common eye emergencies - .net framework

Common Eye

Emergencies

Ocular Trauma

Medical Ophthalmic

Emergencies

History of ocular trauma

• 1908-1913 Work-related

– 30 % IOFB ie metal chips from grinding

• WW1-WW2 Explosives, shrapnel etc

• 1950-1976 Road traffic accidents

– Windscreen injuries, seatbelt law

• 1987-dateSport, recreation

– Ice hockey, racket sports,

Impact

How many?

4500 admissions in the UK236 lead to loss of vision

50% injuries at home

Nature?

Blunt 80%Perforating 18%

IOFB 1%

Trauma

• Blunt

– Lid avulsion

– Periorbital haematoma

– Blow-out fractures

– Hyphaema

– Sphincter rupture

– Iridodialysis

– Retinal detachment

– Choroidal rupture

– Globe rupture

• Sharp

– Lid laceration

– Globe laceration or

perforation

• Intraocular foreign bodies

– Globe penetration

• Chemical burns

• Non accidental injury

Blunt injuries

• Mechanical waves are transmitted through the globe

• Damage can occur to all intraocular structures

Blunt injuries

• Mechanical waves are transmitted through the globe

• Damage can occur to all intraocular structures

Lid lacerations

• Check that the rest of the eye is OK

• Management:

– Lacerations crossing lid margin, medial canthus, lacrimal apparatus, levator complex or those associated with globe perforations should be referred to the ophthalmologist

– All other lacerations may repaired with 6/0 monofilament

– Remember tetanus

Periorbital haematomas

• Causes:

– Direct blow to orbital region

• Management: – Check for other ocular damage eg orbital floor fracture, globe

perforation, hyphaema, fundal examination

– If bony injury suspected X-Ray

– Cold compresses

– Analgesia

Periorbital haematoma

Blow-out fracture

• Causes:

– Direct blow to orbital region

• Symptoms:

– Orbital pain, pain on ocular movements, diplopia, paraesthesia over maxilla

• Signs:

– enophthalmos

– restricted eye movements

– bony tenderness

– surgical emphysema

– sensation over V2 distribution

Blow-out fracture

• Management:

– CT scan

– Refer to ophthalmology/max-fax

Blow-out fracture

Restriction in upgaze

Enophthalmos

Hyphaema

• Causes:

– Direct blow to the eye

• Symptoms:

– Blurred vision, watering, photophobia

• Signs:

– Blood in the anterior chamber

Hyphaema

• Management:

– rook for globe perforation

– refer to ophthalmology

– occasionally admitted

– bed rest

– topical steroids

– reduce intraocular pressure

– secondary bleeds may need surgical evacuation

Hyphaema

Sphincter rupture Iridodialysis

Ruptured globe

• Causes:

– High velocity injury, blunt or sharp

• Symptoms:

– Severe pain, loss of vision

• Signs:

– Subconjunctival haemorrhage, full thickness scleral and corneal

lacerations, prolapse of intraocular contents, reduced intraocular

pressure

Ruptured globe

• Management:

– Tetanus prophylaxis

– X-RAY

– Plastic shield

– Urgent ophthalmology referral

– 1’ repair: restores integrity of globe

– 2’ repair: attempt to restore function

Scleral laceration

Iris prolapse

Corneal perforation and cataract

Intraocular foreign bodies

Inert Toxic

Gold Platinum

Silver Glass Stone Plastic

Copper Thorn Twig Wood Soil Hair

follicle

Lead Zinc

Aluminium

Iron

Intraocular foreign bodies

• Causes:

– High velocity object

• Symptoms:

– Mild to moderate pain, vision may be unaffected

• Signs:

– May be minimal, entry site may not be obvious

• Management

– X ray

– Referral to ophthalmologist

• Systemic antibiotics (Ciprofloxacin)

• Referral to vitreoretinal surgeon

IOFB: iris hole IOFB: on retina

FB: subconjunctival

Chemical burns

• Causes:

– Alkalis: rapid penetration

– Acids: aggregate with proteins

• Symptoms:

– Pain, red, photophobia, blurred vision

• Signs:

