia with or without oral antibiotics. Most effusions will resolve within 3–6 months with active non-intervention. Surgical intervention is reserved for chronicity, recurrence or impending complication of otitis media. There is much debate surrounding absolute indications for intervening.

Under pressure, several sequelae may occur in otitis media. By far the most important implications of prolonged or recurrent infections are the serious consequences for the growth and learning of a child. Complications of otitis media are associated with direct spreading of infection, and include:

• mastoiditis
• meningitis
• Bezold’s abscess (neck abscess)
• sigmoid sinus thrombosis
• apicitis
• tympanic membrane perforation.

All these are, hopefully, prevented with early intervention. Prompt otolaryngological referral is advised.

Chronic otitis media with effusions (OME)

Most effusions will resolve within 3–6 months with active non-intervention. Surgical intervention is reserved for chronicity, recurrence or impending complication of otitis media. There is much debate surrounding absolute indications for intervening.

Cholesteatoma

A cholesteatoma is a benign skin growth in an abnormal location within the ear. The skin-lined sac increases in size, leading to infection and bony destruction. It is dangerous because of its location near the tympanic membrane and its tendency to expand and cause destruction of neighbouring structures. Its clinical significance is in recalcitrant discharging ears and its destructive process.

Complications of untreated cholesteatoma include those listed in Table 27.2. Complete surgical removal is urgent, essential and unavoidable.

TABLE 27.2 Complications of cholesteatoma

Pathology Symptom/sign
Erosion of ossicles Deafness
Erosion of facial nerve Facial palsy
Sigmoid sinus thrombosis/hydrocephalus Meningism
Erosion of labyrinth Balance difficulties
Infection petrous apex Gardener’s sign
Tegmen bone erosion Brain abscess/meningitis

Bell’s palsy

Bell’s palsy is the most common palsy. Full recovery is the normal outcome with active non-intervention. It is important to note that it is a diagnosis of exclusion, and therefore a careful history and examination is paramount. The aetiology is thought to be viral (herpes virus) in nature; however, steroids and anti-viral medication are still controversial in the literature.

Therapeutic approaches include:4

• acyclovir plus prednisolone
• vitamin therapy (including vitamin B12, B6 and zinc), which may help nerve growth
• relaxation techniques
• electrical stimulation acupuncture (more trials needed).

Otosclerosis

Otosclerosis is a bone disease of the otic capsule resulting in abnormal deposition of bone around the otic capsule. The presenting symptom is deafness, more commonly from stapes fixation (preventing ossicular mobility). More rare is ossification of the cochlea, which renders the hair cells inactive. There is a slight female preponderance and it is therefore thought to be associated with hormonal fluctuation. When suspected, audiogram and referral are warranted.

RHINOLOGY

The nose is the organ of olfaction (smell), and has several important functions besides olfaction, including cleansing inspired air, humidification and warming. Functionally it has an external and an internal part (Fig 27.8). The external part contains bone and cartilage and acts to prop open the portal for air movement. The internal nose is highly vascular, particularly over the turbinates, to allow warming of air, and plays a role in nasal defence. Unfortunately, engorgement may also cause obstruction. Problems of the nose surround difficulties in the normal physiology of the nose. The two most commonly dealt with by doctors include epistaxis and sinusitis.

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FIGURE 27.8 Anatomy of the nose

EPISTAXIS

Otherwise known as nose bleeding, epistaxis is a common problem. It is most commonly idiopathic in origin. In very basic terms, it may be divided into anterior and posterior bleeding. Anterior bleeding is by far the most common presentation and can be precipitated in children by nose picking, repeated blowing or other trauma. Most anterior bleeding will stop spontaneously with pressure alone (with or without cotton wool pledget). A confluence of small vessels on the anterior septum, known as Little’s area, is the most common site of bleeding, and is very amenable to cauterisation in the absence of any bleeding diathesis.

Posterior bleeding is more common in older hypertensive patients and is more difficult to manage, not uncommonly requiring hospital admission and review. Neoplastic cause or coagulation defect should be considered.

