Learn — Skin, eye & ENT

13 notes · 29 questions on the topic

Skin lesions — wheal, vesicle, papule, macule

Dermatological diagnosis rests on naming the lesion correctly, because the primary lesion — the one that appears first on previously normal skin — narrows the diagnosis before any test is done. Primary lesions are described by whether they are flat or raised, solid or fluid-filled, and by size, with 1 cm as the dividing line for most pairs, while secondary lesions are the changes that follow from scratching, infection or healing.

Flat lesions: a macule is a flat, non-palpable change in colour of 1 cm or less (freckle, early measles rash, petechia) and a patch is the same thing larger than 1 cm (vitiligo, melasma, a hypopigmented anaesthetic patch of leprosy).
Raised solid lesions: a papule is 1 cm or less (wart, insect bite, acne), a nodule is larger than 1 cm and extends deeper (lipoma, erythema nodosum), a plaque is a flat-topped elevation larger than 1 cm often formed by papules coalescing (psoriasis, lichen planus), and a tumour is a large mass.
Fluid-filled lesions: a vesicle is 1 cm or less and contains clear fluid (chickenpox, herpes simplex, early contact dermatitis), a bulla is larger than 1 cm (burn blister, pemphigus, bullous impetigo), a pustule contains pus (acne, folliculitis, pustular psoriasis) and a cyst is a sac of fluid or semisolid material.
A wheal is a transient, oedematous, itchy raised lesion with a pale centre and a red flare that comes and goes within 24 hours and leaves no mark — the lesion of urticaria; an individual wheal lasting more than 24 hours, burning rather than itching, or leaving bruising, suggests urticarial vasculitis and needs a biopsy.
The single most important bedside test is blanching: press a glass over the rash, and a lesion that does not blanch is purpura (petechiae if 2 mm or less, ecchymosis if large) from bleeding into the skin, whereas an erythematous rash blanches. A non-blanching rash with fever is meningococcal sepsis until proven otherwise.
Secondary lesions and what they tell you: scale (psoriasis, fungal infection), crust (dried exudate in impetigo), erosion (loss of epidermis only, heals without a scar), ulcer (loss into the dermis or deeper, heals with a scar), fissure, excoriation from scratching, lichenification from chronic rubbing, atrophy, and scar or keloid.
Named signs that convert a description into a diagnosis: Nikolsky sign, where firm lateral pressure shears the epidermis away, is positive in pemphigus vulgaris, staphylococcal scalded skin syndrome and toxic epidermal necrolysis; Auspitz sign is pinpoint bleeding when a psoriatic scale is lifted; the Koebner phenomenon is lesions appearing along a scratch in psoriasis, lichen planus and vitiligo; Darier sign is urticaria on rubbing a lesion in mastocytosis.
The arrangement is as informative as the lesion: grouped vesicles on an erythematous base in a dermatome are herpes zoster, linear lesions suggest an external cause or Koebner phenomenon, target or iris lesions are erythema multiforme, annular lesions with an active scaly edge are tinea, and an anaesthetic hypopigmented patch is leprosy until proven otherwise.
Documentation should be reproducible by the next nurse: site and distribution, number, size in millimetres, colour, shape and border, surface and consistency, arrangement, and whether it blanches; the patient's palm with the fingers together is about 1% of body surface area and is a useful field measure for extent.

Contact dermatitis

Contact dermatitis is inflammation of the skin caused by something that touched it, and it comes in two forms with quite different mechanisms — irritant contact dermatitis, a direct non-immunological chemical injury that can affect anyone on first exposure, and allergic contact dermatitis, a type IV delayed cell-mediated hypersensitivity that appears 24 to 72 hours after re-exposure in someone who has already been sensitised. It is the commonest occupational skin disease and it is an occupational hazard of nursing itself, since repeated hand washing, glove use and disinfectants are among its leading causes.

