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Ophthalmic emergencies

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Presentation on theme: "Ophthalmic emergencies"— Presentation transcript:

1 Ophthalmic emergencies
Rahul Chakrabarti Ophthalmology HMO


3 Case 1: Sudden visual loss
70 yo female brought to emergency by neighbour. She reports that half an hour previously her vision in right eye has suddenly been lost. There has been no improvement since. The eye is not painful or red. Past ophthalmic history: early cataracts in both eyes. Past history: angina, hypertension. Both well controlled with medication.

4 Further history Moderate to severe headaches for previous 3 months
Chewing food produced ache in her jaw Scalp tenderness when brushing hair Felt generally unwell during this period of time

5 Examination Acuity : hand movements right eye, 6/9 left eye
Profound relative afferent pupillary defect Ophthalmoscopy of left eye normal Right optic disc abnormal Remainder of right retina normal


7 Giant cell arteritis 5-10% of all anterior ischaemic optic neuropathies 90% are “non-arteritic” ION Occlusive granulomatous vasculitis Untreated eventual loss of vision in both eyes Age 50 or older Clinical features Loss of vision Headache, scalp tenderness Jaw claudication Neck pain Weight loss/malaise/ night sweats Myalgia – association with polymyalgia rheumatica Double vision Short posterior ciliary artery vasculitis  ischaemic necrosis of optic nerve head

8 Signs Ix Reduced VA (<6/60) Relative afferent pupil defect
Field deficit Altitudinal loss Swollen, pale disc +- disc haemorrhages, cotton wool spots Superior + inferior optic disc swelling Tender, thickened, nodular temporal vessels/absent pulses CN 3/4/6 palsies Ix Elevated ESR (mean 70)/CRP Temporal artery biopsy Within 10 days of steroids

9 Treatment Prognosis Bottom line Immediate
Methylprednisolone 1g IV daily for 1-3 days Oral prednisolone 1-2mg/kg daily High dose steroid for months Side effect prophylaxis Prognosis Risk of second eye – 10% if treated, 95% if untreated Complications: TIA, CVA, neuropathies, thoracic artery aneurysms Bottom line Arrange urgent inflammatory markers Seek advice Safer to start treatment if any delay

10 Non-arteritic AION Insufficient circulation to crowded optic nerve  local oedema, compromised circulation Associations Diabetes, hypertension, disc morphology (small cup, crowded disc) Smoking, hyperlipidaemia, anaemia, OSA Mean age 60yo Acuity usually better than 6/60, altitudinal field loss common No associated symptoms ESR, CRP, platelets – normal Lower risk to other eye – 20% at 5 yrs Treatment No proven benefit anything in particular Aspirin 75mg / day Optimising risk factors

11 Case 2 : Sudden vision loss (2)
45 yo female referred from oncology unit with sudden, painless vision loss in her right eye. Progressive loss of upper vision in right eye Past history of metastatic lung carcinoma Past ophthalmic history – nil signifcant, but noticed blurred vision over past 8 weeks Painless visual loss No headache, jaw claudication, pain on EOM

12 Examination Acuity 6/6 right, light perception only left
Pupils equal and round RAPD present right eye Full range of extraocular motility

13 Bullous shifting exudative RD inferiorly
Subretinal amelanotic choroidal mass Vitreous clear

14 Retinal detachment Retina has 2 layers
Separation of neural retina from pigment epithelium due to fluid entering this potential space (sub-retinal space) Most cases are rhegmatogenous (tear/ hole in neural retina) Non rhegmatogenous Much less common Tractional: pulled off by membranes (eg proliferative DR) Exudative: breakdown of blood-retinal barrier (eg choroidal tumours, uveitis) Usually less extensive detachment Pathogenesis Vitreous is more firmly attached to retina in certain places Periphery Optic disc Bloood vessels

15 Rhegmatogenous retinal detachment
Commonest form of RD Due to vitreous liquefaction + break in retina Clinical features Flashes, floaters Peripheral field loss (early) Curtain-type field defect Loss of central vision (macula) Loss of red reflex Vitreous – PVD, vitreal pigment +/- blood Retinal breaks U-shaped, round holes Upper temporal quadrant in 60% Detached retina Looks grey, balloons forward Retinal blood vessels on the surface Unilateral convex, corrugated dome

16 Vitreous detachment Vitreous liquefies due to aging Collapse inwards
Floaters Traction on retina at points of firmer attachment Flashes Floaters – vitreous opacities 2 possible outcomes Posterior vitreous detachment (PVD) Retinal tear Fluid can then can access to sub-retinal space Retinal detachment Loss of visual field in this area Extension to macular = loss of central vision