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FIGURE 27.9 Severe postoperative epistaxis

SINUSITIS

The sinuses are located in the bony make-up of the face, and include the paired maxillary, ethmoid, frontal and sphenoid sinuses. Their role continues to be debated in the literature and includes resonance of sound, facial strength without mass, humidification and warming of inspired air, and other functions. The clinical significance is vastly different and focuses on pain and discharge. Sinusitis may be acute or chronic and in simple terms occurs after mucus accumulation in the sinuses, which often becomes infected, leading to pain, discharge and nasal obstruction. Odontogenic origin must also be a consideration. The mechanism of blockage may be due to obstruction of the natural sinus drainage pathway, failure of muco-ciliary clearance or thickened inspissated mucus. The most common infection is bacterial, with Streptococcus pneumoniae and Haemophilus influenzae the most common. Viral infection can implicate narrow drainage pathways in sinusitis. Fungal infection warrants urgent referral.

Acute treatment centres on supportive therapy with fluid, antibiotics and nasal irrigation. Severe cases and any complications may require surgical intervention. Complications involve surrounding structures such as the orbit (periorbital cellulitis) and brain (meningitis, abscess). The timing and type of surgery depends on the individual case presented. The aim is to relieve pain, prevent complications and restore the sinus to its natural function. Functional endoscopic sinus surgery (FESS) has revolutionised surgical access, minimising external scarring and allowing greater access to all the sinuses.

Food and inhalant sensitivity can present as chronic sinusitis, with comparable culprit lists. Once again, dairy is a common food culprit, along with oranges, nuts and seeds. Only a small proportion of cases will be identified on IgE testing.

It should be noted that IgA-deficient patients have more allergies/sensitivities, and IgA deficiency should be excluded in all patients with chronic sinusitis.

Herbal treatments

Herbal medicines have a role to play in reducing symptoms from both acute and chronic respiratory conditions. Gathering evidence suggests that herbs have antiviral and antimicrobial activity to assist in the management of infection, antipyretic and diaphoretic activity to manage fevers, and anti-inflammatory activity. Mucillaginous herbs soothe and repair mucous membranes. Immuno-modulatory activity is a common feature.

Common herbs used are:5,6

• licorice root (Glycyrrhiza glabra)—antiviral, anti-inflammatory
• Echinacea spp whole plant (Echinacea spp)—immunomodulating
• thyme leaf (Thymus vulgaris)—antimicrobial, antiviral
• sage leaf (Salvia officinalis)—antiseptic
• olive leaf (Oleo europa)—antimicrobial, antiviral
• yarrow (Achillea millefolium)—diaphoretic.

VESTIBULAR DISORDERS

HISTORY

Vestibular disorders are difficult to pinpoint, and history remains the best tool for diagnosis. It includes conditions such as benign paroxysmal positional vertigo (BPPV), vestibular neuronitis, migrainous vertigo and Ménière’s disease. The history should consider periodicity, duration and associated and possible precipitating factors. It is important to distinguish true vertigo from lightheadedness, generalised malaise and blackouts.

True vertigo is always:

• due to asymmetry in vestibular apparatus
• transient
• worse with head movement.

Periodicity of attacks:

• Single episode versus recurrent attacks.

Duration of attacks:

• True vertigo lasting seconds to a minute is virtually pathognomonic of BPPV.
• First ever episode of true vertigo with nausea/vomiting lasting 24–72 hours is likely to be vestibular neuronitis.
• Recurrent episodes of vertigo lasting hours to days is likely to be endolymphatic hydrops (e.g. Ménière’s disease) or migraine, depending on associated symptoms and past history.

Associated symptoms:

• Endolymphatic hydrops includes episodes of vertigo with low-frequency hearing loss, tinnitus and aural fullness.
• Past history of migraine may be associated with vestibular migraine.
• Cerebellar infarction may not have associated neurological signs, and if presenting as isolated vertigo needs to be distinguished from vestibular neuronitis.

Precipitating factors:

• BPPV is always induced by head movement (vertigo induced by rolling over in bed is the most classic).

EXAMINATION

Eye movements should be followed closely. Check visual smooth pursuits and saccades (rapid eye movements). An abnormality suggests central cause of vertigo.

