• 7 EOM (4 rectus muscles + 2 obliques + levator)
  • Inferior rectus bound to lower lid retractors via Lockwood ligament.
    • Recession (weakening) lowers retractors/LL
    • Resection (cut) elevators retractions/LL


  • Blood supply: Muscular br of ophthalmic a –> anterior ciliary a –> ANTERIOR SEGMENT
  • Ophthalmic artery –> Central retinal artery
  • Main venous supply: superior ophthalmic vein
    • Runs through superior orbital fissure outside the apex


  • Parasympathetic innervation –> sphincter pupillae (constrict) + ciliary muscle (accommodation, regulates flow of aq humor). Travels with branch of CN 3 lower division (n. to inf oblique)
  • Nerves to the rectus mm + SOB enter the muscle 1/3 of the distance from the origin
  • * CN IV is outside of the muscle cone; not affected by RBB

Other eye basics:

  • Orbital fat stops about 10 mm from the limbus
  • Tenon capsule: principal orbital fascia, forms envelope within which the eye moves (baseball glove, baseball)
    • Fuses posteriorly with the optic nerve sheath; anteriorly with intermuscular septum 3 mm from limbus
  • Sclera is thinnest just posterior to the 4 rectus mm insertions
  • Thinnest walls of orbit:
    1. Lamina papyracea
    2. Maxillary bone (especially medial to infraorbital canal)
  • Orbital apex
    • Involves optic canal and part of superior orbital fissure: optic n. and a. + CN 3, CN 6, and nasocilliary nerve (branch of V1)
    • V1 branches: NFL


  • Frontal, ethmoid, sphenoid, MAXILLARY
  • Decreases weight of the skull, functions as resonators for the nose
  • Can be asymmetric and vary in size and shape
  • Expands as we grow
  • Ethmoid sinus
    • Not present at birth
    • Ethmoiditis common cause of orbital cellulitis and SPA
  • Sphenoid sinus
    • Optic canal is located immediately superolateral to sinus wall thus sphenoid sinus injury can –> VA or VF deficit
  • Maxillary sinus
    • Roof forms floor of each orbit. Maxillary bone is thinnest medial to infraorbital canal.
  • CT and MRI are main imaging studies for ocular disorders

Computed Tomography – CT

  • Usually obtained in 3-mm cuts, less for greater detail

  • Trauma, thyroid eye disease, FBs, orbital cellulitis

  • Benefits

    • Good view of bone

    • Better spatial resolution (easier to locate lesion)

    • Less motion artifact (quick scan)

    • Metallic FBs

    • Less expensive

  • Disadvantages

    • CI in pregnancy

    • Limited view of orbital apex

  • Contrast (iodine):

    • Inflammation

    • Infection

    • Note: Avoid in patients with allergy to iodine or with renal dysfunction

Magnetic Resonance Imaging – MRI 

  • Usually obtained in 3-mm cuts, less for greater detail

  • Multiple sclerosis, optic neuritis

  • Benefits

    • Better tissue contrast / more soft tissue detail 

    • No ionizing radiation

    • Can be used in pregnant women, kids

    • Good view of orbital apex

  • Disadvantages

    • CI: Metallic FBs, pacemaker, aneurysm clips

    • Longer scan, $

    • Claustrophobia

  • T1 best for anatomical detail of orbit

  • T2 shows blood brighter than melanin (differentiating melanotic lesion vs hemorrhage)

  • Contrast (gadolinium) enhances (looks bright on MRI) vascularized lesions

    • SE: Nephrogenic systemic fibrosis in patients with severe renal failure (stage 4+)

CT or MR Angiography (CTA/MRA)

  • Imaging arteriovenous malformations, aneurysms, and AV fistulas

  • CCF –> CTA

  • Everything else –> MRA

  • Can manifest at any point during one’s life
  • Most are evident on ultrasound before birth
  • Key: The more severe the abnormality, the earlier it occurred

Anophthalmia: Complete absence of eye tissue. Three types, all involve issue with optic vesicle. Rare.

