FEU-NRMF MD2022

OPHTHALMOLOGY – OCULAR EMERGENCIES

Lecturer: Dr. Jesus F. Marin (November 2020) INSTRUMENTATION
References: Lecture Video + PPT 2020; Manual; PARBS
[no proofreading use at your own risk!]

PRESENTATIONS OF OCULAR EMERGENCIES

Emergency Referral

Instruments for: illumination, magnification, and spreading the lids outwards

Acute/Symptomatic White/Externally
Red Eye Non-Seeing Eye OCULAR EMERGENCIES
TRUE EMERGENCIES
Common conditions presenting with a red congested eye:
Intervention is critical within minutes:
- Ocular Infection, Inflammation, Acute Angle Closure Glaucoma,
1. Chemical burns of the globe
and Trauma
2. Central Retinal Artery Occlusion

THE ACUTE RED EYE

URGENT CONDITIONS
• Infection
Intervention is need within one to several hours:
• Inflammation 1. Acute Angle Closure Glaucoma
• Glaucoma 2. Endophthalmitis
• Trauma – Blunt or Penetrating/Perforating 3. Penetrating Injuries of the Globe

ACUTE RED EYE: DIFFERENTIAL DIAGNOSES SEMI-URGENT CONDITIONS

Summary of the distinguishing features of 3 of the more common causes of Intervention can be effectively administered within days or even a week:
red eye: 1. Acute Exophthalmos
Conjunctivitis Iritis/Uveitis Glaucoma 2. Retinal detachment endangering the macula
Injection Superficial Ciliary Ciliary 3. Blow-out Fracture of the orbit
Discharge Mucoid, Purulent Serous Serous 4. Optic Neuritis
Cornea/AC (+) Infiltrates (+) Flare/Cells Bedewed 5. Ocular Tumors (e.g. Retinoblastoma)
Pupils Normal Constricted Mid-dilated
IOP Normal Low High TRUE OCULAR EMERGENCIES
Vision Normal Decreased/ Decreased/ ARTERIAL OCCLUSIVE DISEASE
Moderate Severe

BASIC INFORMATION
Elicited medical history will commonly bring to light conditions that can produce
the clinical signs and symptoms:
▪ Demographic Data ▪ Medical/Surgical History
▪ Chief Complaint ▪ Medications/Allergy
▪ Evolution of illness (laterality, duration & tempo, mechanism of
injury, associated s/sx) Common Presentation: OVERALL PALLOR OF THE INVOLVED AREA/S
OF THE RETINA
From PARBS: Questions to ask
▪ Is the visual loss transient or persistent? CENTRAL RETINAL ARTERY OCCLUSION
▪ Is the visual loss monocular or binocular? ▪ TRUE OPHTHALMIC EMERGENCY
▪ What was the tempo? Did the visual loss occur abruptly, or did ▪ Sudden painless visual loss
it develop over hours, days, or weeks? ▪ “Cherry-red Spot,” generalized retinal edema & opacification
▪ What is the patient’s age? Medical condition? ▪ Precipitating Factors:
▪ Did the patient have documented normal vision in the past? ▪ Arteriosclerosis ▪ Hypertension
▪ Diabetes ▪ Embolization
EYE EXAMINATION ▪ Increased IOP
▪ Must be treated within 45-90 minutes (Golden Period)
Basic 5-point examination:
▪ Treatment:
▪ Gross Examination ▪ EOM Evaluation
o Carbogen, brown paper bag breathing
▪ Visual Acuity ▪ Ophthalmoscopy
o Efforts to decrease IOP and dislodge the embolus/clot
▪ IOP Determination
- Digital Massage
Extended eye exam:
- IV Acetazolamide
▪ Confrontation Test ▪ Periorbita Exam
- Anterior Chamber Paracentesis
▪ Periorbita Exam ▪ Fundoscopy
o Pharmaceutical: Systemic Antithrombotic Agents
▪ Anterior Chamber Assessment

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o Surgical (only try if medical treatment does not work): PRESENTATION
- Core Vitrectomy with direct CRA Massage ▪ Sudden unilateral eye pain with ipsilateral headache & vomiting
- Panretinal Photocoagulation for neovascularization ▪ History of iridescent vision (may infer earlier bouts of increased
- Anti-VEGF Tx to prevent formation of new BVs IOP and subsequent corneal edema or bedewing)
▪ Blurring of vision
CHEMICAL BURNS ▪ Red eye
▪ Hazy cornea
▪ Mid-dilated, sluggish to non-reactive pupil
▪ Shallow anterior chamber
▪ Increased IOP ( usually in the range of 30+ to 50+ mmHg)