Irritant contact dermatitis accounts for the large majority of cases; it burns and stings more than it itches, stays sharply confined to the area of contact, needs no prior sensitisation, and is caused by soaps and detergents, wet work, alcohol rubs, acids and alkalis, solvents and cement.
Allergic contact dermatitis itches intensely, appears 24 to 72 hours after exposure, and characteristically spreads beyond the exact area of contact and sometimes to distant sites — that spread is the discriminator from irritant dermatitis.
Common allergens in India: nickel in jewellery, watch straps and clothing fasteners; parthenium (Congress grass), which causes an airborne contact dermatitis on the exposed face, neck and arms and can be mistaken for a photodermatitis; potassium dichromate in cement, affecting masons' hands and feet; paraphenylenediamine in hair dye and in black henna; rubber accelerators such as thiurams in gloves; and fragrances and preservatives in cosmetics.
The two glove reactions must be separated because the management differs completely: a type IV allergy to rubber accelerators causes an itchy eczematous rash on the hands over a day or two, while a type I IgE-mediated allergy to natural rubber latex protein causes immediate itching, weals, rhinitis, wheeze and, rarely, anaphylaxis within minutes; the latter demands a latex-free environment for that person.
The acute picture is erythema, oedema, vesicles and weeping; the chronic picture is dryness, scaling, fissuring and lichenification, and secondary bacterial infection shows as pustules, honey-coloured crusting and pain.
Diagnosis is largely from the pattern and the history — the site tells the allergen, and improvement away from work or on holiday points to an occupational cause; patch testing is the confirmatory test for allergic contact dermatitis, applied to the back and read at 48 hours and again at 96 hours, and it is not done on actively inflamed skin or while the patient is on systemic corticosteroids.
Treatment begins with identifying and removing the cause, since no drug will work while exposure continues; then generous and frequent emollients, a topical corticosteroid of a potency matched to the site (a mild preparation such as hydrocortisone on the face and flexures, a potent one on the palms and soles), wet wraps for acute weeping lesions, and antibiotics only for proven secondary infection.
Oral antihistamines help sleep but do little for the itch of allergic contact dermatitis, because that itch is not histamine-driven; a short course of oral corticosteroid is reserved for severe or widespread disease.
Occupational prevention for nurses: use nitrile rather than latex gloves, wear gloves only when indicated and for as short a time as possible, dry hands completely before gloving, prefer alcohol handrub to repeated washing when hands are not soiled, apply emollient after every wash and at the end of every shift, and report the condition to occupational health so that it is documented and compensable.
Chronic hand dermatitis in a healthcare worker is not a cosmetic problem — broken skin cannot be decontaminated reliably, so it is an infection control issue as well as a personal one.

Scabies

Scabies is infestation of the skin by the mite Sarcoptes scabiei var. hominis, whose fertilised female burrows into the stratum corneum and lays eggs there; the rash and the itch are a delayed hypersensitivity reaction to the mite, its eggs and its faeces rather than to the burrowing itself. It is spread by prolonged skin-to-skin contact, so it runs through households, hostels, orphanages and hospital wards, and WHO recognises it as a neglected tropical disease because untreated infestation leads to streptococcal skin infection, acute post-streptococcal glomerulonephritis and rheumatic heart disease in endemic communities.

The hallmark is intense itching that is worst at night and in the warmth of bed, with more than one member of the household itching — the family history is often more diagnostic than the rash.
The lesion to look for is the burrow, a short grey wavy line, in the finger web spaces, the flexor wrists, elbows, anterior axillary folds, around the umbilicus and the belt line, the buttocks, and the genitalia, where firm itchy scrotal or penile nodules are almost diagnostic in men and the areolae are involved in women.
Distribution differs by age: adults are spared above the neck, whereas in infants, in the very elderly and in the immunosuppressed the scalp, face, palms and soles are involved, and in infants the lesions are often vesicular or pustular on the palms and soles.
The incubation period explains the treatment rule: itching starts 4 to 6 weeks after a first infestation because sensitisation takes that long, but within 1 to 3 days on re-infestation, so contacts who are not yet itching are already infested and must be treated at the same time.
Permethrin 5% cream is first-line: applied to cool dry skin over the whole body from the neck down in adults, and including the scalp and face while avoiding the eyes and mouth in infants, the elderly and the immunosuppressed, with attention to web spaces, under the trimmed fingernails, the umbilicus and the genitals; left on for 8 to 12 hours (usually overnight), washed off, and repeated after 7 days to kill mites hatching from surviving eggs. It is reapplied to the hands after any hand washing during those hours.
Oral ivermectin 200 micrograms per kg is the alternative, repeated after 1 to 2 weeks; it is convenient for outbreaks and institutions but is not used in pregnancy or lactation or in children under 15 kg. Sulphur ointment 5% for 3 consecutive nights is the safe option in pregnancy and in young infants, and benzyl benzoate is effective but irritant and must be diluted for children.
Every household member, sexual contact and close contact is treated on the same day whether or not they itch, because staggered treatment simply passes the mite back and forth.
Environmental measures: clothing, bed linen and towels used in the previous 3 days are machine washed hot and dried in a hot dryer or ironed, and items that cannot be washed are sealed in a plastic bag for at least 3 days, since the mite dies within about 2 to 3 days away from the human host; fumigation of the house is unnecessary.
Post-scabetic itch persists for 2 to 4 weeks after successful treatment because the hypersensitivity outlasts the mite; it is treated with emollients, an antihistamine and a mild topical corticosteroid, and repeated scabicide application is avoided as it causes irritant dermatitis and is mistaken for treatment failure. Genuine failure is suspected only when new burrows or new lesions appear after 4 weeks.
Crusted (Norwegian) scabies occurs in immunosuppressed, HIV-positive, elderly, institutionalised and neurologically impaired patients, or after topical steroid misuse; it carries thousands to millions of mites in thick hyperkeratotic crusts, the itch may be minimal, and it is extremely contagious — the usual source of a ward or care-home outbreak. It needs isolation with contact precautions, gowns and gloves, a keratolytic to lift the crusts, repeated topical scabicide and multiple doses of oral ivermectin.
Complications: secondary infection with Staphylococcus aureus and group A Streptococcus causing impetigo, cellulitis and abscess, and downstream post-streptococcal glomerulonephritis and rheumatic fever; eczematisation and, in India, misdiagnosis and treatment with topical steroids, which produces the atypical picture of scabies incognito.