  • Primary, secondary, and consecutive
  • Orbital development is partly dependent on normal ocular development. In anophthalmia, there’s no eye thus there’s the orbital tissues are also hypoplastic.

Microphthalmia: Small eye with an axial length < 2 SD below the mean AL for that patient’s age.

  • Most have no potential for vision.
  • Treatment focus: cosmetic appearance
    • Progressively larger conformers until patient can be fitted for prosthesis.

Craniofacial clefting / Craniofacial abnormalities 

  • Goldenhar syndrome
  • Treacher Collins-Franceschetti syndrome
  • Crouzon syndrome (proptosis…)


  • Very common: dermoid and epidermoid cysts

Hamartoma: benign overgrowth of tissue made primarily of mature cells that are normally found in that location

  • Think: “You normally hammer a nail with a hammer.”

Choristomas: overgrowth of tissue made of cells that are NOT normally found in that location

  • Think: “Chor-azy!”
  • Dermoid cysts, epidermoid cysts, dermolipomas, teratomas

Dermoid cyst

  • Present at birth, grows SLOWLY with time, painLESS
  • Freely mobile or fixed to periosteum
  • Path: Lined by keratinized stratified squamous epithelium with adnexal structures in the wall (ex of choriostomas)
  • Common location: lateral brow adjacent to frontozygomatic suture > medial UL
  • If @temporal fossa, get CT to rule out dumbbell expansion through a suture
    • “Dumball dermoid cyst” –> pulsating proptosis with chewing 
  • CT: cyst is well-defined with enhancing wall (bright) with nonenhancing (dark) lumen
    • Think: halo-like
  • Long-standing dermoids (adulthood) can erode orbital bones
  • Tx: surgical excision. Keep cyst wall intact – rupture of cyst –> acute inflammatory process


  • Solid tumor, located within conjuncitva on LATERAL side of eye
  • May extend to levator or EOMs
  • Google picture 


  • Rare, arise from all 3 germinal layers (ectoderm, mesoderm, endoderm), usually cystic
  • Classic presentation: severe unilateral proptosis at birth
  • If confined to orbit: benign > malignant

Midfacial (Le Fort) Fractures

  • All involve the maxilla and must extend posteriorly through the pterygoid plates (I –> III more severe)
  • Le Fort I – no orbital involvement 
  • Le Fort II – involves lacrimal and maxillary bones + medial orbital floor
  • Le Fort III – medial, floor, and lateral walls involved.
  • Ophtho not primary


  • Key: Surgical indications: large Fracture size, muscle Entrapment, Enophthalmos
    • Think: Pay the FEE

Orbital Floor Fracture

  • Rule of thumb: Always consider when there’s been a periorbital blow forceful enough to cause ecchymosis
  • Signs:
    • +/- Periorbital erythema, edema;
    • Diplopia
    • Enophthalmos – occurs in large fractures (orbital soft tissues prolapse into maxillary sinus)
    • Hypoesthesia (infraorbital nerve distribution V2)
    • Emphysema of the orbit and eyelids – more commonly in medial wall fx
      • Don’t blow nose to prevent orbital emphysema
    • Note: Diplopia can also be due to orbital edema or hemorrhage (should improve in 1-2 wks), damage directly to EOM or their innervation
  •  Inferior rectus entrapment
    • Increased IOP in upgaze compared to primary gaze
    • Limited vertical movement
    • Vertical diplopia
    • Pain in inferior orbit
  • Management
    • CT – Use coronal and sagittal views. Assess fracture size and EOM involvement (entrapment).
    • Observation > Surgery
    • If there’s a possibility of surgery, usually wait 5 – 10 days to allow edema and hemorrhage to decrease prior to deciding if diplopia requires surgery. Can use oral steroids to aid in this. Exception: Kids with trapdoor fracture (inferior rectus entrapment) + OCR –> urgent repair to release muscle and prevent fibrosis
    • Surgical indications:
      • Diplopia (up or downgaze) within 30 degrees of primary position. May improve after 2 weeks. If not, consider surgery.
      • Enophthalmos >2 mm
      • Large fractures involving at least 50% of the orbital floor
      • Time frame – within first 2 weeks (scar tissue formation, contracture of prolapsed tissue )unless urgent indication
      • May need strabismus surgery in the future

Zygomatic Fracture

  • Zygomaticomaxillary complex (ZMC) fracture
  • “Quadripod fracture” – zygoma fractured at 4 of its articulations with adjacent bones
  • Can involve the orbital floor. Can lead to globe displacement or diplopia.

