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Ophthlmolgy Henry Rocha (hr430@cam.ac.uk)A g e n d a RedFlag ANATOMY Basic anatomy and examination of the eye COMMON PRESENTATIONS: • SUDDEN VISION LOSS • GRADUAL VISION LOSS • RED EYE •TODAY, BUT NOTES GIVEN AT THE END OF SLIDES)Anatomy ANTERIOR POSTERIORE x a m in a tio n E• EyelidsSSESSMENT • Cornea • Pupilnctiva ADDITIONAL ASSESSMENTS • Visual Fields • Pupil response • Direct/indirect ophthalmoscopy • Fluorescein • Colour vision Su dden Vision oss ImeiteOphthorefAis<6/60VPainful p ti c Neuritis Hx:28 F, sudden painful LOV in the Reye. She also reports increased urinary frequency and urgency along with tingling down the L leg CAUSES: INVESTIGATIONS + MANAGEMENT: • Multiple Sclerosis – sensory loss, ataxia, spastic• Urgent referral to Eye Clinic + Neurology (within weakness +/- internuclear ophthalmoplegia 1W) • Diabetes • MRI of brain and orbits with gadolinium • Syphilis contrast FEATURES: • High-dose steroids • Unilateral decrease in VA over hours to days • Recovery usually takes 4-6 weeks • Dyschromatopsia • Pain worse on eye movement • 65% normal fundus • RAPD • VF defects – central scotoma, arcuate or altitudinal field defects Anterior Ischaemic Op tic Neuropathy (AION) Non- Arteritic arertc AION AIONArteritic A I O N CLUES IN HISTORY: • Female (>60 years old) • Unilateral throbbing headache • Jaw claudication and scalp tenderness • Systemically unwell • Sudden painful unilateral visual loss (VA < 6/60, high risk of fellow eye involvement) MANAGEMENT: • Immediate referral • ESR + CRP • Temporal arterybiopsy • High dose steroids ASAPNon-Arteritic A I O N CLUES IN HISTORY: • Sudden – NOT PAINFUL, unilateral dVA (>6/60) • VF defects – superior or inferior altitudinal defect • Look for vascular risk factors e.g. HTN, diabetes • Small crowded optic disc (small/absent optic cup) MANAGEMENT: • Urgent referral • Manage co-morbidities and treat underlying causeAqueous Fluid Production & Drainage Aqueous Fluid Production • Produced by the non- pigmented epithelium of the ciliary body Aqueous Fluid Drainage: • 90% is through the Trabecular Meshwork Pathway (TM → Schlemm’s Canal → episcleral veins) • Uveoscleral pathway (10%) – ignore for UKMLA SBA purposes cute Angle Closure G la u c o m a Hx:40 F, presents with a red L eye and significant nausea. She also reports a significant headache, blurry vision and photophobia. On examination, you note that her L pupil is dilated and does not respond to light. MANAGEMENT: • Immediate ophthalmology referral CLUES IN HISTORY: • Medical: No guidelines for initialmanagement • Sudden severe pain: may be ocular or but can lie patient supine + use glaucoma headache eyedrops + IV acetazolamide • Symptoms worse with mydriasis (pupil dilation • Surgical: Definitive management is eg. when in a dark room) BILATERAL laser peripheral iridotomy • Haloes around lights • Semi-dilated non-reacting pupil • Hard, red-eye • Hypermetropia – small eyeball • Systemic upsetCupto Dic RatioPainessRetinal Artery O cc lus io n (C R A O B R A O ) Hx:65M vasculopath presents with sudden LOV of L eye which came on suddenly 6 hours ago and is still ongoing. CLUES IN HISTORY: • Vasculopathic history – thrombus formation • History of smoking, GCA or vasculitis • History of amaurosis fugax • CRAO – RAPD, BRAO – typically no RAPD MANAGEMENT: BRAO • Immediate call with Ophthalmology • CRAO – ocular massage, AC paracentesis, IOP-lowering medications and rebreathing into paper bag(?) CRAO = central RAO; BRAO = branch RAO CRAORetinal Vein O c c lu s ion (CRVO/BRVO) Hx:60M vasculopath presents with sudden painlessLOV of L eye which came on suddenly 6 hours ago and is still ongoing CLUES IN HISTORY: • Sudden painless dVA • Vasculopathic history – thrombus formation • Hyperviscosity history – eg. thrombophilia etc. • ‘Blood and thunder’ or ‘stormy sunset’retina • Haemorrhages + cotton wool spots • Non-ischemic CRVO + BRVO – no RAPD • Ischemic CRVO – RAPD BRVO MANAGEMENT: • Urgent referral to ophthalmology within 1 week • Anti-VEGF or Ozurdex for macular oedema • Laser PRP for neovascularization – since ischemia drives neovascularization CRVOPapilloedema Hx:65M presents with a 2d history of transient visual loss. Upon further questioning he reports a month history of worsening headaches (worse in the morning/when coughing) CLUES IN HISTORY: MANAGEMENT: • Bilateral + painless