Fig 1. Macular hole. the vitreous cortex at the macula. Tests Amsler grids (p428) reveal visual distort- ion; optical coherence tomography (OCT, \201 g 2) diagnoses and stages macular holes. Fluoresce- in angiography (FA) helps diff ere ntiate macul ar holes from cystoid macular oedema and choroi- dal neovascularization (CNV). Treatment In stage 1, see what happens (no treatment if there is spontaneous resolution or Quresh Mohamed FCROphth. no progression). Surgery: a vitrectomy is done to remove the vi treous and the internal limiting membrane over the hole is peeled. An air bubble is introdu ced to nudge (tamponade) the macula back into position. The patient spends 1 \200\2232 post -op weeks face down. Series of patients have been variously reported, with hole closure rat es of \211 95% ( 67% improve by \211 2 lines of visual acuity). Success is also possible if the hole is long-standing (>6 months). Fig 2. Stage 4 hole (optical coher- ence tomography). However, in some patients, more than one operation is needed to close the hole, and adverse eff ects may occur: macular retinal pigment epithelium changes, retinal detachments, iatro genic retinal tears, enlargement of the hole, macular light toxicity, postoperative intraoc ular pressure spikes. Many patients develop cataracts (76% of cases requiring extraction wi thin 2 years). Patients not suitable or not wishing for this need visual aids (eg to read). The eye in diabetes mellitus \200\207Keep BP <150/85mmHg and all the major diabetic retino pathies are less com- mon.1 Diabetes can be bloody and blinding \200\224the leading cause o f blindness in those aged 20 \200\22365 (UK). Almost any part of the eye can be aff ected: mainly cata- ract and retinopathy. 30% of adults have ocular problems when diabetes pre- se nts. At presentation, the lens may have a higher refractive index producing relative myopia . On treatment, the refractive index reduces, and vision is more hypermetropic, so don \200 \231t correct refractive errors until diabetes is controlled. Structural changes Diabetes a ccelerates formation and progress of age- related cataract. Typically this is premature sen ile cataract, but young diabet- ics can also be aff ected at presentation; here the lens ha s taken up a lot of glucose which is converted by aldolase reductase to sorbitol. Diabetes causes ocular ischaemia, which can cause new blood vessel forming on the iris (ru- beosis), and, if these block the drainage of aqueous \202 uid, glaucoma may result. Retinopathy P athogenesis: microangiopathy in capillaries, precapillary art- erioles and venules causes o cclusion leakage. Vascular occlusion causes ischaemia new vessels in the retina, opti c disc, and iris, ie proliferative retinopathy. New vessels can bleed (vitreous hemorrhage) . Retraction of \201 brous tissue running with new vessels heightens risk of retinal deta chment. Occlusion also causes cotton wool spots (ischaemic nerve \201 bres). Vascular lea kage: As pericytes are lost, capillaries bulge (microaneurysms) and there is oedema & hard exudates (lipoprotein & lipid \201 lled macrophages). Rupture of microaneurysms at the ne rve \201 bre level causes \202 ame shaped hemorrhages; when deep in the retina, blot he morrhages form. 446 \200 y g o o m a h t h p O l l \200\207Presymptomatic screening enables timely laser photocoagulation. Screen by regular eye exam or retinal photography. Screen all diabetic patients annually in the community, by dilated fundus photography which is then reviewed by a trained screening service. Referral s are then made accordingly. Lesions are mostly at the posterior pole and can be easily see n by ophthalmoscope. Non-proliferative diabetic retinopathy (NPDR) is rated as mild, modera te or severe depending on the degree of ischaemia. Signs comprise micro- aneurysms (seen as \200\230dots \200\231), hemorrhages ( \202 ame shaped or \200\230blots \200\231) hard e xudates (yellow patches), engorged tortuous veins, cotton wool spots, large blot hemorrhage s (the latter 3 are signs of signi \201 cant ischaemia). NPDR can progress to sight-threat ening proliferative retinopathy. Proliferative diabetic retinopathy (PDR): Fine new vessels appear on the optic disc, retina and can cause vitreous hemorrhage. Maculopathy: Leakage f rom the vessels close to the macula cause oedema and can signi \201 cantly threaten vision (clinically signi \201 cant macular oedema). It can exist with otherwise mild retinopathy . \200\207Refer those with maculopathy, severe NPDR, or proliferative retinopathy urgently f or assessment2 and treatment (eg photocoagulation) to protect vision. Treatment Good contro l of diabetes prevents new vessels forming. \200\230Meta- bolic memory \200\231 eff ects m ean that early good control of diabetes with insulin pays dividends later. 