Orbital Apex Fracture

  • Orbital apex: optic canal and part of superior orbital fissure: optic n. and a. + CN 3, CN 6, and nasocilliary nerve (branch of V1)
  • These fractures can also involve superior orbital fissure outside of apex due to proximity (LFTs – V1 x2, trochlear nerve CN 4)
  • CT – Look for fractures at/near optic canal

Orbital Roof Fracture

  • Etiology: blunt trauma, missile injury, falls
  • Younger > Older pts
    • @Younger pts: frontal sinus has not pneumatized yet. In older patients, the frontal sinus absorbs part of the impact diffusing the force preventing extension of the fracture to the orbital roof
  • Likely to involve intracranial process (CSF rhinorrhea, subperiosteal hematoma, ptosis, intracranial injury…)
  • EOM entrapment rare
  • Diplopia more likely d/t hematoma, edema. or contusion of orbital structures
  • Most don’t require surgical repair. If so, by neurosurgery.

Medial Orbital Fracture

  • Aka Naso-orbital-ethmoidal fractures (NOE)
  • Etiology: face hitting solid surface
  • Avulsion of anterior ethmoidal a. –> severe epistaxis
  • Type I
  • Type II
  • Type III (more severe) – break or avulsion of medial canthal tendon


  • Imaging: CT (avoid MRI)
  • Removal:
    • Composed of vegetable matter
    • Easily accessible in the anterior orbit
  • Observation (common)
    • Inert, smooth edges, located posteriorly
    • Ex: BBs (FYI can do MRI)


  • Etiology: spontaneous (d/t tumor or blood dyscrasia), after surgery or trauma
  • If vision compromised by compression of optic nerve or elevated IOP –> blocks arterial perfusion, urgent lateral canthotomy and cantholysis


Traumatic Optic Neuropathy (TON)

  • Occurs due to 1 of 3 mechanisms

    • Direct injury to the optic nerve

    • Orbital pressure > arterial perfusion pressure –> disruption of blood supply to optic nerve

    • Indirect injury: force @frontal brow (may have LOC) –> orbital apex –> optic canal

  • Must assess

    • APD –> TON (however difficult to assess for if pt has received narcotics)

    • “Tight” globe / Intraorbital pressure –> urgent canthotomy, cantholysis

      • Trauma –> retrobulbar hemorrhage or edema –> proptosis, ptosis, EOM motility deficit, elevated IOP (hence “tight”)

  • Management: no clear treatment known currently; observation > high-dose steroids vs surgery

  • Infectious
    • Pre-septal vs post-septal cellulitis (bacterial > fungal, parasitic)
(Everything else “Non-Infectious Inflammation)
  • Autoimmune
    • TED, IgG4 disease
  • Vasculitis
  • Ganulomatous (sarcoidosis)
  • NSOI – Nonspecific orbital inflammation
    • Dx of exclusion, no known local or systemic cause


Most commonly bacterial; 3 key mechanisms
  1. Direct spread from adjacent infected structures (sinusitis in pre and post septal > dacryocystitis, dacryoadenitis)
  2. Direct inoculation from trauma or a skin infection
  3. Hematologic spread from a distant site

