Ophthalmology: Anatomy Physiology and Pharmacology

👁️ Ophthalmology anatomy, physiology and pharmacology — the foundation page for the Ophthalmology chapter. The eye is small, but its anatomy explains almost every eye presentation — why a blowout fracture causes double vision, why some drops can trigger acute glaucoma, why a third nerve palsy with a big pupil is an emergency. Many systemic drugs harm the eye, and some eye drops cause systemic effects. This page covers the structures, how vision works, and the drugs used in and around the eye.
Your four questions for every eye problem: Which part of the eye or visual pathway is affected? Is vision, the pupil or eye movement affected — and is it sight-threatening? Could a drug (local or systemic) be the cause? Is this a treatment I can start, or does it need an ophthalmologist?

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The Orbit

• Bony orbit — seven bones forming a cone pointing backwards.
  • Floor (maxilla) — thin — blowout fracture after a blow from a ball or fist: infraorbital nerve numbness (cheek and upper lip), restricted upgaze with vertical diplopia (inferior rectus entrapment — urgent in children: "white-eyed blowout" with vomiting and bradycardia), enophthalmos.
  • Medial wall — paper-thin lamina papyracea (ethmoid) — ethmoid sinusitis spreads into the orbit (orbital cellulitis in children); surgical emphysema after nose-blowing with a fracture.
  • Roof — anterior cranial fossa above.
• Openings:
  • Optic canal — optic nerve (II) and ophthalmic artery.
  • Superior orbital fissure — III, IV, VI, V1 (ophthalmic division) and the superior ophthalmic vein — lesions here (or in the cavernous sinus) cause multiple cranial nerve palsies with forehead numbness.
  • Inferior orbital fissure — infraorbital nerve and vessels.
• Orbital septum — fibrous sheet from the orbital rim to the eyelids — separates preseptal (periorbital) cellulitis (lids only — oral antibiotics) from orbital cellulitis (behind the septum — proptosis, painful or restricted eye movements, reduced vision, RAPD — emergency: IV antibiotics, CT, ENT and ophthalmology).
• Proptosis — thyroid eye disease (commonest — bilateral or unilateral; enlarged extraocular muscles), orbital cellulitis, tumours (lymphoma, metastases), carotid–cavernous fistula (pulsatile, bruit, red eye).
• Venous drainage — ophthalmic veins drain to the cavernous sinus (no valves) — facial infections can spread (cavernous sinus thrombosis).

Eyelids

• Functions — protect the eye, spread the tear film with blinking, drain tears towards the puncta.
• Muscles:
  • Levator palpebrae superioris — oculomotor nerve (III) — main lid elevator — complete ptosis in third nerve palsy.
  • Müller's muscle (superior tarsal) — sympathetic — 1–2 mm of elevation — partial ptosis in Horner's syndrome.
  • Orbicularis oculi — facial nerve (VII) — closes the eye — can't close the eye in Bell's palsy (exposure keratopathy).
• Causes of ptosis — ageing (levator aponeurosis disinsertion — commonest), III palsy, Horner's, myasthenia gravis (fatigable, variable), myotonic dystrophy, mitochondrial myopathy (CPEO), congenital (amblyopia risk in children).
• Lid glands:
  • Meibomian glands (in the tarsal plate) — oil layer of tears — blockage causes a chalazion (painless lump); blepharitis (meibomian gland dysfunction) — warm compresses, lid hygiene.
  • Glands of Zeis and Moll (lash follicles) — infection causes a stye (external hordeolum).
• Lid position — entropion (inturning — lashes rub the cornea) and ectropion (outturning — watering, exposure) — common in older people; surgery.
• Lid lumps — basal cell carcinoma is the commonest malignant lid tumour (lower lid, medial canthus — pearly, ulcerated, lash loss); sebaceous gland carcinoma mimics chalazion (recurrent "chalazion" — biopsy).
• Lid lacerations involving the margin or the medial canthus (canaliculus) — ophthalmic repair.

Tears and the Lacrimal System

• Tear film (three layers):
  • Lipid (outer) — meibomian glands — slows evaporation.
  • Aqueous (middle) — lacrimal gland — nutrients, antimicrobials (lysozyme, IgA), washing.
  • Mucin (inner) — conjunctival goblet cells — helps tears spread and stick.
• Lacrimal gland — in the superolateral orbit; parasympathetic supply from the facial nerve (greater petrosal nerve → pterygopalatine ganglion) — a proximal facial nerve lesion reduces tear production.
• Drainage — puncta (medial lids) → canaliculi → lacrimal sac → nasolacrimal duct → inferior meatus of the nose.
  • Congenital nasolacrimal duct obstruction — sticky, watery eye in infants — most resolve by 12 months (massage; probing if persistent).
  • Acquired obstruction — watering eye in older adults; dacryocystitis (painful swelling at the medial canthus — antibiotics, later DCR surgery).
• Dry eye disease — evaporative (meibomian gland dysfunction — commonest) or aqueous-deficient (Sjögren's, ageing, drugs — anticholinergics, antihistamines, isotretinoin, beta-blockers); symptoms worse with screens, wind and air conditioning; reflex watering is common in dry eye.
• Schirmer's test — filter paper measures tear production.
• Corneal exposure — Bell's palsy, thyroid eye disease, sedated ICU patients (lid taping, lubricants).

