Opthalmology Flashcards

Question

Corneal abrasion management

Answer 1

Topical anaesthetic drops (tetracaine, oxybuprocaine) interfere with Na ions entering nerve cells, reducing impulse generation and pain perception. WARN patient that it may sting on application and to let you know when the stinging stops. Usually wears off within 20 minutes - NOT prescribed as pain relief ONLY prescribed for eye examination as can slow corneal healing. Usually heals on its own, pain settles over 24-48 hours, take simple painkillers as needed Eye can feel gritty for several weeks Risk of eye infection - give chloramphenicol eye ointment QDS for 5 days (pull down lower eyelid and apply 1cm strip, blink to spread medication) Eye patch IF necessary for several hours Sunglasses might help photophobia and avoid touching/rubbing the eye AVOID contact lenses Lubricant eye drops PRN. Recurrent corneal erosion syndrome - treat as corneal abrasion but with long term eye lubricant use (eye drops and ointments) regular use at night, artificial tears throughout the day to provide a barrier between the lid and cornea preventing blister tearing/sticking. Continue for several months even once asymptomatic

Answer 2

Pathology: Foreign object becomes lodged under the eyelids or in the eye Rust rings - may form around foreign bodies that contain iron, typically those that are metallic. Salt in tears interacts with the Fe forming rust in the eye. The reaction begins within 2-4 hours of the foreign body embedding into the eye. Complete rust ring formation can be after 8 hours. The ring may persist even after foreign body removal, staining the cornea. Residual rust can also migrate to the surface within 24 hours usually. Aetiology: Fingernails, hairbrushes, dust particles, grit, accidental traumas, metals etc.

Answer 3

``` Foreign body sensation/foreign body still present Painful eye Red eye Watery Photophobia Rust rings ``` Investigation/diagnosis: Eye examination using topical anaesthetic (EVERT EYELID) - Snellens chart, appearance, movements, visual fields, PEARL size, fluorescein staining, slit lamp (abrasions), flip the eyelid!! Pupil, equal and reactive to light = PEARL

Answer 4

Management: Topical anaesthetic drops (tetracaine, oxybuprocaine) interfere with Na ions entering nerve cells, reducing impulse generation and pain perception. WARN patient that it may sting on application and to let you know when the stinging stops. Usually wears off within 20 minutes - NOT prescribed as pain relief ONLY prescribed for eye examination as can slow corneal healing. Once confirmed, moisten a cotton bud with saline drops and gently remove the foreign body with a cotton bud, sweeping from the conceal surface Only use a needle to remove if you have been trained and have appropriate magnification If unable to remove, apply eye patch and refer to ophthalmologist for removal It is likely you may cause corneal abrasion via removal techniques if the object is difficult to remove Referrals: Unable to remove foreign body Rust rings present Visual acuity or fields are affected (blurred vision or blind spots) Pupil concerns - unequal or unreactive to light Bleeding from eye or around eye Clear or bloody fluid coming from the eyeball

Answer 5

Background: Can be infectious or not Common condition, more frequent in those wearing contact lenses Bacterial keratitis is the most common form. Pathology: Inflammation of the cornea Aetiology: Noninfectious - eye injury, contact lenses, foreign body in eye, swimming with contact lenses Bacteria - pseudomonas aeruginosa and staph. Aureus are the most common causes, usually in people who improperly use contact lenses Fungi - fungal keratitis caused by aspergillus candida or fusarium, usually in people who improperly use contact lenses or from outdoor exposure Parasites - acanthamoeba in those with contacts (swimming lakes, wooded areas) Viral - herpes simplex virus, often progresses to keratitis from conjunctivitis Risk factors: Contact lenses

Answer 6

``` Red eye Pain and irritation Blurry or vision changes Photophobia Difficulty opening the eye Discharge +/- hypopyon (leukocyte collection at bottom of anterior chamber in severe cases) Round corneal infiltrate or ulceration Excessive tearing ``` acanthamoeba keratitis bacterial keratitis

Answer 7

Investigation/diagnosis: Scrape or test for underling culture Eye examination: Snellens chart, appearance, movements, visual fields, PEARL size, fluorescein staining, slit lamp (abrasions), flip the eyelid!! Pupil, equal and reactive to light = PEARL Management: Urgent referral to ophthalmology Can lead to corneal ulcers and destruction of the stroma leading to perforation Treat cause - antibiotics/antifungals/antivirals etc. Severe cases - corneal transplant

Answer 8

Background: Eye disorder leading to progressive damage of the optic nerve, loss of nerve tissue resulting in vision loss Most common form is primary open angle glaucoma Acute angle closure glaucoma - rare medical emergency, can cause vision loss within 24 hours, affects 1 in 1000 people in their lifetime. Can be acute or chronic. Types: Primary open angle glaucoma (chronic simple glaucoma) Acute angle closure glaucoma Secondary glaucoma Congenital glaucoma - rare but usually present at birth or develops shortly after. Caused by eye abnormality