Preseptal Cellulitis

  • Anterior to the septum
  • Can progress to a localized abscess
    • Resident case: 4 yo with SPA but dx was pre-septal as globe was intact (ocular exam wnl)
    • Key: exam! VA, APD, color, proptosis, EOM.
  • Key: May have severe periorbital erythema and edema but the globe is not involved (infection surrounding the eye that has not penetrated the “wall”) 
    • White and quiet (no chemosis), PERRL (no APD), VA wnl, full motility
  • Peds – commonly due to gram positive cocci
  • Treatment: oral > IV antibiotics (common examples)
    • Adults
    • Kids
      • Sinusitis – Augmentin (amoxicillin clavulanate)
    • Trauma – Staph aureus –> responds to penicillins i.e. Unasyn (ampicillin-sulbactam)
  • CT scan if no improvement within 48 hours on abx

Postseptal Cellulitis

  • Posterior to the septum
  • Abscesses usually localize to the subperiosteal space next to the infected sinus
    • Not all SPA require surgical drainage; guidelines by Garcia and Harris – observe unless any are present:
      • 9 years or older
      • Frontal sinusitis
      • Non-medial SPA
      • Large SPA
      • Suspicion of anaerobic infection (gas in abscess on CT)
      • Infection of dental origin (more likely anaerobic)
      • Evidence of chronic sinusitis (nasal polyps)
      • Acute optic nerve or retinal compromise
  • Etiology:
    • Extension from nearby infected structures (sinuses, face, eyelids, teeth)
    • Trauma, surgery
    • Bacteremia –> septic embolization
    • Intraorbital – endophthalmitis, dacryoadenitis
  • If not treated appropriately, risk of posterior spread (RARE) –> blindness, cavernous sinus thrombosis, cranial neuropathy, brain abscess, or death
  • Treatment – IV antibiotics –> oral abx
    • Adults
      • Usually involve multiple organism –> broad spectrum
      • Ex: CiVil war (IV Ceftriaxone, Vancomycin)
    • Peds
      • Usually d/t single gram positive organism
      • IV Unasyn
    • Erythromycin ung (corneal exposure, chemosis)
  • Nasal decongestants may help to drain infected sinus




  • Most common and virulent fungal disease to involve the orbit
  • Fungi –> sinus or nasal cavity –> orbit
  • Invade blood vessels –> thrombosing vasculitis –> tissue necrosis –> further fungal invasion
  • Immunocompromised patients
  • Presentation: proptosis + orbital apex syndrome
  • Dx: biopsy of necrotic tissue
    • Path: Nonseptate, large branching hyphae that stain with hematoxylin-eosin 
  • Tx: IV anti-fungal (amphotericin B)
  • Acute
  • Chronic – slow destruction of sinus and adjacent structures
  • Allergic aspergillosis sinusitis – immunocompetent patients + nasal polyps + chronic sinusitis
    • +/- eosinophila, elevated IgE
    • About 20% of patients with AAS initially present with orbital signs
  • Dx: biopsy
    • Path: septate branching hyphae of uniform width


  • Developing countries
  • Cysts can form within orbit
  • Echinococcosis (dog tapeworm)
    • Rupture of cyst –> progressive inflammation
  • Cysticercosis (pork tapeworm)

Necrotizing Fasciitis 

  • RAPID, severe, potentially vision or life-threatening bacterial infection @ subcutaneous soft tissues
    • Group A beta-hemolytic streptococcus most common (*Use Clindamycin – effective against the toxins)
    • Can lead to toxic shock syndrome
    • 30% mortality rate
  • Immunocompromised > Immunocompetent
  • Tx: early surgical debridement + IV abx

Orbital Tuberculosis

  • Pulmonary focus –> hematogenous spread –> orbit
  • Usually u/l. Uncommon.
  • Tx: anti-TB mgmt


Thyroid Eye Disease (TED)