Cornea, Conjunctiva and Sclera

• Cornea — the clear front window:
  • Provides about two-thirds of the eye's focusing power (about 43 dioptres) — refractive surgery reshapes it.
  • Avascular — oxygen from tears and air (contact lens overwear causes hypoxia and neovascularisation); transparency depends on regular collagen and a dehydrated stroma.
  • Layers — epithelium (regenerates within days — abrasions heal quickly), Bowman's layer, stroma (90% — scars here are permanent), Descemet's membrane, endothelium (pumps water out — doesn't regenerate; loss causes corneal oedema — Fuchs' dystrophy, surgical trauma).
  • Most densely innervated tissue in the body (V1) — abrasions and ulcers are very painful; corneal reflex — afferent V1, efferent VII (lost early in cerebellopontine angle tumours).
  • Keratitis risks — contact lenses (Pseudomonas, Acanthamoeba — tap water and swimming), HSV (dendritic ulcer), herpes zoster ophthalmicus, trauma, dry eye, exposure — urgent ophthalmology.
• Conjunctiva — thin vascular membrane covering the sclera (bulbar) and lining the lids (palpebral); conjunctivitis — infective (bacterial — purulent; viral — watery, follicles, preauricular node, very contagious) or allergic (itch, papillae); subconjunctival haemorrhage (painless, harmless — check BP and INR if recurrent).
• Limbus — the corneoscleral junction — ciliary (circumcorneal) injection (redness concentrated at the limbus) suggests serious disease — keratitis, anterior uveitis, acute angle-closure glaucoma — rather than conjunctivitis.
• Sclera — tough white coat; episcleritis (mild discomfort, sectoral redness — benign, self-limiting) vs scleritis (severe, boring pain, tender, deep violet redness — associated with rheumatoid arthritis and vasculitis (GPA) — urgent ophthalmology; risk of perforation).

Uvea and Aqueous Humour

• Uveal tract — pigmented, vascular middle layer:
  • Iris — controls pupil size — sphincter pupillae (parasympathetic — III — constricts) and dilator pupillae (sympathetic — dilates).
  • Ciliary body — ciliary muscle (parasympathetic — accommodation) and ciliary epithelium (makes aqueous humour).
  • Choroid — highly vascular — supplies the outer retina (photoreceptors).
• Uveitis:
  • Anterior (iritis) — painful red eye, photophobia, small pupil, ciliary injection, cells and flare in the anterior chamber (hypopyon if severe) — associated with HLA-B27 (ankylosing spondylitis, reactive arthritis, IBD, psoriasis), sarcoidosis, JIA (asymptomatic — children need screening), Behçet's, herpes — topical steroids and cycloplegics (ophthalmology).
  • Intermediate and posterior — floaters, blurred vision — sarcoidosis, MS, toxoplasmosis, TB, syphilis, CMV (immunosuppressed).
• Aqueous humour:
  • Production — ciliary epithelium (active secretion — Na⁺/K⁺-ATPase, carbonic anhydrase, beta-adrenergic and alpha-2 receptors — the targets of glaucoma drugs).
  • Flow — posterior chamber → through the pupil → anterior chamber → drainage angle.
  • Outflow — trabecular meshwork → Schlemm's canal (conventional — most) and uveoscleral outflow (through the ciliary muscle — increased by prostaglandin analogues).
  • Functions — nourishes the lens and cornea, maintains eye shape and pressure.
• Ocular melanoma — the commonest primary intraocular malignancy in adults (choroid) — often found on routine eye examination.

Intraocular Pressure and the Drainage Angle

• Normal intraocular pressure (IOP) — about 10–21 mmHg; depends on the balance of aqueous production and outflow; measured by tonometry (Goldmann applanation); corneal thickness affects readings.
• Glaucoma — progressive optic neuropathy with characteristic optic disc cupping and visual field loss; raised IOP is the main modifiable risk factor (but "normal-tension glaucoma" exists).
• Primary open-angle glaucoma — the angle is open but outflow through the trabecular meshwork is reduced — painless, slowly progressive peripheral field loss (central vision lost late) — risk factors: age, family history (first-degree relatives — free NHS eye tests from 40), Black African or Caribbean ancestry, myopia, diabetes, steroids. Detected by optometrists (IOP, discs, fields).
• Primary angle-closure glaucoma — the peripheral iris blocks the angle:
  • Risk factors — hypermetropia (small eye, shallow anterior chamber), older age, women, East Asian ancestry, growing cataract.
  • Triggers — pupil dilation — dim light, anticholinergics, antihistamines, tricyclics, sympathomimetics, dilating eye drops, topiramate (different mechanism — ciliary body swelling).
  • Acute attack — severe eye pain, headache, nausea and vomiting, haloes around lights, red eye, fixed mid-dilated pupil, hazy cornea, rock-hard eye — emergency (see Ophthalmology emergencies).
  • Definitive treatment — laser peripheral iridotomy (both eyes) or lens extraction.
• Secondary glaucoma — steroids, uveitis, trauma, neovascular (diabetes, CRVO), pigment dispersion.
• Congenital glaucoma — large cloudy eyes (buphthalmos), watering, photophobia in infants.

