ocular emergencies and urgencies...• axial myopia (> -3 d increases the danger 10 fold) •...

3/29/2016

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OCULAR URGENCIES AND

EMERGENCIESRosmary Sanchez O.D., M.B.A.

Common Urgencies and Emergencies

1. Trauma:1. Chemical burns

2. Open globe trauma

2. Infectious:1. Endophthalmitis

2. Orbital cellulitis

3. Neurological:1. Acute third nerve palsy (rule out intracranial aneurysm)

4. Glaucomatous:1. Angle closure glaucoma

5. Retinal:1. Macula on rhegmatogenous retinal detachment

6. Vascular:1. Central retinal artery occlusion2. Ischemic optic neuropathy

Case Presentation

• Splash of drano in right eye

about 15 min ago.

• Started washing eye since then

• Gross examination:

• Cornea: sloughing of epithelium,

edema

• Scattered limbal ischemia

• Why just a gross examination at

this point?

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Chemical Burns

• Range from mild epithelial defects to complete opacification and destruction of tissue

• Alkali injuries are typically more severe than acid injuries

• Incidence: 7.7 -18% of all ocular traumas

• > young males and > at work

• The severity of the a chemical injury depends on the chemical substance• pH• Volume

• Toxicity of the chemical (degree of penetration and cell injury)

• Duration of contact

Chemical Burns

• Alkali Burns

• Cause saponification of the fatty acids

in cell membrane.

• Subsequently, destruction of the

proteoglycan ground substance and

collagen fibers of the stromal matrix.

• Stronger alkali substances may

penetrate into the anterior chamber

in 15 minutes.

• Secondary conditions: glaucoma,

cataracts, and uveitis.

• Acid Burns

• Limited to superficial layers of the

cornea causing protein coagulation.

• Coagulated proteins can act as a

barrier to further acid penetration

• Hydrogen molecules damage the

ocular surface by altering the pH.

• Anions cause protein denaturation,

precipitation, and coagulation

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Chemical Burns

• Classification

• Modified Hughes/Roper Hall

classification

• Based on the degree of corneal

involvement

• Limbal ischemia

• Dua classification

• Limbal involvement (in clock hours)

• Percentage of conjunctival involvement

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Chemical Burns

• Immediate Management:

• Copious irrigation with sterile isotonic solution

until pH is neutral.

• Tap water, although hypotonic, is an appropriate

substitute.

• Instill topical anesthetic (proparacaine or lidocaine

4%) to facilitate irrigation and relieve pain.

• Irrigate under eyelids to remove chemical

residue completely.

• In cases of acid burns, debridement of

devitalized corneal epithelium should be done.

Chemical Burns• Medical Management:

• Inflammation: Steroid

• Pred-Forte every 1hr or Durezol every 2hrs then taper

• Recommended only for the acute phase

• Usage should be guarded and followed closely

• Infection:

• Broad spectrum antibiotic

• Pain:

• Cycloplegics, lubrication (preferred ointments and PF)

• Collagenase inhibitors:

• Topical acetylcysteine 10% or 20% every 4 hours

• Tetracyclines such as Doxycycline 50 mg BID

• High dose of ascorbic acid ~2g/day

• Bandage contact lens

• Amniotic membrane

• Surgical therapy:• Limbal stem cell transplantation

• Corneal transplantation

Case Presentation

Presentation:

• 102F fever.

• Painful eye movement, OS

• MHx: Previous sinusitis infection

• Restricted ocular motility, OS

• BCVA: 20/20 OD; 20/50 OS

• Chemosis

• Proptosis

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Orbital Cellulitis

Life threatening infection of the orbital

soft tissues behind the orbital septum

Orbital Cellulitis

Pathogenesis:• Extension from periorbital structures

• Paranasal sinus

• Face and eyelids

• Lacrimal sac (dacryocystitis)

• Teeth (dental infection)

• Extension of pre-septal cellulitis

• Exogenous causes:

• Trauma - within 72 hours of injury that penetrates the septum

• Surgery

• Endogenous causes:

• Bacteremia with septic embolization

• Intraorbital causes:

• Endohthalmitis

• dacryoadenitis

• Sinusitis:• H. influenzae (children)

• S. pneumoniae

• S. aureus

• Other streptococci

• Moraxella catarhalis

• Anaerobic

• Post trauma/Post-surgical• S. aureus

• Anaerobic

Orbital Cellulitis

• Presentation:

• Fever (102 F or greater)

