Opthalmology Lecture (Notes)

Gross structure of the eye A B C D E F G R H I J K L F’ M N • – Sclera (A’ cornea) – Choroid – Cilliary body & processes – Iris – Retina – Optic disc – Macula lutea – Fovea centralis – Vitreous body / humour – Aqueous body / humour – Lens – Suspensory ligament – Pupil – Optic nerve – Retinal artery – Retinal vein The eyelids Normal eyelid closure requires an intact nerve supply to the orbicularis occuli muscles (facial nerve). Eyelid opening is affected by the levator palpebrae superioris supplied by CN III Functions: • Protection of the eye from mechanical trauma, extremes of temperature and bright light. • Maintenance of the normal pre-corneal tear film that is important for maintenance of corneal health and clarity. • The conjunctivae From the limbus to the margins of the eyelids Very thin and easily damaged Function – produces the inner (mucous) layer of the tear film from goblet cells • The tear film Consists of 3 layers: • The mucoid layer lies adjacent to the corneal epithelium. It improves the wetting properties of the tears. It is produced by the goblet cells in the conjunctival epithelium. • The watery (aqueous) layer is produced by the main lacrimal gland in the supero-temporal part of the orbit and accessory lacrimal glands found in the conjunctival stroma. This aqueous layer contains electrolytes, proteins, lysozyme, • immunoglobulins, glucose and dissolved oxygen (from atmosphere) The oily layer (superficial layer of the tear film produced by meibomian glands - modified sebaceous gland) of the eyelid margins. This oily layer helps maintain the vertical column of tears between the upper and lower lids and prevents excessive evaporation. The tears normally flow away through a drainage system formed by the puncta (inferior and superior), canaliculus (inferior and superior), the common canaliculus, opening into the lacrimal sac, the nasolacrimal duct (which drains into the nose). • The cornea 0.5mm thick, transparent mesh of collagen fibres covering the anterior 1/6 of the eye Contains many nerve endings (very sensitive to touch) Structure Has 5 layers (outside to inside) 1. Epithelium - stratified squamous epithelium with layers of regular arrangement. 2. Bowman’s layer – Basement membrane of the epithelium 3. Stroma - consists of approximately 90% of total corneal thickness. Consists of lamellae of collagen, cells, and ground substance. 4. Descemet’s membrane - the basement membrane of the endothelium. 5. Endothelium - a single layer of cells lining the inner surface of descemet’s membrane. Cannot regenerate and if damaged allows water into the eye --> opacity Function Is the main refractive layer of the eye & is transparent due to 3 factors • Has no blood supply (receives nutrients from the aqueous) • The collagen fibres have a specific arrangement • It is dehydrated (due to cation channels in the endothelial layer) • The sclera Made of the same collagen of the cornea but is opaque due to a different arrangement of fibres It is hydrated and has blood vessels across the surface (episclera) Optic nerve leaves the globe through the lamina cribrosa (at the back) • The iris Part of the uvea (continuous with the cilliary body and the choroids) Anterior layer is variable in pigment (gives eye colour), posterior layer is similar to choroids Contains radial and sphincter muscle fibres that allow the pupil to dilate and constrict Mydriatics Dilate the pupil by paralysing the cilliary muscle (cycloplegia) bec parasympatholytic Except phenylephrine (sympathomimetic) NB: pupil dilation may precipitate acute angle closure glaucoma in predisposed patients Uses • Enhance examination of lens, vitreous and fundus. Short acting agents preferred : tropicamide, cyclopentolate, phenylephrine. (Note topical phenylephine especially 10% may cause elevation of bp. Use 2.5%). • Cycloplegia - enhances more accurate refraction especially in children. Cyclopentolate or rarely atropine. • To relieve spasm of ciliary muscle and iris sphincter in treatment of Iritis/Iridocyclitis & severe corneal epithelial defects Drug Atropine Homatropine Cyclopentolate Tropicamide Time MaxEffect 1-2 hours 40 minutes 25 minutes 20 minutes Duration of Max Effect 8-48 hours 50 minutes 50 minutes 15 minutes Patient able to read 3-4 days 6 hours 3 hours 45 minutes Miotics Constrict of pupil (miosis). Associated with cyclotonia (spasm of ciliary muscle). Also reduce IOP, therefore used in treatment of glaucoma. Generally parasympathomimetics. Accommodation normal 10-14 days 36 hours 18 hours 4 hours Pilocarpine - causes direct stimulation of iris sphincter and ciliary body. Used in treatment of glaucoma or to constrict pupil (after dilation). Choline esters - Acetylcholine, very short acting used mainly to constrict pupil in intraocular surgery eg cataract (when required) carbachol: long acting Anticholinesterases - eserine (short acting), Phospholine Iodide (Ecothiopate) (long acting) • Anterior chamber and anterior chamber angle Anterior chamber is between the cornea & the iris (anterior segment = all anterior to lens) Posterior chamber is between the iris and the lens Anterior chamber angle – angle between the iris and cornea (can be open, narrow or closed) The angle contains the drainage mechanism for the aqueous • Trabecular network --> • Schlemm’s canal --> • Aqueous veins --> • Episcleral veins If the angle is closed --> impaired drainage & increased IOP --> closed angle glaucoma • The Lens Is clear and avascular (supported by the Posterior aqueous humour) Lens Epithelium Lens Cortex Suspended from the cilliary body by the Capsule zonule (suspensory ligament) It continues to grow with age. New fibres Anterior Lens produced by the epithelium migrate to Lens Capsule the nucleus Nucleus 65% water, 35% protein. Water content decreases with age, making the lens less pliable. As the lens becomes more rigid with age accommodation decreases = presbyopia Diagram showing a cross Has a high protein content. If the protein is section through the human lens, the main structures are denatured --> sugars --> osmotic indicated. effect --> water enters lens, disrupting structure --> opacity = cataract Structure Capsule – surrounds entire lens to hold its contents together Epithelium – only at the front Cortex – produced by the epithelium Nucleus – in centre • Cilliary Body Comprised of: Pars plicata (raised = functional part) Pars plana (flat = little function so used as surgical point of entry) The anterior termination of the retina into the cilliary body is the ora seratta Function § Makes and influences the production of aqueous humour Low plasma concentration, high ascorbic acid Normal volume 0.3mls Produced by ultra-filtration from the cilliary processes in the posterior chamber Inflammation of anterior uvea --> proteins leak from iris circulation to aqueous --> plasmoid aqueous § Accommodation - near response (accommodation, convergence & papillary constriction) Lens needs to become more convex for focussing on near object Cilliary muscle is circular so must contract to reduce tension on zonules (suspensory ligaments) • The vitreous Is attached weakly around the optic disk and strongly at the aura serata Serves very little function – is mainly a space filler Is a clear gel (Avascular with 99% water with a specific, clear arrangement of collagen fibres) Degenerates with age in the core (liquefaction) è tears the posterior attachment & runs between the retina & capsule, vitreous collapses --> black patches in the vision = floaters = posterior vitreous detachment (PVD - 75% of ppn at some point) è If abnormal attachments between the retina & vitreous --> retinal detachment --> liquid enters behind retina è Rx by removing vitreous to reduce tension on the retina • Retina The vertebrate retina has ten distinct layers. From innermost to outermost, they include: 1. Inner limiting membrane - Müller cell footplates 2. Nerve fiber layer 3. Ganglion cell layer - contains nuclei of ganglion cells and gives rise to optic nerve fibers. 4. Inner plexiform layer 5. Inner nuclear layer 6. Outer plexiform layer 7. Outer nuclear layer 8. External limiting membrane - separates the inner segment portions of the photoreceptors from their cell nuclei. 