124 Pregnancy, d yslipidaemia, BP \200\200, renal disease, smoking, and anemia may accelerate retinopathy. P hotocoagulation by laser is used to treat both maculopathy (focal or grid) and proliferativ e retinopathy (panreti- nal). Intravitreal triamcinolone and anti-VEGF drugs (p439) are use d with laser to treat diabetic macular oedema. See \201 gs 1 & 2. If vitreous hemorrhage is massive and does not clear, vitrectomy may be needed. CNS eff ects Ocular palsies may oc cur, typically nerves III and VI. In diabetic third nerve palsy the pupil may be spared as \201 bres to the pupil run peripheral- ly in the nerve, receiving blood supply from the p ial vessels. Argyll Robertson pupils and Horner \200\231s syndrome may also occur (p424). 1 UKPDS data: N = 1148. Absolute risk for blindness was 3.1 per 1000 patient-years if contro l was tight VS 4.1 for others. There was no diff erence if the BP was lowered by ACE-i or \200 -blockers. 125 2 Fluorescein angiography and optical coherence tomography OCT imaging are important tools here. 447 Fig 1. In this diagram of the retina that is depicted in \201 g 2, where are the le- sion s? In this image of the macular re- gion, a is the foveola, b is the fovea cen- tralis, c i s the parafoveal area, and d is the perifoveal area. 126 See p445 for ana- tomical/histolog ical nomenclature. 127 In day-to-day clinical parlance the word fovea is often used (confus ingly) to refer to fovea centralis and/or the foveola. y g o o m l a h t h p O l The macula is a circle centered on the foveola whose diameter is the distance between the t emporal border of the op- tic disc and the foveola. \200 128 Results of retinal screening in diabetes: when to refer to a surgeon: 1 Maculopathy: If screening shows exudate or retinal thickening within one optic disc diameter of the cent er of the fovea \200 Circinate or other group of exudates within the macula \200 Any micr oaneurysm or hemorrhage within 1 disc-diameter of the center of the fovea, if best visual a cuity is <6/12. 2 There are features of pre-proliferative retinopathy (venous beading; venous loops or reduplications); multiple deep, round or blot hemorrhages. 3 Any unexplained drop in visual acuity. \200 128 4 Proliferative diabetic retinopathy This is treated with panretinal (scatter) laser photo-coagulation (PRP). This type involves tre ating the peripheral retina which is not receiving adequate blood \202 ow. By treating th ese areas, the stimulus driving the neovascular process may be halted. As this treatment in volves many laser applications (eg >1000) it may be divided into \211 2 sessions. NB: panr etinal photocoagulation does not improve vision. It is intended to help prevent blindness. It may cause some loss of peripheral, color, and night vision. Some patients get generalize d blurring of vision which is usually transient but may persist inde \201 nitely. x Fig 3. After the laser. Figs 2 & 3 Prof J Trobe. Fig 2. Retinopathy before the laser. The eye in systemic disease Systemic disease often manifests itself in the eye and, in some cases, eye ex- amination will \201 rst suggest the diagnosis. Vascular retinopathy This may be arteriopathic (arteriovenous nipping: arteries nip veins where they cross \200\224th ey share the same connective tissue sheath) or hypertensive \200\224arteriolar vasoconstric tion and leakage \200\224producing hard exudates, macular oedema, hemorrhages, and, rarely, papilloedema. Thick, shiny arterial walls appear like wiring (called \200\230silver \200 \231 or \200\230copper \200\231). Nar- rowing of arterioles leads to infarction of the sup er \201 cial retina seen as cotton wool spots and \202 ame hemorrhages. Leaks from these appear as hard exu- dates macular oedema/papilloedema (rare). 448 \200 Emboli to the retina cause amaurosis fugax ( \200\230a curtain passing across the eyes \200 \231). Typical cause: atheroma (listen to carotids).1 Arrange urgent carotid Doppler; treat eg by aspirin, statin carotid endarterectomy. Retinal hemorrhages are seen in leukemia; comma-shaped conjunctival hemorrhages and retinal new vessel formation may occur in sickle-cell disease; optic atrophy in pernicious anemia. Note also Roth spots (retinal infarcts) of infective endocarditis (OHCM p144). Metabolic d isease Diabetes: p446. Wilson \200\231s dis- ease (Kayser \200\223Fleischer ring, \201 g 1). Hyperthyroid- ism, and exophthalmos: OHCM p211. In myxoedema, eyelid and periorbital oe dema is quite common. Lens opacities may occur in hypoparathyroidism. Conjunctival and corn eal calci \201 cation may occur in hyperparathyroidism. In gout, monosodium urate deposite d in the conjunctiva may give sore eyes. Granulomatous disorders (TB, sarcoid, leprosy, Cou rtesy of Jon Miles. brucellosis, toxoplasmosis) all produce in \202 ammation in the eye (u veitis). TB, con- genital syphilis, sarcoid, CMV, and toxoplasmosis may all produce choroid oreti- nitis. In sarcoid there may be cranial nerve palsies and lacrimal gland