• Painful eye movement

• Restricted ocular motility

• Decrease in vision

• Proptosis/globe displacement

• Raised intraocular pressure

• Eyelid edema (absence of eyelid crease)

• Conjunctival chemosis

• Severe malaise and headache

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Orbital Cellulitis

Complications:

• Subperiosteal/orbital abscess

• ONH damage and blindness

• Cavernous sinus thrombosis

• Meningitis

• Septicemia (blood infection)

• Death

• Prognosis depends on the organism

and the extent of disease at the time of

presentation

Case Presentation

• 65 yo Asian female

• Ocular pain

• Blurred vision in one eye

• Halos around lights

• With nausea and one episode of vomiting

• Headache

• BCVA: 20/20 OD, 20/50 OS

• IOP: 20 mmHg/63mmHg

• Mid-dilated OS pupil

• Closed angles, OS; narrowed angle, OD

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Acute Angle Closure Glaucoma

• Characterized by a rapid and large increase in the intraocular pressure (IOP), resulting from a sudden blockage of the trabecular meshwork by the iris.

Pathophysiology:

• Pupillary block• Excessive iris-lens apposition impedes the flow of

aqueous from PC to AC, elevating PC aqueous pressure

• Secondary forward bowing of peripheral iris results in occlusion of the TM

• Alternative mechanisms: Plateau iris, ciliary block.

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Risk Factors:

• Age > 40 yo (lens thickness, cataracts)

• Female gender (2x > male gender)

• Family history (first degree relatives)

• Hyperopic individuals

• Anterior chamber depth < 2.5mm

• Race: Inuit 5% > Asian 1.4% > White 0.6%

> Black 0.2%

• Certain medications e.g. Topamax


Acute Symptoms: Acute Signs:

• Ocular pain • Elevated IOP

• Blurred vision • Closed/narrow angle

• Haloes around lights • Corneal edema

• Nausea and vomiting • Conjunctival injection

• Headache (frontal or supraorbital)

• Mid dilated sluggish moving and irregularly shaped pupil

• Iris bombe (typically)

• Glaucomfecken and sectoral iris atrophy – indicators of previous episodes of AACG

• Optic nerve head damage


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Tests:

• Gonioscopy

• To examine the iridocorneal angle

• R/O other causes:

• Glaucomatocyclitic crisis, NV glaucoma, malignant glaucoma, angle mass, iridocorneal endothelial syndrome (ICE)

• Dynamic gonioscopy

• Reversible (appositional closure)

• Irreversible (synechial closure).

• A scan, ultrasound biomicroscopy, anterior

segment OCT


Treatment:

• Topical drops:

• Beta adrenergic antagonists

• Alpha2 adrenergic agonists

• CAI- topical and oral.

• Miotics 1-2% Pilocarpine after IOP starts to normalize

• Hyperosmotics

• Topical corticosteroids

• Globe compression and dynamic gonioscopy


Surgical Treatment:

• Laser peripheral iridotomy (LPI)

• If laser iridotomy cannot be performed:

• Surgical irdectomy

• Peripheral iris may be flattened with a laser iridoplasty

• Pupillary block may be relieved with a laser pupilloplasty.

The fellow eye shares the anatomic predisposition for

increased pupillary block.

• Recommended to do a peripheral iridotomy.

• 50% chance of developing an acute attack in the untreated fellow eye

within 5-10 years

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Case Presentation

Symptoms:

• Double vision (vertical and

horizontal)

• Severe ptosis, OD

• Ipsilateral frontal headache

• Dilated pupil, OD

• Down and out position, OD

Pupil Involving Third Nerve Palsy

Isolated CN3 palsy with pupil involvement should be considered an ophthalmic

and neurosurgical emergency (95-97% is caused by an aneurysm in PCA)

Pupil Involving Third Nerve Palsy

Imaging:

• Computed tomography angiography (CTA)

• Magnetic resonance angiography (MRA)

• Common catheter angiography (CCA)

Highly and equally sensitive in diagnosing of 95% of 3 mm intracranial aneurysm or larger

Early intervention can improve return of neural function and avoid a catastrophic rupture, which carries a significantly high rate of mortality

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• 54 yo female.

• Flashes of light and floaters since yesterday, OS

• Darkness over one half of visual field OS

• BCVA: 20/20 OD, OS

• Shaffer’s sign “tobacco dust” pigmented cells in

the vitreous

• And:

Case Presentation

Rhegmatogenous Retinal Detachment

• Full thickness retinal defect caused

by liquefied vitreous passing through

a retinal break into a potential

epithelioretinal interspace between

the sensory retina and the RPE.

