Ophthalmic emergencies.RC

Report
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
▫
▫
▫
▫
▫
▫
Conjunctival injection or blanching
Haemorrhage, corneal abrasions
Corneal oedema
Perilimbal ischaemia (blanched vessels)
Raised IOP
Hughes’ classification: Grades 1 to 4
• Clinical Fx
 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

similar documents