swelling. Co llagen and vasculitic diseases These also cause in \202 ammation. Conjuncti- vitis is foun d in SLE and Reiter \200\231s syndrome; episcleritis in polyarteritis nodosa and SLE; scler itis in rheumatoid arthritis; and uveitis in ankylosing spondylitis and Reiter \200\231s sy ndrome (OHCM p552). In dermatomyositis there is orbital oede- ma with retinal hemorrhages. Beh et \200\231s syndrome causes uveitis & retinopa- thies. Temporal arteritis leads to is chaemic damage to the optic nerve. Keratoconjunctivitis sicca/Sj gren \200\231s syndrome ( OHCM p724). There is re- duced tear formation (Schirmer \201 lter paper test), producing a gritty feeling in the eyes. Decreased salivation also gives a dry mouth (xerostomia). It occurs in association with collagen diseases. Pilocarpine and cevimeline help sicca feature s and topical ciclosporin helps moderate or severe dry eye.129 Silicone nasolacrimal puncta l plugs help maintain tears on the eye surface for longer HIV/AIDS Those who are HIV +ve ma y get CMV retinitis (often despite highly active antiretroviral \200\224), 130 with retina l spots ( \200\230pizza pie \200\231 fundus, signifying su- per \201 cial retinal infarcti on) + \202 ame hemorrhages involving ever more of the retina. This may be asymptomatic or cause blindness; it implies AIDS and \200\201CD4 count. IV ganciclovir or its prodrug (or al valganciclovir) are used. 131 Cotton wool spots may indicate HIV retinopathy (may presen t before full AIDS); it is a microvasculopathy, not a retinitis. Candidiasis of the aqueous and vitreous is hard to treat. Kaposi \200\231s sarcoma ( \201 g 1 p607) may aff ect the lids or conjunctiva. Other causes of retinopathy (hemorrhages, microaneurysms, hard exu- da tes) 132 radiation; carotid artery disease; central or branch retinal vein occlu- sion; ret inal telangiectasia/Coats \200\231 disease; Leber \200\231s miliary aneurysms. 1 Causes of amaurosis fugax: giant cell arteritis, orbital schwannomas, meningiomas, ocular small vesse l disease, Churg \200\223Strauss vasculitis, antiphospholipid syndrome, arrhythmias, dys \201 brinogenemia, uveitis \200\223glaucoma \200\223hyphaema syndrome post-cataract extract ion. 69,133 \200\223138 y g o o m a h t h p O l l Fig 1. Kayser \200\223Fleischer ring. A swollen optic nerve head is called papillitis (there are many causes). Papilloedema is sw ell- ing of the optic disc that is non-in \202 ammatory and caused by raised intracranial pressure. Papil- loedema is usually though not always bilateral. In \201 gs 2 & 3, the di sks are swollen forwards and also outwards into the surrounding retina. Disc margins are hi dden and in places retinal vessels are con- cealed, because oedema has impaired the trans- lucency of the disc tissues. The retinal veins are congested and there are a few hemorrhage s at 9 o \200\231clock in \201 g 2. \200\207Whenever you see these appear- ances, get he lp. Measure the BP, and look in the other eye. Any hypertensive changes or haemor- rhages? Or signs of central retinal vein occlusion? (p435). Bilateral disc changes suggest intracra nial hypertension (ICP \200\200). Is there headache \200\224worse in the mornings, centered in the frontal region, and are aggravated by bending down? In young obese women, think of benign intra-cranial hypertension. (=pseudoneuritis = pseudo- Pseudopapilloedema papillitis ; see \201 g 4) is usually associated with hyper metropia astigmatism or tilted disks, as in this patient below (from a 12-yr-old boy referred for \200\230?brain tumor \200\231 ). The disc margins are blurred and the disc appears elevated. Its cup may be ab- sent but there is no true oedema and veins are of normal size and pulsate (transmitted from a nearby artery). It is usually bilateral and symmetrical and does not change over time. Fluorescen ce angiogra- phy (FA) distinguishes it from papilloedema or optic neuritis/papillitis (ther e is no contrast leakage). Opaque myelinated nerve \201 bres may be confused with papillo edema ( \201 g 5). Other causes of swollen disks include optic neuritis (p434) and disorde rs of the nerve sheath (eg a meningioma, as seen in the MRI image, \201 g 6). Optic nerve head drusen ( \201 g 7) are multiple hyaline bodies extending beyond the disc margins. Ab normal branching of the retinal vessels is often present. The nerve head is usually small ( bilateral \200\230crowded disc \200\231). If the hyaline material is buried in the disc su bstance, diagnosis is confusing, especially if a \201 eld defect is also present. NB: opt ic atrophy in the contralateral eye is the Foster \200\223Kennedy syn- drome (eg from menin gioma of the optic canal in the eye with optic atrophy; in practice, the usual cause is con sequential ischaemic optic neuropathy). Nystagmus suggests a lesion in the posterior fossa; Sixth nerve palsy may be a false localizing sign. Homonymous \201 eld defects may accomp any compression of the supra-geniculate or poste- rior visual pathway by a glioma, meningio ma, or AV malformation. 