Other tests:

• high-frequency head impulse test—abnormality is pathognomonic of peripheral vestibular disorder (vestibular neuronitis in the acute setting)
• head shake test—enhances ability to detect unidirectional nystagmus
• cerebellar testing—standard assessment (e.g. past-pointing, heel–shin, dysdiadochokinesis)
• hyperventilation test—excludes anxiety disorder or may be concomitant
• Unterberger (Fukuda stepping) test—diagnostic of peripheral vestibulopathy
• ability to stand:

• with eyes open, in acute setting, usually excludes cerebellar disorder
• when absent with eye closure but present with eyes open, suggests vestibular disorder

• Dix-Hallpike manoeuvre—pathognomonic of BPPV when positive with classical torsional nystagmus and vertigo following a brief latency period (Fig 27.10).
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FIGURE 27.10 Dix-Hallpike manoeuvre. The patient’s head is turned 45° to the right. The patient is then brought into the supine position with the neck extended below the level of the examination table and observed for nystagmus and symptoms of vertigo.

Organise formal audiology in all cases.

BENIGN PAROXYSMAL POSITIONAL VERTIGO

Benign paroxysmal positional vertigo (BPPV) is the most common cause of recurrent vertigo. It is seen more often in females than in males, and occurs in all ages. In the elderly population it commonly occurs spontaneously; in younger patients it is more common after traumatic injury. The feeling commonly occurs after rapid head movement leading to movement of loose otoconia in the posterior semicircular canal, resulting in a brief transient episode of vertigo lasting only seconds. Episodes recur with any movement that causes fluid shift in the affected canal—rolling in bed, hanging out the washing on the line, opening a high cupboard, and so on.

Generally there are no examination findings apart from positive Dix-Hallpike manoeuvre.

The treatment uses the Epley manoeuvre, with a good cure rate (80%+). This often expedites recovery rather than waiting for spontaneous remission (up to 18 months).

It may recur months to decades later and is treated in the same manner.

Rarely, surgical intervention is required, to occlude the posterior semicircular canal.

VESTIBULAR NEURONITIS AND LABYRINTHITIS

Vestibular neuronitis is a relatively sudden onset of unilateral vestibulopathy presenting with vertigo and nausea/vomiting. It is the most common cause of first ever acute fulminant episode of vertigo with nausea and vomiting.

Vertigo with nausea and vomiting with the additional symptoms of hearing loss with or without tinnitus indicates acute labyrinthitis.

There is no gender predilection, and the average age of presentation is approximately 40 years.

The aetiology is likely to be viral or ischaemic, but is largely uncertain. It disrupts the superior and/or inferior vestibular nerve input to one vestibule, resulting in sudden severe vertigo with nausea.

There are no cochlear symptoms or signs, no neurological symptoms or signs, and a positive high-frequency head impulse test (diagnostic). The patient usually recovers completely within weeks. Recovery requires good compensation (by normal proprioception, vision and other inputs).

Treatment is to encourage compensation with early mobilisation once the vertigo and nausea settle.

Symptomatic relief with medications such as PR stemetil, p.o. or sublingual benzodiazepine or prochloroperazine should be limited, to avoid lack of compensation, toxicity and suppression of contralateral vestibular apparatus.

The patient is often referred for vestibular physiotherapy if not compensated within 4–6 weeks or if the patient has poor compensatory mechanisms (e.g. patient with walking stick, poor eyesight).

MIGRAINOUS VERTIGO

Migrainous vertigo is more difficult to manage, with a recurrent type of vertigo with or without headache. It is often associated with a family history of migraines, and is a common cause of recurrent vertigo (variably described as second or third behind BPPV). It occurs in all ages, with a predilection for migraine sufferers.

Comments about food-related reactions and cytokines also apply in migrainous vertigo. Inhalants such as cigarette smoke and petrochemicals in the form of cosmetics and perfume should also be considered. Fumes travel up the nose and through the cribriform plate directly to the brain. For the chemically sensitive, and/or those with migraine genes, migrainous vertigo is a common and distinctly unpleasant experience.

Like migraines, migrainous vertigo is thought to be a vascular phenomenon, with the vertigo lasting minutes to days with or without headache. The patient shows only transient neurological signs, with possible central signs on visual assessment. There are often very different serial electronystagmography (ENG) and caloric testing.

A trial of classic migraine management is best for prevention, including trigger identification and lifestyle modification.

