adjusted as needed What to do if there is no sound \200 Check the hearing aid is not switched to \200\230O \200\231 or \200\230T \200\231 \200 Check the batteries are not dead, or put in upside d own \200 Check the mold is not clogged with wax \200 Check the tubing is not wet (dry w ith hairdryer) or twisted What to do if there is a whistling or squealing noise (feedback) \200 Occurs when the ear mold is not snug, allowing sound to escape into the microphone \200 Worse at high volumes \200 Check that the ear mold is a good \201 t (return to audiologist if not), and is inserted correctly Ensure there is not excess earwax impeding \201 t \200 Try turning the volume down Main taining the hearing aid \200 Handle carefully \200 Keep the hearing aid dry, away from strong heat or light \200 Use a clean dry tissue to clean, never a damp cloth \200 Use wax remover on a regular basis If the ear mold is separate (eg behind-the-ear) then periodi cally remove and wash with warm soapy water, ensuring it is totally dry before reconnecting it. This page intentionally left blank 556 CHAPTER 21 Ears Tinnitus The perception of a sound in one or both ears, without an external stim- ulus. Int ermittent or continuous. Varying kinds of noises (ringing, humming, buzzing, occasionally o ther noises) and at varying pitches. Large spectrum of disease. More common in men than wom en and incidence rises with age. Up to a fourth of older people may experience intermittent symp- toms. About a sixth of these will \201 nd it bothersome, and 1:20 will be disa- bl ed by it. A fourth of patients will get worsening symptoms with time. Tinnitus can be due to actual sounds that are generated by local structures: \200 Vascular structures (aneurysmal vessels, vascular tumors, etc. \200\224 generate a pulsatile or humming noise that may worsen with exercise) Muscle spasms (palatal or middle ear muscles \200\224 generate a clicking noise. Usually indicates underlying neurological disease) Eustachian tube may be patulous (can occur after dramatic weight loss) resulting in a roaring sound Joints (eg temporomandibular joint, cervical spine joints) More commonly, the noise is gene rated from somewhere within the auditory pathway (cochlear organ, nerve, brain stem or audi tory cortex) after some sort of damage or injury. The following are associated with tinnitu s: \200 Hearing loss \200\224 a very common cause in older people. Mechanism unclear \200\224 may be akin to phantom limb pain. Note tinnitus may precede deafness. May be assoc iated with conductive (eg wax accumulation) or more commonly sensorineural deafness (includ ing presbyacusis). Treatment of deafness (with hearing aid or occasionally cochlear implant ) often results in improvement of tinnitus Drugs \200\224 many commonly prescribed drugs in older people can either cause or exacerbate tinnitus (see Box 21.1 ) Vascular disease \200\224 microvascular damage to the auditory system, or a stroke affecting the auditory cortex. Modify vascular risk factors to limit progression Infection \200\224 eg chronic otitis media. Treat the cause, but may have residual problems Other \200\224 M ni re \200\231s disease, diabetes, thyroid disease, Paget \200\231s dis ease, brain tumor (intracanalicular and cerebello-pontine), trauma, and autoimmune disease. Treat underlying cause History \200 Obtain a description of tinnitus. This may indicate cause, eg pulsatile nois e is often vascular; clicking noise is often due to palatal muscle spasms; high-pitched con tinuous noise is usually due to sensorineural hearing loss; low-pitched continuous noise is more commonly seen (but not exclusive to M ni re \200\231s disease) Screen for possible causes (drug history, ear disease, noise exposure, injury etc.) Examination Should include full head and neck examination, cranial nerve examination, auscu ltation for bruits and inspection of the auditory canal. TINNITUS 557 Investigation Check FBC, glucose, and thyroid function. Refer to specialist for full audi- ometric assessment and possible imaging especially if unilateral (MRI angiography). Treatment \200 Dif \201 cult and frustrating \200\224 often best done in specialist cli nics with multidisciplinary team support Stop all ototoxic medication and avoid in future \200 Assess whether caffeine, aspartame sweetener, alcohol, nicotine and marijuana worsen tinnitus and avoid if so Treat the cause wherever possible \200 Strong association with insomnia and depression, b oth of which worsen the suffering and should be treated. Some evidence to suggest that antidepressants ( SSRIs) may help even when there is no overt depression Many other treatments have been tried (eg lidocaine, magnetic and ultrasonic stimulation, m elatonin, Ginkgo biloba , niacin, and zinc) but limited evidence they work and adverse effe cts common Hearing aids are useful if