Answer 9

Pathology: Primary open angle glaucoma - fluid pressure inside the eye increases, due to increased resistance through the trabecular meshwork in the eye, increasing pressure may cause damage to the optic nerve and causes a loss in nerve fibres Normal intraocular pressure is 10-21mmHg Advanced glaucoma leads to blindness Acute angle closure glaucoma - with age the lens becomes larger, pushing the iris forward and narrowing the space between the iris and cornea. As this angle narrows the fluid from the eye is blocked from the drainage system. This suddenly increases the intraocular pressure. Although the attack often only affects one eye, the other may be at risk as well. Aetiology: Secondary glaucoma - result of eye injury or underlying conditions such as uveitis Acute angle closure glaucoma - narrow drainage angle

Answer 10

Acute angle glaucoma - more common in those >40 YO often between 60-70 YOs. long sighted, women, southeast asian and inuit people. More likely to come on whilst pupils are dilated. Medications like eye drops, SSRIs, TCAs, ipratropium topiramate and ranitidine cause pupil dilation. ``` primary glaucoma: Family history (up to 10 fold) Age 60+ African and hispanic people Thin corneas Myopia (short sighted) Increased ocular pressure >21mmHg Possibly HTN/diabetes ```

Answer 11

Primary open angle glaucoma - develops slowly, asymptomatically until significant vision loss is reached, usually loss of peripheral vision (tunnel vision) and eventual loss of central vision Subacute or intermittent Acute closed angle glaucoma - intermittent attacks of burning, haloes without pain, attack may end when going into brighter rooms due to pupil constriction pulling the iris away from drainage channels. Attacks can last a few hours then symptoms improve. With each attack vision may be damaged further. ``` Acute angle closure glaucoma - blurred vision, haloes, coloured rings around lights, severe sudden pain in one eye, can radiate to severe headache, red eye, nausea and vomiting, generally unwell, hazy cornea, worsening symptoms. Hard eyeball Fixed pupil Dilated pupil Hazy cornea Circumcorneal erythema ```

Answer 12

Eye vision screening, routine or due to visual disturbance, visual fields test Fundoscopy - optic disc cupping, optic nerve health Ocular pressure estimate (non-contact tonometry, uses puff of air to measure corneal response) Goldmann applanation tonometry - gold standard for measuring ocular pressure. Device applies pressure to the cornea to determine intraocular pressure

Answer 13

Background: Characterised by double vision, sunken ocular globes, loss of sensation of the cheek and upper gums due to infraorbital nerve injury Two broad categories of blowout fractures - open door (large, displaced and comminuted) and trapdoor (linear, hinged and minimally displaced) Trapdoor fracture - Seen in children and young adults due to elasticity of the orbital floor. Fractures may be subtle and are associated with high risk of tissue entrapment The floor of the orbit is the most common portion to sustain fracture Pathology: The orbit holds the eye in place and protects the eyeball Following trauma, the muscles, fat and connective tissue can be bruised and displaced. If enough volume is lost from the orbit, the eye sinks back into the orbit (enophthalmos) causing cosmetic and functional concern If eye muscles are impacted by fracture then eye motility and possibly double vision is affected Children <7 years have thinner bones and have not fully developed the maxillary sinus, making them more likely to break the orbital bone as the floor bone. Trapdoor fracture - fracture of the orbital floor where the inferiorly displaced blowout fracture recoils back to its original position and potentially entraps contents of the orbit. Aetiology: Trauma to the eye/orbital region Risk factors: Children <7 YOs

Answer 14

Presentation: Most commonly bruising, tenderness and swelling around the eye Diplopia Cheek numbness, nose or teeth Disruption of smooth contour of orbital floor on palpation Reduced eye motility especially up and downward movements Air under skin around the eye Trapdoor fracture - pain with eye movements, N+V, diplopia Investigation/diagnosis: Eye examination - Snellens chart, appearance, movements, visual fields, PEARL size, fluorescein staining, slit lamp (abrasions), flip the eyelid!! Pupil, equal and reactive to light = PEARL

Answer 15

All patients need a follow up with ophthalmology within 1 week of fracture Advice to avoid blowing nose, can use nasal decongestants to prevent orbital emphysema. Most fractures heal spontaneously without significant consequence Surgery indicated if there is enophthalmos >2mm on imaging, diplopia on primary or inferior gaze, entrapment of extraocular muscles or fracture involving >50% of the orbital floor. Surgery is rarely performed immediately, can be safely postponed for up to 2 weeks if needed for swelling to subside. Usually provides permanent cure but sometimes provides only partial relief from diplopia or sunken eye.

Answer 16

Management: Treatment usually started if pressure is >24mmHg Eye drops to reduce intraocular pressure - topical prostaglandin analogue to increase aqueous outflow e.g. latanoprost or topical B blocker reducing aqueous secretion e.g. timolol Laser - stimulate biochemical change to improve outflow of fluid form the eye Surgery - trabeculectomy (channel ‘bleb’ is created from which fluid drains from the eye) Acute angle closure glaucoma Emergency referral to ophthalmology, do NOT cover with eyepatch or leave in darkened room, this dilates pupil and worsens symptoms, NICE first line - lie patient flat, head NOT supported by pillows as may relieve pressure Pilocarpine eye drops constricting pupils helping fluid drainage Acetazolamide orally 500mg, analgesia and antiemetic if needed Beta blocker and steroids to reduce fluid production and inflammation (timolol) Mannitol IV to reduce fluids. Once attack has ceases - preventative measures such as laser (peripheral iridotomy) to assist drainage or surgery (surgical iridectomy), often done for both eyes not just the symptomatic one Sometimes eye drops are needed longer term for intraocular pressure control