– Epithelial loss, conjunctival injection and chemosis, limbal ischaemia, corneal clouding, uveitis

Chemical burns

• Management:

– Copious irrigation with 0.9%Na Cl for at least 30min or until neutral pH

– Referral to ophthalmologist

– Admission dependent on extent of burn

– Topical and oral vitamin C

– Cycloplegia, topical steroids and antibiotics

Substance Chemical pH

Common alkalis

Oven cleaning fluid Sodium hydroxide 14

Drain cleaning fluid Sodium hydroxide 14

Plaster Calcium hydroxide 14

Fertilizers (some) Ammonium hydroxide 13

Common acids

Battery fluid Sulphuric acid 1

Lavatory cleaner Sulphuric acid 1

Bleach Sodium hypochlorite 1

Pool cleaning fluid Sodium hypochlorite 1

Alkali burn

Non-accidental injury

• The problem

– 35% of serious eye injuries occur in children <12 yrs

– 4% of children attending eye casualty have been abused

–• Who?

– Most children are under 3 years of age

– Parents tend to be young, single, from poor social circumstances with a history of being abused

Non-accidental injury

• Mechanism

– Shaking

• Hallmark

– Injuries in different stages of healing eg retinal haemorrhages

• The consequence

– 15% will have permanent physical problems

– Virtually all abused children have permanent emotional problems

Non-accidental injury

Medical Emergencies

• Orbital cellulitis

• Microbial keratitis

• Endophthalmitis

• Corneal melts

• Acute anterior uveitis

• Acute angle closure glaucoma

• Central retinal artery occlusion

• Anterior ischaemic optic

neuropathy

• Giant cell arteritis

• Papilloedema

• Accelerated hypertension

• Eye Movement disorders

–Acute III nerve palsy

–VI nerve palsy

• Posterior vitreous detachment

• Retinal detachment

Orbital cellulitis

• Causes:

– Infection from neighbouring structures usually air sinuses

– Infection behind the orbital septum

• Symptoms:

– Frontal headaches, fevers, rigors, diplopia, loss of vision

• Signs:

– Pyrexia, lid swelling, proptosis, chemosis, limitation of ocular movements, optic nerve compression

• Complications:

– Blindness, intracranial abscesses

Orbital cellulitis

• Management:

– This is a potentially life threatening condition

– Admit for high dose intravenous antibiotics

– Urgent CT scan

– FBC, blood cultures

– ENT opinion

Orbital cellulitis

Microbial keratitis• Causes:

– Gram +ve and -ve organisms e.g. Pseudomonas, pneumococcus, Staph, E.coli, acanthamoeba

– Secondary to corneal injury eg foreign body, contact lenses, loose sutures or corneal anaesthesia / exposure

• Symptoms:

– Pain, red, discharge, photophobia, reduced vision

• Signs:

– Corneal epithelial defect, localised white infiltrate in the stroma, hypopyon

• Management:

– Refer to ophthalmologist for admission

– Corneal scrapes and intensive topical antibiotics

– Isolation cubicle

Microbial keratitis

Endophthalmitis• Causes:

– Post-operative (Staph sp., Strep sp.)

• Symptoms:

– Red, pain, reduced vision, usually 3-5 days post-op

• Signs:

– Conjunctival injection, anterior chamber activity, hypopyon,

vitritis, hazy view of the fundus

• Management:

– Urgent referral to ophthalmologist for admission

– Aqueous tap / vitreous biopsy and intravitreal antibiotics

– Intensive topical antibiotics

– Systemic antibiotics

Acute angle closure glaucoma• Causes:

– Hypermetropia, hypermature cataract

• Symptoms:

– Pain, reduced vision, haloes around lights, headache, nausea, vomiting

• Signs:

– Reduced vision, red eye, corneal oedema, mid-dilated pupil, closed drainage angle

• Management

– Refer to ophthalmologist

– Lower intraocular pressure

• Medical: Systemic acetazolamide, mannitol, topical pilocarpine and β-Blockers

• Laser: Nd-YAG iridotomy

• Surgical: Iridectomy

Acute angle closure glaucoma

Retinal Detachment• Causes

– Usually as a result of a retinal tear (rhegmatogenous)