hearing loss \200\224 the increased awareness of the background sound tends to make the noise less apparent Masking techniques involve wearing a \200\230white noise \200\231 generator, rather like a hearing aid that aims to distract the patient from the tinnitus by reducing the contrast b etween the tinnitus signal and background noise, improving the plasticity of the central au ditory cortex and thereby facilitating a reduction in perception of the sound Mainstay of treatment is aimed at adjusting patients \200\231 perception of the tinnitus, t rying to habituate them to the noise and limiting the negative emotions it generates. Inclu des tinnitus retraining therapy, biofeedback, stress reduction techniques and cognitive and behavioral therapy Tinnitus support groups can be helpful ( M www.tinnitus.org.uk ) Box 21.1 Drugs causing or exacerbating tinnitus \200 Aspirin (high dose) \200 Other NSA IDs \200 Loop diuretics \200 ACE inhibitors \200 Calcium channel blockers \200 Doxa zosin \200 Aminoglycoside antibiotics \200 Clarithromycin \200 Quinine and chloroquin e \200 Carbamazepine \200 Tricyclic antidepressants \200 Benzodiazepines \200 PPIs \200 Some chemotherapy agents 558 CHAPTER 21 Ears Vertigo De \201 nition Vertigo is the hallucination of movement. A sensation of rotatory m otion either of the patient with respect to the environment ( \200\230its like being on a r oundabout \200\231), or the environment with respect to the patient ( \200\230the room is s pinning \200\231). The key element is a feeling of motion, without which a clinical diagnos is of vertigo should not be made. Understanding vertigo The vestibular system comprises the temporal bone labyrinths (compose d of the semicircular canals, the saccule, and the utricle), the vestibular nerve and the c entral vestibular structures in the brainstem. Normally, there is a constant input from bot h ears updating the central structures on head position. In the brainstem they are integrat ed with inputs from the visual cortex and from proprioceptive receptors (most important are neck and ankles). Any interruption of this signal leads to an excess of information from the good side, and s o an acute feeling of dizziness and nausea (vertigo) along with disruption of the vestibulo -ocular re \202 ex (which will cause nystagmus). This situation continues until either inp ut is restored, or the vestibular system adapts to the altered balance of signals. Adaptation means that: Vertigo is not a chronic condition. Multiple recurrences may occur, but a complaint of longstanding continuous dizziness is not vertigo. Vertigo rarely occurs with slowly progressive conditions (eg acoustic neuroma) as adaptation occurs along the way All vertigo is made worse by head movement \200\224 if not, then seek an alternative diagnosis The use of vestibular sedatives should be limited to the acute phase for symptom relief only \200\224 prolonged use will delay adaptation. 2There is no indication for long-term use of prochlorperazine. Causes (Table 21.1 ) \200 Around half of all patients complaining of dizziness will have vertigo (see b \200\230Dizziness \200\231, p.114) Over all ages, 80 % of vertigo arises from peripheral structures (the ears) and 20 % from central structures (the brain) Peripheral vertigo is due to benign positional paroxysmal vertigo in up to 50 % Central vertigo is usually due to stroke \200 The proportion of central vertigo increases with age, because of the increased incidence of stroke Table 21.1 Common causes of vertigo Condition Features Cause Treatment Resolves spontaneously but may recur Epley \200\231s maneuver may help (see b \200\230HOW TO Perform Epley \200\231s maneuver \200\231, p.562) Mild episodes lasting less than a minute, recurring frequently over weeks to months Calcium debris in semicircular canal Usually idiopathic May be preceded by minor head traum a Benign paroxysmal positional vertigo (BPPV) High-dose steroids acutely may speed recovery Treat with vestibular sedatives only while vo miting, then allow adaptation to occur May have recurrent (milder) episodes Ischaemia of vestibular apparatus, often proceeded by a viral respiratory tract infection Acute onset of severe vertigo, lasting hours to days Associated nausea, vomiting and postur al instability Patient in bed, refuses to move head Acute vestibular failure (labyrinthitis) Symptomatic treatment of acute attacks Betahistine is a labyrinthine vasodilator Diuretics may reduce attack frequency Surgical options include grommet insertion, transtympanic genta micin, endolymphatic decompression and vestibular nerve sectioning Dilation of endolymphatic space in the canals \200\224 primary cause still unknown M ni re \200\231s disease Recurrent episodes of violent vertigo, vomiting, tinnitus, ear fullness (lasting up to 12hr ) and \202 uctuating hearing loss TIAs