Answer 17

Grey thickened film across the lens is NOT a cataract - it is the corneal arcus and is not usually a cause for concern Formed from cholesterol deposits building up during ageing leading to the grey ish ring presentation around the iris Typically related to the slowdown in lipid metabolism as the patient ages, however, if presenting before age 40 could indicate more sinister pathology. Can indicate atherosclerosis, high cholesterol, hypertension and other conditions if in those under age 40 The condition itself is not harmful to vision or eye health but it is wise to get blood tests screening for cholesterol, LFTs, U+Es, and measure blood pressure

Answer 18

Background: Gradual progressive clouding and thickening of the lens of the eye Major cause of treatable blindness worldwide Usually an age related condition common in >65 YO most common in women Rarely it can be congenital (juvenile cataract) Cataracts can obscure other pathologies such as AMD or glaucoma Pathology: Eye lens is made mostly of water and protein fibres Clouding of vision occurs when lens proteins (crystallins) clump together, resulting in poor light refraction and therefore worsening sight Aetiology: Clumping of the crystallin proteins within the optic lens ``` Risk factors: Smoking Alcohol consumption Diabetes Steroid treatment UV exposure Poor nutrition and socio-economic status ```

Answer 19

Build up of brown-yellow pigment (lens proteins) Grey cloudy appearance on the PUPIL (NOT the iris) Decreased visual acuity - blurred vision Gradual painless loss of vision (rapid with diabetic cataracts) Difficulty reading Failure to recognise faces Problems watching TV Reduction in colour intensity Diplopia in one eye (advanced) Starbursts around lights, especially at night time Investigation/diagnosis: Eye examination - visual acuity, colour vision Loss of red reflex CN II exam

Answer 20

Ophthalmology referral for surgery based on level of visual impairment, how it affects their life, willingness to have surgery, comorbidity which may benefit from surgery, diabetic retinopathy, diplopia, change in colour perception or where complications (secondary glaucoma or uveitis) is likely. Faster referral - diabetics, colour vision damage Surgery is an intraocular lens implant (IOL) by LA/GA and is the only effective management, has low morbidity and mortality with high success rates One rare but serious complication of surgery is endophthalmitis - inflammation of the inner eye usually from infection, can lead to loss of vision or the eye itself. Treated with intravitreal antibiotics injected into the eye. Urgent referrals: Suspected AMD, particularly with vision distortion or rapid changes (diabetic retinopathy) Sinister pathology is suspected Vision loss is bilateral Pain or erythema in eye or additional visual symptoms e.g. flashes Rapid visual deterioration, progressive or new deterioration Mononuclear patients or those who already have poor vision in one eye. Any vision loss in the ‘good’ eye requires urgent assessment

Answer 21

Background: Onset <6 months Juvenile cataracts Has a risk of amblyopia (lazy eye) Pathology: Eye lens is made mostly of water and protein fibres Clouding of vision occurs when lens proteins (crystallins) clump together, resulting in poor light refraction and therefore worsening sight ``` Aetiology: Congenital infections (TORCH) ```

Answer 22

Presentation: Irregular/partially absent red reflex detected in initial screening (when shining light onto pupils they usually turn red but instead turn white/grey) Presence of leukocoria or white reflex in light or photos Investigation/diagnosis: Eye examination - CN II Screen for TORCH syndrome (congenital infections) - toxoplasmosis, other agents (syphilis, parvovirus, varicella zoster, zika virus), rubella, cytomegalovirus, herpes simplex Red reflex screening in neonates Management: Urgent referral within 4 weeks to ophthalmologist

Answer 23

Background: Abnormality of the coordinated movement of both eyes Congenital - onset <6 months of age or acquired from >6 months of age Exotropia - divergent squint, one eye turned out Esotropia - convergent squint, one eye turned in Hypertropia - upward turn Hypotropia - downward turn Paralytic squint - paralysis of CN III, IV and VI, direction of gaze does affect the size of the squint or presence of the squint. Non-paralytic squint - other cause, size of deviation does not vary with direction of gaze, usually congenital Convergent squint (esotropia) is most common in children, they have a risk of strabismic amblyopia from the brain suppressing deviated images and leading to the visual pathway not developing normally Divergent squint is more common in older children and has less risk of amblyopia Heteropia or manifest squint - slight tendency for gaze to deviate particularly when gazing in the distance or daydreaming. This is usually normal as perfect gaze alignment (orthophoria) is unusual Squint can be intermittent of persistent, most intermittent squints are accommodative in origin Pathology: For single vision, fine coordination of both eye movements is needed (CN III, IV and VI) Misalignment of the eyes results in the retinal image not in corresponding areas of both eyes which can cause diplopia (adults) and amblyopia (children)