Lens, Focusing and Refraction

• Lens — clear, avascular, biconvex, held by zonules from the ciliary body; provides about one-third of focusing power and all of the adjustable focus.
• Accommodation (focusing on near objects) — ciliary muscle contracts (parasympathetic — III) → zonules relax → lens becomes rounder (more powerful); with pupil constriction and convergence (the near triad).
• Presbyopia — age-related stiffening of the lens — reading difficulty from the 40s — reading glasses.
• Refractive errors:
  • Myopia (short-sighted) — eye too long — images focus in front of the retina — concave (minus) lenses; increased risk of retinal detachment, open-angle glaucoma and myopic maculopathy; rising in children (near work, less time outdoors).
  • Hypermetropia (long-sighted) — eye too short — convex (plus) lenses; risk of angle closure; in children — squint and amblyopia.
  • Astigmatism — unequal corneal curvature — cylindrical lenses.
  • A pinhole improves vision reduced by refractive error (not by disease) — quick bedside test.
• Cataract — opacity of the lens — gradual painless blurring, glare, faded colours — ageing (commonest), diabetes, steroids (posterior subcapsular), trauma, UV light, smoking, uveitis, radiation, congenital (rubella, galactosaemia — absent red reflex in a baby is urgent).
  • Treatment — phacoemulsification with intraocular lens implant (day case, local anaesthetic) when vision affects daily life (NICE NG77).
  • Complications — posterior capsule opacification (laser capsulotomy), endophthalmitis (rare — painful red eye with reduced vision days after surgery — emergency), retinal detachment, cystoid macular oedema.
• Lens dislocation — trauma, Marfan syndrome (upwards), homocystinuria (downwards).

Vitreous, Retina and Macula

• Vitreous — clear gel filling the back of the eye; liquefies with age:
  • Posterior vitreous detachment — new floaters and flashes (traction on the retina) — common after 50 and in myopes — needs same-day or next-day examination to exclude a retinal tear.
  • Vitreous haemorrhage — sudden floaters or loss of vision — proliferative diabetic retinopathy, retinal tear, trauma.
• Retina — neural tissue lining the back of the eye:
  • Photoreceptors (rods and cones) → bipolar cells → ganglion cells (axons form the optic nerve); retinal pigment epithelium supports photoreceptors (recycles visual pigment).
  • Optic disc — where ganglion cell axons leave — no photoreceptors (blind spot); swelling (papilloedema — raised ICP; disc swelling — optic neuritis, AION) or cupping (glaucoma).
  • Macula — central retina responsible for detailed and colour vision; the fovea at its centre is packed with cones and has no blood vessels.
• Retinal detachment — flashes, floaters, then a "curtain" or shadow spreading across the vision — emergency (same day) — especially before the macula detaches ("macula-on").
• Age-related macular degeneration — the commonest cause of blindness registration in the UK:
  • Dry (geographic atrophy) — slow central loss — no proven treatment in the UK (low vision aids; stop smoking; AREDS supplements may slow intermediate disease).
  • Wet (neovascular) — sudden central distortion (straight lines look wavy — Amsler grid), blurring — urgent referral (within 1 week — rapid access) for anti-VEGF injections.
• Diabetic retinopathy — microaneurysms, haemorrhages, exudates, cotton wool spots → proliferative (new vessels — bleeding, detachment) and maculopathy (the commonest sight-threatening form) — NHS Diabetic Eye Screening (annual or 2-yearly retinal photography for everyone with diabetes aged 12+).
• Hypertensive retinopathy — arteriolar narrowing, AV nipping, flame haemorrhages, cotton wool spots, papilloedema (malignant hypertension — emergency).

Blood Supply of the Eye

• Ophthalmic artery — the first branch of the internal carotid artery — enters through the optic canal; branches:
  • Central retinal artery — supplies the inner retina; an end artery — occlusion causes sudden painless profound loss of vision: pale retina with a cherry-red spot at the fovea (the fovea is supplied by the choroid) — a form of stroke — urgent stroke pathway (and exclude giant cell arteritis in older people).
  • Posterior ciliary arteries — supply the choroid (outer retina) and the optic nerve head — giant cell arteritis occludes them — arteritic anterior ischaemic optic neuropathy (pale swollen disc, sudden visual loss) — high-dose steroids immediately (the other eye is at risk).
  • Cilioretinal artery (present in some people) — from the choroidal circulation — may spare central vision in central retinal artery occlusion.
  • Lacrimal, ethmoidal and muscular branches; anterior ethmoidal artery — nosebleeds (see ENT page).
• Amaurosis fugax — transient monocular visual loss ("curtain coming down") from emboli (carotid stenosis, AF) — a TIA — urgent stroke assessment and carotid imaging.
• Venous drainage — central retinal vein and ophthalmic veins → cavernous sinus.
  • Retinal vein occlusion — "stormy sunset" / "blood and thunder" haemorrhages (CRVO) — risk factors: age, hypertension, diabetes, glaucoma, hyperviscosity — manage risk factors; anti-VEGF for macular oedema; neovascular glaucoma risk.
• Retinal circulation is the only place where small vessels can be seen directly — signs of hypertension, diabetes, emboli (cholesterol Hollenhorst plaques), raised ICP and vasculitis.

How We See — Photoreceptors and Visual Function

• Rods — about 120 million; peripheral retina; very sensitive — night and peripheral vision; contain rhodopsin (needs vitamin A — deficiency causes night blindness and xerophthalmia — a major cause of childhood blindness worldwide).
• Cones — about 6 million; concentrated at the fovea; colour (red, green and blue cone types) and fine detail; work in bright light.
• Phototransduction — light isomerises retinal (11-cis to all-trans) → activates transducin → closes sodium channels → photoreceptor hyperpolarises → signal to bipolar and ganglion cells.
• Dark adaptation — takes about 20–30 minutes (rhodopsin regeneration) — impaired in vitamin A deficiency and retinitis pigmentosa (inherited rod–cone dystrophy — night blindness, tunnel vision, bone-spicule pigmentation).
• Colour vision deficiency — X-linked red–green (about 8% of men, 0.5% of women); acquired colour loss — optic neuritis (red desaturation), ethambutol, macular disease.
• Visual acuity — mainly foveal function; Snellen (6/6 normal — fraction of distance the patient reads at versus a normal eye) or LogMAR charts.
• Binocular vision — the brain fuses images from both eyes (depth perception); misalignment (squint) in children causes amblyopia ("lazy eye") if not treated before about 7–8 years (patching, glasses, atropine penalisation).
• UK driving standard (DVLA, group 1) — read a number plate at 20 metres (about 6/12 binocular acuity, with glasses if needed) and an adequate binocular visual field (at least 120° horizontally) — field loss from glaucoma, stroke or retinal disease must be reported.