cause stuttering symptoms (see b \200\230Vertebrobasilar insuf \201 ciency (VBI) \200\231, p.117). Stroke will cause abrupt onset, prolonged symptoms Vertigo is most common symptom, usually associated with other neurology (eg ataxia, diplopia, visual loss, slurre d speech, motor or sensory impairment) Cerebellar stroke can cause vertigo alone After stroke, slow improvement is normal, but often residual defects Modify vascular risk f actors (see b \200\230Vascular secondary prevention \200\231, p.308) to prevent recurrence Vertebrobasilar stroke V E R T G O I 5 5 9 560 CHAPTER 21 Ears Vertigo: assessment History \200 This is the most important diagnostic tool in vertigo, a nd should be open questions with clari \201 cation Describe the dizziness \200\224 is it a sensation of movement of self or the room (likely vertigo) or a light-headed feeling (less likely vertigo). A non-speci \201 c description d oes not exclude vertigo Establish if likely peripheral (abrupt onset and cessation with nausea, vomiting and tinnit us) or central (more prolonged, less severe, less positional episodes. Usually with other n eurological symptoms and signs) Ask about onset, severity, duration, progression and recurrence to narrow down cause (see Table 21.1 ) Ask about provoking factors \200\224 may be spontaneous, or brought on by changes in middl e ear pressure (sneezing, coughing) or head/ neck position (question carefully to distingui sh this from orthostatic symptoms) Ask about associated symptoms, eg tinnitus and hearing loss (is it worse during an attack) Ask about predisposing factors, eg vascular risk factors, recent infections, headache, otot oxic drugs, ear discharge, deafness, tinnitus, etc. Ask about psychiatric symptoms (eg low mood) \200\224 these are rarely offered spontaneously Examination \200 General examination (including cardiovascular examination) \200 Postur al blood pressure measurements \200 Neurological examination \200 Examine eye movements for pursuit and saccades. Abnormalities in a patient with balance complaints suggests a cerebellar origin Head and neck examination including otoscopy (to assess auditory canals and tympanic membranes) Gait assessment \200 Hearing test (see b \200\230HOW TO Assess hearing \200\231, p .550) \200 Vestibular assessment (see b \200\230HOW TO Examine the vestibular system \200\231, p.561) VERTIGO: ASSESSMENT 561 HOW TO Examine the vestibular system This is hard to do directly \200\224 it largely relies on testing the integrity of the vestibulo-ocular re \202 ex. \200 Test eye movem ents with the head still, looking for nystagmus (the eyes drift slowly towards the bad side, and the rapid correction phase is towards the good side). Visual \201 xation will suppress a peripheral nystagmus, but not a central. Periph eral lesions cause horizontal nystagmus in both eyes; central lesions cause nystagmus in an y direction that is more prolonged and severe Try to provoke vertigo and nystagmus by gently \202 exing, extending, rotating and laterally bending the cervical spine Check visual acuity with a Snellen chart both with the head still, and with the patient slo wly shaking their head. If acuity is > 4 lines worse with head shaking this suggests impair ment Ask the patient to \201 x gaze on the examiner \200\231s nose, while the examiner turns t he head rapidly to one side or the other. The patient should be able to keep gaze \201 xe d. If there is a peripheral vestibular problem the gaze may drift during rotation to that s ide, which is manifest by a catch-up saccade back to the point of \201 xation. When done properly this test has a better than 80 % sensitivity and speci \201 city for vestibular h ypofunction Ask the patient to shake their head, and then check for nystagmus \200\224 if it is present, this implies unilateral impairment Nystagmus after 30sec of hyperventilation can be an indicator of a vestibular schwannoma Hallpike maneuver \200 Tests for BPPV (50 \200\22380 % sensitive) \200 Sit the patient up, and stand behind them \200 Hold their head turned 45 to one side \200 Keep holding the head at this angle and rapidly lie the patient down so the hea d is 30 below the level of the couch, looking down to the \202 oor (steps 1 and 2 of t he Epley \200\231s maneuver, see b \200\230HOW TO Perform Epley \200\231s maneuver \200\231, p.562) Ask about symptoms, while watching for nystagmus (towards the \202 oor) BPPV can be diagnosed con \201 dently when the nystagmus is latent (occurs after a few seconds), transient (stops after less than 30sec) and fatiguable (lesse ns with repeat testing) If any of these features are absent, the vertigo is likely to be due to another cause Repeat with the head turned in the other direction 562 CHAPTER 21 Ears Vertigo: management Some speci \201 c treatments depending on cause (see Table 21.1 ). Symptomatic relief