visual loss – note headache • BP – rule out malignant hypertension is still painful • Immediate action • Enlarged blind spot • MRI + MR venography • Possible 6th nerve palsy • IIH – Acetazolamide + weight loss CAUSES: • IIH • SOL • Decreased CSF absorption/Increased CSF production • Look out for Cushing's triadWet Age-Related Macular Degeneration (10%) Hx:83M referred GP with a new-onset inability to see objects near to him, especially at night. On fundoscopy, the doctor notices well-demarcated red patches. PMHx of HTN and he is a life-long smoker CLUES IN HISTORY: • Painless + sudden dVA • Main risk factors: >75YO, smoking, HTN • Wavy lines = metamorphopsia (use Amsler Grid) • Red hue = vitreous haemorrhage • Visual hallucinations = Charles Bonnet syndrome MANAGEMENT: • Urgent Ophthalmology referral within 1 week • Anti-VEGF injections to reduce neovascularization • Laser photocoagulation may be considered • No preventative treatment and no cure G a du al Vision L o ss • Dry AgrelatedacuarDegenerain • ataacts • PrimaryOpenngeG aucoma(PAO G) • Retinopathy– DM TN+RO PD r yAge-Related Macular Degeneration (90%) Hx: 77M presents to GP because he cannot read the newspaper properly, especially at night time. Symptoms vary in intensity each day. The doctor performs a fundoscopy that shows the presence of small accumulations of extracellular material between layers of the eye. The examination is otherwise normal. He has no relevant past medical history and he is a life-long smoker. CLUES IN HISTORY: • Painless + gradual dVA • Main risk factors: >75YO, smoking, HTN • Wavy lines = metamorphopsia (use Amsler Grid) • Visual hallucinations = Charles Bonnet syndrome MANAGEMENT: • Urgent Ophthalmology referral within 1 week • Stop smoking + AREDS2 vitamin combination + can slow progress (no beta-carotene) • No preventative treatment and no cureCataracts Hx:83F is complaining of poor vision, which has been gradually progressing for the last few years. On examination, there are obvious cataracts in both eyes, but best corrected visual acuity is only slightly reduced at 6/9. She has no past ocular history. CLUES IN HISTORY: • Painless + gradual dVA • Can complain of loss of contrast, glare and haloes around lights • RF: smoking, age, trauma, diabetes, long-term steroids, metabolic diseases etc • Absent red reflex MANAGEMENT: • Refer for phacoemulsificationsurgery (if QoL is affected) rimary O p e n Angle G la u c o m a Hx:55YO, British Ghanian woman reports to her optometrist for a routine eye check and gets referred to ophthalmology with a cupped optic disc and increased IOP CLUES IN HISTORY: • Painless + gradual irreversible loss of vision • Insidious onset – often asymptomatic on Dx •age, genetics, HTN, DM, corticosteroidsmyopic, • Optic cup: disc ratio is important (>0.6-0.7) MANAGEMENT: • Refer to Ophthalmology for confirmation (tonometry, perimetry etc) • 360 degrees SLT for patients with IOP >=24mmHg • Medical – topical prostaglandin analogues (1 line) • Can add beta-blockers/carbonic anhydrase inhibitors etc • Surgery in refractory cases ypertensive Retinopathy Hx:57M +Hx of HTN has routine optometrist visit, gets referred due to retinal changes CLUES IN HISTORY: MANAGEMENT: • Asymptomatic – eventually loss of vision • Refer to Ophthalmology for confirmation • Lower BP iabetic Retinopathy Hx:57M +Hx of HTN and DM sees GP with gradual and painless loss of vision over the past year CLUES IN HISTORY: • Usually gradual + painless loss of vision • RFx = poor diabetic control, long DM duration, • Smoking, hyperlipidaemia, HTN MANAGEMENT: • Referrals: ⚬ BDR – annual screen GP/optometrist ⚬ NPDR – within 6 weeks ⚬ PDR – Urgent within 1 week • Control glucose + BP + lipid levels • NPDR - monitor • PDR – PRP laser +/-anti-VEGF injections etinopathy of Prematurity Hx:Premature infant – infant born before week 32, weight < 1500g, oxygen treatment MANAGEMENT: • Laser therapy • Cryotherapy – older therapy and being phased out • Anti-VEGF approved in the US etinitis Pigmentosa (RP) CLUES IN HISTORY: • Young, female with strong family history • Tunnel vision due to loss of peripheral retina • Reduced night vision initially and then full blindness – disease of rods (then cones) MANAGEMENT: • No specific treatment;using UV sunglasses may delay the start of symptoms R e dE ye ImmediaeOphthoreferralif painful • Conjunctivitis • Ep(Sclerts) • Keraits • Anterior veiis • Pre(Orbital)Cellulitis+dophthalmitis • Tau ma Conjunctivitis PURULENT DISCHARGE SEROUS DISCHARGE ITCHY VIRAL BACTERIAL ALLERGIC • Usually caused by • Usually caused by: Staph, Strep, H. • History of atopy and presents Adenovirus (80%) influenzae with watering eyes (bilateral) • Self-limiting • Neonates: Chlamydia, N. gonorrhea • Eyelid + conjunctival oedema • If purulent – take swab (chemosis) • Topical chloramphenicol (not if pregnant) • Antihistamines, if severe= topical steroids En tro p ion vs. E ctro p ion • Entropion and ectropire conditionsthat affect your eyelid • Entropion —eyelid turns iaues youryelahes torub ganstthecornea • Ectropion —eyelid turns out and does not touch your eye Keratitis, Epi(scleritis) andAnterior Uveitis PRESENTATION • Painful, photophobia, blurry • Painful, photophobia, • Episcleritis = mild discomfort vision, foreign body • Scleritis = very painful,possible blurry vision sensation VA loss • Ciliary injection • Possible hypopyon • Hypopyon • Corneal opacity (use fluorescein) Keratitis, Epi(scleritis) andAnterior Uveitis CAUSES • Pathogens = HSV/VZV, P. Many causes including: • Episcleritis = unknown • HLAB27 such as ANK aeruginosa, • Scleritis = RA/SLE SPON acanthamoeba • Inflammatory: Sarcoid + • Foreign body Bechet’s • Infectious: TB, VZV, Lyme Keratitis, Epi(scleritis) andAnterior Uveitis MANAGEMENT • Immediate referral • Topical 10% phenylephrine to differentiate • Immediate referral • No steroids for HSV episcleritis vs scleritis ⚬ Topical Cycloplegics • Episcleritis – coolcompresses+lubricants + oral + steroids NSAIDs • Scleritis – immediate referral for same-day assessment + oral NSAIDs + possible oral glucocorticoids if severe Orbital Inflammation PRE-ORBITAL CELLULITIS • Extends from skin infection/trauma ORBITAL CELLULITIS ENDOPHTHALMITIS • Swollen eyelid skin + erythema + low-grade fever • Extends from dental/sinus abscess • Normal vision + normal • Severe swelling of deeper tissue • Interior eye infection – Post Op/IVI EOM, no exophthalmos, no • Reduced vision + painful + proptosis, RAPD, • Staph <6 weeks; P. acnes >6 weeks RAPD colour desaturation • Pain + swelling + reduced vision • Refer to secondary care for • Immediate referral • Immediate referral assessment + PO Abx ⚬ IV Abx (cef + metro + fluclox) ⚬ Intravitreal Abx (flucloxacillin) Physical + Chemical Trauma SUBCONJUNCTIVAL CHEMICAL INJURY GLOBE RUPTURE HAEMORRHAGE • Painless + self limiting • Alkali worse than acid • Teardrop pupil • Often no sign of trauma • Wash your eye • Immediate referral • Look out for HTN/anticoag • Immediate referral ⚬ Surgery ⚬ Steriod +/-abxThank ou! D ip lop ia • Stabismus • Canialnervepasies • Myashe nagravs • Thyroidyed sease trabismus (squint) Ocularmisalignmentthatismostcommonlyfound in children(accommodativeesotropia) CLUES IN HISTORY: • Usually quite straightforward • Corneal light reflex can help to diagnose squint MANAGEMENT: • Glasses to correct refractive error • Patching normal eye – improves amblyopia (<7 years) • Surgery Cranial Nerve Palsies CN III: MR/IR/SR/IO CN VI: LR CNIV: SO • Down + out at rest (unable to • Turns in at rest • Diplopia looking down adduct eye) • Unable to abduct eye (stairs/books) • Complete ptosis • Ischaemia + trauma + • BOOT WOOG • Dilated pupil (if aneurysm) congenital • Congenital + trauma + • Ischaemia + PCA aneurysm ischaemia yasthenia G ra v is Hx:35F, periods of fatigue and limb weakness that is worse in the evenings, eyelids droop alternately, double vision, difficulty swallowing however her pupils are normal and reactive. CLUES IN HISTORY: • Ptosis, can get ocular movement palsies too • Multiple diagnostic tests – edrophonium test, repetitive nerve stimulation, anti-AChR • CT chest – thymic hyperplasia/ thymoma • FVC monitoring in crisis MANAGEMENT: • Pyridostigmine • Thymectomy • Crisis – IVIG/PEX + ventilation hyroid E y eDisease Hx:50 F, Hx of Graves disease presents with double vision and red swollen eyes which appear to be ‘popping out.’ She smokes 1 pack/day and has been doing so for the past 30Y CLUES IN HISTORY: • Orbital fibroblasts + anti-TSHR • RFx: smoking, females • Eyelid retraction + lid lag • Red eye + diplopia + restricted motility • Most common cause of exophthalmos MANAGEMENT: • CT/MRI (thickening of EOM bellies) • Stop smoking + topical lubricants • Euthyroid status • Surgery (orbital decompression)