9. Photoreceptor layer - Rods / Cones 10. Retinal pigment epithelium 2 types of photoreceptors Rods – mainly in peripheral area, give night vision Cones – mainly in macula, give colour vision Structure – 2 main layers Retinal pigment epithelium –deep to the photoreceptors giving metabolic support Neural retina – layers include the photoreceptors, relays and nerve fibres Fovea – only cones, nerve cells moved to the side (giving dent shape) & no vessels on surface • Choroid Between sclera and retina Mainly a layer of fenestrated vessels that supply the outer 2/3 of the retina Separated from the retina by Bruch’s membrane (prevents the retina becoming oedematous) Drusen – are small localized thickenings of Bruch’s membrane • Optic nerve & Optic Disc Nerve fibres running across the retina converge on the disc and leave through the lamina cribrosa Optic disc - As the fibres turn 90o to exit the globe they appear pink/orange The optic cup is the section with no nerve fibres in and its size depends on the size of the disc and the number (and size) of the nerve fibres. It is white because you are seeing the lamina cribrosa of the sclera Cup size increases in glaucoma because nerve fibres die --> larger cup:disc ratio • Understand the diagnostic agents used to enable eye examination Diagnostic agents Fluorescein. For distinguishing breaks in epithelial surface of cornea. Rose Bengal stains damaged cells, useful for looking for dry spots on cornea & conjunctiva. Local anaesthetic agents: Cocaine powerful anaesthetic, 5 mins to work. May induce temporary clouding of corneal epithelium, pupil dilation, delirium. Amethocaine - rapid effect (1min). No pupil dilation but stings on administration and produces vasodilation. Benoxinate - slower acting but no irritation or corneal damage. May be used as combination with Fluorescein for tonometry. Proxymethocaine (Ophthaine) - rapid anaesthesia in 20 seconds. Does not sting. Short acting but not strong action. Lignocaine Used as combination with Fluorescein for tonometry. Ophthalmoscopy • To explain how to use the ophthalmoscope and how to optimally visualise the fundus. Red reflex – should show retina a back of eye If limited = opacity somewhere in path of light (cornea, aqueous, lens, vitreous) If absent = may not be possible to visualise fundus (dense cataract or vitreous haemorrhage) Anterior Segment – check for opacity, floaters, foreign bodies Optic Disc Medial to fovea (approx 20o from line of view) Note the: Colour – should be pink/orange (may be dark red or pale) Cup – ratio of cup to disc (normal = 0.3) Contour – is the disk raised, swollen or flat (do you need to change focus to see it?) Peripheral retina Ask the patient to look up, down, left and right Macula & Fovea Ask the patient to look directly at the light • To outline the normal fundal anatomical landmarks and common ophthalmic abnormalities. Disc Colour Cup Contour The vessels Number Size (engorged?) Anyeursms Haemorrages Silver wiring The retina Colour (pigment) Exudates (hard/soft) Detatchment Degeneration Atrophy Nasal vessels Swollen disc Disc atrophy Cotton wool spots Silver wiring (chronic HT) AV nicking (chronic HT) Roth spots (Cotton wool spot surrounded by haemorrhage) Hard exudates Drusen Dot, flame & blot haemorrhages Optic Disc Swelling • To know the possible presenting symptoms & investigations of a patient with a swollen optic disc Unilateral S&S - reduced acuity & colour vision, visual field defect, blurred disc margins Causes – vascular, inflammatory, demyelination, hereditary, infiltrative (lymphoma), infective (toxoplasmosis) Ix – visual fields, FBC, glucose, ESR, coag and infection screens. Bilateral S&S - normal or severely reduced acuity, transient (papiloedema), decreased colour vision, enlarged blind spot Causes – raised ICP, malignant hypertension, papilopathy (diabetic), infiltrative, toxic Ix - BP, glucose, FBC, U&E, creature, ESR, visual fields • To learn about some causes of optic disc swelling. Optic neuritis Retrobulbar pain especially on eye movement, associated with globe tenderness Disc may not be swollen Relative afferent pupillary defect Red desaturation Central scotoma on field-testing May have had other transient neurological symptoms Risk of developing MS Papilloedema – MUST BE BILATERAL Symptoms include transient visual obscuration May also have splinter haemorrhages, exudates, cotton wool spots & retinal folds near the disc Enlarged blind spots Gradually progressive field loss – generalised constriction Eventual atrophic changes Arteritic anterior ischaemic optic neuropathy (AION) Temporal headache associated with jaw claudication, weight loss, myalgia Visual loss caused by inflammatory infarction of posterior cilliary artery Raised ESR and CRP Needs urgent Rx with high dose steroids (continue for 2 yrs) Temporal artery biopsy should be performed within a week of starting treatment Non-arteritic aion Infarction of PCA as for AAION ESR not raised 50% of patients hypertensive No associated systemic symptoms Optic atrophy End stage eye disease Associated with apd Visual Field Examination • To outline the visual pathway. The optic impulses run as follows: Retina Optic disc (through lamina cribrosa) forms the Optic nerve (then myelinated and surrounded by dura and CSF - and through optic foramen) Optic chiasm (1/2 fibres decussate) Optic tract Lateral geniculate body (thalamic nuclei) Optic radiations Superior fibres rotate 90o to medial & pass through parietal lobe Inferior fibres rotate 90o to lateral & pass through the temporal lobe as the skirt round the temporal horn of the lateral ventricle Fibres then revert as they enter the occipital lobe & run to the cortex Visual cortex – areas 17 & 18 • To explain how to examine visual fields. Perimetry = measurement of visual field Can be static i.e. stationary stimuli of various size or illumination or kinetic i.e. moving stimuli to test limit of field for that stimulus. Scotoma Relative - an area in the field where sensititivity is reduced Absolute - an area where there is no perception of the stimulus e.g. blind spot from optic nerve head. Confrontation testing § Position patient correctly and explain clearly § Screen for hemianopia and inattention hemianopia with both eyes open. § One eye at a time § Test 4 quadrants gross function by presenting 1 & 2 fingers and asking to count § Screen all 4 quadrants by diagonal movements. White hat pin (then red) § Test patient reliability by identifying blind spot. • To explain the different types of field abnormalities possible. Retinal defects arcuate scotoma (Bjerrum scotoma or nerve fibre bundle defect) DD : lesions at disc margin e.g. drusen nasal step (left) paracentral scotoma (right) Enlarged blind spot e.g. papilloedema, myopic peripapillary atrophy Peripheral field constriction e.g. glaucoma, retinitis pigmentosa, poisons, bilateral occipital lobe infarcts, hysteria Central scotoma e.g. macular degeneration, optic neuritis, toxic amblyopia Defect crossing axes Retinal pathology, e.g. detachment (usually unilateral, May be bilateral if pathology in both eyes) Altitudinal defect eg ischaemic optic neuropathy, occlusion 1st order branch retinal artery or vein Bitemporal hemianopia Lesion at optic chiasm Bitemporal superior quadrantinopia - pressure from below chiasm commonly pituitary tumours (adenomas) Bitemporal inferior quadrantinopia - pressure from above chiasm e.g. craniopharyngioma (in young) Meningioma (over 30’s) Incongruous hemianopia Lesion in the optic tract before the lateral geniculate body Uneven hemianopia, usually larger defect on temporal side The lesion is on the contralateral side to the field defect Superior Quadrantinopia After the LGB the inferior fibres (superior image) rotate 90o to lateral The fibres must pass through the temporal lobe to bypass the temporal horn of the lateral ventricle A lesion in the temporal lobe will affect these fibres (also often causes paresis / paralysis) The lesion is on the contralateral side to the field defect Inferior Quadrantinopia After the LGB the superior fibres (inferior image) rotate 90o to medial The fibres pass through the parietal lobe A lesion in the parietal lobe will affect these fibres The lesion is on the contralateral side to the field defect Homonymous hemianopia The fibres rejoin & rotate back in the occipital