in the short term can be achieved with vestibular sedatives: \200 Anticholinergics (eg hyoscine patch 1mg/24hr) \200 Antihistamines (eg c yclizine 50mg tds, cinnarizine 30mg tds) \200 Phenothiazines \200\224 usually sedating ( eg prochlorperazine 10mg tds) \200 Benzodiazepines (eg diazepam) if unable to take antich olinergics (asthma) May also bene \201 t from antiemetics (eg metoclopramide, domperidone). These drugs are not for long-term use, and rarely bene \201 cial in BPPV as attacks are so short lived. Most vertigo will resolve with vestibular adaptation, leaving only brief feel ings of imbalance on rapid head turns. Some however, will develop chronic dysfunction, in which case man- agement is directed towa rds facilitating adaptation and development of coping strategies \200\224 vestibular rehab ilitation . This is done by physiothera- pists or ENT specialist nurses and adopts a holist ic approach. It involves a series of habituating exercises performed regularly to enable ad apta- tion via compensation to occur. In addition to vestibular rehabilitation, consider sp ectacles to improve visual acuity, exercise to improve muscle strength, and a walking stick to aid peripheral balance. Speci \201 c maneuvers (see b \200\230HOW TO Perform Epley \200\231s maneuver \200 \231, p.562) and exercises are used for BPPV. HOW TO Perform Epley \200\231s maneuver (See also Figs. 21.1 \200\223 21.6 . ) \200 Aims to clear debris from the posterior semicircular canal \200 Requires the patient to be fairly \202 exible \200 Premedication with a vestibular sedative is advised in seve rely affected patients Stand behind the patient, \201 rmly holding the head between your hands Make movements quickly and smoothly, holding each position for at least 30sec The procedure takes approximately 3 \200\2235min 1. With the patient upright, turn the head 45 to the affected side 2. Lie the patient do wn, with the head still turned until they are reclined beyond the horizontal (as in the Hallpike maneuver) 3. With the patient still recl ined beyond horizontal, rotate the head through 90 , with the face upwards 4. Keeping the head still, ask the patient to roll on to their side 5. Rotate the head so t he patient is facing downwards 6. Keep the head at this angle, and raise the patient to sit ting position 7. Finally, rotate the head so it faces the midline with the neck \202 exed (looking forward, and downwards) VERTIGO: MANAGEMENT 563 Fig. 21.1 With the patient upright, turn the head 45 * to the affected side. Fig. 21.2 Lie the patient down, with the head still turned until they are reclined beyond t he horizontal (as in the Hallpike maneuver). 564 CHAPTER 21 Ears Fig. 21.3 With the patient still reclined beyond horizontal, rotate the head through 90 * , with the face upwards. Fig. 21.4 Keeping the head still, ask the patient to roll on to their side. Fig. 21.5 Rotate the head so the patient is facing downwards. VERTIGO: MANAGEMENT 565 Fig. 21.6 Keep the head at this angle, and raise the patient to sitting position. Finally, rotate the head so it faces the midline with the neck \202 exed (looking forward and down wards). This page intentionally left blank 567 Chapter 22 Eyes The ageing eye 568 Visual impairment 569 Blind registration 570 HOW TO Optimize vision 570 Visual hallucinations 571 Cataract 572 Glaucoma 574 Age-related macular degeneration 576 HOW TO Use an Amsler grid to detect macular pathology 578 The eye and systemic disease 579 Drugs and the eye 580 Eyelid disorders 582 568 CHAPTER 22 Eyes The ageing eye Vision is a complex activity which involves eye function, cognition, rea- so ning, and memory. With increasing age the chance of visual impairment increases because of: \200 Changes due to senescence \200 Changes due to cumulative exposure to environmenta l toxins \200 Changes in associated functions (cognition, hearing, etc.) \200 Increasin g incidence of many eye diseases Visual impairment is not inevitable \200\224 there is con siderable diversity both in visual decline and in compensatory adaptations. There is a tend ency for patients to blame failing vision on age, and so not to seek help. However some cha nges may be age related (but corrective action may be available, eg glasses) or else impair ment may herald the onset of treatable disease. Prompt identi \201 cation and treatment ma y make all the difference between independence and dependence. Distinguishing what is \200 \230normal \200\231 and when to refer to a specialist is key. Changes in vision with age Visual acuity often decreases \200 Multifactorial \200\224 ch anges in macula, lens, and cornea \200 May be corrected (eg glasses) \200 Consider eye disease if deterioration is rapid Visual \201 elds \200\224 peripheral vision less sensi tive \200 Although formal \201 eld-testing normal \200\224 consider cerebrovascular disease