Answer 24

Aetiology: Palsy/dysfunction in cranial nerves CN III, IV and/or VI Sometimes can be caused by disorder to the external ocular muscles Manifest squint - muscle strength inadequate to maintain alignment, stimulus to maintain alignment is weak (blurred vision) or problems with neurological pathways Risk factors: Disorders affecting the brain such as Down’s syndrome, hydrocephalus, space-occupying lesions, stroke, graves disease Trauma Presentation: Reduced visual acuity Diplopia Asthenopia (eye strain, fatigue or pain) particularly in the afternoon or end of the day Low school performance or issues Walking difficulties Manifest squint - one eye covered and movement of uncovered eye takes up fixation Latent squint (phoria) - one eye covered, no squint in the other eye, then covering is removed and there is movement of the previously covered eye abnormal red reflex - light shone into eye

Answer 25

Screening tests - corneal reflection (light reflex test; should fall centrally and symmetrically on each cornea, will be asymmetrical with squint), ocular alignment test Cover test Cover-uncover test Management: 3Os Optical - diagnosis and treatment (spectacles) or refractory erros (reduce risk of anisometropic amblyopia) Othoptic - patching the good eye encouraging use of the squint eye Operations - resection and recession of rectus muscles to correct alignment

Answer 26

Background: Age-related macular degeneration is one of the most common causes of blindness in the UK Can be wet (10%) or dry (90%) macular degeneration Wet AMD progresses more rapidly and carries a worse prognosis and often progresses to bilateral disease Pathology: The macula is located in the retina in the centre at the back of the eye globe. It contains a concentrated area of rods and cones called the fovea which is vital for central vision. It is made of four layers, the choroid (contains blood vessels), Bruch’s membrane, retinal pigment epithelium and then photoreceptors Degeneration and defective changes in the macula cause atrophy of the retinal pigment epithelium WET AMD - aberrant vessels grow from choroid into the neuro-sensory retina and leak, causing oedema and rapid loss of vision. DRY AMD - Drusen and degenerative changes at the macular (small yellow deposits of fatty proteins accumulating in the retina)

Answer 27

``` >50 YO Family history Smoking Caucasian Diet high in saturated fats (meats, butter, cheese) Overweight HTN ``` Presentation: Deteriorating central vision (loss of central fields) - scotoma (central patch of vision loss) Ophthalmoscopy - pigment, drusen +/- bleeding at the macula DRY AMD - Drusen and degenerative changes at the macular (small yellow deposits of fatty proteins accumulating in the retina) WET AMD - aberrant vessels grow from choroid into the neuro-sensory retina and leak, progresses rapidly Amsler grid - blurry, wavy lines, dim areas Atrophy of the retinal pigment epithelium

Answer 28

Investigation/diagnosis: Optical coherence tomography - scans retina and macula Slit lamp biomicroscopic fundus exam - specialist exam Ophthalmoscopy Fluorescein angiography - blood supply, oedema and neurovascularisatoin Visual exam using Amsler grid, snellen chart Management: Smoking cessation, vitamin supplements (C, E, Zinc) can slow progression Diet rich in green vegetables and fruits Wet AMD - anti-VEGF intravitreal injections (ranibizumab, bevacizumab, pegaptanib) once monthly Laser photocoagulation intravitreal steroid injections

Answer 29

Background: Can be with increasing age or cicatricial (trauma) Common in older adults, generally affecting the lower eyelid only but can affect the entire length of the eyelid if severe, usually only one segment sags away from the eye Pathology: Lower eyelid turned out due to natural loss of muscle tones and orbital fat in older age Excessive tearing can occur due to lack of proper drainage and tears may pool/overflow the eyelid constantly Sensitivity to light may occur due to the surface of the cornea being irritated Secondary infection due to the exposed conjunctiva can lead to keratitis Aetiology: Natural loss of muscle tone with age Risk factors: Increasing age

Answer 30

Presentation: Usually lower eyelid section or entire eyelid pulling downwards away from the eye, turning out to expose inner eyelid margins Watery or teary eyes Excessive dryness - gritty, sandy Irritating - stagnant tears or dryness causing irritation, burning and redness Sensitivity to light Infection or keratitis Investigation/diagnosis: Clinical diagnosis Eye exam ``` Management: Artificial tears Lubricating eye ointments Treating secondary infections Surgical correction PRN ```

Answer 31

Pathology: Eyelid turned inward, generally only the lower eyelid due to atrophic changes in the affected eyelid Exacerbated often by the inturning of eyelashes causing conjunctiva and corneal irritation Aetiology: Atrophic changes in lower lid retractors due to trachoma infection (common in africa, asia) Congenital Risk factors: Family history Living in africa or asia Presentation: Lower eyelid usually turned inwards, eyelashes inverted Reported irritation of the eye, redness, pain Foreign body sensation Corneal damage

Answer 32

Investigation/diagnosis: Clinical diagnosis Eye exam Management: Artificial tears Lubricating eye ointments to relieve irritation Surgery to correct eyelid - if left untreated can cause damage to the cornea, eye infections and vision loss

Answer 33

Pathology: The central retinal vein runs through the optic nerve and drains blood from the retina, there are four branches that converge to form the central retinal vein, blockage in one can cause problems in one area whereas blockage in the central vein causes drainage problems in the whole eyeball. Occlusion leads to venous stasis - increased viscosity, fluid and blood stagnate and leak from blood vessels into the retina tissue This forces the layers of the retina apart (serous retinal detachment) and affects the retinas ability to respond to light Aetiology: Thrombosis or external pressure on the retinal vein causing vessel occlusion External pressure due to hypertensive or sclerotic changes in the central retinal artery in the optic nerve head Occlusion of the central retinal vein at its exit from the eye by raised intraocular pressure (e.g. chronic glaucoma)

Answer 34