lobe A lesion in the occipital lobe (“geniculocalcine tract”) before the cortex will cause a homonymous hemianopia The lesion is on the contralateral side to the field defect Macula sparing homonymous hemianopia The macula area of the cortex receives blood supply from both the middle and posterior cerebral arteries A vascular lesion will produce a macula sparing homonymous hemianopia, as the macula receives supply from the other (providing only one area affected) The lesion is on the contralateral side to the field defect Eye Movements & Orthoptics • To understand the role of the Orthoptist in the investigation, diagnosis and management of patients with ocular motility disorders Orthoptics – “straight eyes” Binocular vision – using the eyes together as a pair Simultaneous perception – each eye perceives the world simultaneously Fusion – 2 images become 1 Stereopsis –fused image seen as 3D • To know the actions of the different extra-ocular muscles. SR LR SR MR IR D C A B E F • IO LR SO Muscle Medial rectus (MR) Lateral rectus (LR) Superior rectus (SR) Inferior rectus (IR) Superior oblique (SO) Inferior oblique (IO) IR Inn CN III CN VI CN III CN III CN IV CN III Primary action Adduction Abduction Elevation Depression Intortion Extortion Secondary Action Tertiary Action Intortion Extortion Depression Elevation Adduction Adduction Abduction Abduction To learn how different cranial nerve palsies affect the eye. III rd nerve palsy (picture shows right CN3 palsy) Affects the MR, IR, SR, IO, pupil SO and IR spared Eye points down and out Ptosis Dilated pupil (efferent defect – more evident in bright light, no afferent defect) Causes: Congenital, Nuclear or Cavernous sinus disease. Vasa nervosum obstruction (medical). The pre-ganglionic parasympathetic pupillary fibres travel peripherally in the third nerve and therefore tend to be spared in the case of obstruction of the vasa nervosum but affected if the nerve is compressed from without by a tumour. Pupil-sparing third nerve palsies are therefore said to be 'medical' (common in elderly hypertensive diabetics for example) and pupil-affecting third nerve palsies are 'surgical' (usually caused by an aneurysm of the posterior communicating artery. Intra-cranial aneurysm (surgical) – non pupil sparing Management So many muscles are affected the Rx of the diplopia is usually a black patch. IV th nerve palsy SO affected Eye unable to look down and in on affected side (picture shows right CN4 palsy) Hence, vertical diplopia most marked on looking down and in Bilateral cases may occur with head injuries Causes Congenital - most common, caused by a lax superior oblique tendon and therefore not a true palsy Vasa nervosa obstruction - elderly hypertensive diabetic Closed head injury - false localising sign Intra-cranial diseases in the posterior fossa, including surgery. Management If it doesn't get better on its own, is by surgery to the other oculomotor muscles to try to make up the function of the fourth nerve. VI th nerve palsy LR palsy (abducens palsy) Eye may drift medially on affected side due to pull of MR (see picture – right palsy) Causes (6 causes worth knowing) 1. Vasa nervosum infarction (the commonest cause). 2. Nuclear. The seventh nerve must always be affected since it winds around the sixth nerve nucleus. The pyramidal tract may also be involved (Millard-Grubler syndrome). 3. False localising sign. The sixth nerve has a long intra-cranial course and can be easily stretched during rapid head decelerations. 4. Raised intra-cranial pressure. 5. Gradenigo's syndrome. Ear or mastoid infection spreading to the petrous temporal bone can inflame the sixth nerve which hooks over its tip. 6. Cavernous sinus disease. The sixth nerve lies below all the other nerves in the cavernous sinus, and so can be affected separately. The commonest cause of this is a naso-pharyngeal carcinoma extending upwards into the cavernous sinus. Treatment Treatment of sixth nerve palsy is to wear a black patch until it gets better; or to have an injection of Botulinum Toxin to straighten the eye whilst waiting for it to get better; or to transpose the other rectus muscles to make up the function of the lateral rectus. VII th nerve palsy May cause exposure as eye sphincter affected so test corneal sensation is intact • To know the normal pattern of eye movements. Five movement systems have been identified. These are the Smooth pursuit - primary position into the limits of the other 8 positions of gaze. Versions should be tested first, followed by ductions. Saccadic – constant movements from one area of the field of view to another with the eyes moving as a pair. As seen in reading Vestibular – eye movements to counteract the motion of the body. Controlled by the vestibular system. If this fails à nystagmus Optokinetic – a combination of smooth pursuit and saccade. E.g. for watching a train out of the window Vergence - the eyes rotate based on the distance to the object to keep the object in both foveas. In the near extreme à “cross eyed” • To understand human visual development. At birth - vision is very basic and a child is unable to follow an object At six weeks - the visual cortex begins to function. From this period that amblyopia (lazy eye) can develop. From six weeks to six months - the development of vision is very rapid and if there is any obstruction to vision in this period the resulting amblyopia is very dense and irreversible. If problems occur with vision in this period, nystagmus tends to develop. From six months to about 7-8 years - the macula develops and the visual cortical development continues. Disturbances of binocular vision in this period result in amblyopia, which is not very dense. After this period - obstructions to vision generally do not result in amblyopia but can interrupt binocularity. • To know the different clinical patterns of eye movement disorders that commonly present in the eye clinic. Squint (Strabismus) A misalignment of the visual axes is known as a manifest squint or strabismus. Squints fall into two types Concomitant squints (mostly children), remains the same in all positions of gaze. These derive from supra-nuclear abnormalities of gaze or binocularity. Usually onset 3-4 years Inconcomitant squints (mostly adults), changes based on the positions of the eyes. These squints derive from lesions affecting the occulomotor nerve nuclei, the nerves themselves or the eye muscles. Manifest squint (Heterotrovia) A manifest squint occurs when one or other of the visual axes is not directed towards the fixation point & is visible all the time. 2 outcomes are possible Diplopia – double vision if the squint develops after 7yrs Suppression – the image from the squinting eye is ignored (if before 7yrs) à amblyopic (lazy eye). The cover/uncover test • The patient fixes on a target that can be seen with each eye individually i.e. if one eye has very poor vision, a target that can be seen with this eye (this is especially important when testing without glasses). • One eye is covered with an occluder, and you look for any movement of the uncovered eye to fix on the target. • The cover is then removed (can repeat over the same eye to confirm the findings) • This is then repeated, on the other eye • The test is repeated for near, distance & light, with and without glasses. Results If the un-covered eye makes a movement to fix when the other eye is covered, a manifest squint has been detected. The direction of the movement determines the type of manifest squint. Behind the occluder, the covered eye will have also made a corresponding movement. When the cover is removed, the eyes will go back to the original squinting position. Manifest squints end in ‘tropia’ and the squinting eye must be specified i.e. right esotropia. When describing results of the cover test, you are looking at where the eyes start off from. • ESOTROPIA - un-covered eye moves outwards to fix (it started off in an inwards / convergent position – as in picture – left esotropia) • EXOTROPIA - un-covered eye moves inwards to fix (it started off in an outwards) • HYPERTROPIA - If the un-covered eye moves downwards to fix • HYPOTROPIA - If the un-covered eye moves upwards to fix • No movement - seen when either eye is covered, there is no manifest squint