One retrospective review found that migraine treatments were effective in about 90% of patients with migraine-associated vertigo.7 Treatments included:

• dietary changes—reduction or elimination of aspartame, chocolate, caffeine or alcohol
• lifestyle changes—exercise, stress reduction and relaxation techniques, improvements in sleep patterns
• vestibular rehabilitation exercises.

Migraine medications including pizotifen or propranolol can help in repeat events. Other medications that may be useful include benzodiazepines, tricyclic antidepressants, selective serotonin reuptake inhibitors (SSRIs), calcium channel blockers and antiemetics.

MÉNIÈRE’S DISEASE

Ménière’s disease is a disorder of the inner ear caused by endolymphatic hydrops (increased volume and pressure of the endolymphatic sac). Its incidence is approximately 100/100,000, with a usual onset in early to mid-adulthood, with no male/female preponderance. There are multiple postulated theories (e.g. viral infection causing release of saccin, leading to fluid retention and endolymphatic hydrops, expressing as clinical episodes), but the common feature is an enlarged endolymphatic sac.

During an episode, the patient classically has:

• low-frequency hearing loss
• tinnitus
• aural fullness
• vertigo (often of hours’ duration).

The prognosis is variable, with contralateral involvement in 20% of patients by 20 years of age. The condition rarely reaches the stage of Tumarkin crises or Lermoyez syndrome.

Confirming the diagnosis includes obtaining an audiogram, caloric testing, MRI (to exclude other inner ear pathology) and ENT referral. Treatment centres on reducing the absorption of fluid into the endolymphatic sac.

For an acute attack:

• diazepam 5 mg IV with or without prochlorperazine 25 mg suppository, or IM
• betahistine 8 mg p.o. t.d.s. if persistent.

Example of a stepwise approach:

• low-sodium diet (< 1500–2000 mmol/day)—Ménière’s disease has many features in common with migrainous vertigo. It is a hybrid allergic disorder, but is also subject to many of the problems afflicting the modern Western diet. The role of sodium is significant; however, the dietary balance of sodium and potassium is a consideration. In a primitive diet, the ratio of potassium to sodium was 10:1 or more. The modern diet has reversed this and it is now 1:2 at the very best. For those with salt-retaining genes and an allergic diathesis, Ménière’s is a logical consequence
• magnesium supplementation—magnesium deficiency is made all the worse by the consumption of calcium tablets without magnesium balance. Magnesium depletion is a common agricultural problem in the developed world. The ideal dietary ratio of calcium to magnesium is 3:2. In dairy products, the balance is closer to 8:1 or even 16:1. This adds a relative magnesium deficiency to an already absolute deficiency. Magnesium supplements have a distinct role to play in Ménière’s disease
• avoidance/treatment of precipitants in some cases (e.g. food additives, antihistamines)
• avoidance of tobacco and coffee
• diuretics—hydrochlorothiazide/amiloride
• vestibular suppressants
• ventilation tube ± Meniett® device
• intratympanic gentamicin
• anxiety management
• surgical options for intractable cases.

TONSILLAR AND PERITONSILLAR DISORDERS

The tonsils and adenoids are congregations of lymphoid tissue in the oropharynx. They play an important role in immunology and memory for infection and, consequently, are implicated in mucosal defence. They are most active in childhood and therefore are often considered an entity of childhood illness.

Most commonly, tonsillar and peritonsillar disorders are part of a child’s development, and surgical intervention is not often required. Infection or tonsillitis is the most common complaint of the tonsils. Symptoms and their frequency and severity often dictate treatment. It is important to assess for obstructive symptoms and, in children, for poor behaviour with morning ‘hangover’, and in adults, for daytime somnolence, poor sleep hygiene, cardiovascular comorbidity and Epworth Sleepiness Scale (Fig 27.11). Formal sleep studies may be required before making a decision on surgery.

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FIGURE 27.11 Epworth Sleepiness Scale

In patients who ‘rebound’ or re-present with tonsillitis, it is important to consider the likelihood of being ‘under-antibioticised’, or the likelihood of being ‘under-analgesed’. A duration of more than 3–4 days, trismus, referred unilateral otalgia and/or previous peritonsillar abscess may suggest peritonsillar abscess (quinsy).

For patients with these conditions presenting less acutely, consider sleep-disordered breathing, recurrent tonsillitis affecting school/university or work, recurrent peritonsillar abscess or suspicion of malignancy, as key reasons for referral to ENT.