▪ A true ocular emergency GOALS OF TREATMENT

▪ Important to establish the nature of the offending agent ▪ Dehydrate the vitreous ( most important; to quickly lower
▪ ALKALI agents are more serious than acid – penetrate deeper down the pressure and allow the other agents to start working)
and need longer treatment in terms of irrigation ▪ Constrict pupil/decongest the peripheral angle
▪ IMMEDIATE irrigation needed – should be initiated before arrival ▪ Improve outflow/decrease aqueous production
at the ER (e.g. immediate tap water irrigation)
AGENTS USED
ALKALI VS. ACID
▪ Anticholinergic (e.g. Pilocarpine)
Alkali Acid
▪ Betablockers (e.g. Timolol/Betaxolol)
More damaging Dissociates in water to form
Pilocarpine & Timolol – would only work after high-risk
hydrogen ion
ischemia is lessened
Reacts with fats to form soaps Weak acids cause less severe
▪ Carbonic Anhydrase Inhibitors (e.g. Diamox)
damaging cell membranes – damage
increased penetration into tissues ▪ Osmotic Agents (e.g. Glycerol/Mannitol) – Monitor urine
Higher pH = Greater damage Damage seen unless pH is ≤2.5 output and make sure patient will have diuresis esp. with Mannitol
(pH: 11 or 11.5) since it draws fluid to the intravascular space → may precipitate
CaOH → KOH → NaOH → Sulfurous Acid → Hydrochloric, hypotensive crisis esp. in the elderly → may lead to demise
NH4OH Phosphoric, Sulfuric
SURGICAL MANAGEMENT
INITIAL EMERGENCY CENTER MEASURE
▪ Topical Anesthesia (and lid retractor)
▪ Copious Irrigation – with several liters of normal saline solution
for a period of 2 hours or even as long as 12 hours
▪ Check for Foreign Bodies
Remember that the patient may come to you because of a mixture of
problems that he encountered because of the industrial accident.
done after controlling the IOP;
EC TREATMENT FOLLOWING IRRIGATION Left: Laser Iridotomy; Right: Peripheral Iridectomy (using a knife)
▪ Topical Cycloplegics From PARBS:
▪ Topical Antibiotics IRIDOTOMY
▪ Patch Eye ▪ Involves the use of surgical instruments – or more often, a
▪ Prompt Referral to an ophthalmologist laser – to punch a tiny, half-millimeter hole in the iris through
which the trapped fluid can drain
URGENT CONDITIONS IRIDECTOMY
ACUTE ANGLE CLOSURE GLAUCOMA ▪ Similar procedure to iridotomy and usually performed for
similar reasons. The difference is that rather than creating a
hole in the iris, the surgeon removes part of it.

PRIMARY CAUSE: PUPILLARY BLOCK

Right: the break in the peripheral iris circumvents the pupillary block and
allows the aqueous fluid to flow into the anterior chamber → opens up angle
and allow aqueous flow in the normal routes of excretion

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ACUTE IRIDITIS/IRIDOCYCLITIS/UVEITIS

CONJUNCTIVITIS
Questions to ask to establish conjunctivitis
▪ Is the involvement unilateral or bilateral?
▪ What was the tempo? Did the redness and/or discharge occur
abruptly or over hours, days, or weeks?
▪ Inflammatory disease; usually monocular ▪ What is the patient’s age, activities, and medical condition? Was
▪ Precipitated by: stress, resistance breakdown, or thunderstorms there any exposure?
▪ Associated with brow ache and photophobia ▪ Is there pre-auricular lymphadenopathy?
▪ Can be seen by the slit-lamp; not by the ophthalmoscope ▪ Is there significant visual loss? Transient or permanent?