``` Risk factors: >60 YOs HTN Hypercholesterolaemia Raised eye pressure (glaucoma) Diabetes Smoking Thrombophilic disorders ``` Presentation: Leaking, swollen vessels, bleeding seen on fundoscopy Reduced vision in affected eye Unilateral painless loss of vision (unless complicated by glaucoma) May be asymptomatic if blockage is small

Answer 35

Investigation/diagnosis: Fundoscopy - flame and blot haemorrhages, optic disc oedema, macula oedema Bloods - FBC (LEUKAEMIA), ESR, serum glucose Blood pressure Eye exam - visual acuity Management: It is not possible to treat or remove occlusions in retinal veins, management focussed on minimising damage, reduce risk of further occlusion and treating complications anti-VEGF intraorbital injections stops abnormal blood vessels growing then leaking and bleeding into retina Steroids intraorbital injections (often repeated regularly) Panretinal photocoagulation PRP laser treatment sometimes used to branch retinal vein occlusions and can be helpful to central vision

Answer 36

Background: Ophthalmic emergency Occurs to 1 in 100,000 a year Pathology: Blockage of the blood flow through the central retinal artery which supplies blood to the retina Branch of the ophthalmic artery from the internal carotid Aetiology: Embolism/atherosclerosis is the most common cause Ophthalmic causes include severely raised intraocular pressure GCA - vasculitis affects the ophthalmic or central retinal artery reducing blood flow

Answer 37

``` Risk factors: Increasing age Family history Smoking Alcohol intake Diabetes HTN Poor diet Inactivity Obesity GCA ``` Presentation: Sudden, painless loss of vision Usually unilateral Relative afferent pupillary defect - pupil constricts more when light is shone into the other eye in comparison to when light is shone into the affected eye directly, as ischaemia means it does not detect the input as well Fundoscopy reveals a pale retina with attenuation of vessels and a cherry red spot

Answer 38

``` Investigation/diagnosis: Fundoscopy Clinical diagnosis Eye examination Bloods - ESR if GCA indicated Temporal artery biopsy if GCA indicated ``` Management: Emergency hospitalisation for specialist management Ocular massage Remove fluid from anterior chamber to reduce intraocular pressure Inhaling carbogen to dilate artery Sublingual isosorbide dinitrate Long term - manage reversible risk factors and secondary prevention of CVD

Answer 39

Background: Ophthalmic emergency Pathology: Separation of the neurosensory layer of the retina from the choroid layer, causing traction of the retina and potentially leading to retinal tearing Aetiology: Retinal tear allowing vitreous fluid to fill the space most commonly (rhegmatogenous) Fibrosis and proliferation leading to scar tissue pulling the retina off (traction) Accumulation of subretinal fluid leading to retinal detachment (serous) ``` Risk factors: Increased age Myopia - severe nearsightedness Proliferative diabetic retinopathy Severe HTN Family history Previous cataract surgery Ocular trauma ```

Answer 40

Sudden onset of floaters and flashes in vision Loss of vision (PAINLESS) Blurred and distorted vision Fundoscopy can show fluid under the retina, tear in retina or lines of detachment Investigations/diagnosis: Eye examination - visual acuity, visual field tests Fundoscopy Management: Same day referral to specialist, urgency dependent on clinical suspicion, changes in visual acuity, visual field loss or fundoscopy findings Cryotherapy or laser photocoagulation to achieve permanent adhesion between the retina and RPE. This prevents recurrence of fluid in 95% of cases and stops retinal detachment progression

Answer 41

Pathology: Inflammation of the optic nerve, in patients with MS often presents with acute demyelinating optic neuritis (ADON) ``` Aetiology/risk factors: MS - acute demyelinating optic neuritis (ADON) Diabetes Vitamin deficiency (B12) Syphilis ``` Presentation: Sudden painless loss of vision, varying severity over hours or days Eye pain, around the eye particularly with movement Impaired colour vision - Dyschromatopsia - reds appear less red, ‘red desaturation’ Uhthoff’s phenomenon - transient worsening of vision with increased body temperature

Answer 42

Investigation/diagnosis: MRI of brain and orbit Bloods - autoantibodies, HbA1c, syphilis serology, U+Es, vitamin B12, intrinsic factor Management: Refer to ophthalmologist or neurologist (asses risk of developing MS - look for demyelination) Recovery usually over 2-6 weeks however 38-50% of ADON develop MS within the next 15 years High dose methylprednisolone for 72 hours, then 1mg/kg daily for the next 11 days which may briefly delay onset of MS

Answer 43

Background: A syndrome or sign of a potentially more serious condition Pathology: Loss of axons and shrinkage of myelin leading to widening of the optic cup Aetiology/Risk factors: Increased intraocular pressure (glaucoma) Chronic papilloedema Ischaemia (retinal artery occlusion, GCA) Toxins (tobacco, methanol, lead, arsenic, quinine, carbon bisulfide) MS Syphilis External pressure on optic nerve (tumours, pagets disease of bone)