On examination, general signs of infection or inflammation are evident, with fever and tachycardia the most common. The patient may have cervical lymphadenopathy, trismus (moderate to severe increases suggestive of quinsy in acute setting), erythema of tonsils, crypt debris in tonsils or purulence of tonsils. Confluent slough over the tonsils increases the suggestion of Epstein-Barr virus (EBV; mononucleosis).

Abdominal (spleen/liver) examination and generalised lymphadenopathy is palpated for when suspicious of EBV mononucleosis.

Severe infections should be referred, and flexible nasopharyngolaryngoscopy by an ENT surgeon is possible if there is concern regarding obstructed breathing, deep neck space infection, supraglottitis, epiglottitis or lingual tonsillitis.

PERITONSILAR ABSCESS (QUINSY)

Quinsy is inflammation of the peritonsillar space with suppuration. Classically it occurs between the ages of 15 and 40 years, but it is possible at any age. Inflammation of the tonsils can lead to peritonsillar space infection adjacent to acute tonsillitis. This may lead to abscess formation, with resultant swelling of the unilateral peritonsillar space, oedema, fluctuance, deviation of uvula and trismus.

If untreated, extension of infection into any of the other deep neck spaces is possible. Prompt treatment is therefore recommended. After the first quinsy, there is a 25% risk of subsequent quinsy; a second quinsy increases that risk to 50% risk of subsequent quinsy. A third quinsy almost always (90% risk) gives a subsequent quinsy.

Treatment is by acute drainage (incisional drainage or repeated aspiration under local anaesthetic).

‘Hot’ tonsillectomy (removal of the tonsils while they are acutely infected) is controversial and rarely seen these days. Supportive therapy must include antibiotics (with a probiotic), fluids and analgesia. More recently, the use of steroids has helped settle severe infections more rapidly.

LARYNGITIS

Laryngitis is an acute inflammation of the larynx due to overuse, inflammation or infection. It may be acute or chronic, and presents with hoarseness. The patient may also complain of sore throat, fever, dry cough, trouble swallowing and trouble breathing.

Acute laryngitis

Causes of acute laryngitis incude viral URTI, vocal abuse and irritants such as cigarette smoke. Treatment includes the following:

• resting the voice
• hot lemon and honey drinks
• avoidance of tobacco and alcohol
• steam inhalation
• simple analgesia for pain.

Referral is required if symptoms persist for longer than four weeks.

Chronic laryngitis

Risks for chronic laryngitis include smoking, excessive alcohol consumption and overuse of the voice. Chronic hoarseness requires examination of the vocal cords to exclude benign nodules or carcinoma.

Benign nodules may respond to conservative measures such as ceasing smoking, voice rest and speech therapy. They may require surgical removal.

Exclude gastro-oesophageal reflux disease, a common hidden cause of hoarseness. Refer for specialist assessment.

Herbal treatments

Common herbs used are similar to those for sinusitis.8

Traditional Chinese medicine

Laryngitis refers to inflammation of the larynx, which can be acute or chronic. For both conditions, in TCM they fall into the category of ‘Hou Yin’, which means ‘loss of voice due to throat problem’. For acute conditions, the invasion of pathogenic wind-cold or wind-heat is the major cause of blockage at the throat area. In chronic conditions, it is due to a yin deficiency failing to nourish the throat area. The primary treatment for acute laryngitis is to expel wind-cold or wind-heat; for chronic laryngitis the treatment is nourishing yin.

TCM herbs:9,10

• platycodon root (Platycodon grandiflorum)
• figwort root (Scrophularia ningpoensis)
• dwarf lilyturf tuber (Ophiopogon japonicus)
• Vietnamese sophora root (Sophora tonkinensis)
• isatis root (Isatis indigotica).

INFECTIOUS MONONUCLEOSIS

An acute inflammation of the tonsils often caused by Epstein-Barr virus (classical) is called infectious mononucleosis. There are two peaks of primary infection: at age 1–5 years and in adolescence. Most children seroconvert by 5 years of age, so clinical disease usually manifests in adolescents or young adults who failed to seroconvert in childhood.