17 Principles of management
Position patient so dependent fluid moves away from macula Urgent referral for surgery Relief of vitreoretinal traction Vitrectomy or indenting eye wall from outside (suture explant : scleral buckling) Augmented by injection of silicone oil or gas Closure of retinal break Drainage of subretinal fluid Needle puncture through sclera + choroid Adhesion of detached retina to RPE External cryotherapy or internal laser  inflammation of choroid + retina  adhesion of layers


19 Key points Flashes and floaters common
Most will be PVD Should have a dilated exam to exclude tears Check confrontation visual fields If loss more suspicious for detachment Urgent referral

20 Case 3: Acute red eye 64 year old male presents to emergency with red swollen, watery right eye for the past 2 days, but now sudden deterioration of vision. No significant medical history No past ophthalmic history Saw LMO yesterday Impression of viral conjunctivitis, Commenced chloramphenicol drops Minimal relief. Vision now much worse.

21 Further history Severe pain in the right eye since for last 3 hours
Associated frontal headache, malaise

22 Examination Visual acuity- counting fingers only in right eye, 6/6 in the left eye Right afferent pupillary defect Oval shaped pupil, fails to react to direct or consensual



25 Acute angle closure glaucoma
Differentials Iritis Conjunctivitis Acute corneal problems Fluorescein stain

26 Acute angle closure glaucoma (AACG)
Glaucoma – progressive optic neuropathy 1% over 40 yo, 3% over 70 yo Primary open angle glaucoma (POAG) – 1/3 Secondary glaucoma – 1/3 AACG Usually primary Risk factors Epidem: Age >40, female, Chinese, SE Asians Anatomical: Pupil block, crowding of AC angle  prevents access to trabecular meshwork

27 Clinical features of AACG
Pain (periocular, headache, abdominal) Blurred vision Haloes Nausea / vomit Ipsilateral Red eye Raised IOP (usually 50-80mmHg) Corneal oedema (hazy cornea) Diminished red reflex Fixed semi-dilated pupil Due to iris ischaemia Contralateral angle is narrow Bilateral shallow AC

28 Acute congestive angle-closure glaucoma
Signs Ciliary injection Complete angle closure Severe corneal oedema Dilated, unreactive, vertically oval pupil Shallow anterior chamber Treatment Topical anti-glaucoma drops Diamox Laser peripheral iridotomy

29 Approach to treatment of AACG
Immediate Systemic – acetazolamide 500mg IV stat (then 250mg oral, qid), analgesia, anti-emetic Carbonic anhydrase inhibitor – decreased aqueous production Ipsilateral eye B-blocker (eg timolol 0.5% stat, then bd) Decreased aqueous production Pilocarpine 2% (reverse the pupil block) Parasympathomimetics – ciliary contraction  opens trabecular meshwork Sympathomimetic (eg apraclonidine a2 agonist 1% stat)  decreased aqueous production + increased outflow Hourly IOP check Definitive management – Bilateral Nd-YAG Peripheral iridotomy B blockers – diminish function of ciliary epithelium


31 Case 4: The swollen, painful eye
21 year old female presents to emergency with increasing swelling and pain of the right eye region for past 10 days. Associated diplopia in up and left gaze Systemic symptoms: productive cough, fevers over this time No significant past medical or ophthalmic history B blockers – diminish function of ciliary epithelium


33 Examination Acuity – Right 6/18, left 6/6 Proptosis – 5mm on the right
No RAPD Pain on all movements of right eye Limitation of elevation, adduction right eye, with accompanying diplopia Anterior segment Dilated conjunctival vessels in right eye Normal left eye examination

34 Orbital vs Periorbital cellulitis
Orbital cellulitis = ophthalmic emergency S.pneumoniae, S.aureus, H influenzae Risk Fx: sinus disease, local infection, trauma (septal perforation), ENT/ ophthal surgery Hx: FEVER, MALAISE, PAINFUL, SWOLLEN orbit O/E: Swollen lids +- chemosis, Proptosis, Painful eye movements, Optic nerve function (VA, colour, RAPD) Complications: Local- keratopathy, raised IOP, CRVO, CRAO Systemic- orbital abscess, cavernous sinus thrombosis, meningitis, cerebral abscess!


36 Treatment of orbital cellulitis
Admit Vital signs FBE, Blood cultures CT- orbit and sinuses IV Fluclox 1g qid or Cefuroxime 1g tds PLUS Metronidazole 500mg tds Majority need drainage of collection – diagnostic and therapeutic


38 Periorbital cellulitis
Not an emergency, it’s not in the orbit! Similar organisms Much less severe Risk FX: local infection, URTIs Fx: fever, malaise, swollen lids, but no proptosis, pain on eye movement or optic nerve deficits INV: not necessary usually RX: oral fluclox 500mg qid for a week + metronidazole 400mg tds for a week

39 Case 5: Trauma A 26 year old male is brought to emergency late at night with sudden blurred vision and pain in the right eye after being assaulted. He states he was struck with a glass bottle to the right side of his face in an assault. Past medical and ophthalmic history are unremarkable.