  • Classic signs
    • Most common: eyelid retraction  (u/l or b/l)
    • Proptosis
    • Restrictive extraocular myopathy
    • Lid lag in downgaze (von Graefe sign)
    • Compressive optic neuropathy –> vision loss
    • Exposure keratopathy
    • Conjuncitval erythema over the insertions of rectus muscles/ chemosis
  • Common sx:
    • Dull, achy pain
    • Diplopia (prisms, strabismus surgery)
    • Photobia
    • Blurry vision
  • Can occur in hyper (Graves – 90%), hypo (Hashimoto), or euthyroid states. Course of eye disease does not parallel disease state.
    • Think – it has a mind of its own! Independent of thyroid state.
  • Dx: 2 of 3 present
    1. Presence of immune-related thyroid dysfunction
    2. One or more typical ocular signs (see above)
    3. Radiographic evidence of TED (muscle enlargement, tendon sparing)
      • Inferior rectus > Medial > Superior > Lateral 
  • If only orbital sx present, observe.
  • Possible cause: orbital fibroblasts (express CD40 receptors) –> inflammation
    • Neural crest –> orbital fibroblasts
  • Tx: TED is self-limiting disease
    • Active disease (lasts longer in smokers) –> quiescent phase. Reactivation occurs in ~10% of patients (tx: IV steroids).
    • Establish euthyroid state
    • Mgmt depending on severity
      • More mild: quit smoking, oral selenium, lubrication
      • More severe: steroids, OScE, immunomodulators (?Rituximab)
    • Most patients with TED –> supportive care
  •  Pearls
    • Eyelid retraction
    • Most common cause of u/l or b/l proptosis
    • F >>M
    • Smoking is a risk factor
    • Order of surgery: orbital decompression –> strabismus surgery –> eyelid retraction repair
      • OScE


IgG4 Disease

  • Multiorgan disease
  • Mass-forming lesions
    • IgG4-expressing plasma cells with inflammatory T lymphocytes infiltrate various organs –> MASSES!
  • Tx: Responds well to steroids


  • Type III hypersensitivity reaction 
  • Often associated with systemic vasculitis

Giant Cell Arteritis

  • Ophthalmic emergency
  • Affects the aorta, branches of the external and internal carotid, and vertebral aa
  • Vision loss
    • –> CRAO
    •  –> Ischemic optic neuropathy
  • Ischemia of CN –> Diplopia
  • HA, jaw claudication, scalp tenderness, mailaise
  • Elevated ESR, CRP, and platelets
  • Dx: TA biopsy
  • Tx: steroids

Granulomatosis with polyangiitis (GPA) aka Wegener Granulomatosis

  • Necrotizing granulomatous vasculitis (small vessel), cANCA
  • Respiratory tract, kidneys
  • Extension to sinuses –> orbits
    • Can lead to bony erosion
  • 25% have scleritis
  • Tx: Immunosuppresion (cyclophosphamide)

Polyarteritis nodosa

  • Retinal and choroidal infarction


  • African American or Scandinavian descent
  • Lungs most commonly involved overall. Lacrimal gland most commonly affected within the orbit (b/l)
  • Path: Noncaseating epithelioid histiocytes in a granulomatous pattern
  • Dx
    • Biopsy of lacrimal gland
    • CXR or CT (hilar adenopathy, pulmonary infiltrates)
    • Labs: SCE, lysozyme, calcium

Nonspecific Orbital Inflammation (NSOI)

  • Lymphoid + fibrotic infiltrate
  • Diagnosis of exclusion
  • ?Immune-mediated
  • Frequent locations (1 most common):
    1. EOM (may have thickening of EOM tendons in contrast to TED)
    2. Lacrimal gland
    3. Anterior orbit
    4. Orbital apex
    5. Diffuse
  • Tx: Responds well (and fast) to steroids

  • EOM enlargement
    • Tendons involved: NSOI
    • Tendons spared: TED


Removal of the entire globe while preserving other orbital tissues.


  • Pathology of entire globe and optic nerve (can aid in diagnosis)

  • Lower risk of sympathetic ophthalmia

  • In primary intraocular tumors, prevent metastasis (melanoma, retinoblastoma)

    • In retinoblastoma, surgeon should obtain longer segment of optic nerve to ensure complete removal of tumor

  • Removal of a blind, painful eye

    • Neovascular glaucoma

    • Chronic uveitis

    • Previous trauma

    • Note: for a nonpainful, disfigured eye consider trial of a cosmetic scleral shell before eye removal

  • Sympathetic ophthalmia: delayed hypersensitivity immune response to uveal antigens –> immune response

    • Can essentially occur any time after ocular trauma/penetration


Removal of intraocular contents. Leave sclera, EOM, and optic nerve intact (crushed).