449 Fig 2. Papilloedema. y g o o m l a h t h p O l Fig 3. Papilloedema. Fig 4. Pseudopapilloedema. Fig 5. Nerve \201 bres mimicking papilloedema. Fig 6. Meningioma of left op- tic nerve sheath. We thank Mr J F Cullen FRCS for permission to use the images. Fig 4 Reproduced from Brain \200\231s Diseases of the Nervous System, OUP. Fig 7. Optic drusen. Tropical eye disease Xerophthalmia & keratomalacia These indicate vitamin A lack, eg if poo r, weaned early on to vitamin A de \201 cient milk products, alcohol abuse, steator- rhoea or a food-fad or intolerance ( \200\234dairy products make me sick \200\235). Peak inci dence: 2 \200\2235yrs; 40 million children worldwide. Signs: Night blindness (nyctalopia), tunnel vision, poor acuity, and dry conjunc- tivae (xerosis). The cornea is unwettable and loses transparency. Small foamy plaques (Bit t \200\231s spots, \201 g 1) occur, raised from interpalpebral conjunctiva. Vitamin A reverses these changes. Early corneal xerosis is reversible. Corneal ulceration and perforation can occur. In keratomalacia there is massiv e sof- tening of the cornea perforation and extrusion of the intraocular contents. Tests : Visual \201 elds tests; dark-adapted electroretinography (bilateral \200\201amplit- ud es \211\210 diminished rod function);139 plasma vitamin A \200\201. \201\227: Just hand out the vitamins? 1 It \200\231s not so simple. \201\201Every Bit t spot is a stain on th e soul of the body politic, and as each represents a failure of education and politics, we are all implicated. \200\207Examine the cultural web that led to the de \201 ciency, and try to take whatever steps are necessary to correct it. Trachoma Caused by Chlamydia tracho matis (serotypes A, B, or C). It is spread mainly by \202 ies, where it is hot, dry, and dusty and the people are poor, living near their cattle. 400 million people are aff ected; 100,000,000 are children. Staging: 1 There is lacrimation. Follicles under the upper lid gi ve a \201 ne granu- lar appearance ( \201 g 2 \200\2233). 2 There is intense erythema. T he follicles are larger and underneath both lids. A \201 ne pannus and capillaries grow d own towards the cornea. 3 The follicles rupture and are replaced by scar tissue. The pannus is more advanced. The cornea may ulcerate. 4 Scar tissue distorts the lids and causes entr opion. Eyelashes scratch the cornea, which ulcerates. Drugs: Mass anti-trachoma treatment: tetracycline 1% eye ointment 12-hrly for 5 days each month for 6 months. In active disease use 8-hrly for 6 weeks + tetracycline 250mg/6h PO for 14 days. Azithromycin (20mg/kg stat) is 78% ef- fective in children and is a preventive that can be repeated 6 \200\22312 monthl y. 141,142 Lid surgery: Eg lid margin splitting + tarsal plate fracture + everting sutures. Prevention: Good water; wash face often; azithromycin. Onchocerciasis (river blindness) Th is is caused by nematode micro \201 lariae (Onchocerca volvulus), transmitted by black \202 ies of the Simulium species. Of the 20 \200\22350 million people aff ected, 95% live i n Africa. It may cause blindness in 40% of some populations. Unless the eye is aff ected, p roblems are mostly in the skin. Fly bites result in nodules from which micro \201 lariae a re released, to invade conjunctiva, cornea, ciliary body, and iris (rarely retina or optic nerve, \201 g 4). Sometimes they may be seen swimming in the aqueous or dying in the ante rior chamber. Micro \201 lariae initially excite in \202 ammation; \201 brosis then occ urs around them; if in the cornea, corneal opacities (nummular keratitis) occurs. Chronic i ritis causes synechiae cataracts and a \201 xed pupil. Tests: Skin snip tests, triple- antigen serology; PCR. \201\227: Get expert help. Ivermectin2 is the chief micro \201 lar icide, 150 g/kg PO stat every 6 \200\22312 months, until adult worms die (OHCM p443). In lightly infected expatriates, the \201 rst 3 doses are advised to be monthly, with observ ation in hospital after dose 1 (reactions are common in expatriates). Macro \201 laricides : doxycycline 200mg/day for 4wks (or for 2wks if with rifampicin) is under trial. 139,140 M acro \201 lariae are adults living in lymphatics. Steroids: OHCM p443. 450 y g o o m a h t h p O l l 1 For children: retinol palmitate 50,000U IM monthly until eyes are normal (adult dose 100, 000U, weekly to start with); or oral retinyl palmitate 200,000U PO. \200 -carotene (a pro- vitamin) 1.2 \211\210 106 U PO, is as eff ective, and cheaper. Avoid \200\200vitamin A in pregnancy (vitamin A embryopathy). 