41 Globe rupture Clinical Features Anterior rupture Posterior rupture
Herniating iris, oozing aqueous, vitreous, lens Severe subconjunctival haemorrhage hyphaema Posterior rupture Suspect if deep AC but low IOP compared to other eye


43 Treatment of Penetrating FB, Globe rupture
Prepare patient for urgent surgery Imaging Plain XR Ocular ultrasound Orbital + facial bone CT High risk of endophthalmitis Clear plastic shield Systemic ABx: Ciprofloxacin, po, 750mg bd Tetanus is required Take to theatre for primary repair

44 Potential problems Corneal abrasion Acute and chronic glaucoma
Traumatic cataract Vitreous haemorrhage Retinal damage Commotio retinae Choroidal rupture Orbital blow-out fracture

45 Orbital compartment syndrome
Globe and retrobulbar contents encased within a fascial cone, bound by 7 rigid bony walls Anteriorly – medial and lateral canthal tendons attach eyelids to orbital rim Small increases in orbital volume  forward movement of globe  rapid rise in orbital tissue pressure If intraorbital pressure > central retinal artery pressure  ischaemia Classically in retrobulbar haematoma (post op, trauma)

46 Symptoms of acute orbital compartment syndrome
Eye pain Diplopia Loss of visual acuity Reduced ocular motility Proptosis

47 Examination Proptosis Ecchymosis of eyelids Chemosis Ophthalmoplegia
Afferent pupillary defect Decreased fields Papilloedema Increased IOP Reduced acuity

48 Lateral canthotomy Perform lateral canthotomy, as follows.
Clean the area with sterile saline. Inject approximately 1 mL of lidocaine 1-2% with or without epinephrine into the lateral canthus. Apply a hemostat/clamp with one side anterior and one side posterior to the lateral canthus and advance until the rim of the bony orbit is felt. Clamp for seconds. Perform the lateral canthotomy by carefully cutting through the crushed, demarcated line to the orbital rim/lateral fornix to avoid traumatizing the orbit, as in the image below. Cantholysis is performed by identification and disinsertion of the inferior crus of the lateral canthal tendon, which should allow free mobility of the lower lid margin.

49 Orbital blow-out fractures
Floor (maxilla) > medial wall (ethmoid) Clinical features Soft tissue bruising/ oedema, surgical emphysema Enophthalmos Altered infra-orbital sensation Reduced ocular motility – vertical diplopia Investigation Facial XR CT (2mm coronal slices): prolapsed extraocular muscles, haemorrhage


51 Indications for surgical intervention in orbital floor fractures
Immediate Persistent oculocardiac reflex Young patient with white eye “trap-door’ fracture Significant facial asymmetry < 2 weeks Persistent symptomatic diplopia Significant enophthalmos Hypoglobus Progressive infra-orbital hypoaesthesia Decreased HR when traction on EOM / compression of eyeball Due to trigeminal afferents + vagus n synapse via afferents from trigeminal going to visceral motor nucleusof vagus n


53 Chemical injuries Alkalis- liquefactive necrosis – penetrate further than acids (coagulative necrosis) Alkalis pH 14 : NaOH, oven cleaners, drain cleaners, plaster, fertilisers Acids pH 1: H2SO4, battery fluid, toilet cleaning fluid, bleach (Na hypochlorite) Prognostic factors Agent, how much cornea is involved Limbal involvement Associated blunt trauma, thermal injury Complications Corneal opacification Conjunctival scarring Ectropion, corneal ulcers

54 Chemical injuries Hx Clinical Fx What, when, how much Wearing PPE
Sx: burning, itchy, gritty, vision loss Mx: did they irrigate it Clinical Fx Conjunctival injection or blanching Haemorrhage, corneal abrasions Corneal oedema Perilimbal ischaemia (blanched vessels) Raised IOP Hughes’ classification: Grades 1 to 4 1 is clear cornea, no limbal ischaemia, good prognosis 4 is opaque cornea, 50% limbal ischaemia, poor prognosis

55 Treatment of Chemical injuries
Immediate- copious irrigation (anything will do except acid/ alkali, water preferable!) Evert lids- remove particulate matter Admit px Topical Abx (preservative free chlorsig qid) Topical cycloplegia tds Topical lubricant (preserve free- celluvisc, 4/24 + paraffin nocte) Oral simple analgesia If raised IOP  acetazolamide 250mg, qid + timolol 0.5% bd

56 Tips from the bosses Test the VA with and without pinhole
Angle-closure glaucoma is uncommon If the patient’s pain does not disappear with anaesthetic drops, the cause is likely to be from deeper to the cornea Never start a patient on steroid drops without ophthalmology input

57 References jpg 2. 3. 4. 5. gr/614&page=GR_AG

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