The Visual Pathway and Field Defects

Lesion site	Field defect	Typical causes
Optic nerve	Monocular loss, central scotoma, RAPD, reduced colour	Optic neuritis (MS), ischaemic optic neuropathy, compression, glaucoma (arcuate defects)
Optic chiasm (crossing nasal fibres)	Bitemporal hemianopia (superior first if from below)	Pituitary adenoma (from below), craniopharyngioma (from above — inferior first), meningioma
Optic tract	Incongruous contralateral homonymous hemianopia	Tumour, stroke (rare)
Temporal lobe (Meyer's loop)	Contralateral superior homonymous quadrantanopia ("pie in the sky")	Stroke, tumour, temporal lobe surgery
Parietal lobe	Contralateral inferior homonymous quadrantanopia ("pie on the floor")	Stroke, tumour
Occipital cortex	Contralateral congruous homonymous hemianopia, often with macular sparing	Posterior cerebral artery stroke (macula has dual MCA and PCA supply)

• Visual pathway — retina → optic nerve → chiasm (nasal retinal fibres — temporal fields — cross) → optic tract → lateral geniculate nucleus (thalamus) → optic radiations (temporal and parietal lobes) → primary visual cortex (occipital).
• Pupil fibres leave the optic tract before the lateral geniculate nucleus (to the pretectal nucleus) — so cortical blindness spares the pupil light reflexes.
• Bilateral occipital infarcts — cortical blindness, sometimes with denial (Anton's syndrome).
• See the Neuro-ophthalmology page for clinical detail.

Pupils and Their Nerves

• Pupillary light reflex:
  • Afferent — optic nerve (II) → pretectal nucleus (both sides).
  • Efferent — Edinger–Westphal nucleus → parasympathetic fibres in the oculomotor nerve (III) → ciliary ganglion → short ciliary nerves → sphincter pupillae — both pupils constrict (direct and consensual).
• Relative afferent pupillary defect (RAPD) — swinging torch test — the affected pupil dilates when the light swings to it — optic nerve disease or extensive retinal disease (not cataract or refractive error).
• Sympathetic pathway (three neurones) — hypothalamus → brainstem and spinal cord to T1 → (1st order) → sympathetic chain → superior cervical ganglion (2nd order — passes the lung apex) → along the internal carotid artery (3rd order) → dilator pupillae and Müller's muscle.
  • Horner's syndrome — miosis, partial ptosis, (anhidrosis — depends on level), apparent enophthalmos — causes: Pancoast tumour, carotid dissection (painful Horner's — emergency), lateral medullary stroke, cervical cord lesions, neck surgery, cluster headache.
• Abnormal pupils:
  • Third nerve palsy with a dilated pupil — compression (posterior communicating artery aneurysm, uncal herniation) — emergency CT angiography; the pupillary fibres run on the outside of the nerve.
  • Pupil-sparing third nerve palsy — usually microvascular (diabetes, hypertension).
  • Holmes–Adie (tonic) pupil — young women, large pupil that reacts slowly, absent ankle reflexes — benign.
  • Argyll Robertson pupils — small, irregular, accommodate but don't react to light — neurosyphilis (also diabetes).
  • Drugs — pinpoint pupils (opioids, organophosphates, pilocarpine); dilated (anticholinergics, sympathomimetics, cocaine, amphetamines, tricyclic overdose, mydriatic drops, nebulised ipratropium — accidental).
  • Physiological anisocoria — up to 1 mm difference, equal in light and dark.

Eye Movements — III, IV and VI

• Six extraocular muscles — "LR6 SO4, the rest 3":

  Muscle	Nerve	Main action (testing position)
  Lateral rectus	VI	Abduction
  Medial rectus	III	Adduction
  Superior rectus	III	Elevation (best in abduction)
  Inferior rectus	III	Depression (best in abduction)
  Inferior oblique	III	Elevation (best in adduction)
  Superior oblique	IV	Depression in adduction (looking down and in — reading, walking downstairs); intorsion

• Third (oculomotor) nerve palsy — eye "down and out", complete ptosis, ± dilated pupil.
• Fourth (trochlear) nerve palsy — vertical diplopia worse looking down and in (stairs), head tilt away from the affected side — trauma (long thin intracranial course), congenital, microvascular.
• Sixth (abducens) nerve palsy — horizontal diplopia worse looking towards the affected side, failure of abduction — microvascular, raised intracranial pressure (a "false localising sign" — long intracranial course), tumours, MS, Wernicke's.
• Conjugate gaze — the medial longitudinal fasciculus links VI and III nuclei — lesion causes internuclear ophthalmoplegia (failure of adduction with nystagmus of the abducting eye — MS in the young, stroke in the old).
• Restrictive causes of diplopia — thyroid eye disease (inferior and medial recti — restricted upgaze), blowout fracture; neuromuscular — myasthenia gravis (fatigable, variable, pupils normal).
• Monocular diplopia (persists with the other eye covered) — ocular cause (cataract, refractive) — not neurological.