2 A problem with ivermectin is that it \200\231s a mono therapy micro \201 laricide that has limited eff ect on adult worms, and so needs continui ng for the life span of the adult worm (up to 15yrs).143 451 Fig 1. Bit t \200\231s spots. Reproduced from the British Journal of Ophthalmology, with p ermission from BMJ Publishing Ltd. y g o o m l a h t h p O l Fig 3. Trachoma: (a) dots outline the area to be examined; (b) follicular trachomatous in \202 ammation (>5 follicles in upper tarsal conjunctiva); (c) intense trachomatous (in \202 ammatory thickening in \202 ammation partially obscures numerous follicles; (d) trach omatous scars (white bands or sheets in the tarsal conjunctiva); (e) trachomatous trichiasi s and corneal opacity (lashes rub the cornea, which eventually clouds). Fig 3. Reproduced from the Oxford Textbook of Medicine, with permission from OUP. Fig 4. Left: sclerosing keratitis in a man blinded by onchocerciasis in Nigeria Prof. An - thony Bryceson. Right: Hissette \200\223Ridley fundus & optic atrophy; some central keyho le vision remains. Reproduced from the Oxford Textbook of Medicine, with permission from OU P. Eye trauma 144 \200\207Prevention is the key, eg wearing goggles, or plastic glasses when near small moving objects or using tools (avoids splinters, \201 sh-hooks, and squash-bal l in- juries). Always record acuity (both eyes; if the uninjured one is blind take all inju ries very seriously). Take a detailed history of the event. 452 \200 If unable to open the injured eye, instill a few drops of local anesthetic (tetracaine 1%): after a few mins, comfortable opening may be possible. Examine lids, conjunctiva, cornea, sclera, anterior chamber, pupil, iris, lens, vitreous, fundus, and eye movement. An irregul ar pupil may mean globe rupture. Aff erent pupil defects (p424) do not augur well for sight recovery. Note pain, discharge, or squint. CT may be very useful (foreign bodies may be ma gnetic, so avoid MRI). Penetrating trauma Refer urgently: delays risk of ocular extrusion o r infec- tion. Uveal injury risks of sympathetic ophthalmia in the other eye. \200\207A hi sto- ry of \202 ying objects (eg work with lathes, hammers, and chisels) prompts careful examination + X-ray to exclude intraocular foreign bodies ( skull X- ray or CT to exclude intracranial involvement). \200\207Don \200\231t try to remove a large foreign body (knif e; dart). Support the object with padding. Transportation su- pine. Pad the unaffected eye to prevent damage from conjugate movement. Foreign bodies (FB) ( \201 g 1) Have a low thre sh- old for getting help; FBs often hide, so examine all the eye; for lid eversion see tiny url.com/5jbt7v. FBs cause chemosis, subconjunctival bleeds, ir- regular pupils, iris prolap se, hyphaema, vitre- ous hemorrhage, and retinal tears. If you suspect a metal FB, X-ray th e orbit. With high- velocity FBs, consider orbital ultrasound: pick- up rate is 90% vs 40% for x-rays; skill is needed (not always to hand in busy A&E de- Courtesy of Bristol Eye Hos pital. partments). Removal of super \201 cial foreign bodies may be possible with a tri- a ngle of clean card (chloramphenicol 0.5% drops after, to prevent infection.) Corneal abrasi ons ( \201 g 2; often from small fast-moving objects, eg children \200\231s \201 nger-na ils; twigs.) They may cause intense pain. Apply a drop of local anesthetic, eg 1% tetracain e be- fore examination. They stain with \202 uorescein and should show sign of healing wi thin 48h. Apply chloramphenicol eye ointment and di- late the pupil. Send the patient home with an- algesics. Re-examine after 24h. If still having a foreign body sensation after rem oving the pad, stain again with \202 uorescein. If the cornea stains, repeat the procedur e for another 24h. If it still stains after 48h, refer. NB: meta-analyzes of small corneal abrasions do not favor using pads. 145 \200\223147 Burns Treat chemical burns promptly: ins till anesthetic drops (tetracaine) eve- ry 2min till the patient is comfortable. Then hold lids open and bathe the eyes in copious clean water while the speci \201 c antidote is sou ght. Often the lids close tight from severe pain. Late serious sequelae: eg corneal scarrin g, opaci \201 cation, and lid damage. Alkali burns are more serious than acid. Refer promp tly. Arc eye Welders and sunbed users who don \200\231t use UV protection may damage the co rnea (FB sensation, watering, blepharo spasm). \201\227: Local anesthetic drops every 2min . After dose 2, excruciating pain can vanish. Apply an antibiotic oint- ment and it will re cover in 24h. It is very painful; be generous with analgesia. Finally, remember fat embolus in trauma patients with visual problems. y g o o m a h t h p O l l Fig 1. Corneal FB (center). Fig 2. Corneal abrasion just above the pupil. Bristol Eye Hospital. 