Stevens-Johnson syndrome (SJS)

Stevens-Johnson syndrome is a T-cell mediated severe cutaneous adverse reaction, almost always to a drug, in which keratinocytes die in sheets so that the epidermis separates from the dermis and at least two mucosal surfaces ulcerate. It lies on a single spectrum with toxic epidermal necrolysis, divided only by the area of skin detached: under 10% of the body surface is SJS, 10 to 30% is SJS/TEN overlap and over 30% is toxic epidermal necrolysis. It matters because it is a burn the patient never went near a fire to get, and a ward that treats it as a rash loses the patient to fluid loss, sepsis and blindness.

Detachment decides the name and the prognosis: under 10% of body surface area is SJS, 10 to 30% is SJS/TEN overlap and over 30% is toxic epidermal necrolysis, but the disease and the treatment are the same throughout.
The reaction begins 4 days to 4 weeks after the drug is first started, most often in the second week, so a rash on the first day of a new drug is almost never SJS.
High-risk drugs are allopurinol, the aromatic anticonvulsants (carbamazepine, phenytoin, lamotrigine, phenobarbitone), sulfonamides including cotrimoxazole, nevirapine and oxicam NSAIDs; in India anti-tubercular drugs and dapsone are added, and in children Mycoplasma pneumoniae can trigger it with no drug at all.
A prodrome of fever, sore throat, burning eyes and skin that hurts to touch runs 1 to 3 days ahead of the rash, which starts as dusky macules and atypical targets on the face and trunk; more than 90% of patients have two or more mucosal sites involved, usually mouth, eyes and genitals.
Nikolsky sign is positive, meaning sliding lateral pressure on normal-looking skin shears the epidermis away, and the Asboe-Hansen sign extends an existing blister sideways under thumb pressure.
SCORTEN, scored within the first 24 hours, predicts mortality from seven items: age over 40 years, an underlying malignancy, heart rate over 120/min, detachment over 10% of body surface area, serum urea over 10 mmol/L (about 28 mg/dL), serum bicarbonate under 20 mmol/L and blood glucose over 14 mmol/L (about 252 mg/dL).
The nearest confusables separate on mucosa and timing: staphylococcal scalded skin syndrome spares the mucosa and affects small children, erythema multiforme major gives typical acral target lesions after herpes simplex, DRESS appears 2 to 8 weeks in with facial oedema, eosinophilia and hepatitis, and acute generalised exanthematous pustulosis gives sterile pustules within days.
Withdrawing the culprit drug on the day the rash appears is the single act that lowers mortality; everything after that is burn-unit care — a warmed room, non-adherent dressings, fluid and electrolyte replacement, calorie-dense nasogastric feeding, strong analgesia, and no prophylactic systemic antibiotics.
Ciclosporin has the best evidence among the immunomodulators while systemic corticosteroids and intravenous immunoglobulin remain contested; silver sulfadiazine dressings are avoided because the sulfonamide can be the very class that caused the reaction.

Presbycusis

Presbycusis is the bilateral, symmetrical, gradually progressive sensorineural hearing loss of ageing, caused by degeneration of the hair cells at the basal turn of the cochlea, of the spiral ganglion neurones and of the stria vascularis. It matters because it begins in the high frequencies that carry the consonants, so the patient insists that people are mumbling rather than that he is deaf, and untreated it produces social withdrawal, depression and an established rise in the risk of cognitive decline — which makes the referral a nurse makes a public-health act and not a courtesy.