  • Must rule out an intraocular tumor first!

  • Benefits

    • Quicker surgical time. Less anesthesia.

    • Less disruption of orbital anatomy (EOM, nerves, fat atrophy)

    • Better motility of the prosthesis (EOM remain attached to the sclera)

    • Possible better “outcome” cosmetically

  • Disadvantages

    • Cannot do if intraocular tumor present

    • Increase risk of sympathetic ophthalmia

    • Cannot do full pathology report

  • Eyelid skin is the thinnest skin of the body

  • Has no subq fat layer (unique)

  • Upper eyelid crease: attachments of levator to the orbicularis m

Orbicularis oculi muscle

  • Main protractor of the eyelid

  • CN 7

  • Eyelid closure

  • 3 Parts

    • Pretarsal + preseptal –> involuntary blinking

    • Orbital –> voluntary blinking

Orbital Septum

  • Thin, multilayered sheet of fibrous tissues

  • Origin: periosteum over the orbital rim at the arcus marginalis

  • Can thin with time –> anterior fat protrusion (why older folks have “fatty eyes”)

  • UL – fuses with levator

  • LL – fuses with capsulopalpebral fascia

Orbital Fat 

  • Posterior to orbital septum (key in penetrating traumas – is the septum involved?)

  • UL

    • Anterior to the levator

    • 2 fat pockets: nasal and central

  • LL

    • Posterior to the capsulopalpebral fascia

    • 3 fat pockets: nasal, central, and temporal

  • Fat pockets – think MJ “23” for order


  • Upper eyelid

    • Levator (anterior)

    • Muller muscle/superior tarsal muscle (posterior)

      • –> 2 mm of elevation of the UL 

      • “Knocked out” in Horner syndrome –> mild ptosis

    • Whitnall ligament

      • Runs perpendicular to levator where the levator transitions into the levator aponeurosis

      • Acts as a suspensory ligament (think of it as a hooks to hold curtain)

  • Lower eyelid

    • Capsulopalpebral fascial (LL version of levator aponeurosis)

    • Inferior tarsal muscle (LL version to Muller muscle)

    • Lockwood ligament (LL version of Whitnall ligament)


  • Structural support of the eyelids

  • UL tarsus: 10-12 mm max height (centrally)

  • LL tarsus: 4 mm max height

  • 1 mm thick

  • Tarsus — Medial/lateral canthal tendon — Periosteum

Canthal Tendons

  • The medial and lateral canthal tendons maintain the palpebral fissure

    • Lateral canthal tendon inserts 2 mm higher than medial tendon

  • Lateral canthal tendon weakness –> telecanthus, horizontal lid laxity


  • UL: 100

  • LL: 50

Meibomian Glands

  • Originate in the tarsus

  • UL: 25

  • LL: 20

  • Sebaceous glands that contribute to the lipid layer of the tear film (holocrine secretion)

  • Eyelashes and meibomian glands arise from a common pilosebaceous unit

    • Trauma may lead to eyelash arising from nearby meibomian gland

Eyelid vasculature 

  • ICA –> ophthalmic a –> supraorbital + lacrimal

  • ECA –> arteries of the face

Innervation Summary

  • Levator – CN 3 superior division

  • Muller muscle – sympathetic n. fibers

    • Smooth muscle

  • Orbicularis – CN 7

Common between the two:

  • Congenital

  • Involutional

    • Horizontal laxity

    • Retractor laxity or dehiscence

  • Cicatricial


  • Eyelid puckers outward

  • Can –> chronic conjunctival inflammation, hypertrophy, keratinization

  • Involutional

    • Most common

    • Due to horizontal eyelid laxity at the medial and/or lateral canthal tendons

      • Dx: snapback test, distraction test (pull LL away from globe, + if > 6mm)

    • Retractor laxity or dehiscence

    • Surgical tx:

      • Horizontal lid tightening (LTSP) – Common option!