if distinct homonymous \201 eld defect Multifactorial \200\224 pupil smaller, lens cloudier, and peripheral retina less sensitive Near vision decreases \200 Accommodative power diminishes due to increasingly rigid lens \200 Presbyopia (a lack of accommodation range) is part of normal ageing, begins in middle age and can be corrected with glasses Color vision \200 Retinal receptors unchanged \200 Alterations in color perception may relate to yellowing of the lens altering the light reaching the retina Light adaptation slower \200 Rods and cones may be slower to react to changes in illumina tion, and the pupil may let in less light, requiring brighter lighting for good vision Causes dif \201 culty with night driving in particular \200 Glare may be a problem as th e lens, cornea, and vitreous become less clear, and minute particles scatter light Contrast sensitivity decreases \200 Due to changes in cornea, lens, and retina Floaters \200 Due to aggregation of collagen \201 brils in vitreous \200 Usually normal, but if sudden onset, or large quantity, may indicate retinal detachment or vitreous hemorrhage VISUAL IMPAIRMENT 569 Visual impairment 2.5 % of the UK population has visual impairment not amenable to cor- rec tion by glasses alone. There is considerable social and psychological impact, yet it is und erreported and optimal help is often not delivered. Causes (From blind registration data): \200 Macular degeneration (49 % ) \200 Glaucoma (15 % ) \200 Diabetes (6 % ) \200 Cardiovascular disease (5 % ) 83 % of people who regi ster are > 65 years old. Low-vision clinics are available in most hospitals. Interventions Include: \200 Change glasses prescription (bene \201 ts 10 \200\22320 % ) \200 Explain the disease (often does not cause total blindness, eg with macular degeneration; improve understanding of future) Psychological support (often combined with hearing loss in older people \200\224 beware social withdrawal. Acknowledge problem, discuss fears) Discuss blind registration \200 In some cases, consider guide dogs and learning Braille \200 Take speci \201 c history of certain activities and provide practical advice: \200 Reading \200\224 what do they actually need to read? Advise about good light, magni \201 ers, large print books, photocopy recipes to larger size. Writing \200\224 use black pen on white paper, consider a Millard writing frame or bold line paper, discuss speci \201 c tasks such as checks and pension books. Television \200\224 sitting closer, black and white sets may improve contrast \200 Telli ng the time \200\224 talking watches and clocks \200 Cooking \200\224 improving lightin g in kitchen by removing net curtains, tactile markers for cookers, electronic fullness ind icators on cups Telephoning \200\224 large button telephones \200 Social interaction \200\224 sit with back to the window to improve light on a visitor \200\231s face, discuss accessible holidays Further reading Royal National Institute for the Blind online : M www.rnib.org.uk . SENSE o nline : M www.sense.org.uk . 570 CHAPTER 22 Eyes Blind registration Done by ophthalmologists. Copy of the form goes to social services, GP a nd the of \201 ce for national statistics. Generally there is under-registration \200\224 probably due to stigma and a sense that thi s is the end of the \201 ght, rather than the start of new help and opportunity. De \201 nitions \200 Partially sighted <6/60 in both eyes or reduced \201 elds (eg hom onymous hemianopia) Blind need not mean no vision. Statutory de \201 nition is that the person should be \200 \230so blind as to be unable to perform any work for which eyesight is essential \200\231. Pragmatically it is vision <3/60 or very diminished \201 elds Bene \201 ts to individual \200 Financial \200\224 including personal income tax allowa nce, disability living allowance or attendance allowance, working tax credit or pension cre dit, extra housing or council tax bene \201 ts, carers \200\231 allowance, help towards ca re home fees, free NHS sight test, free NHS prescriptions, lower television license fee, ca r parking and public transportation concessions, exemption from directory enquiries fees Easier access to help from social services \200 Loan of cassette recorder and talking boo ks and newspapers (also available without registration) HOW TO Optimize vision Bigger \200 Magni \201 ers (glasses or contacts, hand magni \201 ers, stand magni \201 ers, illuminated magni \201 ers, reading telescopes). Consider portability, cosmetic aspe cts, and posture required to use Larger print (books, enlarge frequently used items with photocopier) Bolder \200 Contrast ing colors \200\224 eg black on white \200 Use to emphasize written word, door handles, stair edges, etc. \200 Use white cups for dark drinks \200 Put contrasting strips round light \201 ttings Brighter \200 Remove