• “rhegma” – break

• Most common retinal detachment


Risk Factors

• Posterior vitreous detachment

• Axial myopia (> -3 D increases the danger 10 fold)

• Surgery (Post cataract surgery or Yag laser capsulotomy)

• Lattice degeneration (Up to 30% of all RRD. )• The lifetime risk of RD in a patient with lattice is less than 1%.

• RD in one eye • Risk in 2nd eye is 5.8% (first year) and 10% within 4 years.

• Fam hx of RD

• Ocular trauma

• Genetic disorders: Marfans syndrome, sticklers syndrome

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• Small & peripheral:

• laser photocoagulation (or cryotherapy) around the break

• Takes 3 - 14 days for maximal retinal adhesion to be

achieved.

• Larger RRD:

• Vitrectomy

• Scleral buckle

• Pneumatic retinopexy

• CF6 or C3F8 “air/gas bubble” as a tamponade

• Silicon oil

Treatment depends upon the type and size of retinal

detachment:

Eye of a 72-yo woman shows normal yellowing of the

lens due to age-related nuclear sclerotic cataract

Same woman’s other eye shows a more severe

nuclear sclerotic cataract two years after vitrectomy.


Time frame for management:

• The status of the macula is the primary determinant of the emergency.

• If “Mac on” the repair should be performed within 24 hours.

• If “Mac-off” the repair is less critical and can be performed within 7 days.

Case Presentation

• 72 yo WM

• Sudden, severe, painless loss of

vision in right eye

• MHx: left carotid stent (3 weeks

ago)

• Meds: Plavix, Aspirin, Multivitamin

• BCVA:

• CF, OD

• 20/30, OS

• APD

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Central Retinal Artery Occlusion

Presentation:• Sudden, painless, monocular, severe loss of

vision.• May have had previous episodes of amaurosis fugax

• >50 years of age

• Vision acuity from 20/40 to CF

• Retinal appearance:• Opaque, edematous

• cherry red spot

• Narrowed retinal arterioles

• Pallor of ONH and sometimes disc edema.

• Later stages: optic nerve atrophy and neovascularization (controversial)


• Etiology:

• Arterial emboli (cholesterol, fibro-platelet, calcific)

• Thrombotic

• Arteritis: GCA, polyarteritis nodosa.

• Hypercoagulation disorders, collagen vascular, and

inflammatory disorders such as lupus.

• Ocular conditions associated with retinal arterial

obstruction (ONH drusen)

Embolus is the most common cause of

CRAO, accounting for over 2/3 of all

cases. The carotid artery and the heart

are the most common sources.


• Treatment:

• To dislodge the embolus:

• Ocular massage

• Artery dilation to up to 16% due to autoregulation

• Blood flow increase to up to 86%

• Then, lowering IOP

• Anterior chamber paracentesis

• IV acetazolamide

• Vasodilation (inhaling CO2)

• Intra-arterial thrombolysis

• Hyperbaric oxygen therapy

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Systemic evaluation:

• Cardiovascular evaluation

• Hyperviscosity evaluation

• Hypercoaguable evaluation

• Hemoglobinopathies

Vascular work up Suggested

Exclude arteritic cause ESR, CRP, CBC, and platelet

Common vascular

risks factors

Blood pressure

Fasting cholesterol and profile

Fasting blood sugar level

Investigating for

embolic sources

Duplex carotid ultrasound

Echocardiogram

Young patients (<50yo)

w/ no vascular risk

factors

Vasculitic screen (ANA, ENA, ANCA,

ACE)

Hypercoagulable screens

(antiphospholipid antibody, factor V

Leiden, protein C&S)

Myeloproliferative or sickle cell disease

(blood film)

Homocysteine

Systemic and ocular conditions related to retinal artery occlusions:

Systemic cardiovascular disease

HTN, DM, atheromatous disease, cardiovalvular diasease, bacterial endocarditis, myoxoma, arrythmias.

Coagulopathies:

Antiphospholipid antibodies, Protein C deficiency, Protein S deficiency, Antithrombin III deficiency, Elevation of platelet factor 4, Sickle cell anemia, Homocysteine.