The loss is bilateral, symmetrical and high-frequency first, so the audiogram shows a sloping curve falling away above 2000 Hz with no air-bone gap; a loss that is unilateral or clearly asymmetrical is not presbycusis and needs magnetic resonance imaging to exclude a vestibular schwannoma.
Speech discrimination falls further than the pure-tone thresholds predict — phonemic regression — because the consonants s, sh, f, th and k are high-frequency sounds; the patient hears that he is being spoken to but cannot tell the words apart, and background noise makes it far worse.
Schuknecht's four types are asked in the examination: sensory (loss of outer hair cells at the basal turn, an abrupt high-frequency drop), neural (loss of spiral ganglion cells, with speech discrimination out of proportion to the audiogram), strial or metabolic (atrophy of the stria vascularis, a flat audiogram with good discrimination) and cochlear conductive (stiffening of the basilar membrane, a gradually sloping curve).
Recruitment is present, meaning loudness grows abnormally fast once the threshold is crossed; this is why shouting at an elderly patient is both useless and painful, and why the correct technique is to face him, get his attention first, speak slowly at normal volume in a lower pitch and rephrase rather than repeat.
Before the loss is labelled age-related, remove the reversible causes: impacted wax, otitis media with effusion, ototoxic drugs (aminoglycosides, loop diuretics, cisplatin), noise exposure and diabetes, hypertension and smoking, which all accelerate the cochlear damage.
Assessment is by otoscopy, tuning-fork tests and pure-tone audiometry with speech audiometry; the hearing handicap that decides treatment is the speech discrimination score and the patient's own difficulty, not the decibel number alone.
Management is a properly fitted hearing aid with follow-up, assistive devices such as amplified telephones and television loops, and auditory rehabilitation; a cochlear implant is considered when the loss is severe to profound and a well-fitted aid gives no useful speech understanding.
Most patients abandon a first hearing aid within weeks because their own voice sounds boomy and the world sounds noisy, so counselling about a graded wearing schedule, battery care, moisture protection and a review appointment is the intervention that decides whether the aid is used at all.

Otoscope examination

Otoscopy is the inspection of the external auditory canal and the tympanic membrane with a lighted, magnifying otoscope and the largest speculum the canal will take, and it is the single examination that separates a conductive from a sensorineural problem at the bedside. It matters because almost everything treatable in the ear — impacted wax, a foreign body, acute otitis media, an effusion, a perforation, a cholesteatoma — is visible in the ten seconds the otoscope is in the canal, and because a nurse who cannot tell a safe central perforation from an unsafe attic perforation cannot tell a nuisance from an intracranial risk.

Straighten the canal before looking: pull the pinna upwards, backwards and slightly outwards in an adult and in a child over about three years, and gently downwards and backwards in an infant, because the infant's canal runs upwards and its cartilaginous part is not yet developed.
Hold the otoscope like a pen with the ulnar border or little finger braced against the patient's cheek, so that if the child jerks the instrument moves with the head instead of tearing the canal, and examine the normal ear first in a child in pain.
The normal tympanic membrane is pearly grey, translucent and slightly concave, with the handle of the malleus running downwards and backwards to the umbo at the centre, the short lateral process bulging above it, and the cone of light spreading anteroinferiorly — at 5 o'clock in the right ear and at 7 o'clock in the left.
The membrane is divided into the pars tensa below and the small pars flaccida or Shrapnell's membrane in the attic above the lateral process, and into four quadrants by a line along the handle of the malleus and another at right angles to it through the umbo; the posterosuperior quadrant is the dangerous one, because the incudostapedial joint and the chorda tympani lie behind it, and a ventilation tube is therefore placed in the anteroinferior quadrant.
Read the disease from the drum: acute otitis media gives a red, bulging drum with the landmarks and light reflex lost; otitis media with effusion gives a retracted, dull amber or grey drum with a fluid level or bubbles and reduced mobility; a central perforation of the pars tensa with mucoid, odourless discharge is the safe tubotympanic type of chronic suppurative otitis media, whereas an attic or marginal perforation with scanty foul discharge and granulation is the unsafe atticoantral type with cholesteatoma.
Pneumatic otoscopy with a Siegle's speculum, in which the drum is watched while the pressure in the canal is alternated, is the most useful bedside test for a middle-ear effusion; a drum that does not move indicates fluid behind it, a perforation or ossicular fixation.
Never syringe or irrigate an ear when a perforation, a grommet, a previous mastoid operation or a vegetable foreign body such as a pea or a seed is possible — water drives infection into the middle ear and swells vegetable matter — and never attempt to remove a foreign body blindly with forceps, which pushes it against the drum.
Otoscopy is one half of the examination: complete it with tuning-fork tests, tests of facial nerve function, palpation for mastoid and tragal tenderness, and inspection of the postauricular sulcus, because the ear that looks discharging and the ear that is dangerous look the same until you look at the attic.

Laryngoscope

The laryngoscope is the instrument used to bring the larynx into view, either indirectly with an angled mirror held in the oropharynx or directly with a rigid blade, a flexible fibreoptic scope or a video laryngoscope. It matters twice over: it is the diagnostic instrument for hoarseness, stridor, dysphagia and vocal cord palsy, and it is the instrument on which every intubation depends, so the nurse who prepares the trolley and hands over the blade decides how fast an airway is secured.