453 Contusions and intraocular hemorrhage Our eyes are protected by our bony orbital ridges. Se vere contusions from large objects may damage the eye, but smaller objects such as champagn e corks, squash balls, and airgun pellets (p720) cause local contusion, eg result- ing in l id bruises and subconjunctival hemorrhage (if the posterior limit of such a hemorrhage cann ot be seen, consider fracture of the orbit). Both usually settle in 2 weeks. \200\207Get e xpert help with all injuries penetrating the eyeball. Intraocular bleeds: \200\207Get expe rt help: acuity may be aff ected. Blood is often found in the anterior chamber (hyphaema, \201 g 1, p413): small amounts clear spontaneously but if \201 lling the anterior chambe r, evacuation may be needed. It is often recognizable by pen-torch examination. Even small hyphaemas must be carefully evaluated (so refer): it may signify serious injury. Late compl ica- tions: Glaucoma; corneal staining. Pain suggests glaucoma or re-bleeding. Secondary he morrhage: This may occur within 5 days and may produce sight-threatening secondary glaucoma . Sometimes the iris is paralyzed and dilated due to injury (called traumatic mydriasis). T his usually recovers in a few days but sometimes it is permanent. Vitreous hemorrhage will cause dramatic fall in acuity. There will be no red re \202 ex on ophthalmoscopy. Lens dis location, tearing of the iris root, splitting of the choroid, detachment of the retina, and damage to the optic nerve may be other sequelae; they are more common if contusion is caus ed by smaller objects rather than large. Blows to the orbit: Blunt injury (eg from a footba ll) can cause sudden \200\200 in pressure within the orbit, and may cause blowout fracture s with the orbital contents herniating into the maxillary sinus. Tethering of the inferior rectus and inferior oblique muscles causes diplopia. Test the sensation over the lower lid skin. Loss of sensation indicates infra-orbital nerve injury, con \201 rming a blowout fra cture. CT may show the depressed fracture of the posterior orbital \202 oor. Fracture red uction and muscle release is necessary. 148 Types of major injury, and prognosis The ocular trauma score (OTS) gives prognostic information: to get the score, assign a point value fo r initial visual acuity from row 1 of the table. Then subtract the appropriate points for e ach diagnosis from subsequent rows. A patient with an initial visual acuity of <6/60, scler al rupture, and retinal detachment has a score of 80 \200\22323 \200\22311= 46. Higher OTS scores indicate a better prognosis. For exact details of how, see asotonline.org/ots.html; but note that some 2008 data suggest that OTS may be over-pessimistic. 149 y g o o m l a h t h p O l Visual acuity (p412) No light perception Light perception/hand movement only <6/60 6/50 \200\2236/15 >6/12 60 70 80 90 100 \200\22323 \200\22317 \200\22314 \200\22311 \200\22310 Globe rupture Endophthalmitis Perforating injury Retinal detachment Aff erent pupillary def ect (Marcus Gunn pupil) In one series, the chief injuries were corneal wounds (68%), lens injury (50%), retinal les ions (50%), vitreous hemorrhage (25%), and endophthal- mitis (14%). Multiple foreign bodies causing perforating injury with retained posterior segment foreign body occurred in 7%. Ou tcome was worse if acu- ity was aff ected, presence of a large foreign body, or there was b acterial endophthalmitis or proliferative vitreo-retinopathy. 149 Blindness and partial sight The pattern of blindness around the world diff ers considerably , depending on local nutrition and economic factors. 90% of the world \200\231s blind live in developing countries \200\224and 80% would not be blind if trained eye personnel, medici nes, oph- thalmic equipment, and patient referral systems were optimized. The diseases resp onsible for most of the blindness in the world are trachoma, cataract (50% of the world \200\231s blindness), glaucoma, keratomalacia, onchocerciasis, and diabetic retinopathy (se e BOX). In the past smallpox, gonorrhea, syphilis, and leprosy (10% of those aff ected were blind) were also common causes of blindness. 454 DVLA: see p527 \200 Rates of blindness are higher than 10/1000 in some parts of Africa and Asia, but in the UK and the USA rates are 2/1000. Blindness may be voluntarily registered in England, registrat ion making one eligible for certain concessions. Although the word blind suggests inability to perceive light, a person is eligible for registration if their acuity is less than 3/60 , or if >3/60 but with substantial visual \201 eld loss (as in glaucoma). There are 350, 000 people registered blind in the UK. Criteria for partial sighted registration: acuity is <6/60 (or >6/60 with visual \201 eld restrictions). Causes of blindness These have chang ed considerably in the UK over the last 70 years. Whereas in the 1920s ophthalmia neonatoru m (p36) was responsible for 30% of blindness in English blind schools, this is now a rare b ut treatable disease. Retrolental \201 broplasia was common in the 1950s, mostly aff ecti ng pre- mature infants: monitoring of intra-arterial oxygen in premature babies tries to pr event this. With