Systemic vasculitis:

Polyarteritis nodosa, temporal arteritis, Kawasaki's syndrome, Wegener's granulomatosis, Susac's disease, systemic lupus erythematosus

Oncologic:

Metastatic tumors, leukemia, lymphoma

Infective diasease:

Syphilis, HIV

Trauma:

Direct ocular compression, penetrating injury, retrobulbar injection, orbital trauma, Purtscher's disease

Ocular conditions:

Preretinal arterial loops, optic nerve drusen, necrotizing herpetic retinitis, toxoplasmosis

Other causes:

Oral contraceptives, pregnancy, drug abuse, migraine


• The only true emergency would be if the patient comes within 97 min of the

event and to rule out giant cell arteritis in patients older than 50 years.

• If GCA: steroid therapy is recommended immediately and scheduled for temporal artery

biopsy.

• Otherwise, etiology evaluation is generally recommended as an outpatient basis.

• Time is tissue!!!

• Prognosis:

• Life expectancy: 5.5 years

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Case Presentation

• 78 yo WF

• Sudden and painless decrease in vision for 2 days, OD

• New onset of headaches for three days that gets worse

after combing hair

• Joint pain

• General malaise

• RAPD

• BCVA: 20/300 OD, 20/30 OS

• After DFE and HVF:

Arteritic Anterior Ischemic Optic Neuropathy

• Inflammatory and thrombotic involvement of the short posterior ciliary arteries (SPCA’s) with resultant optic nerve head occlusion and infarct of retina

• Caused by Giant cell arteritis (GCA)

• chronic medium and large sized arteries vasculitis that affect the superficial temporal arteries and ophthalmic arteries

• Approximately 0.5-27 cases per 100,000 people aged 70 years or older

• Incidence is higher for Caucasians and European descent

• Females 3x > males


Systemic presentation:

• Headaches • New onset headaches

• Most common systemic complaint

• Localized to the temporal side of the head

• Jaw claudication

• Scalp tenderness (combing hair)

• Night sweats

• Fever

• Arthralgia

• ≥ 60 yo• 90% of affected individuals >65 yo

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Ophthalmic presentation:

• Amaurosis fugax (30%)

• Visual field defect (commonly altitudinal)

• APD

• Pale swollen disc often with flame-shaped

hemorrhages

• Optic cupping and atrophy occur later as the edema

resolves


Management

• Laboratory testing:

• Erythrocyte sedimentation rate (ESR)

• ≥ 47 mm/h

• Normal in 13% of GCA patients

• C-reactive protein (CRP)

• ≥ 2.45 mg/dl

• CBC with differential = anemia of chronic inflammation

ESR + CRP 99% sensitivity, 97% specificity for

GCA


Treatment

• Systemic corticosteroids

• Immediate IV steroid therapy

• 2 weeks or until symptoms resolve and ESR, CRP normalize

• Slow taper of oral prednisone for ~ 24 months.

• Temporal artery biopsy (gold standard)

• Once visual loss occurs, it is rarely recovered.

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Case Presentation:

• Blowout Fracture

Case Presentation

• Penetrating Ocular Injury

Case Presentation

• Perforating Ocular Injury

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Risk Factors for Open Globe Trauma

Take Home Message

• Have a clear pre-determined plan of action

• Be prepared with an emergency kit:

• Litmus strips

• IOP lowering medications

• BP kit

• Thermometer for suspected cellulitis

• Fox shield and tape

• CPR responder pack

• Epinephrine pen

• Calm demeanor in the face of emergency is critical because patients feel

worse and loses confidence if the doctor appears anxious

Take Home Message

• Knowledge of local professionals who can help and know how to refer:

• Ophthalmologist with specialty

• Emergency room

• Internal medicine

• Neurology

• Radiology

• Infectious disease specialist

• Document, document, document

• If it is not in the chart, it was not done

• Appropriate follow up care

• Phone calls to patient as well as specialty doctors will enhance the quality of care

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LASIK Emergency - Presentation

• ER physician calls about 29 yo AF post op week #2 after LASIK OU with a 20/20

result OU whose 5 year old child had struck her in the eye with a “piece of metal”

• Vision on presentation: 20/CF at 2’

• Symptoms: significant pain and photophobia

LASIK Emergency – Physical Exam

• Corneal tissue appeared heaped up over visual axis

LASIK Emergency - Management

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LASIK Emergency – Follow Up

• Presentation 20/CF • Post reposition, cleaning, smoothing, and epithelial debridement

• 2 Days post op

• UCDVA 20/20

• PROMPT repositioning and smoothing critical to prevent permanent tissue folds

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ocular emergencies and urgencies...• axial myopia (> -3 d increases the danger 10 fold) •...

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