Indirect laryngoscopy uses a warmed angled mirror placed against the soft palate while the patient sits upright, leans forward, opens the mouth and lets the tongue be held forward in gauze; the mirror is warmed to stop it fogging and tested on the back of the hand, and the patient is asked to breathe quietly and then to say a long "eee" so that adduction of the cords can be seen.
In the mirror image the larynx is seen vertically inverted: the anterior commissure appears at the top of the mirror and the arytenoids and posterior structures at the bottom, which is the point candidates lose marks on.
The flexible fibreoptic nasopharyngolaryngoscope is passed through the nose in an awake, seated patient after topical decongestant and anaesthetic; it is the test of choice when the gag reflex defeats the mirror, in children, and when the airway must be looked at without disturbing it.
Direct laryngoscopy under general anaesthesia is done in the sniffing-the-morning-air position — the neck flexed on the chest and the head extended at the atlanto-occipital joint — which lines up the oral, pharyngeal and laryngeal axes; it allows biopsy, foreign-body removal and microlaryngeal surgery.
Blade choice follows anatomy: the curved Macintosh blade sits in the vallecula and lifts the epiglottis indirectly, while the straight Miller blade picks up the epiglottis directly and is preferred in infants, whose epiglottis is large, floppy and omega-shaped and whose larynx sits higher and more anteriorly, at about C3 to C4 rather than the adult C5 to C6.
The view obtained is graded by Cormack and Lehane: grade I the whole glottis, grade II only the posterior glottis or arytenoids, grade III only the epiglottis, grade IV neither epiglottis nor glottis; grades III and IV define a difficult laryngoscopy and are the point at which a bougie, a video laryngoscope or a supraglottic airway is called for.
The nurse's preparation is a checklist: consent and nil by mouth, suction working and within reach, oxygen and a bag-valve-mask, two working laryngoscope handles with the correct blades and spare bulbs and batteries, endotracheal tubes in three sizes with a stylet and bougie, a cuff syringe, tape, capnography and monitoring, and a difficult-airway trolley with a tracheostomy set nearby.
Placement is confirmed by a sustained capnography trace first, then by equal chest movement and bilateral air entry with no gurgling over the epigastrium; the paediatric uncuffed tube size is roughly the age in years divided by four plus four, and the depth at the lips is about three times the tube size.
After a direct laryngoscopy or biopsy the patient stays nil by mouth until the gag reflex has fully returned, is nursed sitting up and watched for stridor, hoarseness, bleeding, surgical emphysema and respiratory distress; the specific complications to warn about are dental and lip trauma, laryngospasm and laryngeal oedema.

Acute epiglottitis

Acute epiglottitis, more accurately supraglottitis, is a rapidly progressive bacterial inflammation of the epiglottis, aryepiglottic folds and arytenoids, classically caused by Haemophilus influenzae type b. It is a true airway emergency because the loose tissue on the lingual surface of the epiglottis swells within hours into a cherry-red mass that falls back over the glottis, and because the manoeuvres that feel most natural to a nurse — laying the child flat, holding him down and putting a spatula on the tongue — are the ones that convert partial obstruction into complete obstruction.

The classic picture is a child of about 2 to 6 years, and increasingly an adult, who becomes ill over a few hours with a high fever, severe sore throat and a toxic appearance, and who is sitting up, leaning forward on the hands with the chin thrust out and the mouth open — the tripod or sniffing position.
The four Ds are drooling (saliva is too painful to swallow), dysphagia, dysphonia with a muffled hot-potato voice, and distress with soft inspiratory stridor; a barking cough is conspicuously absent, and that absence is the discriminator from croup.
Croup, or acute laryngotracheobronchitis, is the differential and is not the same disease: it affects 6 months to 3 years, is viral (parainfluenza), comes on over days with a barking seal-like cough and hoarse voice, causes little drooling, shows the steeple sign of subglottic narrowing on an anteroposterior neck film, and responds to nebulised adrenaline and dexamethasone.
A lateral soft-tissue neck radiograph shows the thumb sign of the swollen epiglottis with ballooning of the hypopharynx, but the film is taken only if the child is stable and only with a doctor escorting him; a child in respiratory distress goes to theatre, not to the X-ray department.
Do not examine the throat with a spatula, do not take blood, do not attempt cannulation, do not lay the child supine and do not separate him from his parent, because crying and struggling can precipitate laryngospasm and complete obstruction; keep him upright on the parent's lap and give oxygen by whatever route he tolerates, including blow-by.
Definitive management is a controlled airway before anything else: the child is taken to the operating theatre with an anaesthetist and an ENT surgeon present and a tracheostomy set open, and is intubated under inhalational anaesthesia with a tube half a size to one size smaller than usual, after which cultures and cannulation are done.
Antibiotic treatment is an intravenous third-generation cephalosporin, ceftriaxone or cefotaxime, for about 7 to 10 days, with humidified oxygen, intravenous fluids and sedation on the ventilator; most children can be extubated in about 48 to 72 hours once a leak develops around the tube and the swelling has settled.
The Haemophilus influenzae type b conjugate vaccine, given in India within the pentavalent vaccine at 6, 10 and 14 weeks, has made paediatric epiglottitis rare, so an unimmunised or partially immunised child is the one at risk, and rifampicin prophylaxis for four days is offered to unimmunised young household contacts.