Basic Eye Assessment

• Visual acuity — always first (and documented — medicolegal) — each eye separately, with glasses or pinhole; if unable to read the top letter — count fingers, hand movements, perception of light.
• Pupils — size, shape, reactions, RAPD.
• Visual fields — confrontation (red pin for central scotoma and chiasmal lesions); formal perimetry.
• Eye movements — H-pattern, diplopia, nystagmus.
• Anterior segment — lids, conjunctiva, cornea (fluorescein stains epithelial defects green under blue light — abrasions, ulcers, dendritic herpes ulcer), anterior chamber (hypopyon, hyphaema), pupil.
• Red reflex — absent or white in cataract, retinoblastoma (leukocoria), vitreous haemorrhage — newborn and 6–8 week checks.
• Fundoscopy — optic disc (colour, cup, swelling), vessels, macula, retina — dilated examination is best.
• Amsler grid — distortion or missing areas — macular disease.
• Colour vision — Ishihara plates — optic nerve disease, ethambutol monitoring.
• Intraocular pressure — tonometry (optometrist or ophthalmology); a stony-hard eye on gentle palpation in acute angle closure.
• Red flags — sudden loss of vision, painful red eye with reduced vision, photophobia, chemical injury (irrigate immediately — before anything else), penetrating trauma, new diplopia with headache, flashes and curtain.

Getting Drugs into the Eye

• Routes:
  • Topical drops and ointments — most eye treatment; the cornea is a barrier (lipophilic epithelium, hydrophilic stroma); a drop is about 50 microlitres but the eye holds only about 10 — one drop is enough; separate different drops by 5 minutes; ointments last longer but blur vision (use at night).
  • Periocular and intracameral injections — subconjunctival, sub-Tenon's steroid; intracameral antibiotic at cataract surgery (cefuroxime).
  • Intravitreal injections — anti-VEGF, steroids, antivirals — reach the retina.
  • Systemic — oral acetazolamide, steroids (GCA, uveitis, optic neuritis), antivirals (herpes zoster ophthalmicus), antibiotics (orbital cellulitis, endophthalmitis).
• Systemic absorption of eye drops — drops drain through the nasolacrimal duct to the nasal mucosa and are absorbed directly into the circulation (bypassing first-pass metabolism) — timolol drops can cause bronchospasm and bradycardia.
  • Reduce it — punctal occlusion (press on the inner corner of the eye for 1–2 minutes) or simply closing the eyes after instillation.
• Preservatives (benzalkonium chloride) — damage the ocular surface with long-term or frequent use — preservative-free drops for frequent dosing, dry eye and long-term glaucoma therapy if intolerant.
• Contact lenses — remove before drops (preservatives absorb into soft lenses); don't wear during eye infections.
• Adherence — technique is often poor (especially older people with arthritis or tremor) — drop aids, teaching, simplified regimens, combination drops.
• Expiry — most multidose bottles are discarded 28 days after opening.

Glaucoma Drugs

Class	Mechanism	Side effects and cautions
Prostaglandin analogues (latanoprost, bimatoprost, travoprost) — once daily at night; first-line drops	Increase uveoscleral outflow	Darkening of the iris (permanent, brown), eyelash growth, periocular skin darkening, periorbital fat loss, red eye; caution in uveitis and after complicated cataract surgery (macular oedema)
Beta-blockers (timolol, betaxolol)	Reduce aqueous production	Systemic — bronchospasm (avoid in asthma, caution COPD), bradycardia, heart block, hypotension, fatigue; masking hypoglycaemia
Carbonic anhydrase inhibitors — topical (dorzolamide, brinzolamide); oral or IV acetazolamide	Reduce aqueous production	Topical — stinging, bitter taste; acetazolamide — paraesthesia, fatigue, hypokalaemia, metabolic acidosis, kidney stones, avoid in sulfonamide allergy and severe renal or hepatic impairment
Alpha-2 agonists (brimonidine, apraclonidine)	Reduce production, increase outflow	Allergic follicular conjunctivitis (common), dry mouth, fatigue; contraindicated in infants (CNS and respiratory depression); caution with MAOIs
Miotics (pilocarpine)	Parasympathomimetic — constricts the pupil and pulls the iris from the angle; increases trabecular outflow	Brow ache, dim and blurred vision (especially at night), myopic shift; mainly used in angle closure
Rho kinase inhibitor (netarsudil)	Increases trabecular outflow	Red eye, corneal deposits

• NICE NG81 — for ocular hypertension and open-angle glaucoma, selective laser trabeculoplasty (SLT) is offered as a first-line option (with IOP of 24 mmHg or more); otherwise a generic prostaglandin analogue; add or switch classes if the target isn't reached; surgery (trabeculectomy, minimally invasive glaucoma surgery) for progression.
• Acute angle-closure glaucoma — emergency drugs (pending laser iridotomy):
  • IV acetazolamide (500 mg) then oral.
  • Topical beta-blocker (timolol), alpha-agonist (apraclonidine), steroid; pilocarpine once IOP starts to fall (the ischaemic iris doesn't respond at very high pressure).
  • Analgesia and antiemetics; lie the patient supine; IV mannitol or oral glycerol if refractory (specialist).
• Combination drops (e.g. timolol with dorzolamide, brimonidine or a prostaglandin) — fewer drops, better adherence, less preservative exposure.