      • Medial spindle procedure

        • To fix mild medial ectropion with punctal eversion

      • Lower eyelid retractor repair (advance retractors to inferior border of tarsus)

        • Capsulopalpebral fascia + inferior tarsal muscle
  • Congenital

  • Cicatricial

    • Injury to eyelid skin –> deficiency of skin –> ectropion

      • Examples of injuries: burn, trauma, chronic skin inflammation, scarring from zoster

    • Management

      • Treat underlying issue, protect cornea

      • Surgery if needed (may use skin graft)

      • Goals: release traction + correct shortening of anterior lamella with skin graft

  • Paralytic

    • CN 7 paralysis or palsy

    • Lagophthalmos –> corneal issues

  • Mechanical


  • Inversion of eyelid

    • +/- Trichiasis

  • Involutional

    • Horizontal laxity

    • Retractor laxity or dehiscence

    • ** Orbicularis override

      • Test: Correct the eyelid position then have patient squeeze tight. If that leads to –> entropion then d/t orbic override.

    • Surgical tx:

      • Horizontal lid tightening (LTSP)

      • Lower eyelid retractor repair (advance retractors to inferior border of tarsus)

      • ** Orbic myectomy

  • Cicatricial

    • Many causes

      • Autoimmune  – pemphigoid

      • Inflammatory – Stevens-Johnson syndromej

      • Infectious – trachoma, herpes zoster

      • Traumatic – burn, scarring

      • Topicals (glaucoma drops, particularly miotics may lead to chronic conjunctivitis –> vertical conj shortening)

    • Key dx to differentiate involutional vs cicatricial entropion: use your finger to return lid to normal position

      • Involution: lid will stay in position you moved it to

      • Cicatricial: lid will NOT stay/correct; posterior side of lid may have scarring

  • Acute spastic entropion 

    • Due to ocular irritation or inflammation

    • Occurs most often in patients who had undx (likely involutional) eyelid changes pre-op

    • Usually resolves when underlying irritation/inflammation treated

    • Can use botox to temporarily paralyze the overriding orbic


  • Acquired misdirection of eyelashes
  • Treatment based on pattern of eyelashes (segmental vs diffuse) + “health” of posterior lamella (entropion also present?)
    • Eyelashes only involved
      • Epilation – expect recurrence ~3 – 8 weeks
      • Electrolysis – destroys hair follicle (definitive tx however can recur)
      • Argon laser
      • Full-thickness pentagonal resection
    • If +entropion, correct entropion (will secondarily improve trichiasis)


  • Can occur at UL or LL

  • –> Exposure of sclera between the limbus and the eyelid margin

  • Can lead to lagophthalmos, exposure keratopathy

  • Can have local, systemic, or CNS causes

    • Parinaud syndrome – example of CNS lesion (midbrain, vertical gaze palsy)

  • TED is the most common cause of both UL and LL retraction

    • Lateral flare 

  • Can be induced by strabismus surgery

    • Recession of superior rectus (near levator)

    • Recession of inferior rectus (near capsulopalpebral fascia

  • Tx based on cause

Chalazion (Usually painLESS)

  • * Obstruction of meibomian glands (@internal hordeolum) –> focal inflammation –> chalazion

    • Meibomian gland: oil-producing sebaceous glands within the tarsal plate

      • The oil is important component of the tear film

      • If plugged, the oil can’t be excreted. Instead is pushed into the tarsus –> acute  inflammatory response

  • Common!

  • Associated with rosacea and chronic blepharitis

  • Treatment:

    • Frequent warm compresses, lid hygiene

    • Topical abx (ex: maxitrol)

    • +/- Oral doxycycline or tetracycline for long-term suppression of meibomian gland inflammation or ocular rosacea

    • +/- I&D through conj and tarsus to remove gunk + cyst wall 

    • Less commonly used: steroid injection (can lead to depigmentation of overlying skin)

  • Send to path if atypical or recurrent (sebaceous cell carcinoma)

Hordeolum (PAIN!)