Answer 44

Presentation: Gradual loss of vision Pale optic disc Widening of optic cup Investigation/diagnosis: Eye examination Fundoscopy Bloods - autoantibodies, syphilis screening, inflammatory markers Review of medications and substances (smoking, alcohol, occupational exposure) Management: Treat underlying condition Optic atrophy related to optic neuritis may be limited using steroids Complication - visual loss Prognosis - irreversible condition, treatment aimed at limiting progression

Answer 45

Background: Diabetes is the most common cause of blindness in people under 65 YOs Blood vessels in the retina are damaged by prolonged exposure to hyperglycemia causing progressive deterioration in the health of the retina Nonproliferative - background/preproliferative retinopathy - does not include neovascularization Proliferative type - includes neovascularization Diabetic maculopathy is a separate condition and can coexist Pathology: Hyperglycemia leads to damage to the retinal small vessels and endothelial cells. Increased vascular permeability leads to leakage from the blood vessels, blot haemorrhages and the formation of hard exudates Hard exudates are yellow/white deposits of lipids in the retina Damage to blood vessel walls leads to microaneurysms and venous beading (where the walls of the veins are no longer straight and parallel - look like string of beads/sausages). Microaneurysms are where weakness in the wall causes small bulges. Damage to nerve fibres in the retina causes fluffy white patches to form on the retina called cotton wool spots Intraretinal microvascular abnormalities (IMRA) - dilated and tortuous capillaries in the retina act as a shunt between arterial and venous vessels Neovascularization - growth factors released in the retina causing development of new blood vessels Aetiology: Insulin resistance or lack of production (type I or II diabetes)

Answer 46

Nonproliferative - background/preproliferative retinopathy - mild (microaneurysms), moderate (microaneurysms, blot haemorrhages, hard exudates, cotton wool spots, venous bleeding), severe (blot haemorrhages + microaneurysms in 4 quadrants, venous beating in 2 quadrants, intraretinal microvascular abnormality in any quadrant) Proliferative type - neovascularization and vitreous haemorrhages Diabetic maculopathy - macular oedema and ischaemic maculopathy, hard exudates (waxy yellow lesions with distinct margins arranged in clumps or rings) Complications - retinal detachment, vitreous haemorrhage, rubeosis iridis (new blood vessel formation in the iris), optic neuropathy, cataracts

Answer 47

Investigation/diagnosis: Eye examination Fundoscopy Management: Laser photocoagulation anti-VEGF intravitreal injections (ranibizumab and bevacizumab) Vitreoretinal surgery (keyhole surgery on eye) for severe disease

Answer 48

Background: Damage to small blood vessels in the retina relating to systemic HTN Pathology: Increased blood pressure chronic or acute leads to increased intraocular pressure >21mmHg causing damage to the retinal blood vessels leading to leaking of vessels and oedema Aetiology: Chronic HTN Malignant HTN Risk factors: HTN

Answer 49

Grade 1 - changes of early HTN retinopathy are subtle with generalised arteriolar narrowing Grade 2 - development of areas of focal narrowing, compression of venules at sites of arteriovenous crossing (AV nipping/AV nicking) Grade 3 - development of features similar to those of diabetic retinopathy, retinal haemorrhages, hard exudates, cotton wool spots Grade 4 - all features of grade 3 + optic disc swelling, headache, eye pain, reduced visual acuity, FND Silver wiring or copper wiring - walls of the arterioles become thickened and sclerosed causing twisting and coiling of arteries Arteriovenous nipping - arterioles cause compression of veins where they cross. This is due to sclerosis and hardening of the arterioles and sclerosis Cotton wool spots - ischaemia and infarction in the retina causing nerve fibre damage Hard exudates - damaged blood vessels leaking lipids into the retina