net curtains \200 Use high power bulbs (eg 15 0W not 60W incandescent; a wider range of high luminescence \200\230low energy \200\231 la mps is now available) Use directable light sources (eg angle poise lamps) VISUAL HALLUCINATIONS 571 Visual hallucinations Management varies with the cause. Organic brain disease \200 Lewy body dementia (occur in 50 \200\22380 % ; usually well fo rmed, eg animals). Also occurs in dementia of Parkinson \200\231s disease. Can respond dramatically to cholinesterase inhibitors Anoxia, migraine and delirium \200\224 treat the underlying cause \200 Focal neurologica l disease (especially occipital and temporal lobe \200\224 range from unformed lines and lights, etc. to complex) Occipital lobe seizures \200\224 treat with anticonvulsants Drugs \200 Common with dopamine agonists and anticonvulsants (usually mild and unformed). Try reducing the dose, watching for rebound in symptoms Overdose of anticholinergic drugs such as antihistamines or tricyclic antidepressants Use of amphetamines and LSD \200 Alcohol withdrawal Psychiatric disease Visual hallucinations occasionally occur with schizophrenia (auditory m ore common). Charles Bonnet syndrome \200 Diagnosis of exclusion \200 No other psychiatric symptoms or diseases present \200 Occurs with bilateral visual loss (typically secondary to catara cts or glaucoma) as a \200\230release phenomenon \200\231 These are usually well formed, vivid, and occur in clear consciousness \200 Insight is us ually present \200 Duration is usually seconds to a minute or so \200 May be simple ( \202 ashes, shapes) or complex (recognizable images) \200 Non-threatening \200\224 the p atient \200\231s reaction is often one of curiosity or amusement Probably under-estimated as patients reluctant to tell doctors for fear of being labeled as \200\230mad \200\231 Not related to psychiatric problems \200 Reassurance is often all that is required, but s ymptoms may be improved by enhancing vision 572 CHAPTER 22 Eyes Cataract Term used to describe any lens opacity. The most common cause of treatable blindne ss worldwide. In the UK it is largely a disease of the older population: 65 % of people in their 50s and everyone > 80 have some opaci \201 cation. This is probably caused by cumula tive exposure to causative agents rather than senescence per se. Causes \200 Exposure to environmental agents (eg UV light, smoke, blood sugar) \200\224 more exposure with increasing age Ocular conditions (trauma, uveitis, previous intraocular surgery) \200 Systemic condition s (eg diabetes, hypocalcaemia, Down \200\231s syndrome) \200 Drugs (especially steroids \200\224 ocular and systemic) Symptoms \200 Painless visual loss which varies depending on whether unilateral/ bilateral and severity/position of the opacity Commonly begins with dif \201 culty in reading, recognizing faces, and watching television May be worse in bright light or be associated with glare around lights Signs \200 Reduced visual acuity \200\224 usually gradual \200 Diminished red re \202 ex on ophthalmoscopy \200 Change in the appearance of the lens (appears cloudy brown or white when viewed with direct light) Beware co-existing conditions: pupil responses are normal, and the patient should be able t o point to the position of a light source Management \200 Optimizing visual conditions 2New glasses prescription may delay need for surgery. \200 Surgical removal of opaci \201 ed lens \200 No effective medical treatm ent When to treat? Tailor treatment to the individual. Depends on visual requirements of patien t, severity of cataract, and presence of other ocular disease (worsens outcome from surgery ). Roughly speaking <6/18 in both eyes is likely to bene \201 t from surgery, but an elder ly person who does not read much may be quite content with this visual level. Conversely, s omeone who wishes to continue driving, or needs precise vision for other reasons may wish f or surgery much sooner. Previously surgeons waited for the cataract to \200\230ripen \200 \231 to aid extraction \200\224 this is no longer the case. Have a frank discus- sion abou t risks and bene \201 ts with each individual. CATARACT 573 What the surgery involves \200 Usually done as a day case under local or topical anesthes ia \200 Patient must be able to lie fairly \202 at and still. Patients with dementia ma y need sedation or general anesthesia (altering risk/bene \201 t); consider heart failure, chest disease and spinal deformity \200\224 can they lie \202 at? If not, then the surg eon may be able to adapt the procedure It is not necessary for patients to discontinue medications. The procedure may be done safely while a patient is taking aspirin, and even warfarin Generally a safe and well tolerated procedure \200 Phacoemulsi \201 cation is most commo nly used in the UK (small cut in eye to access lens that is