Meniere disease

Meniere's disease is idiopathic endolymphatic hydrops — a distension of the endolymphatic compartment of the inner ear from over-production or defective absorption of endolymph, in which periodic rupture of Reissner's membrane lets potassium-rich endolymph mix with perilymph and poisons the hair cells and vestibular nerve endings. It matters because the attacks are violent and unpredictable, because each one leaves a little more permanent hearing loss behind, and because the patient can be thrown to the ground without warning, so the nurse's first concern in an attack is not the vertigo but the injury it can cause.

The diagnostic picture is a tetrad: episodic rotatory vertigo lasting from about 20 minutes to several hours, fluctuating sensorineural hearing loss, a low-pitched roaring tinnitus and a sense of fullness or pressure in the affected ear, with nausea, vomiting and horizontal-rotatory nystagmus during the attack but never any loss of consciousness.
Hearing loss is sensorineural, usually unilateral at the outset, and begins in the low frequencies with a rising audiogram curve that fluctuates between attacks; over years it stops fluctuating and settles into a flat, permanent, moderate to severe loss.
Recruitment is characteristically positive, so loudness grows abnormally fast and the patient is intolerant of loud sound; this is a cochlear sign and separates Meniere's disease from the retrocochlear pattern of a vestibular schwannoma.
Investigation is pure-tone and speech audiometry between and during attacks, a caloric test that typically shows reduced or absent response (canal paresis) on the affected side, electrocochleography with a raised summating to action potential ratio, the glycerol dehydration test, and magnetic resonance imaging of the internal acoustic meatus to exclude a vestibular schwannoma.
Two named variants are asked: Lermoyez syndrome, in which hearing improves as the vertigo begins, and Tumarkin's otolithic crisis or drop attack, in which the patient is suddenly thrown to the floor without warning and without losing consciousness — a hazard that bans driving, ladders, swimming alone and working at heights.
The acute attack is treated with bed rest in a quiet, dimly lit room with the head still, a vestibular sedative such as prochlorperazine, promethazine or dimenhydrinate, an antiemetic, intravenous fluids if vomiting is persistent, and reassurance that the attack will pass.
Long-term control is built on salt restriction, because sodium load drives the hydrops — a low-salt diet with avoidance of caffeine, alcohol, tobacco and monosodium glutamate — together with a diuretic such as hydrochlorothiazide with amiloride or acetazolamide, betahistine to improve cochlear microcirculation, and attention to stress and sleep.
When medical treatment fails, the ladder is intratympanic dexamethasone, then intratympanic gentamicin as a chemical labyrinthectomy that abolishes vertigo at the cost of some hearing, then endolymphatic sac decompression, vestibular neurectomy where hearing is worth preserving, and labyrinthectomy only in an ear whose hearing is already destroyed.

Epistaxis — management

Epistaxis is bleeding from the nasal cavity, and about 90 per cent of it is anterior, arising from Little's area on the anterior part of the nasal septum where Kiesselbach's plexus is formed by the anastomosis of the anterior ethmoidal, sphenopalatine and greater palatine arteries with the septal branch of the superior labial artery. It matters because the two ends of the spectrum look alike at first: the child with a picked septum stops with finger pressure, while the elderly hypertensive or anticoagulated patient with a posterior sphenopalatine bleed swallows litres unseen and arrives in shock, so the nurse's first job is always to decide which of the two is in front of her.

