Ophthalmic emergencies.RC

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Ophthalmic emergencies

Rahul Chakrabarti

Ophthalmology HMO

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.

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

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

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

• Signs

▫ 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

• Treatment

▫ Immediate

 Methylprednisolone 1g IV daily for 1-3 days

 Oral prednisolone 1-2mg/kg daily

▫ High dose steroid for 12-24 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

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

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

Examination

• Acuity 6/6 right, light perception only left

• Pupils equal and round

• RAPD present right eye

• Full range of extraocular motility

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

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

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

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

• 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

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.

Further history

• Severe pain in the right eye since for last 3 hours

• Associated frontal headache, malaise

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

Acute angle closure glaucoma

• Differentials

▫ Iritis

▫ Conjunctivitis

▫ Acute corneal problems

 Fluorescein stain

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

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

Acute congestive angle-closure glaucoma

Signs

• Severe corneal oedema •

Ciliary injection

• Dilated, unreactive, vertically oval pupil

Shallow anterior chamber

Treatment Topical anti-glaucoma drops

Diamox

Laser peripheral iridotomy

• Complete angle closure

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

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

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

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!

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

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

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.

Globe rupture

• Clinical Features

▫ Anterior rupture

 Herniating iris, oozing aqueous, vitreous, lens

 Severe subconjunctival haemorrhage

 hyphaema

▫ Posterior rupture

 Suspect if deep AC but low IOP compared to other eye

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

Potential problems

• Corneal abrasion

• Acute and chronic glaucoma

• Traumatic cataract

• Vitreous haemorrhage

• Retinal damage

▫ Commotio retinae

▫ Choroidal rupture

• Orbital blow-out fracture

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)

Symptoms of acute orbital compartment syndrome

• Eye pain

• Diplopia

• Loss of visual acuity

• Reduced ocular motility

• Proptosis

Examination

• Proptosis

• Ecchymosis of eyelids

• Chemosis

• Ophthalmoplegia

• Afferent pupillary defect

• Decreased fields

• Papilloedema

• Increased IOP

• Reduced acuity

Lateral canthotomy

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

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

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

Chemical injuries

• Hx

▫ 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

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

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

References

• 1.http://img.medscape.com/pi/emed/ckb/neurology/113

4815-1162916-669.jpg

• 2. http://www.eyeatlas.com/box/310.htm

• 3. http://www.eyeatlas.com/box/315.htm

• 4. radiopaedia.org/cases/blowout-orbital-fracture

• 5.http://www.djo.harvard.edu/site.php?url=/physicians/ gr/614&page=GR_AG

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