Answer 50

``` Investigation/diagnosis: Eye exam Blood pressure Fundoscopy Keith-Wagener classification (grade 1-4) ``` Management: Focused on controlling blood pressure and reversible risk factors (smoking cessation, lipid levels, exercise and diet, alcohol reduction)

Answer 51

Background: Optic disc swelling is a general term usually referring to papilloedema secondary to raised intracranial pressures. Pathology: Depends on underlying cause ``` Aetiology/Risk factors: Intracranial space-occupying lesions (tumours) Sinus thrombosis Hydrocephalus Meningitis or encephalitis Optic neuritis (MS) Malignant HTN Uveitis ```

Answer 52

Optic disc margins are blurred Small haemorrhages may be present Signs of underlying pathology Investigation/diagnosis: Eye examination Vitals - BP, temperature, neck stiffness, Bloods - CRP, ESR, viral serology, cultures, G+S History for clinical diagnosis/red flags (headaches, neck stiffness etc.) CT/MRI scan

Answer 53

Find and treat underlying cause tumours surgery/chemotherapy etc. Raised intracranial pressure: Early involvement of neurosurgeon or neurologist Elevate head of bed to 30 degrees Correct hypotension with fluid resus (3% hypertonic saline to increase blood osmolality encouraging water movement into blood away from intracranial compartments) Hyperventilation inducing to lower ICP (induces hypocapnic vasoconstriction; causes PaCO2 decrease, leading to arterial vasoconstriction thus lowering cerebral blood flow, blood volume and ICP) Mannitol (might induce hypovolaemia; monitor serum osmolarity) or dexamethasone to reduce ICP (with tumours must discuss with senior before giving these) Avoid pyrexia, manage seizures (increases ICP) CSF drainage with intraventricular catheter and monitor ICP Analgesia and sedation - usually IV propofol, etomidate r midazolam with morphine/alfentanil Neuromuscular blockade to avoid further ICP increase from intrathoracic pressure increases

Answer 54

Background: Embryonal tumour of the retina Most common malignancy of the eye in children Onset is gradual between third month of pregnancy and 5 years of age Patients with bilateral disease are presumed to have the heritable form even though only 25% of patients have an affected parent 60% of patients have non-heritable form, normal life expectancy once eye cancer is cured. Hereditary form is associated with increased risk of non-ocular cancers particular Ewing’s sarcoma, olfactory neuroblastoma and osteosarcoma Increased risk of soft tissue and bone sarcomas persists for decades after retinoblastoma diagnosis Pathology: Cancer develops from cells with cancer-predisposing variants of Rb1 gene on chromosome 13 (recessive mutation) Aetiology: 40% cases are hereditary mutations on chromosome 13 on the b1 gene

Answer 55

Presentation: Abnormal pupil appearance - leukocoria (white pupillary reflex to light) Vision deterioration, red and irritated eye Faltered growth or delayed development Squint/strabismus Heritable disease - usually present before 12 months of age Nystagmus Family history Asymmetrical red eye reflex Eye enlargement Investigation/diagnosis: Eye examination Red reflex test by ophthalmoscope Genetic testing Bi-dimensional ocular USS and MRI (preferred over CT to avoid radiation exposure) Staging - groups A-E depending on tumour size and invasion

Answer 56

Referral urgently (2WW) for those with leukocoria, new squint or change in visual acuity, family history of retinoblastoma Royal london hospital and birmingham children’s hospital are UK centres for ophthalmology Photocoagulation for small tumours Cryotherapy Transpupillary thermotherapy Plaque radiotherapy Systemic chemotherapy, Periocular chemotherapy, ophthalmic artery chemotherapy External beam radiotherapy Enucleation as a last resort to prevent spreading Regular follow up needed depending on the case and specialist centre for several years after management - MRI screening every 6 months for 5 years (heritable disease) Those with known Rb1 gene should be screened every 3-4 weeks until 6 months of age then less frequently until age 3, clinical examination every 3-6 months until age 7 and eventually biennial for life

Answer 57

Background: AKA Graves’ orbitopathy Inflammation of the eye muscles, eyelids, tear glands, fatty tissue causing the eye to become uncomfortable, swollen, red and pushed forward (bulging) Around ¼ of people with Graves’ disease will develop thyroid eye disease Pathology: Autoimmune condition causing attack on surrounding eye tissue leading to inflammation around and behind the eye In most patients these autoantibodies also attack the thyroid gland causing Graves’ disease Aetiology: Autoimmune condition Risk factors: Graves’ disease Smoking - double risk increase for those with Graves’ disease

Answer 58

Eyes are protruding forward Red, swollen eyes Reportedly uncomfortable eyes, feeling of foreign bodies or gritty Photophobia New bags under eyes Pain in or behind the eye especially when moving eyes Difficulty moving eyes Rare - vision changes (diplopia or reduced vision) Investigation/diagnosis: Bloods - autoantibodies, TFTs, U+Es Thyroid examination eye examination

Answer 59

Smoking cessation Liquid tears and eye lubricant drops for symptoms Symptoms tend to worsen for the first 6-12 months but then stabilize If symptoms are severe then steroid or immunosuppressive intraocular injections can be given Control hyperthyroidism 6 month course of selenium supplements 100mcg BD (mild cases) can but OTC Decompression surgery, eye muscle or eyelid surgery for extreme cases with pressure on the optic nerve or visual disturbances Prisms on spectacles can help diplopia for those not eligible for surgery

Answer 60

Background: Rare condition resulting from disruption of the sympathetic nerves supplying the eye Triad of ptosis, miosis and hemifacial anhidrosis Congenital horner syndrome is associated with heterochromia (different colour iris on affected side) Pathology: Depends on underlying cause Sympathetic nerves arise from the spinal cord in the thorax (preganglionic) and enter into the sympathetic ganglion at the base of the neck and exit as post ganglionic nerves which travel into the head, running alongside the internal carotid artery Aetiology: Central lesions - 4Ss: Stroke, multiple Sclerosis, Swelling/tumours, Syringomyelia (cyst in the spinal cord) Preganglionic lesions - 4Ts: Tumour (pancoast tumour), Trauma, Thyroidectomy, Top rib (cervical rib misplaced) Postganglionic lesion - 4Cs: Carotid aneurysm, Carotid artery dissection, Cavernous sinus thrombosis, Cluster headache

Answer 61

``` Presentation: Ptosis Miosis Hemifacial anhidrosis Enophthalmos (sunken eye) ``` Investigation/diagnosis: CXR CT/MRI of head Cocaine eye drops (stops noradrenaline reuptake at NMJ) - normally cause pupil dilation, but will NOT in horner syndrome (apraclonidine alternative) Management: Diagnosis and management of underlying condition