present. Latent squint (Heterophoria) In latent squint both eyes are directed towards the fixation target (normal when fixed) But deviate on dissociation. Therefore… Only seen when BV is disrupted Very common – seen in 90% of population Latent squint is usually exophoria or esophoria The alternate cover test This is used to determine the presence of a latent squint, (90% of the population) • The patient fixes on a target that can be seen with each eye individually. • One eye is covered with an occluder. • The occluder is rapidly moved from one eye to the other, allowing the patient time to fix each time. (Ensuring fixing properly and each eye is completely covered) • You are observing the movement of each eye as the occluder is moved from that eye across to the other, i.e. looking for movement of the covered eye just as the cover is removed. • Repeat for near, distant and light Results Both eyes will move in turn either nasally, temporally, or vertically, or not at all if they have no latent squint. As the cover is removed, that eye will make a movement to fix, and the now covered eye will also make a corresponding movement under the cover. As the cover is then moved back to the other eye, the eye under the cover will also make a movement to fix again. When the cover is completely removed, both eyes will return to ‘straight’. Latent squints end in ‘phoria’. When describing the responses, you are looking for the direction in which each eye starts off. • ESOPHORIA - If each eye moves outwards to fix, they started off in an inwards • EXOPHORIA If each eye moves inwards to fix, they started off in an outwards Vertical phorias are different. One eye will move up and the other will move down in all cases, so you need to specify which eye starts off where – it doesn’t matter which eye you specify with a vertical latent squint, only that the direction and eye is correct! • If the right eye starts off in elevated position / moves downwards then the left eye will have to move up– Right hyper phoria OR left hypo phoria. • If the left eye starts off in elevated position / moves downwards then the right eye will have to move up– Left hyper phoria OR right hypo phoria. Causes of Squint Esotropia Primary esotropia can be classified as constant or intermittent and accommodative or nonaccommodative (the angle of deviation is increased when accommodation is exerted) Intermittent: Early-onset esotropia: This is a squint that develops before 6 months of age and is very large & therefore obvious. Strong hereditary element and amblyopia is very common. Rx with surgery. Related to accommodation: The esotropia may be associated with uncorrected hypermetropia. Additional accommodative effort and associated accommodative convergence causes the eye to deviate medially. When the hypermetropic correction is worn, the eyes are straight and binocular single vision is demonstrable. Related to fixation distance: may be only at near or distant Constant: Infantile (starts <6 months) Idiopathic (starts > 6months) Related to accommodation, in which correction of the hypermetropia reduces the size of the esotropia but does not eliminate it Stress induced, due to sensory deprivation or divergence insufficiency Exotropi Primary exotropia may be constant or intermittent (more common). Deviation is classified based on if manifest for distance or near fixation. Constant exotropia may be infantile in origin. Intermittent Divergent squint: Usually when tired. Starts at a very early age and is associated with closing one eye in bright light. Rx surgery for cosmesis Secondary exotropia - Infants with pathological unilateral visual loss from birth. Constant non-paralytic unilateral exotropia in a child under 1 year should always be considered symptomatic until proven otherwise. Prompt referral is indicated. Paralytic squint May be congenital or acquired and is classified according to the underlying cause Neurogenic lesions account for the majority of palsies (CN 3, 4, 6) Mechanical restriction is caused by factors that interfere with the muscle contraction or relaxation or otherwise prevent free movement of the globe. Myogenic causes of limited eye movements are those which directly affect the muscles e.g. myasthenia gravis, inflammation, dysthyroid disease or trauma. Management of squint Refractive error Convex lenses (+ in hypermetropes) relax the accommodation and helps convergent deviatation Concave lenses (- in myopes) induce accommodation and help divergent deviations Prism lenses The apex of the prism should always point the same way as the deviation Esotropia needs a base out prism Exotropia needs a base in prism Surgery Shortening / extending the extraoccular muscles to make the eyes look straight Can be functional or cosmetic • To understand what amblyopia is and how it may treated during the visual development period Amblyopia - a reduction of vision in one eye Can be due to Stimulus deprivation – causing eye not to develop fully Strabismus – brain suppresses the image from the squinting eye Anisometropa – a difference in the refractive error between the eyes Management Can be treated if within critical period (before 7yrs) Occlusion of the good eye forces the other to develop, time depends on severity of defect Examination of Pupillary Light Reflexes • To outline the underlying neuronal pathways. Light Reflex Pupil Constriction Pupil dilatation & Muller’s muscle Through cavernous sinus Cilliary ganglion Cilliary Ganglion To sweat glands on face Int Carotid Ext Carotid Red Nucleus Edinger Westphal Nucleus Superior cervical ganglion Common Carotid Spinal cord C8-T1 Sympathetic cervical chain Superior colliculus Parasympathetic Sympathetic Accommodation reflex Near response = convergence, accommodation and miosis. Afferent pathway is CN II Processed through prestriate cortex (area 19) and the Edinger-Westphal nucleus Efferent pathway is Inferior division of CN III Reflex mydriasis Pupil dilatation is sympathetic control A1 adrenoceptors à contraction of radial muscles à dilatation • Understand how to test the pupillary responses Examination: § Look at pupil size, shape and symmetry (asymmetry = anisocoria), in dim ambient light. § Test light reflex and consensual. Note: distance fixation target. § Swinging flashlight test to examine for a relative afferent pupil defect (RAPD). § Accommodative reflex • To explain about the different types of pupillary abnormalities. Small pupils Horner’s Syndrome: (Lesion of sympathetic pathway) • Classic triad - Small pupil (more pronounced in the dark), partial ptosis, apparent enophthalmos, may also be loss of sweating on face, • Causes • 1st order – CNS (tumour, h’age, MS, syphilis), C-spine (tumour, syringomyelia) • 2nd order – cervical rib, pancoast, aneurysm, LN, atypical TB, trauma • 3rd order – ICA aneurysm, migraine, idiopathic Light-near dissociation (Argyll Robertson reaction) • Failure to constrict to light with a retention of the response to near • Midbrain lesions - pretectal in Parinaud’s, large pupils, Light-near dissoc, upgaze palsy, often a pinealoma. Argyll-Robertson, neurosyphilis: small, irregular and difficult to dilate • Peripheral neuropathies - diabetes, amyloidosis • Systemic disorders - Wernicke’s encephalopathy • Aberrant regeneration after IIIrd palsy Argyll robertson pupils (Congenital syphilis) • Pupils often small and irregular, Sluggish light responses, Light near dissociation • May be blind from optic atrophy Bilateral small pupils • In unconscious patient consider - Opiates, Brain stem infarct. • Uveitis • Congenital miosis Unequal Iris abnormalities: • Trauma - dilated as sphincter tears • Surgery - peripheral or broad iridectomy • Posterior synechiae - uveitis (pilocarpine) • Coloboma - congenital, not fused at midline, infero-nasal defect in iris Unequal size • Normal in 20% of population Large pupils CN III palsy • As mentioned earlier (down & out gaze, ptosis, enlarged pupil) Fixed dilated: • (Trauma) with AACG (also red eye, corneal oedema, hard eye etc) • Mydriatic agents • CN III compression by SOL (PCCA) or CN III infarct (usually pupil sparing) - DM • Uncal herniation from subdural haematoma • Adie’s syndrome (see below) Holmes-Adie’s Pupil: • Unilaterally dilated pupil in fit young person. Reacts poorly if at all to light (efferent defect). Slow and tonic near response. Some light near dissociation • Holmes-Adie syndrome - if impaired knee and ankle jerks in women only! • Due to post-ganglionic denervation of parasympathetic. Problems with responses Afferent pupillary defect (Marcus Gunn pupil) The pupil doesn't dilate appropriately to the level of light reaching it. Results in one pupil appearing larger than the other (relative afferent pupillary defect - RAPD) Damage to the afferent pathway means no direct or consensual response on shining light at affected eye. Both pupils respond appropriately on shining light on other side (as long as unilateral; defect) Optic nerve lesion or extensive retinal lesion eg optic neuritis, glaucoma, total retinal detachment. Efferent defect No direct response due to damage to efferent pathway Consensual response in tact proves no afferent defect Optometry • To understand the principles of measuring and recording vision Vision – the level of detail that an eye can resolve unaided Visual acuity – the patient’s ability to resolve fine detail once refractive errors have been corrected Usually measured with a Snellen chart View at 6m (max distance at which the eye can accommodate) Record by what line the individual can correctly read (can account for errors e.g. 6/24 + 2) Can be affected by crowding (in amblyopes & dyslexics) Can also be done with a LogMAR chart (Bailey-Love chart) View at 4m – read until no correct responses are made on a line 5 letters on each line, uses a Log scale Recorded as a decimal (6/6 = 0.0, 6/60 = 1.0, 6/5 = -0.1) Near visual acuity Measures the ability to focus & accommodate on a close line of text Should be read at 40cm Sizes in Times New Roman point size (6 = normal, 8 = newsprint, 24 = large print books) Should be quoted as e.g. N10 at 40cm In children…. Preferential looking (for young babies) Cardiff cards (pre verbal children) Kay’s Pictures (for young verbal children) • To understand the different types of refractive error and the basic theory of lenses used to correct them Natural focusing The cornea naturally has a focusing ability of 40D and the Lens 20D So the natural power of the eye is 60D Normal eye length = 22.2mm --> focus on fovea ^ macula Artificial lenses Convergence – light is bent in with a convex lens (positive power) Divergence – light is bent outward with concave lens (negative power) Myopia is short sightedness Can be due to axial length > 22.2 or refractive power of eye > 60D Both cause image to fall in front of retina Correct with a spherical concave (negative) lens to diverge the light Hypermetropia (hyperopia) is long sightedness Can be due to axial length < 22.2 or refractive power of eye < 60D Both cause image to fall behind the retina Correct with a spherical convex (positive) lens to converge the light Astigmatism Due to the lens or cornea not being round, but instead elliptical Causes two focusing points on the retina, these may fall in front or behind the retina Correct using 2 lenses to correct the 2 planes seperatley Prescription e.g. +3.00 / -0.75 x 180 +3.00 means hypermetropia -0.75 in a plane of 180o Presbyopia Due to aging of the lens the ability to accommodate decreases Usually noticed once it drops to 3 dioptres – making reading difficult without glasses Loss of ability to accommodate also occurs when lens is removed in cateract surgery (implant cannot accommodate) • Identify the associations between refractive error and pathology Myopia Causes Large eye Cateract Diabetes Mellitus Accomodation spasm (pseudomyopia) Congenital glaucoma Assoc with Retinal detachment Macular haemorrhages Cataract Myopic chorioretinal degeneration Down’s syndrome Keratoconus (conical cornea) • Hypermetropia Causes Small eye Retinal detachment Orbital tumours Macula oedema Assoc with Narrow angle glaucoma Concomitant squint Amblyopia of disuse To be aware of the different types of contact lenses and the indications for their use Indications Visual - anisometropia, high myopia, irregular cornea, scarring, keratoconus Occupational - sports, theatre, film, armed forces Cosmetic - to avoid glasses, to change eye colour Medical - therapeutic Psychological - cannot accept wearing glasses Types Soft lenses – used in high street opticians Flexible, good initial comfort, large diameter = secure fit, safe for sport Can split, dehydrate if left out, expensive Silicon hydrogel – new generation soft lens for extended/continuous use Rigid gas permeable lenses (RGPs) – used by hospital eye service Fixed shape, durable, easy to clean, good for all day, small diameter so less corneal invasion, gives smooth occular surface from irregular corneas Poor initial comfort and small diameter = prone to fall out Assessment Patient must understand concept and care of lens Keratometry used to measure curvature of cornea Slit lamp used to examine health of cornea, lids and tear film Then calculate refraction required • To be aware of the main contact lens complications Giant papillary conjunctivitis (GPC) Corneal abrasion & ulcers Corneal hypoxia Infective keratitis Neovascularisation Solution hypersensitivity • To understand the reasons for visual impairment in the young, employable and elderly age groups of patients. Children 5% of LVA patients are under 16 years old Main cause - Congenital cataracts Others - Optic atrophy (often secondary), Albinism, Buphthalmos, Myopia, RoP In other countries common causes mainly diseases. E.g. cataract, paediatric glaucoma. Adults 25% of LVA patients are in the employable age group Main Cause - Diabetic retinopathy Others – Myopia, Uveitis, Corneal dystrophies, Macular degenerations, Retinitis pigmentosa Elderly 70% of LVA patients are retired / elderly age group Main cause - Age related macular degeneration (dry / wet) Others – Glaucoma, Inoperable cataract, Diabetic retinopathy and maculopathies • To understand the relevant terminology / definitions relating to optometric refraction, contact lens types and Low vision devices. Visual impairment A person who is ‘substantially and permanently handicapped’ by defective vision caused through ‘congenital defect, illness or injury. General guidelines VA 3/60 to 6/60 Upto 6/24 with moderate fields contraction VA 6/18 or better if severe field loss Severe visual impairment A person ‘so blind that they are unable to perform work for which sight is essential’. ( National Assistance Act 1948 ) Guidelines VA less than 3/60 VA 3/60 to 6/60 and with constricted visual fields VA 6/60 to 6/24 but very constricted fields LVI RVI CVI • letter of visual impairment referral of visual impairment certificate of visual impairment To understand the relevance of information quoted to GPs via the GOS18 form and gain an understanding of the reasons for referral GOS18 Form used by Optometrists to relay information to the GP and hospital eye service (HES) Referral: sign of injury, disease or abnormality and treatment or further investigation required, or unsatisfactory level of VA even with corrective lenses. Referral implies transfer of responsibility to GP Information: screening and monitoring diabetics and patients with glaucoma Section 1: completed by optometrist Patients details Sight test details and acuities Disc appearance, IOPS and visual fields Points of interest Section 2: completed by GP Relevant clinical and social history BP, urinalysis, provisional diagnosis • To know the different types of low vision devices (e.g. hand magnifiers, stand magnifiers, telescopic aids etc) Electronic devices For children CCTV Bar magnifier Compact devices Dome ‘bright’ magnifier Software for PCs Bifocal spectacles with high adds for reading Voice activated devices Distance binoculars Screen / scanner readers Distance monoculars Braille keyboards For adults Non-optical devices Hand magnifiers HM Talking books/watches Stand Magnifiers SM Typoscopes Illuminated HM / SM Bump-ons High reading adds ie, strong reading glasses Illumination Binoculars/ monoculars Tinted lenses Spectacle mounted devices Kitchen aids Reverse contrast text Trauma • To assess a patient with ocular trauma. Examination Take a thorough history & record exactly what happened Measure the visual acuity (in chemical injury washout first) Examine the eye systematically from the outside lids to the retina, including