Anterior bleeding from Little's area is by far the commonest, is usually unilateral, visible and controllable with pressure; posterior bleeding, typically from the sphenopalatine artery or Woodruff's plexus in an older, hypertensive or anticoagulated patient, comes down both nostrils and into the throat, is not controlled by pinching, and needs packing and admission.
First aid is Trotter's method and the sequence must be exact: sit the patient upright and leaning forwards, pinch the soft cartilaginous part of the nose — not the bony bridge — firmly and continuously for 10 to 15 minutes without releasing to look, breathe through the mouth and spit any blood out rather than swallowing it, with an ice pack over the bridge of the nose or ice sucked in the mouth for reflex vasoconstriction.
Never tilt the head backwards; blood then runs into the pharynx where it is swallowed, causing nausea and vomiting and concealing the true blood loss, or is aspirated into the airway.
In heavy bleeding, resuscitation comes before the nose: assess airway, breathing and circulation, give oxygen, take the pulse and blood pressure lying and sitting, secure two wide-bore cannulae, send a full blood count, coagulation screen and group and crossmatch, and start fluids, because a patient can exsanguinate through the nose.
If pressure fails, the bleeding point is anaesthetised and shrunk with a pledget of a topical vasoconstrictor and local anaesthetic, then cauterised chemically with a silver nitrate stick applied to the vessel — and only one side of the septum is cauterised at a sitting, because cautery of both sides at once can perforate it.
An anterior nasal pack of ribbon gauze impregnated with paraffin or bismuth iodoform paraffin paste is layered in from the floor of the nose backwards and upwards, or a nasal tampon or inflatable balloon is used; the pack stays 24 to 48 hours, the patient is admitted or reviewed, and an antibiotic is considered because a retained pack risks sinusitis and toxic shock syndrome.
A posterior bleed needs a postnasal pack (Bellocq's) or a balloon catheter, always with admission, oxygen and pulse oximetry, because a posterior pack causes hypoxia and vagally mediated bradycardia and hypotension; failure at this stage is treated by endoscopic sphenopalatine artery ligation or cautery, anterior ethmoidal artery ligation or embolisation.
The cause must be found while the bleeding is being stopped: local causes include nose-picking and trauma, a foreign body (unilateral foul discharge in a child), deviated septum, rhinitis, sinusitis, atrophic rhinitis and tumours, and systemic causes include hypertension, anticoagulants and antiplatelets, liver disease, leukaemia, thrombocytopenia, dengue and other haemorrhagic fevers and hereditary haemorrhagic telangiectasia.
Aftercare prevents the recurrence: no nose-blowing, picking, straining, hot drinks, alcohol or heavy lifting for about a week, saline or petroleum ointment to keep the septum from crusting, sneezing with the mouth open, humidified air, treatment of the blood pressure, and a clear plan for anticoagulation rather than an unrecorded decision to stop it.

Tinnitus

Tinnitus is the perception of sound — ringing, buzzing, hissing or roaring — in the ear or the head in the absence of any external acoustic stimulus. It is a symptom and never a diagnosis, and it matters clinically for two reasons: it is the earliest warning of cochlear damage from noise and from ototoxic drugs, which is the one form the nurse can prevent, and when it is unilateral or pulsatile it points to a tumour or a vascular lesion rather than to an ageing cochlea.

Subjective tinnitus, heard only by the patient, accounts for almost all cases and arises from disordered activity in the cochlea and auditory pathway; objective tinnitus, which the examiner can hear with a stethoscope over the ear, neck or orbit, is far rarer and is either vascular (a glomus tumour, an arteriovenous malformation or a carotid bruit, giving a pulsatile noise synchronous with the pulse) or muscular (palatal or middle-ear myoclonus, giving a clicking sound).
The commonest causes follow the hearing loss: impacted wax, otitis media with effusion, noise-induced hearing loss, presbycusis, otosclerosis, Meniere's disease, head injury and vestibular schwannoma; tinnitus almost always accompanies a hearing loss, so every patient with tinnitus needs otoscopy and an audiogram.
The ototoxic drugs asked in the examination are the aminoglycosides (gentamicin, streptomycin, amikacin, kanamycin), loop diuretics (furosemide, especially given as a rapid intravenous bolus), salicylates including aspirin, quinine and chloroquine, cisplatin, vancomycin and erythromycin.
Reversibility differs and is the discriminator: tinnitus and hearing loss from aspirin, quinine and loop diuretics are usually dose-related and settle when the drug is stopped, whereas damage from aminoglycosides and cisplatin is to the hair cells and is permanent — which is why the tinnitus must be reported the day it appears.
Assessment is otoscopy, tuning-fork tests, pure-tone audiometry with tinnitus pitch and loudness matching, and imaging when the tinnitus is unilateral, pulsatile or accompanied by asymmetrical hearing loss or neurological signs.
No drug cures tinnitus; management is to treat the treatable cause, fit a hearing aid where there is hearing loss because amplification of ambient sound alone masks the tinnitus, and use sound therapy or maskers, tinnitus retraining therapy to build habituation, and cognitive behavioural therapy, which has the best evidence for reducing the distress it causes.
Practical advice that helps immediately: avoid total silence, which makes tinnitus louder, by using low background sound at night; protect the ears from loud noise; cut caffeine, nicotine and alcohol if the patient notices a link; treat insomnia, anxiety and depression, which drive the suffering more than the loudness does.

Profound hearing loss

Profound hearing loss is a hearing threshold worse than 90 decibels in the better ear, which means that ordinary speech is inaudible even when amplified and the patient depends on visual and tactile communication or on a cochlear implant. In a child it is not primarily an ear problem but a language problem, because the auditory cortex only develops if it is stimulated in the first few years of life, so every month between a failed newborn screen and a fitted device is a month of language that cannot be recovered later.