UVEITIS CONJUNCTIVITIS: DIFFERENTIAL DIAGNOSES

VIRAL
Bilateral
Serous to mucoid discharge
Predominantly lymphocytic cellular
response
(+) Pre-auricular lymphadenopathy
Self-limiting
acute, swollen, lot of redness,
and tearing, & follicular reaction
Symptoms Signs Epidemic Keratoconjunctivitis
Photophobia Ciliary Injection – blurring of vision may appear
Deep ocular pain Miosis after 1 week of healing → may
Reflex lacrimation Flare and Cells require use of steroids
Mild to moderate visual reduction Endothelial Precipitate
Floaters Synechiae
formation of synechiae and Iris Nodules
nodules at the later stages ▪ Koeppe (pupil)
BACTERIAL
▪ Busacca (iris)
Monocular Pic below: perforation
Mucopurulent to Purulent
IRIDITIS/UVEITIS MANAGEMENT
Discharge
▪ Uveitic Work-up
Predominantly segmenter cellular
▪ Anti-Inflammatory Agents
reaction
o Steroids
(-) Pre-auricular lymphadenopathy
o NSAIDs
Requires antibiotic treatment
▪ Cycloplegics
o Tropicamide/cyclopentolate ulcers of the cornea and more
o Atropine sulfate often associated with stye or kuliti,
▪ Anti-Infectives (as indicated) angular blepharitis, matting of
lashes, secretions at the tips of the
CILIARY INJECTION SUPERFICIAL/CONJUNCTIVAL meibomian glands (pic on the
INJECTION right)
Usually connotes deep intraocular Superficial ocular affliction ALLERGIC/HAYFEVER/IRRITATIVE
pathology Associated with asthma, allergic
Violaceous Bright red rhinitis, exposure to noxious
Perilimbal Peripheral stimulants
Does not blanch on pressure or Blanches with pressure or Itchiness or burning sensation
with adrenaline adrenaline Stingy discharge with copious
i.e. Uveitis Glaucoma i.e. Conjunctivitis/Blepharitis serous secretion and swelling
Papillary Reaction
Tx: isolation from triggers,
supportive

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OPHTHALMIA NEONATORUM
▪ Group of neonatal conjunctivitis and their temporal presentation
▪ Important to take note how long or when the discharge started:
o Chemical Conjunctivitis (acute with silver nitrate)
o Gonorrheal (Hyperacute; within 1-3 days)
o Staphylococcal (within 1-2 weeks)
o Chlamydial (usually >2 weeks; 2-4 weeks)
▪ Management is directed towards the offending agent
FEU-NRMF MD2022
Tips on Examining the Traumatic Eye:
▪ Topical anesthesia may facilitate evaluation
▪ Be wary of the possibility of perforation or rupture before attempting
better tissue exposure
▪ If needed, retract and fix lids over the orbital rim and not on the
globe!
BIRMIINGHAM EYE TRAUMA TERMINOLOGY SYSTEM (BETTS)

CONJUNCTIVITIS MANAGEMENT
VIRAL BACTERIAL
Grams/Giemsa Stain Grams/Giemsa Stain
Supportive Appropriate Antimicrobials
▪ Anti-inflammatory
▪ Decongestants
▪ Sulfacetamide
BLUNT TRAUMA
ENDOPHTHALMITIS
▪ Severe inflammatory condition of the uvea
▪ Etiology:
o Intraocular Surgery
o Infection/Inflammation of the posterior segment
Projectile hits the front of the eye → causing an immediate anterior-
o Trauma
posterior compression of the eye with a sideward expansion → causing injury
o Leaking glaucoma filtering bleb
to the lens, peripheral iris and retina, vitreous, and even the optic nerve itself
o Endogenous source
▪ Presents with:
▪ Sphincter pupillae muscle may be
o acute redness and congestion
ruptured resulting in semi dilated pupil
o associated with pain
that does not react to light
o inflammatory response in the anterior segment
(IRIDOPLEGIA)
(e.g. cells, flare, hypopyon)
▪ Iris may be torn from its insertion to the
o rapidly progressive visual loss
scleral spur causing IRIDODIALYSIS
▪ Management
▪ Tear a portion of the lens zonule,
o Vitreous culture (to establish dx)
causing the lens to become subluxated
o Antibiotic therapy: Intravitreal, Systemic, and Topical
o Vitrectomy (in severe cases and visual loss)