pupil reactions Dilate pupils for fundal examination +/- radiological investigation Photograph for medicolegal purposes • Main causes of loss of vision due to trauma Corneal scarring & anterior segment damage from alkali burn Severe disrupted globe from penetrating injury Unrecognised intraoccular metallic foreign body causing siderosis bulbi Compressive optic neuropathy from retrobulbar haemorrhage Traumatic optic neuropathy from optic canal bony or shearing injuy • To understand the types of ocular injury that can be sustained & their management. Chemical Injury Immediate wash out, pH check with litmus, anaesthetic drops, irrigate for 5mins then pH, repeat until normal Check acuity, inspect eye though slit lamp Rx; antibiotics, vitamin c, cycloplegia and steroids Blunt Injuries Traumatic Hyphaema – blood in anterior chamber Traumatic Iritis – white cells in ant. Chamber (on slit lamp) + pain and photophobia Orbital haematoma • Eyelid echymosis, superficial lacerations cause bleeding, exclude perforation • Retrobulbar haemorrhage, sight threatening if untreated • Treat with canthotomy or cantholysis Retinal bruising – blurred vision / loss of central vision from rupture on macular Traumatic optic neuropathy – steroids and / or decompression Orbital floor fracture – soft tissue entrapment limits eye movements, causes diplopia Blow out fracture • Periocular bruising • Subcutaneous emphysema • Infraorbital anaesthesia/paraesthesia • Diplopia • Enophthamos • Radiological evidence of fracture and sequalae - muscle, soft tissue entrapment Sharp Injuries Urgent assessment, exploration and rule out perforating injury. Repair asap Superficial corneal injury Red photophobic watering painful eye Foreign body – remove with cotton bud or needle Abrasion – Pain, FB sensation. Stain with fluorescein and use slit lamp. Corneal foreign bodies History: grinding injury Examination: metallic FB, rust ring, ± anterior uveitis Removal:topical anaesthesia, antibiotics, cycloplegia Caution: penetrating injury, internal damage, subtarsal FB Acute Visual Loss and Retinal Disorders • To understand the causes of acute visual loss. Painless Vitreous haemorrhage Visual loss according to size of bleed; small bleed gives floaters, large bleeds cause gross loss of vision. Caused by; proliferative retinopathy (abnormal new vessels on retinal surface, which spontaneously rupture), retinal detachment, trauma, AMD Vascular Occlusion (see later) CVA and Migraine (acephalgic – no headache) Migraine – may see zigzag lines / scintillating scotoma with temporary loss of vision CVA affecting visual pathway Retinal Detachment PVD – Posterior Vitreous Detachment Posterior aspect of vitreous body separates from retina into vitreous. Can be due to trauma or spontaneous, especially in myopes S&S; Photopsia (flashing lights) from retinal traction. Floaters from haemorrhage into vitreous Rx; If tear, laser seal, if not reassure RD – Retinal Detatchment RPE and retina separate, normally due to fluid between them If due to full thickness tear of retina then rhegmatogenous vertical detatchment. If due to neoplasm or inflammation then exudative RD If from membranes growing in vitreous pulling on retina the tractional RD S&S; photopsia +/- floaters with gradual blurring of vision Rx; Urgent surgical re-attachment 6/52 left before retina completely dead. Painful Giant cell / Temporal Arteritis Inflammation of the lining of large & medium arteries S&S; Visual disturbance and headache in the elderly, anterior optic nerve occlusion, sudden visual loss, jaw claudication, myalgia, arthalgia. Can have temporal tenderness. Diagnosis by temporal artery biopsy, ESR & CRP will increase Rx; Prompt treatment with steroids can prevent permanent blindness. Optic Neuritis / Retrobulbar Neuritis Young adults, female>male, sudden visual change (washed out colours or loss of vision), eye pain esp. on movement Typical – idiopathic, MS Atypical – infectious / post infectious (viral), granulomatous, autoimmune, inflammation of orbit, sinuses or meniges Associated with recent viral illness or demyelination . Diagnosis – MRI for ‘light-up’ nerves and plaques Rx; Steroids but ONLY for bilateral, otherwise analgesia, and rest Idiopathic Infracranial Hypertension (benign) Usually overweight females (although can be in slim, and children) Usually causes progressive field loss but also sudden loss Transient visual obscuration and headache, uni / bilateral precipitated by movement Field loss and swollen disc, Often in obese females Must exclude thyroid and venous sinus thrombosis or space occupying lesion haemorrhage from pituitary tumour Rx; weight loss, remove meds (nsaids, tetracyclines etc.), acetozolamide treatment, can insert surgical shunt, or optic nerve sheath fenestration. Eyelids & Adnexal Diseases, • The conditions that lead to eyelid and adnexal infections. Acute Dacryocycstits Infection of the lacrimal sac Most common in adult females Present as watering eye with tender tear sac, may eventually form an abscess & burst Rx – surgical incision (canaliculotomy) and antibiotic Meibomian gland infection (meibomitis) Initially redness along line of gland when eyelid everted è Abscess with swelling & redness of whole eyelid è Can burst to skin or conjunctiva è Gland becomes distended & cystic with graulation è Cyst may then become infected Rx – local heat (steam), antibiotics, once cyst can surgically remove Stye Infection of the lash root Eyelid may swell and become painful, yellow point eventually forms Rx – hot steaming and gentle epilation, Abx if recurrent problematic Blepharitis Chronic inflammation of the lid margins (usually due to staphylococcal infection) Eyes become red rimmed with fine scale (similar to seborrhoeic dermatitis) Rx – avoid rubbing eyes, keep skin & scalp clean & dandruff free, topical Abx may help, local steroids help flare-ups Orbital cellulitis Deeper than the lids and much more serious Eyelid swelling, pyrexia, malaise, diplopia, visual loss – URGENT REFERRAL REQUIRED • To understand the term ‘ptosis’. Drooping of one upper lid In children is usually congenital In adults is either congenital or 3rd nerve palsy Causes Pseudoptosis – small eye, atrophic eye, lid retraction on other side Mechanical – inflammation, tumour or excess skin Myogenic – myasthenia gravis Neurogenic – horners syndrome, CN III palsy Drugs – guanethidine eye drops Congenital – look at photos, check FH Management Depends on cause Always exclude myasthenia gravis and corneal anaesthesia before considering surgery • To understand the symptoms & management of a dry eye Causes Systemic – sarcoidosis, rheumatoid arthritis (Sjogren’s syndrome) Trachoma (chlamydial conjunctivitis & keratitis) Neuroparalytic keratitis Exposure keretitis Old age Signs & Symptoms Sore, tender eye Microfilaments of mucous across eye visible with slitlamp Ix Schirmer’s Test Time taken for a strip of filter paper to wet (between globe & lower eyelid) Tear film break-up time Using slitlamp – time without blinking for tear film to break up Management Depends on the cause Artifical tear drops and ointments (for overnight use) are available • List the main drugs that can be used for dry eyes Tear substitutes Hypromellose: Cheap and effective in most simple cases of dry eye. Drops. Liquiflim: Contains polyvinyl alcohol, useful in Mucus deficiency states. Drops. Tears Naturale: if hypromellose not enough Viscotears. Available as liquid gel. Acetylcysteine. Mucolytic. May be combined with hypromellose. • To know eye lid conditions such as entropion, ectropion and trichiasis. Entropion In turning of the eyelid, common in elderly patients Causes soreness & irritation & can --> corneal scarring & loss of vision Managed by surgery Ectropion Out turning of the lower eyelid, common in elderly patients Causes overflow of tears & conjunctival infection --> rubbing --> worsening Managed by surgery Trichiasis Ingrowing eyelashes (although eyelids in correct position) May be due to trauma or chronic infection Lashes rub on the cornea --> irritation & 2o infection Can be treated by hair removal (although will grow back unless destroy roots) • To examine patients in the eye clinic with eye lid pathologies such as basal cell carcinoma or squamous cell carcinoma. Basal cell carcinoma Most