  • Acute infection (staph)

  • Two types

    • @ Glands of Zeis (external hordeolum aka stye)

      • Clue: commonly at hair follicle!

    • @ Meibomian glands (internal hordeolum)

  • Treatment: more conservative

    • Start: Warm compresses. Usually resolves spontaneously.

      • May need topicals.

Floppy Eyelid Syndrome

  • Chronic papillary conjunctivitis in upper palpebral conjunctiva

  • Clues

    • Ocular irritation, mild mucus discharge especially in the AM

    • Easily everted on exam especially lateral. Lid is mad loose!

  • Associated with obesity, keratoconus, eyelid rubbing, hyperglycemia, sleep apnea, sleeping prone

  • Path: Decreased elastin fibers in the tarsal plate


  • People who pull out hairs often eyebrows or eyelashes

  • Clue: hair that grows at different lengths

Dog Bites

  • Determine partial vs full-thickness involvement

  • Following tetanus and rabies protocol

Eyelid burns

  • Rare. Usually occurs in patients with significant burns.

  • Concern for cicatricial changes (poor prognosis –> eyelid malposition, lagophthalmos, corneal exposure)

  • Options: Lubrication! Moisture chambers, skin grafts, amniotic membrane.


  • Start exam right away especially if told on report that there’s a concern for a leak

  • Want to get a sense of what you’re working with and the severity

    • When to call back-up, specialty service (retina or glaucoma fellow)


  • Trauma, valsalva, cough, rubbing eye

  • PainLESS vision change or distortion

  • Ocular history, meds, recent surgery


  • Vision, pupils, IOP

  • Before checking IOP, do Siedel first

    • Always check bleb in a pt that has one

  • IOP – Applanation for accuracy if possible

  • Anterior chamber status important

    • Deep

    • Shallow (losing aq)

    • Cell/flare

  • Bleb status

    • Siedel

    • Does it look infected (blebitis –> endophthalmitis)

      • Pus

      • White with surrounding conjunctival hemorrhage or engorged blood vessels  (look angry?) “white on red” appearance

  • Do remaining exam: CVF, EOM, slit lamp exam

  • Dilated exam

    • Keys:

      • Vitreous cell indicative of endophthalmitis

      • Choroidal folds indicative of hypotony

        • hypotony= IOP <6.5

        • Clinically definition: IOP low enough –> vision loss


  • Compressive effect on the bleb leak (think of like a leaking wound)

    • Kontur lens.

      • Wear for 4-5 days 24/7. If follow-up is during those 4-5 days, keep on. Do not need to remove Kontur lens to check IOP or Siedel status.

    • Pressure patch if don’t have access to Kontur lens.

    • Suture – hard to do on call.

    • “Glue” / tissue adhesive.

  • 4th generation FQ

  • Aqeous suppressant (beta-blocker, a-adrenergic agonist, CAI)

  • Urgent (surgery)

    • Lens touching the cornea

    • Significance of AC cell

    • Significance of vitreous cell (retina consult)


  • Important: ANY patient with a bleb coming in with a change, must be seen. Blebitis until proven otherwise.

  • Bleb leak + AC cell = Blebitis

  • Hypotony maculopathy = low IOP associated with fundus abnormalities (choroidal folds, optic disc edema, vascular tortuosity)

    • Choroidal folds: Low pressure –> choroid and retina “falls” into the eye –> wrinkling appearance

  • Glaucoma filtering surgery is a risk for hypotony

  • Scenario can also occur in an over filtering bleb

  • IOP on follow-up is important as aqeuous cycles through

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Cherry red spot:

  • CRAO
  • Lipid storage disorders (Tay-Sachs disease, Niemann-Pick disease, Sandhoff diease)


  • TED is the most common cause of upper and lower eyelid retraction + most common cause of UL or BL proptosis