Dilating Drops, Anaesthetics and Stains

• Mydriatics and cycloplegics:

  Drug	Action and duration	Uses and cautions
  Tropicamide	Antimuscarinic — dilates; weak cycloplegia; 4–6 hours	Routine fundus examination (diabetic screening)
  Cyclopentolate	Antimuscarinic — dilates and paralyses accommodation; up to 24 hours	Refraction in children; pain relief in uveitis
  Atropine	Antimuscarinic — up to 7–14 days	Uveitis (prevents posterior synechiae), amblyopia penalisation, myopia control (low dose); systemic toxicity in children
  Phenylephrine	Sympathomimetic — dilates without cycloplegia	Added for wider dilation; caution in heart disease, hypertension and infants (systemic effects)

• Practical points — dilation blurs vision and causes glare for several hours — no driving until it wears off; very low risk of triggering angle closure in narrow-angle eyes (benefits of examination outweigh this — warn patients to seek help for pain, redness and haloes).
• Topical anaesthetics — proxymetacaine, tetracaine (amethocaine), oxybuprocaine — for examination, tonometry, removing foreign bodies and irrigation in chemical injury; never give for home use — repeated use delays healing and causes corneal ulceration and melting.
• Fluorescein — stains areas of missing corneal epithelium green under cobalt blue light — abrasions, ulcers, dendritic ulcers (herpes simplex), Seidel test (leaking aqueous from a penetrating injury); can stain soft contact lenses.
• Anaesthesia for eye surgery — most surgery under local anaesthetic (topical, sub-Tenon's, peribulbar); anticoagulants usually continued for cataract surgery (check local policy).

Antibiotics, Antivirals, Steroids and Lubricants

• Bacterial conjunctivitis — usually self-limiting within 1–2 weeks — lid hygiene and delayed treatment; chloramphenicol drops (or ointment) if severe or persisting; fusidic acid (twice daily — easier for children, pregnancy); no need to exclude children from school (UKHSA).
• Contact lens wearers with a red eye — stop lens wear; same-day assessment for keratitis — topical quinolone (levofloxacin, ofloxacin) covers Pseudomonas; corneal scrapings by ophthalmology.
• Neonatal conjunctivitis (ophthalmia neonatorum, first 28 days) — urgent swabs for gonorrhoea (days 1–5 — risk of corneal perforation) and chlamydia (systemic macrolide) — treat parents.
• Herpes simplex keratitis — dendritic ulcer — topical aciclovir ointment or ganciclovir gel (ophthalmology); never give topical steroids to an undiagnosed red eye (worsens herpes and fungal infection — geographic ulcers, perforation).
• Herpes zoster ophthalmicus — V1 shingles — oral aciclovir or valaciclovir within 72 hours (reduces eye complications); Hutchinson's sign (vesicles on the tip of the nose — nasociliary nerve) predicts eye involvement — same-day ophthalmology if eye symptoms.
• Topical steroids (prednisolone acetate, dexamethasone, fluorometholone) — uveitis, post-operative inflammation, severe allergy, some keratitis — only under ophthalmology supervision:
  • Raised IOP ("steroid responders" — glaucoma), cataract (posterior subcapsular), worsening of herpes simplex and fungal infection, delayed healing.
• Allergic conjunctivitis — antihistamine drops (antazoline, olopatadine, ketotifen), mast cell stabilisers (sodium cromoglicate — regular use), oral antihistamines; cold compresses.
• Ocular lubricants — hypromellose, carbomer gels, sodium hyaluronate, paraffin ointment at night — preservative-free if used more than 4–6 times a day.
• Endophthalmitis (after surgery or injection) — intravitreal antibiotics (vancomycin and ceftazidime) — emergency.

Anti-VEGF and Other Specialist Treatments

• Anti-VEGF intravitreal injections — ranibizumab, aflibercept, faricimab (also blocks angiopoietin-2), brolucizumab; bevacizumab (off-label in some settings):
  • Uses — wet AMD, diabetic macular oedema, macular oedema from retinal vein occlusion, myopic choroidal neovascularisation; retinopathy of prematurity (selected).
  • Repeated injections (monthly to every few months — treat-and-extend).
  • Risks — endophthalmitis (about 1 in 2,000–3,000 injections — painful red eye with reduced vision within days), raised IOP, retinal detachment, inflammation (brolucizumab — vasculitis).
• Intravitreal steroid implants (dexamethasone, fluocinolone) — diabetic macular oedema, RVO, uveitis — raised IOP and cataract.
• Lasers — panretinal photocoagulation (proliferative diabetic retinopathy), YAG capsulotomy (posterior capsule opacification), laser iridotomy (angle closure), SLT (open-angle glaucoma), retinopexy (retinal tears).
• Systemic immunosuppression for uveitis and scleritis — steroids, methotrexate, mycophenolate, adalimumab (NICE TA460).
• Thyroid eye disease — stop smoking, achieve euthyroid state, selenium (mild), IV methylprednisolone (active moderate–severe), mycophenolate, orbital radiotherapy, decompression; teprotumumab (IGF-1R antibody — check UK availability).
• Botulinum toxin — blepharospasm, hemifacial spasm, some squints.
• Gene therapy — voretigene neparvovec for RPE65-associated inherited retinal dystrophy.
• Myopia control in children — low-dose atropine drops, special spectacle and contact lenses, more time outdoors.