then lique \201 ed with an ult rasonic probe). A replacement lens is then folded into the empty lens capsule. Sutures are not usually needed Other methods (extracapsular and intracapsular extraction) are less commonly used Postoperatively the patient will wear an eye shield (usually at night) for a period, and use steroid and antibiotic eye drops Surgery is done on one eye at a time. The poorer-seeing eye is usually done \201 rst. Sec ond eye surgery may be done once outcome from the \201 rst eye is assessed Outcome With no ocular comorbidity, 85 % have a visual acuity of > 6/12 at discharge. Outco me is worse with other eye diseases, eg glaucoma, and in patients with diabetes and cerebro vascular disease. As the replacement lens has a \201 xed focus and is usually chosen to allow clear distanc e vision, the patient will usually require glasses for reading. A new prescription should b e made up a few weeks after surgery, once postoperative in \202 ammation has settled. If s econd eye surgery is planned then glasses are usually issued once both surgeries are comple ted. 574 CHAPTER 22 Eyes Glaucoma Third most common cause of blindness worldwide. 2Leading cause of preventable blin dness in the UK. Early detection can slow/halt progression. De \201 nition Visual loss due to a combination of loss of visual \201 elds and cupping of the optic disc. Usually associated with a rise in intraocular pressure suf- \201 cient to cause damage to the optic nerve \201 bres (either direct mechanical damage, or by ind ucing ischaemia). Intraocular pressure \200 Ciliary body (posterior) makes aqueous, which \202 ows anteri orly through the pupil and drains via the trabecular network in the anterior chamber angle of th e eye Balance of production and drainage determines pressure \200 Wide range of pressures seen in normal adults (detected with tonometry) \200\224 average 15.5mmHg, normal <21mmHg The pressure at which ocular damage occurs is probably highly variable between people Can develop glaucoma with \200\230normal pressure-normal tension glaucoma \200\231 (may be high for that person/other factors such as ischaemia may be relev ant). More common in older patients. Fluctuating BP may be contributory Can have \200\230high \200\231 pressures without glaucoma \200\224 \200\230ocular hyperten sion \200\231 \200 Symptoms depend on rate and degree of rise in pressure. Generally asymptomatic unless advanced or acute Primary ( \200\230chronic \200\231) open-angle glaucoma \200 Most common \200 Failure o f out \202 ow of aqueous causes slow rise in pressure, allowing adaptation, so subtle symptoms No pain, corneal cloudiness, or haloes \200 Slow loss of visual \201 eld, typically in an arc shape ( \200\230arcuate scotoma \200\231) with preservation of central vision (macul a has more nerve cells so is relatively protected). Progresses to tunnel vision, and then b lindness Risk factors \200 Age (1 % in 5th decade, rising to 10 % in 9th decade) \200 African Ca ribbean origin (four times risk) \200 Blood relatives with glaucoma Screening \200 Targ et those at higher risk \200 Combination of ophthalmoscopy (looking for disc \200\230cup ping \200\231), automated perimetry testing (for minor \201 eld defects) and tonometry (for intraocular p ressure) is best \200 Most cases picked up by optometrists \200 Encourage regular eye t ests, and include careful fundoscopy in physical examination GLAUCOMA 575 Treatment \200 Topical treatments (eye drops): B -blockers, eg timolol (decrease aqueous secretion. Can cause systemic B -blockade); prostaglandin analogs eg latanoprost (improve d rainage, may darken iris); A -agonists (decrease aqueous production); carbonic anhydrase in hibitors, eg dorzolamide (decrease aqueous secretion); parasympathomimetics, eg pilocarpine (constrict pupil so will reduce visual \201 eld \200\224 not commonly used) Oral treatments: carbonic anhydrase inhibitors, eg acetazolamide very powerful, with many s ide effects including electrolyte imbalance and paraesthesia of extremities Surgical treatment: trabeculectomy \200\224 operation to improve aqueous out \202 ow. Arg on laser trabeculoplasty (applied to the trabecular meshwork) may be effective. Cyclodiode laser to the ciliary body (decreases production) is used in refractory cases Support group: International Glaucoma Association ( M www.iga.org.uk ) Acute angle closure glaucoma 2Emergency sight-threatening condition \200\224 requires urge nt referral and treatment. \200 Apposition of lens to the back of the iris prevents out \202 ow of aqueous with a rapid rise in pressure Causes red, painful eye with vomiting, blurred vision, and haloes around lights (due to corneal oedema) May be precipitated by pupil dilation, eg at dusk. Pupil constricts when asleep so episodes at night may be aborted by sleep \200 Very rarely can be precipitated by