ORBITAL CELLULITIS
▪ Presents with proptosis, pain, lid swelling, limitation of EOM,
erythema and fever
▪ Different from Pre-septal Cellulitis
CONTUSION HEMATOMA/TRAUMATIC IRITIS/BLACK EYE
▪ Common causes:
o Trauma commonly seen in the ER; hemorrhagic chemosis
o Immunocompromised state ▪ Secondary to blunt ocular injury
o Infection of the paranasal sinuses ▪ Presentation:
▪ Goals of management: 1) establish offending organism through - BOV, photophobia, lacrimation,
diagnostic procedures and 2) imperative and definitive anti- sphincter rupture, iridoplegia
microbial therapy (commonly, multimodal) ▪ Hemorrhagic chemosis sever hypotony
may imply a rupture
▪ Conjunctival injury heals quickly and may mask perforations
From PARBS:
▪ Usually a disease of childhood and due to spread of infection
BLOW OUT FRACTURE OF THE ORBIT
from the ethmoid sinuses
▪ Direct blunt injury
▪ Difference from Pre-septal Cellulitis: No proptosis or limitation
▪ Intact orbital rim
of eye movements!
▪ Presentation: diplopia, hypotropia
▪ Diagnostic modalities:
OCULAR TRAUMA o EOM evaluation
Protective mechanisms of the eye: o Forced duction test
▪ Orbit rim ▪ Blink/Bell’s Reflex You may find a part of a muscle incarcerated,
▪ Lids and lashes ▪ Tears and lacrimal system hence limiting motion of the globes causing diplopia

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o Imaging techniques
▪ Check for the function of the medial wall and optic canal
We usually allot time to see if it will heal by itself or if it will be
persistent and patient will need further treatment → may opt for
surgery – usually after 6 months

LID LACERATIONS
normally occur during fights or trauma
▪ Avoid lid margin retraction Proper Eversion Technique:
▪ Give tetanus prophylaxis 1. Ask the patient to look down.
especially if there are breaks or lacerating injuries in the 2. With thumb and index finger, tug
periorbital [area] downwards on the lashes or lid
▪ Remove superficial foreign bodies margin.
▪ Rule out deeper foreign bodies 3. Push down on the superior edge
▪ Wounds of the eyelid must be carefully cleaned with soap & water of the tarsal plate with the
▪ Lacerations parallel to eyelid margins are closed with fine sutures fingertip or a cotton applicator, at
▪ Vertical lacerations are divided into: the same time, drawing the
o Outer 5/6 of the eyelid (ciliary) margin lashes and lid margin upward.
o Inner 1/6 of the eyelid (lacrimal) margin which 4. Fix the lid at the orbital rim.
avulse the canaliculi leading to the tear sac
important because it contains lacrimal apparatus SUBCONJUNCTIVAL HEMORRHAGE
May be secondary to:
LACERATION REPAIR ▪ Blunt trauma
Ciliary Margin ▪ Valsalva maneuver (e.g. coughing, etc.)
- Place first suture through gray line of the eyelid to align eyelid margin ▪ Hypertension
- Remainder of the eyelid can be closed in layers with catgut sutures for ▪ Bleeding Disorder
the tarsus and silk for the skin ▪ Idiopathic
- Mattress suture with pouted margins to avoid notching at the margin ▪ Management:
o Cold compress
o Reassurance
o Lubricant, Decongestant
not all subconjunctival hemorrhages are benign
From the PPT:

Lacrimal Margin
- Placement of a stent through the canaliculus to remain patent
- Closure of laceration
LACERATIONS OF THE BULBAR CONJUNCTIVA
- Prevention of traction by the orbicularis oculi muscle located lateral to
▪ No globe involvement – rarely require surgical treatment
the laceration
▪ White crescenteric area
to reestablish the drainage of tears using stent sutures that will be
▪ Usually surrounded by
passed on to the ducts
subconjunctival hemorrhage

INJURIES TO THE GLOBE - CORNEA

TRAUMATIC LESIONS/CORNEAL ABRASION
▪ Foreign body sensation, Redness, Tearing, Photophobia, Pain
▪ Highlighted by Fluorescein Dye (under cobalt blue light); w/o the
INJURIES TO THE GLOBE - CONJUNCTIVA
aid of the dye, the opaque area is where the abrasion is
FOREIGN BODY
▪ Frequently lodge at upper tarsal conjunctiva
▪ Upper lid eversion is a must
▪ Removed by directed irrigation stream, spud, cotton tipped
applicator, or needle or fine forceps
▪ Management is completed by prescribing topical antibiotics, esp.
if the foreign object has caused abrasions.