As with tonsillitis, a prodromal fever or malaise accompanied by odonyphagia is common. Confluent exudative and sloughy tonsillitis is classic. Cervical and generalised lymphadenopathy is noted, along with the possibility of a rash, jaundice and/or hepatosplenomegaly. Usually it is self-limiting and very rarely causes significant airway, neurological, cardiovascular or haematological sequelae.

The diagnosis should be confirmed with blood tests for:

• Epstein-Barr virus (EBV) titre IgM and IgG
• full blood examination—lymphocytosis and atypical lymphocytes
• C-reactive protein (CRP)
• liver function tests.

The virus is generally spread among children, adolescents and young adults through salivary contact, and only causes clinical illness when primary infection is delayed until adolescence or beyond. Symptomatic infectious mononucleosis occurs in approximately 50% of young adult cases of EBV infection.

While most people with EBV infection recover fully within a few weeks, Epstein-Barr virus may cause long-term fatigue and is known to be able to induce tumours such as B-lymphoproliferative disease and Hodgkin’s disease.

Prevention

There is no droplet transmission, so isolation is not necessary. Transmission is through saliva, and the virus may be present for months or years after clinical infection.

Advise household contacts to avoid kissing the infected person or sharing cups, eating utensils or toothbrushes with them. Learning stress management techniques helps improve the immune system and may help reduce the risk of viral infection such as EBV.

Acute stage

Rest is essential in the early stages. Graduated increase in activity is to be encouraged after two weeks as tolerated. Splenomegaly occurs in about 50% of cases, so contact sports and heavy lifting should be avoided for two months because of the risk of splenic rupture.

Medication

• Paracetamol or aspirin (not in children).
• Corticosteroids may be needed to relieve obstructive symptoms from tonsillar hypertrophy or neurological complications.
• Prescription of amoxicillin or ampicillin should be avoided if EBV is suspected, as it can cause a pink maculopapular rash if given to a patient with EBV.
• Steroids and antibiotics are reserved for severe cases with superimposed bacterial infection.

Nutrition

• Sore throat and tonsillar hypertrophy can make adequate nutrition difficult to achieve. Soups, soft foods and purees may be needed in the acute phase.
• Avoid fatty foods.
• Avoid coffee and other stimulants, alcohol and tobacco. Alcohol should be avoided completely, particularly if transaminases are elevated.
• Drink 6–8 glasses of fluids, including herbal teas, broths and filtered water daily.
• Eat a predominance of antioxidant-rich fruits and vegetables.
• Eat tofu, fish or legumes for protein.

Supplements

Supplements help to ensure nutritional adequacy and immune support, and may include:

• a multivitamin daily, containing the antioxidant vitamins A, C, E, the B-vitamins, and trace minerals, such as magnesium, calcium, zinc and selenium
• intravenous vitamin C administered by a doctor experienced in the procedure—can be very effective in the acute phase, and will reduce the risk of chronic fatigue syndrome when recovery is prolonged
• omega-3 fatty acids, such as fish oil and flaxseed oil, to help decrease inflammation and improve immunity
• coenzyme Q10, 100–200 mg at night, for antioxidant effect and to counter fatigue and myalgia
• probiotic (containing Lactobacillus acidophilus) for maintenance of gastrointestinal and immune health.

Herbs

A variety of herbs can be useful support for management of infectious mononucleosis. These include:

• Glycyrrhiza glabra (licorice root) 5–15 g daily. In vitro studies suggest that glycyrrhizin may interfere with an early step of the EBV replication cycle.11 It must be used with caution and under professional supervision. If used in high doses for more than two weeks it can cause hypertension, fluid retention and hypokalaemia.
• green tea (Camellia sinensis) (caffeine free)12
• rhodiola (Rhodiola rosea) standardised extract, 100–600 mg daily, for antioxidant, anti-stress and immune activity13
• milk thistle (Silybum marianum) seed standardised extract, 80–160 mg two to three times daily, for liver support, especially if transaminases are elevated14
• elderberry (Sambucus nigra) extract, 1 tablespoonful twice daily, for antiviral and immune activity15
• reishi mushroom (Ganoderma lucidum), 150–300 mg two to three times daily, or tincture of this mushroom extract, 30–60 drops two to three times daily16
• cat’s claw (Uncaria tomentosa) standardised extract, 20 mg three times daily, for inflammation and antiviral activity.17

RESOURCES

Information and patient education

Information and images of ear, nose and throat. http://www.google.com.au/images?client=safari&rls=en&q=ear+nose+and+throat&oe=UTF-8&redir_esc=&um=1&ie=UTF-8&source=univ&ei=M8fcS5T5FNCgkQX1kOjBBw&sa=X&oi=image_result_group&ct=title&resnum=11&ved=0CDUQsAQwCg.