common tumour of the lids (usually lower lid) Slight lump bleeds (--> central crust) with raised hard surround Invasive but only excise to avoid spread into bone Squamous cell carcinoma Resembles BCC and biopsy needed to differentiate Malignant melanoma Highly aggressive but rare Diseases of the Cornea and Conjunctiva • To distinguish the different causes of a red eye and know e.g. different features between a viral, chlamydial and bacterial conjunctivitis. Corneal ulcer / keratitis / abscess S&S; Red eye, Hx of contact lens, FB, cold sores or previous ulcer, photophobia + / - discharge, decreased acuity, pus Use fluorescein to reveal defect Rx; Corneal scrape, anti-retrovirals, NEVER steroids Infective conjunctivitis S&S; Red eye, itch, discharge, crusting, contact Hx, cervical lymphadepoathy Rx; C&S, chloramphenicol hourly 1/7 then qds 1/52 Beware Chlamydia and gonnorhoea as causes Allergic Conjunctivitis S&S; Itchy red eye, atopy, normal vision Rx; Antihistamine +/- steroids Pic – contact dermatitis from topical eye drops Perioccular skin is dry, red and flakey Viral Gritty eyes Watery discharge Follicles Lymphnodes Bacterial Gritty eyes Purulent discharge Lymphnodes Allergic Itchy eyes Stringy discharge Papillae No lymphnodes Sub Conjunctival Haemorrhage S&S; painless, ‘felt something pop’, Hx of coughing or straining. Ix: Check BP, glucose, FBC Causes by trauma, HT or blood dyscrasia (but commonly idiopathic. Sub conjunctival (right) - The edge of the haemorrhage is visible Retrobulbar haemorrhage (left) is red all the way across the sclera (cannot see the edge) Uveitis S&S; red, painful, photophobia, +/- Hx of autoimmune disease or infection, +/- blurring or floaters, decreased acuity, sluggish and or irregular pupils due to sphincter spasm or lens adhesions, raised IOP, circumcilliary redness Rx; topical steroids, cycloplegia and dialatation Episcleritis S&S; red eye, painless / dull mild pain, localised or diffuse, non-tender, no discharge, normal vision Rx; Voltarol +/- indomethacin Scleritis S&S; Painful, red, blurred vision , tender Rx; Non-necrotising – indomethacin Necrotising; Immunosupression Acute angle glaucoma (see glaucoma notes) • Sign Conjunctivitis Keratitis Uveitis Vision Redness Pupil Discharge Pain Normal Conjunctival Normal Yes Discomfort Imapaired Cilliary Constricted Yes Mod-severe Impaired Ciliary Constricted No Ache Acute Glaumcoma Poor Cilliary Dilated No Severe Understand the main drugs used to treat red eye Antibiotics Chloramphenicol - broad spectrum for use in routine conjunctivitis of bacterial origin / prophylaxis in viral cases & ocular trauma - May induce acute allergic reaction. Gentamicin/Soframycin/Norfloxacin/Neomycin/Ofloxacin - for use as alternative. Cefuroxime/Ciprofloxacin used for more severe infections of the cornea. Steroid treatment Modifies the inflammatory response. Topical treatment For anterior structures of the eye and lids. Uses: Blepharitis, vernal catarrh, anterior uveitis (iritis), chronic inflammatory corneal conditions Caution: Only if +ve diagnosis made Complications: Lowers immune response. NEVER use in simple dendritic corneal ulceration as may à worsening & perforation, delays epithelial healing, may increase IOP if susceptible, may cause sub-capsular cataracts Systemic treatment For inflammatory conditions of deeper structures Dangers: Usual systemic problems. Antiallergic agents Opticrom (Disodium Cromoglycate) - severe allergic conjunctivitis or vernal catarrh. Otrivine - Antistin (antihistamine & vasoconstrictor): for mild allergic conjunctivitis Cataracts • The term cataract and the ocular and systemic conditions that cause cataracts. Anatomy The lens is crystalline with an inner nucleus of older inactive cells and an outer cortex. The epithelium is metabolically active; It synthesises protein for lens fibres, transports amino acids and maintains a cation pump to keep the lens clear. At the equator of the lens epithelial cells differentiate into lens fibres (losing their organelles and ability for aerobic metabolism) Zonule filaments suspend the lens cilliary processes to the cilliary muscle. When the muscle contracts the filaments relax allowing the lens to become more convex, with a shorter focal length for reading. Cateract – opacity of the lens of the eye, which occurs when fluid gathers between the lens fibres. The refractive index alters causing light to scatter & vision becomes blurred. Causes of cateract Old age (commonest) Assoc with systemic disease (DM, uveitis, previous ocular surgery) Assoc with systemic medication (steroids, phenothiazines) Trauma & intra-occular foreign bodies Ionising radiation (X-ray), UV Congenital (dominant, sporadic or part of a syndrome, abnormal galactose metabolism, hypoglycaemia) Assoc with inherited abnormality (myotonic dystrophy, Marfan’s syndrome, Lowe’s syndrome, Rubella, high myopia Symptoms and Signs Decreased acuity, both near and distant, glare in sunshine / lights (esp with posterior subcapsular), monocular diplopia, altered colour vision (white and yellow). NO pain. Decreased red reflex +/- central black shadows, white pupil only in advanced cases. • The modern methods used to treat cataract. Treatment Glasses to increase acuity or surgery Surgery Small Incision (most common) – phacoemulsification; fragmentation and irrigation to remove old lens. Intra-occular lens implant inserted. Large Incision – removal of entire nucleus as one piece, cortex aspirated and a rigid or soft implant inserted. Implant power is based on individual needs, can get multi focal lenses now Glaucoma • The normal physiology of aqueous flow in the eye. Intraoccular pressue (IOP) is due to the production of aqueous humour by the cilliary body. Aqueous flows forward over the anterior surface of the lens, through the pupil and drains through the trabecular meshwork into Schlemm’s canal. The alternative uveoscleral pathway drains 10% of aqueous Normal Intra-Ocular Pressure (IOP) = 10-21mmHg (average 16mmHg) Sites of blockage 1. Cilliary block 2. Pupil block 3. Pre-trabecular (neovascular membrane or cellular debris) 4. Trabecular meshwork 5. Post-trabecular (elevated episcleral venous pressure) • The term ‘glaucoma’ and the impact of the disease on patients. Glaucoma - Multifactorial optic neuropathy with characteristic acquired loss of optic nerve fibres Due to increased intra-occular pressure damaging nerve cells (or by normal pressure in patients with vascular disease à occlusion of vessels à ischaemic damage à loss of nerve cells) • The effects of glaucoma on the optic disc and visual fields. The arcuate nerve fibres are most susceptible to damage and so are lost first à Notching of optic disc cup & field defects in the arcuate areas As the disease progresses the entire arcuate areas are lost à arcuate Scotoma The macular papilliary fibres are most resistant to damage and so the macula is the last area of vision to be lost Visual field defects do not tend to cross the horizontal midline Bayonet sign = as the cup increases the vessels become lost as they cross the rim of the disc • To learn about the different forms of glaucoma (acute and chronic). Many ways to divide up; Primary vs Secondary, open vs closed angle, acute and chronic, congenital, juvenile or adult, by IOP (normal tension or hypertensive) Acute angle-closure glaucoma AACG Acute high pressure eye. Risk factors – elderly, hypermetropes, family history Pathogenesis In dark room/environment pupil dilates (iris constricts) to allow more light in The bunching up of the iris causes the drainage angle to block & the iris edge to rest against the lens (more likely in hypermetropes as smaller eyes) = fixed mid dilated pupil The pupillary block prevents aqueous moving from anterior to posterior chambers à pressure builds up and the iris bulges outward This bulging blocks the the drainage angle further impairing draining into the trabecular system The pressure in the anterior chamber increases as fluid cannot drain à The corneal endothelium fails à Hydration of the cornea à clouding of the cornea & Vesicles form on the anterior cornea (very sensitive à pain à N&V The pressure impairs venous drainage on the sclera à red eye (congestion) Symptoms and signs; red eye and pain, blurred vision, halos around lights, headache