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CORNEAL FOREIGN BODY LENS
▪ Management depends on material and depth ▪ Cataract
of cornea: ▪ Subluxated Lens
o Superficial – irrigation or cotton
swab after anesthesia POSTERIOR SEGMENT
o Deep – G 25 needle/spatula or Injuries to Posterior Pole:
fine forceps with slit lamp viewing ▪ Macular Edema/Hole
▪ Removal of the rust ring (pic) formed ▪ Traumatic Macular Edema/Berlin’s Edema
▪ Additional Therapy: ▪ Avulsion/dialysis of vitreous base
o 24-hour Pressure patch over eye ▪ Sclero-choroidal rupture
o Topical antibiotics and cycloplegics ▪ Ret Tears
▪ Intraocular Foreign Body
LACERATIONS/RUPTURES
▪ Penetrating injury
▪ Usually at the limbus or just posterior to recti muscle insertion
most commonly at the weakest portions of the eye or at the
intercalary [area] or the region beneath
▪ Check for hypotony or IOP asymmetry, anterior chamber
depth (shallow AC), irregularity of pupil (peaking pupil), INTRAOCULAR FOREIGN BODY IN THE POSTERIOR SEGMENT
hyphema or even outright prolapse of uveal tissue ▪ Location within the eye
▪ May be accompanied by injury to the iris, lens, or retina o Xray or Ultrasound
▪ Size of the foreign body
Corneoscleral Laceration/Rupture Repair o Roentgen-ray, Ultrasound, CT-Scan
- The lacerated area is exposed by dissecting the cut edges of the ▪ Magnetic Properties
conjunctiva and tenon capsule from o Only nickel and iron may be removed by magnet
the scleral laceration ▪ Tissue Reaction
- Prolapsed uveal tissue is excised o Siderosis
and vitreous removed ▪ MANAGEMENT: Vitrectomy with Foreign Body Removal
- Sclera closed w/ interrupted
sutures ( starting from the
limbus progressing towards center
of the cornea then to the sclera)
- Conjunctiva closed separately

INJURIES TO THE GLOBE – ANTERIOR CHAMBER

IRIS SEMI-URGENT CONDITIONS
▪ Traumatic Iridoplegia RHEGMATOGENOUS RETINAL DETACHMENT
▪ Iridodialysis ▪ Best treated before the macula becomes involved – becomes
▪ Angle Recession ( can be an early or late complication of urgent when threat to this nature is noted
blunt trauma) ▪ Reattachment is achieved by:
▪ Hyphema o Identifying and closing all retinal breaks
o Relieving traction and creating a chorioretinal seal
TRAUMATIC HYPHEMA around breaks through surgery
GRADE 1 Layered blood occupying less than one third of the AC ▪ Surgery performed may be:
GRADE 2 Blood filling one third to one half of the anterior chamber o Scleral buckling or vitrectomy procedure with
GRADE 3 Layered blood filling one half to less than total of the AC retinopexy achieved by diathermy, laser, or
GRADE 4 Total clotted blood, often referred to as blackball or 8-ball cryotherapy
hyphema ▪ Initial Complaint: FLOATERS (from PARBS)

TRAUMATIC HYPHEMA MANAGEMENT Vitreoretinal traction at points of adhesion

↓
1. Light activity or bedrest – to prevent rebleed or painful rise in
Transmission of energy to the retina
pressure ↓
2. Elevate head of bed approximately 30-45° - hyphema settles Break/hole formation relieves traction, but allows liquid vitreous access to
inferiorly, avoid obstruction of vision and facilitate resolution SR space
3. Monocular patch/shield – for protection and to decrease ocular ↓

movement Neurosensory retina separates from RPE

↓
4. Avoid aspirin or ibuprofen
Retina becomes edematous and opaque
5. Cycloplegia/Dilation – ciliary body rest and enhanced posterior ↓
segment visualization Photoreceptor degeneration and atrophy in time