an ever-aging population, the diseases particularly affl icting this popul ation are the common causes of blindness. Nearly two-thirds of the blind population are ove r 65 years of age, and nearly half over 75. Macular de- generation, cataract, and glaucoma are the three commonest causes of blind- ness. Registration In England, responsibility for blind registration lies with the local authority. Application is made by a consultant ophth almologist and is voluntary, not statutory. Registration as blind entitles one to extra tax allow- ances, reduced TV license fees, some travel concessions, and access to talking book s. Special certi \201 cation from an ophthalmologist is necessary for the par- tially sigh ted to receive talking books. At one time it was statutory that the registered blind should receive a visit from a social worker but this is no longer the case, although the social s ervices employ social workers who specialize in care of the blind. The Royal National Insti tute for the Blind1 will advise on aids, such as guide dogs (available if required for empl oyment). It sells talking mobile phones and other helpful gadgets on its website. 150 Speci al educational facilities These provide for visually handicapped chil- dren. Special school s have a higher staff /pupil ratio, specialized equipment, and many have a visiting ophthal mologist. The disadvantage is that the chil- dren may not mix much with other children \200 \224especially if they board. y g o o m a h t h p O l l 1 Royal National Institute for the Blind, 224 Great Portland St, London W1N 6AA (UK 0845 76 6 9999). 455 Common causes of blindness in the world 1 Trachoma 2 Cataract 3 Glaucoma 4 Keratomalacia 5 Onchocerciasis 6 Diabetic retinopathy The most common cause of irreversible blindness and p artial sight in devel- oped countries is age-related macular degeneration. In patients of w orking age, diabetic retinopathy is the leading cause in the West. In a recent survey in Ta ipei City, the leading causes of registrable blindness and low vision were glaucoma, optic neuropathy, diabetic retinopathy, retinitis pigmentosa, and age-related macular degeneratio n. 151 y g o o m l a h t h p O l Color vision and color blindness For normal color vision we require cone photopigments sens itive to blue, green, and red light. The commonest hereditary color vision defect is X- lin ked failure of red \200\223green discrimination (8% \200 and 0.5% \200 aff ected \200 \224so those with Turner \200\231s syndrome have \200 incidence and those with Klinefelte r \200\231s have \200 incidence). Blue \200\223yellow discriminatory failure is more comm only ac- quired and sexes are aff ected equally. Diagnosis: This is by use of colored patte rn discrimination charts (eg Ishi- hara plates, see endpapers). Depressed color vision may be a sensitive indi- cator of acquired macular or optic nerve disease. Monochromatism This may be due to being born without cones (resulting in low visual acuity, absent color vision , photophobia, and nystagmus), or, very rarely, due to cone monochromacy where all cones co ntain the same visual pigment, when there is only failure to distinguish color. Drugs and the eye The eye does not retain drops for as long as ointments and 2-hourly appli ca- tions may be needed. Eye ointments are well-suited for use at night and when crusting a nd sticking of the lids occurs. Allow 5min between doses of drops to prevent overspill. The antibiotic drops most used are not those generally used systemically, eg fusidic acid, chl oramphenicol, neomycin, and framycetin. All eye preparations have warnings not to use for m ore than one month. Mydriatics (=cycloplegics) These dilate the pupil. They also cause cycl ople- gia and hence blur vision (warn not to drive). Pupil dilatation prior to exami- natio n is best achieved using 0.5% or 1% tropicamide which lasts for 3h. 1% cyclopentolate has a n action of 24h and is preferred for producing cyclople- gia (paralysis of the ciliary musc le) for refraction of children. These drugs may be used to prevent synechiae formation in a nterior uveitis. \200\207Over-60s with shallow anterior chambers (especially if a family h istory of glaucoma) may have acute glaucoma triggered, so only use on ophthalmological advi ce. Miotics These constrict the pupil and increase drainage of aqueous. They are used in th e treatment of acute glaucoma (p430). Local anesthetic Tetracaine (0.5% drops) is an exampl e, used to permit examination of a painful eye where re \202 ex blepharospasm is a problem , and to facilitate removal of a foreign body. \200\207It abolishes the corneal re \202 e x so use to treat pain is to risk corneal damage. To relieve pain, give an eye pad, and be generous with oral analgesia. In children use proxymetacaine (it stings less). Steroid and NSAID drops \200\207Steroids are very useful in managing ophthalmic in \202 ammation. The y are dangerous as they may induce catastrophic progres- sion of dendritic ulcers (p416). O phthalmoscopy may miss dendritic ulcers, and slit lamp inspection is essential if steroid d rops are being considered, eg for allergy, episcleritis, scleritis, or iritis. Steroid drop s \200\200intraocular pressure (newer drops less so: eg rimexolone has a low IOP-elevating potential, compa- rable to \202 uorometholone and < dexamethasone & prednisolone acetate ). 