• Posterior vitreous detachment

• Myopia

• Trauma

• Symptoms

– Flashes, floaters, shadow/curtain across vision, painless

• Signs

– Field defect, reduced central vision if detachment has reached macula, visible elevated retina

Retinal Detachment• Complications

– Can lead to complete blindness if untreated

– Once macula detached central vision is lost so the aim is to operate before this occurs

• Surgical management

– External approach (scleral buckle)

– Internal approach (vitrectomy)

Central retinal artery occlusion• Causes:

– Atheroma, embolus (carotid artery or cardiac), arteritis, raised intraocular pressure

• Symptoms:

– Preceding amaurosis, sudden, painless loss of vision or field defect

• Signs:

– Markedly reduced vision, relative afferent pupillary defect, whitening of the retina with cherry red spot, segmentation of retinal vessels, embolus

• Management:

– If within 12 hours, then immediate ocular massage, anterior chamber paracentesis, re-breathing into a paper bag

– If more than 12 hours, no immediate treatment

– ESR, CRP, (FBC)

– Aspirin

Central retinal artery occlusion

Branch retinal artery occlusion

Anterior ischaemic optic neuropathy• Causes:

– Arteritic (giant cell arteritis)

– Non-arteritic (arterio/atherosclerosis)

• Symptoms:

– Sudden, painless loss of vision

• Signs:

– Reduced visual acuity, altitudinal visual field defect, RAPD, pale swollen disc with fine haemorrhages (segmental), later optic atrophy

• Management:

– Exclude giant cell arteritis

• includes history, examination and investigations (ESR, CRP, FBC)

– Screen for hypertension and diabetes

Anterior ischaemic optic neuropathy

Anterior ischaemic optic neuropathy

Giant cell arteritis• Causes:

– Systemic vasculitis, over 60 age group

• Symptoms:

– Temporal headache, scalp tenderness, pain on chewing, general malaise, anorexia and weight loss, girdle pain stiffness and weakness, diplopia, sudden loss of vision

• Signs:

– Tender superficial temporal arteries, VI nerve palsy, anterior ischaemic optic neuropathy (70% chance other eye will get AION if untreated)

• Management:

– Raised ESR and CRP

– Admit

– Commence high dose steroids

– Temporal artery biopsy

Giant cell arteritis

Papilloedema• Raised intracranial pressure

– MUST EXCLUDE A SPACE OCCUPYING LESION

– Idiopathic intracranial hypertension

Accelerated hypertension

• Causes:

– Uncontrolled, undiagnosed systemic hypertension

• Symptoms:

– Asymptomatic, occipital headaches, blurred vision, transient

obscurations

• Signs:

– Cotton wool spots, haemorrhages, optic disc swelling,

hypertensive encephalopathy

Accelerated hypertension

• Management:

– Urgent admission

– In severe cases intravenous sodium nitroprusside

– In milder cases oral nifedipine or atenolol

– Look for secondary causes of hypertension eg renal artery

stenosis, phaeochromocytoma

Accelerated hypertension

Eye movement disorders

• Causes: – Brainstem disorders– Cranial nerve palsies– Hypertension, diabetes – Intracranial aneurysm or cavernous sinus lesion– Myasthenia gravis – Muscle disease

• Symptoms:– Diplopia (III= complicated, IV= vertical, VI= horizontal)– Others

• droopy eyelid, dilated pupil, neurological etc

Eye movement disorders

• Signs:

– IIIn: Partial or complete ptosis, limitation of ocular movements in all directions of gaze other than abduction, dilated pupil if compressive lesion, undilated if ischaemic

• IIIrd nerve palsy + dilated pupil = intracranial aneurysm

– IVn: Head tilt to one side, limitation of depression of the eye when looking down and in

– VIn: Limitation of abduction of affected eye

– Brainstem and muscle disease: Complicated eye movements

IIIn palsy

IIIn palsy

IIIn palsy

• Management:

– Full neurological examination, check BP and BM

– Refer to neurosurgeon, neurologist or ophthalmologist

• MRA, arterial clips

• Patch, fresnel prisms, botulinum toxin, surgery

Intracranial aneurysm

VIn Palsy