Eye Side Effects of Systemic Drugs

Drug	Eye effect and action
Hydroxychloroquine (and chloroquine)	Retinal toxicity ("bull's-eye" maculopathy) — irreversible; risk with dose over 5 mg/kg/day (actual body weight), long duration, renal impairment, tamoxifen — annual screening (OCT and fields) after 5 years of use (after 1 year if additional risk factors — RCOphth 2020)
Ethambutol	Optic neuropathy — reduced acuity and red–green colour loss — check acuity and colour vision before starting; stop if vision changes (dose-related; worse in renal impairment)
Amiodarone	Corneal microdeposits (vortex keratopathy — almost all patients, harmless — haloes); rarely optic neuropathy
Corticosteroids (any route)	Cataract (posterior subcapsular), raised IOP and glaucoma, central serous chorioretinopathy, reactivation of infection
Tamsulosin and other alpha-1 blockers	Intraoperative floppy iris syndrome during cataract surgery — tell the surgeon (effect persists after stopping)
Topiramate	Acute bilateral angle closure and myopic shift (ciliary body swelling) — usually within a month of starting — stop the drug (iridotomy doesn't help)
Anticholinergics, tricyclics, antihistamines, sympathomimetics, nebulised ipratropium and salbutamol	Precipitate angle closure in narrow angles; blurred near vision (cycloplegia)
Vigabatrin	Permanent visual field constriction — field monitoring
Sildenafil and PDE5 inhibitors	Blue-tinged vision, light sensitivity; rarely NAION
Digoxin (toxicity)	Yellow–green vision (xanthopsia), blurring
Bisphosphonates	Uveitis and scleritis (rare)
Isotretinoin	Dry eye, reduced night vision, contact lens intolerance
Phenothiazines (thioridazine, chlorpromazine)	Pigmentary retinopathy (thioridazine), lens and corneal deposits
Linezolid (prolonged)	Optic neuropathy
Checkpoint inhibitors, MEK inhibitors	Uveitis, dry eye; serous retinopathy (MEK)
Pentosan polysulfate	Pigmentary maculopathy
Quinine (overdose)	Sudden blindness (retinal toxicity)
Opioids / organophosphates	Pinpoint pupils

⚠️ Safety Pearl: Never prescribe topical steroid drops for an undiagnosed red eye — they can turn a herpes simplex dendritic ulcer into a perforating corneal ulcer and can quietly cause glaucoma. Leave steroid drops to ophthalmology, where the cornea and pressure can be checked.

Eye Anatomy and Drugs at a Glance

Fact	Why it matters
Thin orbital floor and medial wall	Blowout fractures; ethmoiditis spreads to the orbit
Orbital septum	Preseptal (oral antibiotics) vs orbital cellulitis (emergency)
Levator (III) vs Müller's (sympathetic)	Complete ptosis in III palsy; partial in Horner's
Cornea densely innervated (V1), avascular	Very painful abrasions; contact lens keratitis
Ciliary injection	Keratitis, uveitis, angle closure — urgent
Aqueous — trabecular and uveoscleral outflow	Targets of glaucoma drugs
Hypermetropes and dilation	Angle closure risk
Central retinal artery is an end artery	CRAO — cherry-red spot — stroke pathway, exclude GCA
Posterior ciliary arteries supply the optic nerve head	GCA causes arteritic AION — steroids now
Chiasm — crossing nasal fibres	Bitemporal hemianopia from pituitary tumours
Sympathetic chain over the lung apex and along the carotid	Horner's from Pancoast tumour or carotid dissection
Pupil fibres on the outside of III	Painful III palsy with dilated pupil — aneurysm
Prostaglandin analogue drops	Iris darkening, lash growth
Timolol drops	Bronchospasm and bradycardia — avoid in asthma
Acetazolamide	Hypokalaemia, paraesthesia; angle closure emergency
Topical anaesthetic	Never for home use
Hydroxychloroquine	Annual retinal screening after 5 years
Ethambutol	Check acuity and colour vision
Tamsulosin	Floppy iris at cataract surgery
Topiramate	Bilateral acute angle closure

Spot the Diagnosis

Clue	Diagnosis
Numb cheek and double vision looking up after being hit with a cricket ball	Orbital floor (blowout) fracture
Swollen lids, proptosis and painful eye movements after a cold	Orbital cellulitis
Partial ptosis and small pupil with neck pain after a whiplash injury	Horner's from carotid dissection
Complete ptosis, eye down and out, dilated pupil, headache	III palsy — posterior communicating artery aneurysm
Vertical diplopia worse going downstairs, head tilted	IV nerve palsy
Horizontal diplopia with papilloedema	VI palsy — raised ICP (false localising)
Painful red eye, photophobia, small pupil in a man with back stiffness	Anterior uveitis (HLA-B27)
Red painful eye, haloes, vomiting and fixed mid-dilated pupil after cinema	Acute angle-closure glaucoma
Bilateral blurred vision and eye pain 2 weeks after starting topiramate	Drug-induced bilateral angle closure
Sudden painless loss of vision with a cherry-red spot	Central retinal artery occlusion
Sudden loss of vision, jaw claudication, swollen pale disc in a 75-year-old	Arteritic AION — giant cell arteritis
"Stormy sunset" fundus in a hypertensive patient	Central retinal vein occlusion
Flashes, floaters and a curtain across vision in a myope	Retinal detachment
Straight lines look wavy in an 80-year-old	Wet AMD — urgent anti-VEGF referral
Bitemporal hemianopia with headache and galactorrhoea	Pituitary adenoma (prolactinoma)
Superior homonymous quadrantanopia	Contralateral temporal lobe (Meyer's loop) lesion
Dendritic ulcer staining green with fluorescein	Herpes simplex keratitis — no steroids
Contact lens wearer with painful red eye and corneal opacity	Microbial keratitis — same-day ophthalmology
Vesicles on the tip of the nose with forehead shingles	Hutchinson's sign — eye involvement likely
Brown iris and long eyelashes in one eye on glaucoma drops	Prostaglandin analogue side effect
Wheeze after starting eye drops for glaucoma	Timolol (systemic beta-blockade)
Reduced red–green colour vision on TB treatment	Ethambutol optic neuropathy
Bull's-eye maculopathy in a woman with lupus	Hydroxychloroquine retinopathy
Yellow vision and nausea in an older woman with AF	Digoxin toxicity
White pupil in a baby's photo	Retinoblastoma or cataract — urgent referral