nausea and vomiting Findings; reduced acuity, hazy cornea (due to corneal oedema), vertically dilated fixed pupil, very high IOP (>40mmHg), closed angle. Treatment Medical IV access – pain relief and antiemetic Intensive pilocarpine drops to constrict the pupil (to relieve pupillary block) Drugs (oral/IV) to reduce pressure (B-blocker, prostaglandin analogue) Carbonic anhydrase inhibitor (Acetazolamide) – decreases aqueous production Surgical Laser small holes into trabecular meshwork to improve drainage Laser iridotomy – provides alternative drainage point when pupil dilates Trabeculectomy – if no others work – cut a hole in the trabecular meshwork to drain aqeous to sclera (where it is then absorbed) If pressures still cant be controlled à cycloablation (kill cilliary body) Chronic Primary Open Angle Glaucoma – POAG Normal pressure (can be as low as 12-15 mmHg) Risk factors Family history, Hypertension, Hyperlipidaemia, Diabetes, Myopia, Black race Pathogenesis Exact mechanism unknown Thought to be due to poor/compromised blood supply to retina (as in DM or HT) being compromised further à ischaemic loss of nerve cells across retina à field defects Same changes to optic disc seen as nerve fibres are lost, no red eye as no congestion Will eventually à only central vision remaining = tunnel vision Symptoms & signs; Loss of central vision, peripheral field defects, ‘tunnel vision’ (late stage) Findings; Open angle, IOP 21-40mmHg, disc cupping, enlarged cup disc ratio, arcuate scotoma on fields analysis. Treatment No treatment / cure available Aspirin / clopidogrel / warfarin may help reduce further vascular compromise • To know the current methods to screen patients with glaucoma. Glaucoma Examination Acuity Occular examination (anterior segment and disc) IOP –tonometry, fields Gonioscopy (angle measurement) Screen if FH especially of primary open angle • To learn the different medical therapies to treat elevated intraocular pressure and the know the side-effects of these therapies. Class of agent Beta Blocker Example Timolol, betaxolol Method of action Decreases aqueous production Carbonic anhydrase inhibitor Prostaglandin analogue Acetazolamide, Dorzolamide, Latanoprost, travoprost Decreases aqueous production Increases uveoscleral outflow Alpha 1 agonist Bromonidine Miotic (parasypathomimetic) Pilocarpine (causes cyclotonia) Increases uveoscleral outflow Increases outflow through trabecular meshwork Side effect Bradycardia, bronchoconstriction, depression, impotence Malaise, depression, metallic taste Increases iris pigment, eyelash growth Allergy, dry mouth, fatigue Blurred vision, headache & eye ache Age related macular degeneration • The significance of age related macular degeneration and the effect on a patient’s vision. Commonest cause of central vision 14-25% in > 65s More common in Caucasians, very rare in darkly pigmented skin Initially causes change in visual perception (distortion) Later (in neovascular/wet AMD) the central vision is totally lost, with surrounding distortion and blurring This causes difficulty in reading words, recognising faces & with ADLs Risk Factors - smoking, genetics, age, antioxidant levels Assessment – near & distance visual acuity, reading speed, dilatation & fundosccopy. Photographs of fundus taken to monitor disease. Fluroscein will show up leaky vessels • The different types of age related macular degeneration and their fundal appearances DRY (Atrophic) 90% AMD, but 10-20% severe visual loss in AMD. Features Drusen - accumulation of membranous or lipophilic debris, with amorphous thickening of Bruch’s membrane RPE/Choroidal atrophy Pigmentary changes. à gradual death of the macula Treatment None available WET (Neovascular) 10% of AMD but 80-90% severe visual loss in AMD Features Soft Drusen develop & rupture Bruch’s membrane à neovascularisation from choroidal vessels below à fenestrated – so further exudates AND friable à haemorrhages à detatchment of the RPE or neurosensory retina à fibrovascular scar & loss of retinal tissue à distorted vision & irreversible loss Treatment Laser or PDT to prevent further neovascularisation 90% untreatable as over macula New antiVEGF factors being trialed Diabetic Retinopathy • The significance of diabetic retinopathy and the effect on a patient’s vision. Diabetes affects ~ 2% UK population Diabetics are > 25X than non-diabetics to become blind Most blindness associated with DM is preventable Diabetic retinopathy – commonest cause of VI & blindness in patients in working age (20-65yr olds) Retinal vasculopathy - affects precapillary arterioles, capillaries and venules Risk factors DM – Duration, poor control, pregnancy, renal impairment Age, Smoking, Hypertension, Hyperlipidaemia 2 types Non-proliferative DR (NPDR) or ‘Background’ DR (BGR) Proliferative (PDR) (Diabetic maculopathy is a special retinopathy that may occur with either NPDR or PDR) • The different types of diabetic retinopathy and their fundal appearances Background Retinopathy Normal vision Haemorrhages: dot(small), blot(large) from the venous end of retinal capillaries occur deep in the retina; flame shaped haemorrhages (located in nerve fibre layer) may occur Exudates: yellowish-white deposits with well defined edges; represent precipitation of leaked lipoproteins from diseased retinal vasculature Microaneursyms focal dilatations of retinal capillaries which may leak; usually temp to macula Pre-Proliferative Diabetic Retinopathy Normal vision unless mucula involved Occurs usually after >8-10 yrs dm May be mild, moderate or severe Ischaemia – over large areas Cotton wool spots (CWS): greyish white, poorly defined fluffy edged lesions in the nerve fibre layer; represent axoplasmic accumulations adjacent to retinal nerve fibre microinfarcts Venous changes – looping & dilation / beading (compensation for ischaemia) Arterial changes – arteriolar narrowing & AV nicking – due to atherosclerosis Severe NPDR - large number of dark haemorrhages, irregular calibre variation (beading) and dilatation of retinal veins, and intraretinal microvascular abnormalities. Most patients with severe NPDR will progress to PDR in 12 months Proliferative Diabetic Retinopathy Occurs in ~ 5% of DM (more common in type I) New vessels (NV) in response to significant retinal ischaemia The new vessels… Appear as small tufts of irregularly ramifying vasculature arising from veins Are initially flat but enlarge and move forward into the vitreous Are fragile and likely to bleed with slight traction resulting in pre-retinal and/or vitreous haemorrhage Late PDR changes Retinal fibrosis Traction retinal detachment Iris neovascularisation (rubeosis iridis) & neovascular glaucoma Diabetic Maculopathy Specific type of DR with macular involvement May occur with either NPDR or PDR but more common with type II Leads to visual loss if untreated 3 types which may occur in different combinations Focal: focal leakage from microaneurysms or dilated capillaries resulting in focal retinal thickening and surrounding exudates Diffuse: diffuse leak from dilated capillaries resulting in diffuse retinal oedema which may be associated with some retinal haemorrhages but usually no exudates Ischaemic: due to closure of the perifoveal capillary network; manifests as diffuse oedema plus associated dark haemorrhages. Fluorescein angiography is important in confirming ischaemia • The management of diabetic retinopathy Control of diabetes and other risk factors Reduces progression & severity of retinopathy PRP – PanRetinal Photocoagulation For proliferative DR, reduces vision loss due to bleed and detachment 1500 – 3000 tiny burns in peripheral retina, spares macula, reduced peripheral vision Macular Laser Focal laser – Destroy microanerysms, exudates will slowly resolve Grid Laser – For diffuse macular oedema, low powered laser stops worsening, no improvements, can cause scotoma Vitrectomy Removal of vitreous via trans-pars-plana incision (TPPV) Removes haemorrhage, stops detatchment Future: Anti-VEGFs etc • The features of other DM related eye disease Increased incidence of eyelid infections & cataracts Cranial nerve palsies: III, IV, VI Delayed healing of corneal abrasions; corneal ulcers More severe post-op intra-occular inflammation e.g. cataract surgery Abnormal wound healing