anticholinergic drugs \200 More common in older patients, women, and longsighted indiv iduals \200\224 beware of the vomiting older woman with a red eye On examination cornea is usually cloudy and visual acuity signi \201 cantly reduced (eg counting \201 ngers) Treat urgently with iv acetazolamide, topical glaucoma treatment, and laser iridotomy to re store \202 ow. Treat other eye prophylactically with laser iridotomy to prevent pupillary block 576 CHAPTER 22 Eyes Age-related macular degeneration Age-related macular degeneration (AMD) is the most common cause of adult blind registrations in UK and USA. 2New treatments for early stages make det ection crucial. De \201 nition As it sounds \200\224 age-related degenerative changes affecting the macul a (central part of the retina responsible for clear central vision). Two types: 90 % dry with gradual onset of symptoms (drusen and atrophy of the retinal pigment epithelium) 10 % wet , where symptoms relate to leaking vessels causing distortion or sudden loss of ce ntral vision due to sub-macular hemorrhage (choroidal neovascularization \200\224 new vess els can leak, bleed, and scar causing visual loss in a few months) Prevalence \200 Increases with age \200 25 \200\22330 million worldwide \200 Up to 30 % of > 75s may have early disease, and 7 % late disease Risk factors \200 Cause unknown \200 Age, smoking, family history are strongly associat ed \200 Female sex, Caucasian race, hypertension, blue eyes, other ocular conditions (len s opacities, aphakia) and low dietary antioxidants Symptoms \200 Asymptomatic in early stages, progressing to loss of central vision \200 May also have decreased contrast and color detection, \202 ashing lights and hallucinations Distortion of straight lines is a feature of wet AMD \200 Peripheral vision is normal in absence of other pathology Detection \200 Regular ocular examination \200 Use of Amsler grid in high risk patients (Fig. 22.1 ) Prognosis \200 Dry AMD progresses slowly and rarely causes blindness \200 Wet AMD may p rogress rapidly (blind in under 3 months) and accounts for 90 % of AMD blind registrations. Sudden onset of distortion of central vision should prompt urgent referral Bilateral disease \200\224 42 % with wet AMD will develop this within 5 years AGE-RELATED MACULAR DEGENERATION 577 Prevention \200 Smoking is the most important modi \201 able risk factor \200 A diet r ich in fruit and vegetables reduces risk \200 A combination of B -carotene, vitamins C an d E, and zinc is effective in preventing severe visual loss in established moderate-severe AMD A multicentre study showed that antioxidant vitamins halted progression of dry AMD in around 30 % of patients Management \200 Appropriate for subset of wet AMD only \200 Halts progression so early treatment is desirable \200 Fluorescein angiography should be done within a few days of o nset of symptoms to determine the type and location of neovascular areas Treatment options for neovascular AMD include: \200 Photodynamic therapy \200\224 this t argets sub-foveal neovascular areas (whilst preserving normal retina) by using photosensiti ve drug (vertepor \201 n) along with a non-thermal activating laser. Used in early disease , this therapy can slow or halt progression Anti-angiogenic therapy \200\224 eg ranibizumab \200\224 a recombinant, humanized, monocl onal antibody that neutralizes all active forms of vascular endothelial growth factor A. NI CE recommends its use for wet AMD under certain conditions (eg no permanent damage to the c entral fovea). The cost of ranibizumab beyond 14 injections in the treated eye is met by th e manufacturer Laser photocoagulation is sometimes used for extra-foveal lesions 578 CHAPTER 22 Eyes HOW TO Use an Amsler grid to detect macular pathology Fig. 22.1 Amsler grid. \200 Test one eye at a time \200 Usual reading glasses should be worn, and the grid held at comfortable reading distance Ask the patient to look at the central spot, and not to look away \200 Assess the followi ng: Can all four corners of the grid be seen? \200 Are any of the lines missing, wavy, blurre d, or distorted? \200 Do all of the boxes appear the same size and shape? \200 Any abno rmalities may indicate macular pathology and should prompt referral to an ophthalmologist THE EYE AND SYSTEMIC DISEASE 579 The eye and systemic disease Two of the top four causes for blind registration are due to s ystemic disease \200\224 diabetes and vascular disease. Eye disease develops as a late com plication of prolonged poor control in both cases, and the important message is to strive t o prevent these problems in the \201 rst place. Diabetes Causes retinopathy, cataracts, and \200\230microvascular \200\231 cranial nerve p alsies. Retinopathy \200 Associated with increasing duration of diabetes \200\224 at 20 years, 8 0 % will have some retinopathy