The standard grading of hearing loss by the average threshold in the better ear is: normal up to 25 dB, mild 26 to 40 dB, moderate 41 to 55 dB, moderately severe 56 to 70 dB, severe 71 to 90 dB and profound above 90 dB; profound loss is almost always sensorineural, because a purely conductive loss cannot exceed the roughly 60 dB the middle ear contributes.
Causes divide by timing: prenatal and genetic (about half of congenital deafness, with connexin 26 mutations in the GJB2 gene the commonest non-syndromic form, and Waardenburg, Pendred, Usher and Alport syndromes the named syndromic ones) and congenital infection with rubella or cytomegalovirus; perinatal (prematurity and very low birth weight, birth asphyxia, kernicterus from severe neonatal jaundice, a neonatal intensive care stay with ototoxic drugs); and postnatal (bacterial meningitis, mumps, measles, chronic suppurative otitis media, head injury and noise).
Universal newborn hearing screening uses otoacoustic emissions before discharge with a repeat test, and every baby who fails goes on to brainstem evoked response audiometry, which is the objective measure of threshold in an infant who cannot cooperate; high-risk babies are screened with brainstem audiometry from the start.
The service standard is the 1-3-6 rule: screening completed by one month of age, diagnosis confirmed by three months and intervention with amplification begun by six months — and it is the follow-up of the babies who fail the first screen, not the screening itself, that usually breaks down.
Behavioural tests are chosen by age: behavioural observation audiometry under six months, visual reinforcement audiometry from about six months to two years, conditioned play audiometry from about two to five years, and conventional pure-tone audiometry thereafter, with tympanometry to exclude a middle-ear effusion masquerading as a sensorineural loss.
Rehabilitation starts with a high-powered hearing aid trial; a cochlear implant is offered when the loss is severe to profound in both ears and well-fitted aids give no useful speech understanding, and outcomes are best when the child is implanted before two to three years of age, while an adult who lost hearing after learning to speak does better than one deaf from birth.
A cochlear implant bypasses the damaged hair cells and stimulates the cochlear nerve directly, so it requires a patent cochlea and an intact cochlear nerve; deafness after bacterial meningitis is implanted urgently because the cochlea ossifies within months, and pneumococcal vaccination is given before implantation.
The implant is the beginning of the work and not the end: intensive auditory-verbal and speech therapy, parental training and educational support follow for years, alongside sign language and lip reading, and in India the Assistance to Disabled Persons scheme, the National Programme for Prevention and Control of Deafness and a disability certificate carry the cost and the entitlements.

Rinne and Weber tests

Rinne's and Weber's tests are the bedside tuning-fork tests that separate a conductive from a sensorineural hearing loss: Rinne compares air conduction with bone conduction in one ear, while Weber tests where a fork placed in the midline is heard. A 512 Hz fork is used because 128 and 256 Hz forks are felt as vibration rather than heard and give false results, while forks above 1024 Hz decay too fast to complete the test, and the pair matters because together they localise the lesion before any audiogram is available.

Technique for Rinne's test: strike the fork on a soft surface such as the elbow or knee rather than on metal or bone, which creates overtones; hold the foot of the fork firmly on the mastoid until the patient says the sound has gone, then move the tines about 2 cm from and in line with the external auditory meatus and ask whether it is heard again.
Rinne positive means air conduction is better than bone conduction, which is the normal finding and is also found in sensorineural loss, where both are reduced but the ratio is preserved; Rinne negative means bone conduction is better than air conduction and indicates a conductive loss on that side.
The size of the air-bone gap can be estimated from which fork turns negative: a negative Rinne with a 256 Hz fork corresponds to roughly a 15 dB gap, with a 512 Hz fork about 30 dB and with a 1024 Hz fork about 45 dB.
The false-negative Rinne is the classic trap: in a severe or total unilateral sensorineural loss, the bone-conducted sound crosses the skull and is heard by the opposite normal cochlea, so the patient reports bone conduction better than air conduction in a dead ear; masking the other ear with a Barany noise box unmasks the error.
Technique for Weber's test: place the vibrating fork on the vertex, the middle of the forehead or the upper incisors and ask in which ear the sound is heard — the midline, the right or the left.
Weber is central when hearing is normal or the loss is symmetrical; it lateralises to the poorer ear in a conductive loss, because the blocked ear is not distracted by ambient noise and bone conduction is enhanced, and to the better ear in a sensorineural loss, because the diseased cochlea cannot perceive the sound at all.
Put the two together: a right conductive loss gives a negative Rinne on the right with Weber lateralising to the right, whereas a right sensorineural loss gives a positive Rinne on both sides with Weber lateralising to the left — this pairing is the standard examination question.
Two supplementary fork tests complete the set: the absolute bone conduction test compares the patient's bone conduction with the examiner's assumed-normal bone conduction while the tragus occludes the canal, and it is reduced in sensorineural loss; Schwabach's test does the same by comparison and is shortened in sensorineural loss and lengthened in conductive loss, while Gelle's test assesses stapes mobility and is negative in otosclerosis.
Always look in the ear before interpreting the forks: impacted wax, an effusion or a perforation produces a conductive picture, and tuning-fork tests are a screening tool whose findings must be confirmed by pure-tone audiometry.

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