Answer 62

Pathology: CN III, oculomotor nerve supplies all extraocular muscles aside from the lateral rectus and superior oblique and it supplies the levator palpebrae superioris muscle, responsible for lifting the eyelid When there is a palsy or lesion in CN III the muscles stop receiving signals from the nerve, causing the eye to turn outwards and downwards as only the lateral rectus and superior oblique are still functioning without resistance from other muscles. It also causes ptosis from lack of palpebrae superioris muscle action CN III also contains parasympathetic fibres innervating the sphincter muscles of the iris therefore palsy causes fixed dilated pupils as well. ``` Aetiology: Cavernous sinus thrombosis Posterior communicating artery aneurysm Idiopathic Tumour Raised intracranial pressure Sparing of the pupil suggests microvascular cause - diabetes, HTN or ischaemia ```

Answer 63

Presentation: Ptosis Dilated, non-reactive pupil Divergent strabismus in the AFFECTED eye causing DOWN and OUT positioning ``` Investigation/diagnosis: Eye examination - movements limited Bloods - tumour markers, FBC, iron studies, HbA1C Blood pressure CT/MRI - thrombosis or aneurysm, tumours ``` Management: Identify underlying cause and manage appropriately Most CN III palsies caused by vascular conditions like diabetes may recover completely Maximum improvement usually occurs during the first 6 months after onset but can occur up to 18 months after onset Congenital third nerve palsy is unlikely to resolve spontaneously

Answer 64

Background: Benign condition Unilateral dilated pupil that is sluggish to react to light, has slow dilation of the pupil following constriction. Holmes-adie syndrome is where the holmes-adie pupils are present with absent ankle and knee reflexes Most common in younger women 30-40 YOs Pathology: Damage to the postganglionic parasympathetic fibres Holme-adie syndrome also involves autonomic nerve dysfunction Aetiology: Unknown but may be viral

Answer 65

Presentation: Unilateral dilated pupil that is sluggish to react to light, has slow dilation of the pupil following constriction. Absent ankle and knee reflexes 80% unilateral pupil abnormality Pupil constricted for prolonged amount of time (tonic pupil) Over months-years pupil size diminishes eventually becoming mitotic Investigation/diagnosis: Eye examination - light, accommodation, visual fields, eye movements Management: Corrective spectacles can be prescribed and no other treatment is usually needed Infants <1 YO refer to paediatric neurologist to rule out familial dystonias

Answer 66

Specific finding on neurosyphilis. A constricted pupil that accommodates when focussing on near objects but does NOT react to light. Often irregular shaped, commonly called prostitutes pupil

Answer 67

Pathology: Collection of blood pooling inside the anterior chamber of the eye May cover the iris and pupil, blocking vision partially or completely Vision problems can become permanent if not treated ``` Aetiology: Trauma to eye Increased intraocular pressure Sickle cell anaemia Hemophilia Cancer Abnormal vessels on iris Herpes zoster infection ```

Answer 68

``` Presentation: Painful eye Visual impairment Visible blood in anterior chamber Photophobia Blurry, clouded or blocked vision ``` ``` Investigation/diagnosis: Eye examination Fundoscopy Eye pressure (tonometer) Slit lamp examination CT scan if orbital fracture suspected ``` Management: Mild - self resolving in around one week, take OTC pain medication AVOID aspirin (can increase bleeding risk) Steroid eye drops to limit inflammation Dilating drops to ease pain and encourage drainage Patch over affected eye - encourage dilation Bed rest, head elevated to 40 degrees when sleeping Daily eye pressure monitoring

Answer 69

Background: Myasthenia gravis - autoimmune condition lambert-Eaton myasthenic syndrome (LEMS) - rare autoimmune condition Eye muscle weakness is uncommon in LEMS but more common in myasthenia gravis They are separate autoimmune conditions both where damage to the NMJ occurs and can present slightly similarly Pathology: Autoantibodies attack the NMJ, affecting communication between nerve and muscle cells Causes muscle weakening over time as they receive less and less stimuli Predominantly affects voluntary muscles but involuntary muscles such as eye responses can also be affected Aetiology: Autoimmune disease

Answer 70

``` Presentation: History of LEMS - limb weakness especially with voluntary muscle use Ptosis Diplopia Reduced vision Dry eyes Abnormal eye movements Strabismus Pupillary dysfunction Blurry vision causing headaches ``` Investigation/diagnosis: Eye examination Clinical diagnosis Management: Lubricating eye drops/ointments Corrective spectacles for squints or pupillary dysfunctions Treatment of autoimmune conditions.

Answer 71

CN III - oculomotor nerve Responsible for all extraocular muscles of the eye aside from lateral rectus and superior oblique muscles Also has parasympathetic fibres to ciliary and pupillary sphincter muscles, controlling accommodation reflex Dysfunction: unable to move eye up/down/side to side (DYSCONJUGATE GAZE); ptosis uni or bilateral; loss of accommodation reflex

Answer 72

CN IV - trochlear nerve Responsible for superior oblique extraocular muscle Dysfunction: loss of downward and inner eye movement (DYSCONJUGATE GAZE) (same tests as III oculomotor)

Answer 73

CN VI - abducens nerve Responsible for lateral rectus extraocular muscle Dysfunction: loss of lateral outward eye movement (DYSCONJUGATE GAZE)