152 NSAID drops, eg ketorolac, may obviate the need for some steroid drops. 153 Iatrogen ic eye disease Allergic reactions may damage conjunctiva & cor nea, eg toxic epidermal necr olysis ( \201 g 2, p601) in aspirin allergy (Lyell \200\231s syndrome). Another type of to xic reaction is nystagmus indicating phenytoin toxicity. Dry eyes: Propranolol and oxprenol ol are typical culprits. Corneal deposits: Amiodarone, chloroquine, chlorpromazine, and gol d. Lens opacities: Steroids (including high-dose inhaled) are the typical culprits. Glaucom a: Typical culprit: steroid drops (above), mydriatics and anticholin- ergics (some antipark inson drugs and tricyclics). Papilloedema: Tetracyclines; nalidixic acid; steroids; the Pil l. Retinopathy: The drugs below are culprits if used chronically. \200 Vigabatrin. \200 Ethambutol: Warn patients to report any visual side-eff ects (loss of acuity, color blindn ess). 10% report new visual problems, and in 10% of these the cause is optic neuropathy (w hich may be irreversible).1 \200 Isoniazid: \200\201Red-green perception; pyridoxine co- administration prevents this. \200 Chloroquine (CQ)/hydroxychloroquine (HCQ) can cause (u ntreatable) retin- opathy if high doses are used. Risk of toxicity increases sharply toward s 1% after 6yrs of use, or a cumulative dose of 1000g of HCQ. Risk increases with continued use. Most patients are routinely given 400mg of HCQ daily (or 250mg CQ). This is OK unless short stature (then dose by ideal body weight). Screening schedule: Baseline exam on start ing (maculopathy would be a contraindication). Start annual screening 5yrs (or sooner if th ere are unusu- al risk factors). Newer objective tests, such as multifocal electroretinogra m, spectral domain optical coherence tomography, and fundus auto \202 uores- cence, can be more sensitive than visual \201 elds (which remain useful).154 456 y g o o m a h t h p O l l 457 Obtaining and preparing antibiotic eyedrops Forti \201 ed guttate gentamicin is 15mg/mL (t he normal commercial gentamicin is 3mg/mL); penicillin 5000U/mL, meticillin 20mg/mL, and an tifungals can be obtained from the Chief Pharmacist, Moor \201 elds Eye Hospital (tel. 020 725 33411). Antibiotics can be home-made as follows: Gentamicin forte: Add 2mL of 40mg/mL IV gentamicin to a 5mL bottle of commercial guttate gentamicin (3mg/mL).2 Other antibiotics can be made up using IV preparations to the required concentration using water or normal saline. These are stable for the time recommended for IV solutions in the m anufacturers Data sheets. Penicillin G can be used up to 500,000U/mL. y g o o m l a h t h p O l Eyedrops as a cause of systemic symptoms Drugs applied to the eye may be absorbed through t he cornea and pro- duce systemic side-eff ects \200\224eg bronchospasm or bradycardia in su scepti- ble individuals using antiglaucoma \200 -blocking drops, eg timolol, carteolol, be taxolol \200\224which is cardioselective. \200\207Symptoms may be subtle and insidi- ous \200\224eg gradually decreasing exercise tolerance, or falls from arrhythmias. Serious prob lems are more likely if there is co-morbidity (eg respiratory infection). Other anti-glaucoma drops (p440) cause headaches, and a bitter taste in the mouth; urolithiasis is reported with dorzolamide. Pilocarpine may cause parasympathetic swe ating. Accommodation spasm may lead to brow-ache (worse if <40 years old, or just starting treatment). Other SE: \200\231 \202 u-like syndrome, sweating, urinary frequency; more ra rely: urinary urgency, D&V (or constipation \202 atulence), dyspepsia, \202 ushes, BP \200\200, palpita- tions, rhinitis, dizziness, lacrimation, conjunctivitis, visual disturb ances, ocular pain, rash, pruritus. Even highly selective \200 2-receptor agonists used in glaucoma, eg brimonidine, can cause eff ects such as dry mouth (in 33% of patients), headache, hyperten- sion, fatigue, and dr owsiness. 155 1 Ethambutol eye problems: \200\201acuity (65%), \200\201 visual \201 elds (65%), abnor mal color vision (61%), optic disc pallor (38%), \200\200latency on visual evoked potentia l (65%). 30% showed improved vision on stopping etham- butol in one Korean study; latency for recovery: 5.4 1.7 months. No one with optic disc pallor at the time of diagnosis of optic neuropathy showed visual function improvement.@19145123 2 Mr J Dart FRCS, Moor \201 elds Eye Hospital; see also ncbi.nlm.nih.gov/pmc/articles/PMC2417514/?page=1