Exam-style Scenarios

1. A 68-year-old woman with long-sightedness develops severe right eye pain, haloes, vomiting and blurred vision while watching a film in a dark cinema. The right pupil is fixed and mid-dilated; the eye is red and hard.
Answer: Acute angle-closure glaucoma.

• Emergency ophthalmology; IV acetazolamide 500 mg, topical timolol, apraclonidine and steroid; pilocarpine once IOP starts to fall; analgesia and antiemetic; lie supine.
• Laser peripheral iridotomy to both eyes once settled.
• Avoid anticholinergic and sympathomimetic drugs; check for triggers (e.g. recent dilating drops, topiramate).

2. A 55-year-old man with asthma is started on glaucoma drops and develops wheeze within a week.
Answer: Topical timolol causing bronchospasm.

• Stop the beta-blocker drops; treat the wheeze.
• Switch to a prostaglandin analogue, carbonic anhydrase inhibitor or alpha-agonist, or offer SLT.
• Teach punctal occlusion to reduce systemic absorption of any drops.

3. A 46-year-old woman with SLE has taken hydroxychloroquine 400 mg daily for 7 years. She weighs 58 kg and has eGFR 52.
Answer: High risk of hydroxychloroquine retinopathy.

• Her dose is about 6.9 mg/kg/day (over the 5 mg/kg threshold) and she has renal impairment.
• Ensure annual retinal screening (OCT and visual fields).
• Discuss reducing the dose to 5 mg/kg/day or less with rheumatology; stop if toxicity is found.

4. A 72-year-old man has sudden painless loss of vision in his left eye for 1 hour. Acuity is perception of light; there is a left RAPD and a pale retina with a cherry-red spot.
Answer: Central retinal artery occlusion.

• Treat as an acute stroke — urgent stroke assessment (some centres consider thrombolysis within 4.5 hours).
• Check ESR and CRP and ask about GCA symptoms — high-dose steroids if suspected.
• Investigate the embolic source — carotid imaging, ECG and monitoring for AF, echo; vascular risk reduction.

5. A 30-year-old man who wears soft contact lenses has a painful red right eye, photophobia and reduced vision. Fluorescein shows a small corneal ulcer.
Answer: Microbial keratitis (contact lens related).

• Same-day ophthalmology — corneal scrapings for culture (including Acanthamoeba).
• Intensive topical antibiotics (fluoroquinolone covering Pseudomonas); no steroid drops initially.
• Stop lens wear; bring lenses and case for culture; advice — no swimming or showering in lenses, no tap water.

Key Points

• The orbital floor and medial wall are thin — blowout fractures and orbital cellulitis from ethmoiditis.
• The orbital septum separates preseptal from orbital cellulitis — proptosis, painful eye movements and reduced vision mean orbital.
• Ptosis — levator (III, complete), Müller's (sympathetic, partial); orbicularis (VII) closes the eye.
• Cornea gives two-thirds of focusing power; endothelium doesn't regenerate.
• Ciliary injection means serious disease — keratitis, uveitis, angle closure.
• Aqueous is made by the ciliary body and drains through the trabecular meshwork and uveoscleral route; normal IOP 10–21 mmHg.
• Angle closure — hypermetropes, older, East Asian, dilation by drugs or darkness.
• Central retinal artery occlusion is a stroke; GCA damages the posterior ciliary arteries.
• Rods — night vision (vitamin A); cones — colour and acuity at the fovea.
• Chiasm — bitemporal; temporal — superior quadrantanopia; parietal — inferior; occipital — hemianopia with macular sparing.
• Horner's — Pancoast tumour, carotid dissection; III palsy with dilated pupil — aneurysm.
• LR6 SO4, others III; IV palsy — head tilt and trouble with stairs; VI palsy — false localising sign.
• Glaucoma drugs — prostaglandin (outflow), beta-blocker and CAI (production), alpha-agonist (both), pilocarpine (angle closure); SLT first-line option.
• No topical anaesthetics for home use; no steroid drops for an undiagnosed red eye.
• Systemic drug eye toxicity — hydroxychloroquine, ethambutol, steroids, tamsulosin, topiramate, vigabatrin, amiodarone, digoxin.

Guidelines and Further Reading

• NICE NG81: Glaucoma — diagnosis and management (2022)
• NICE NG82: Age-related macular degeneration; NICE NG77: Cataracts in adults
• Royal College of Ophthalmologists: Hydroxychloroquine and chloroquine retinopathy — recommendations on monitoring (2020)
• Royal College of Ophthalmologists: Ophthalmic services guidance; College of Optometrists clinical management guidelines
• NICE CKS: Red eye, conjunctivitis, herpes zoster ophthalmicus
• DVLA: Assessing fitness to drive — visual disorders
• NHS Diabetic Eye Screening Programme
• BNF — for current doses