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When the vitreous degenerates, pockets of fluid will form → eventually PRESENTATION:
will coalesce → seek a backward course → begins the subsequent ▪ Bilateral = within 15 months (average: 8 months)
detachment of the posterior hyaloid [membrane] → posterior vitreous Unilateral = by 20-30 months (average 25 months)
detachment → when the vitreous detaches, sometimes there are areas that ▪ 90% within 3 years; rare after 7 years
have very adhesive properties → can cause a retinal tear and minute ▪ Signs and symptoms
hemorrhage that may be viewed by the patient as FLOATERS Leukocoria Squint
Can be treated by laser – like providing a barrier – go under [the retinal Photophobia Proptosis
break] causing a subsequent retinal detachment that can be commonly seen inflammation glaucoma
only when the fovea or macula is affected (P.S. sorry I had a hard time photophobia may be misrepresented in babies who rub their eyes and
understanding this part so I suggest that you view the lecture video, start at see some amount of light from photo phosphenes that have remained in the
51:55 onwards) dying cells
what we’d like to see: soapy-white mass tumor at
OPTIC NEURITIS the back of eye in the central areas of the retina (1st pic)
▪ Inflammation of the optic nerve what we don’t want: tumor extending past the sclera
o Invariably leads to MS (2 pic)
nd

o 15-20% of multiple sclerosis present with optic neuritis MANAGEMENT:

o 35-40% of MS will progress to ON ▪ Early diagnosis and tumor ablation (cryo
▪ Clinical Symptoms: vs laser vs radioactive plaque) with
o 70% UNILATERAL, 30% BILATERAL subsequent adjuvant therapy
▪ Triad: ▪ Enucleation/Exenteration
o LOSS OF VISION
o IPSILATERAL EYE PAIN RETINOPATHY OF PREMATURITY
o DYSCHROMATOPSIA (problem with color perception) ▪ Sufficient Cause: IMMATURE RETINAL VASCULATURE
▪ Fundus Signs: ▪ Prematurity + Low Birthweight
▪ Potentiated by excessive oxygen administration
▪ Influenced by maternal and neonatal factors

In examining the patient, important to note if it is already in

▪ Treatment:
Oral Prednisone
o Did not have a better outcome than those given
placebo
o Increased rate of recurrent optic neuritis
o No benefit for typical cases of optic neuritis and may
even predispose patients to further attack
High-dose IV Methylprednisolone + Oral Prednisone
o IV methylprednisolone (250mg QID x 3 days) followed
by oral prednisone (1mg/kg/day x 11 days)
o Sl. Faster recovery of visual function
o Final VA after 6 months did not differ from that of
placebo-treated patients
o Reduced rate of development to MS over a 2-yr follow-
up period
▪ Prognosis: Visual Recovery
o Irreversible optic nerve damage occurs in 80% of
patients, but recovery of Snellen acuity is good
o 65-80%: 20/30 or better
o 45% recover within the first 4 months
o 35% recover near normal acuity at 1 year
o 20% fail to make any significant improvement
the proliferative stage or STAGE 3:
▪ Fibrovascular proliferation on the edge of ridge
▪ Mild, moderate, or severe vitreous
infiltration
▪ 50% chance of progression to stages 4 and 5
and blindness
▪ becomes the critical stage of disease
management
If the neovascularization happens in ≥5 clock hours continuous (or 8 clock
hours in toto or more), this becomes the threshold – a percentage of cases
can go to progressive blindness
PLUS DISEASE
▪ with abnormal iris vessels/tortuosity and engorgement of retinal
vessels ( indicating congestion)
▪ Rush Disease plus disease involving Zone 1 – very rapid
progression
THRESHOLD/PLUS DISEASE
▪ Stage 3 ROP
▪ Zone 1 or 2 in 5 or more continuous clock hours
▪ Zone 1 or 2 w/ 8 cumulative hours of involvement w/ PLUS disease
INTERVENTION W/IN 72 HOURS TO PREVENT EVENTUAL VISUAL LOSS

RETINOBLASTOMA
Objective: ABLATE ISCHEMIC RETINA
▪ Most common intraocular malignancy in childhood Modalities:
▪ Life threatening ▪ Cryotherapy
▪ 1 in 20,000 live births ▪ Laser Photocoagulation (Indirect Ophthalmoscope,
▪ Prognosis is directly related to the size and degree of extension Surgical/Endolaser, Endoptik, Laser Diopexy)
▪ Intraocular = possible cure ▪ Anti-VEGF Therapy
o With orbital extension = poor prognosis
▪ IMMEDIATE OPHTHALMOLOGIC REFERRAL