Medline Plus, Ear, nose and throat. http://www.nlm.nih.gov/medlineplus/earnoseandthroat.html.

Queensland Government, Ear, nose and throat health. http://access.health.qld.gov.au/hid/EarNoseandThroatHealth/index.asp.

ENT colleges

American Academy of Otolaryngology—Head and Neck Surgery. http://www.entnet.org/.

Australian Society of Otolaryngology, Head and Neck Surgery. http://www.asohns.org.au/.

American Academy of Otolaryngology—Head and Neck Surgery. http://www.entnet.org/.

Royal College of Surgeons of Edinburgh. http://www.rcsed.ac.uk/site/630/default.aspx.

ENT UK. http://www.entuk.org/patient_info/.

REFERENCES

1 Black RJ, Cousins V, Chapman P, et al. Ototoxic ear drops with grommet and tympanic membrane perforations: a position statement. Med J Aust. 2007;187(1):62.

2 Taylor PS, Faeth I, Marks MK, et al. Cost of treating otitis media in Australia. Expert Rev Pharmacoecon Outcomes Res. 2009;9(2):133-141.

3 Glasziou PP, Del Mar CB, Sanders SL, et al. Antibiotics for acute otitis media in children. Cochrane Database Syst Rev. 2004;1:CD000219.

4 National Institute of Neurological Disorders and Stroke. Bell’s palsy fact sheet. Last updated 2009. National Institutes of Health. Online. Available: http://www.ninds.nih.gov/disorders/bells/detail_bells.htm#109663050.

5 Mills S, Bone K. Principles and practice of phytotherapy: modern herbal medicine. London: Churchill Livingstone, 2000.

6 Weiss RF, Fintelmann V. Herbal medicine. 2nd edn. Stuttgart: Thieme, 2000.

7 Johnson GD. Medical management of migraine-related dizziness and vertigo. Laryngoscope. 1998;108(1 pt 2):1-28.

8 Blumenthal M, Goldberg A, Brinckmann J, editors. Herbal medicine. Expanded Commission E Monographs. Austin, Texas: American Botanic Council, 2000.

9 Kim H-Y, Shin H-S, Kim Y-C, et al. In vitro inhibition of coronavirus replications by the traditionally used medicinal herbal extracts, Cimicifuga rhizoma, Meliae cortex, Coptidis rhizoma, and Phellodendron cortex. J Clin Virol. 2008;41(2):122-128.

10 Maclean W, Taylor K. The clinical manual of Chinese herbal patent medicines. Sydney: Pangolin Press, 2000.

11 Lin JC. Mechanism of action of glycyrrhizic acid in inhibition of Epstein-Barr virus replication in vitro. Antiviral Res. 2003;59(1):41-47.

12 Chang L-K, Wei T-T, Chiu Y-F, et al. Inhibition of Epstein-Barr virus lytic cycle by (–)-epigallocatechin gallate. Biochem Biophys Res Commun. 2003;301(4):1062-1068.

13 Kelly G. Rhodiola rosea: a possible plant adaptogen. Altern Med Rev. 2001;6(3):293-302.

14 Pradhan S, Girish C. Hepatoprotective herbal drug, silymarin from experimental pharmacology to clinical medicine. Indian J Med Res. 2006;124(5):491-504.

15 Barak V, Halperin I, Kalickman I. The effect of Sambucol, a black elderberry-based, natural product, on the production of human cytokines: I. Inflammatory cytokines. Eur Cytokine Netw. 2001;12(2):290-296.

16 Sanodiya BS, Thakur GS, Baghel RK, et al. Ganoderma lucidum: a potent pharmacological macrofungus. Curr Pharm Biotechnol. 2009;10(8):717-742.

17 Williams J. Review of antiviral and immunomodulating properties of the plants of the Peruvian rain forest with a particular emphasis on Una de Gato and Sangre de Grado. Altern Med Rev. 2001;6(6):567-579.

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