Orbit and Lacrimal System

What is globe displacement, and how are exophthalmos/proptosis and enophthalmos defined and measured?

Globe displacement results from diseases of the orbit changing orbital soft tissue volume or the integrity of orbital walls. Exophthalmos/Proptosis is anterior displacement (forward protrusion) of the globe — "exophthalmos" generally implies an endocrine cause (thyroid eye disease) while "proptosis" implies other causes (orbital mass, inflammation, etc.); pseudo-exophthalmos (from lid retraction, contralateral ptosis, or a large globe in high myopia) must be ruled out. Enophthalmos is posterior displacement of the globe. Both are measured with a ruler or Hertel exophthalmometer, which measures the distance between the corneal tip and the plane of the lateral orbital margin; normal values range from 12-22 mm.

What are the causes of Exophthalmos/Proptosis?

1) Graves' disease: unilateral or bilateral, the commonest cause in adults. 2) Orbital cellulitis: unilateral, the most common cause in children. 3) Orbital tumors: gradual onset, usually unilateral (can be bilateral in lymphoma), with or without associated systemic disease (e.g., neurofibromatosis). 4) Orbital/retrobulbar hemorrhage: acute onset, history of trauma, an ophthalmic emergency due to markedly raised IOP (risk of CRAO). 5) Cavernous sinus thrombosis: life-threatening ophthalmic/neurological emergency, often a complication of orbital cellulitis causing bilateral orbital symptoms. 6) Carotid-cavernous fistula: causes pulsating exophthalmos.

What are the causes of Enophthalmos, and what investigations are used for globe displacement?

Causes of enophthalmos: 1) Orbital fat atrophy (post-traumatic or in old age), 2) cicatrizing tumor metastasis, 3) "blow-out" fracture. Investigations for globe displacement include: CT/MRI of the head and/or orbits, ultrasound of the orbits, and thyroid function tests (to evaluate for Graves' disease).

What is a blow-out fracture, what causes it, and where does it typically occur?

A blow-out fracture is caused by a sudden increase in orbital pressure from an impacting object larger in diameter than the orbital aperture (e.g., a fist or tennis ball), displacing the eyeball. It most frequently involves the floor of the orbit along the thin bone covering the infraorbital canal; the medial orbital wall may also be fractured.

What are the complications of a blow-out fracture?

Since the thin orbital walls separate the orbital cavity from surrounding nasal sinuses, infection can spread from the sinuses to the orbit with nose blowing. Early proptosis occurs due to oedema, emphysema, and hematoma, but enophthalmos can develop later. Large fractures cause globe displacement, while small fractures can cause muscle entrapment with limited ocular motility and double vision requiring surgery. It can also be associated with severe eye injury such as globe lacerations, corneal abrasion, lens dislocation, retinal tear, or traumatic optic neuropathy.

How is a blow-out fracture diagnosed?

1) Visual acuity and pupillary size/reaction must be recorded and monitored. 2) Periocular signs: ecchymosis, oedema, and subcutaneous emphysema. 3) Infraorbital nerve anesthesia affecting the lower lid, cheek, side of the nose, upper lip, and upper teeth/gums if the infraorbital canal is involved. 4) Diplopia, which may result from hemorrhage/oedema restricting globe movement (improves as it resolves), mechanical entrapment of the inferior oblique/inferior rectus muscle or adjacent tissue (causing diplopia in both up- and down-gaze), or direct muscle injury. 5) Enophthalmos. 6) Ocular damage. A coronal CT scan of the orbit is important to diagnose floor fractures and tissue (inferior oblique) entrapment.

How is a blow-out fracture managed?

Patients should be advised to avoid blowing their nose, and prophylactic antibiotics are given. Surgical repair is required if there is muscle entrapment causing diplopia or a large fracture causing marked enophthalmos.

Compare the definitions and etiologies of Preseptal Cellulitis and Orbital Cellulitis.

Preseptal cellulitis is infection of soft tissue anterior to the orbital septum, usually following periorbital trauma or dermal infection (suspect H. influenzae in children, S. aureus or Streptococcus in adults). Orbital cellulitis is inflammation of orbital contents posterior to the orbital septum — an OCULAR and MEDICAL emergency, common in children, the elderly, and immunocompromised patients; usually secondary to sinus/facial/tooth infections or trauma, and can also arise from preseptal cellulitis.

Compare the clinical features of Preseptal Cellulitis and Orbital Cellulitis.

Preseptal cellulitis: fever may be present, moderate-to-severe lid edema, absent conjunctival injection/chemosis/proptosis/pain on eye movement, normal ocular motility and vision, absent RAPD, moderate leukocytosis, normal or elevated ESR. Orbital cellulitis: fever present, marked lid edema, present conjunctival injection/chemosis/proptosis/pain on eye movement, decreased vision, diminished ocular motility ± diplopia, RAPD present in severe cases (a poor prognostic sign), marked leukocytosis, and elevated ESR.

How are Preseptal and Orbital Cellulitis treated, and what are the complications of Orbital Cellulitis?

Preseptal cellulitis treatment: systemic antibiotics (e.g., amoxicillin-clavulanic acid); if severe or in a child aged one year or younger, treat as orbital cellulitis. Orbital cellulitis treatment: hospital admission, blood cultures, orbital CT, IV antibiotics (ceftriaxone + vancomycin) plus oral metronidazole for one week, and surgical drainage of any abscess with close follow-up (especially in children). Complications of orbital cellulitis: 7-11% suffer significant vision loss, optic nerve inflammation, cavernous sinus thrombosis, meningitis, brain abscess, and death (mortality 17-20% without antibiotics) — prompt diagnosis and treatment are essential.

What are the secretory and excretory parts of the lacrimal system?

Secretory part: the main lacrimal gland, accessory lacrimal glands, conjunctival goblet cells, and Meibomian glands. Excretory part: tears drain from the ocular surface through the upper and lower lacrimal puncta via the superior and inferior canaliculi (a common canaliculus is not uncommon) into the lacrimal sac, then flow through the nasolacrimal duct into the nasal cavity behind the inferior turbinate.

What are the three layers of the tear film, and what secretes each layer?

1) Outer oily layer: secreted by the Meibomian glands; prevents/decreases tear evaporation. 2) Middle aqueous (watery) layer: forms the main bulk of the tear film, secreted by the main lacrimal gland and accessory lacrimal glands; has basic secretion (constant lubrication) and reflex secretion (triggered by irritation or emotion). 3) Inner mucous layer: secreted by conjunctival goblet cells; maintains adherence and stability of the tear film on the ocular surface, especially the cornea.

What is Dry Eye Disease (DED), what is its prevalence, and what causes Aqueous Tear Deficiency?

DED describes a breakdown of the ocular surface's tear film coating, ranging from mildly irritating to debilitating; prevalence is estimated at 8-40%, varying by population, and is common (usually mild) above age 40. Aqueous tear deficiency causes: I) Sjögren Syndrome (Keratoconjunctivitis Sicca) — an autoimmune disease causing dry mucous membranes throughout the body, primary or secondary to conditions like rheumatoid arthritis or SLE; lacrimal gland infiltration in sarcoidosis can also reduce tear production. II) Non-Sjögren causes: allergies, age-related hormone decline, pregnancy, thyroid eye disease, certain medications (antihistamines, beta-blockers, diuretics, oral contraceptives, etc.), chemical exposure/injury, eye surgery/contact lens use, neurologic conditions (e.g., trigeminal dysfunction), post-refractive surgery (LASIK/PRK), diabetes, and vitamin A deficiency.

What causes Evaporative Dry Eye Disease, and what is the "mixed" category?

Evaporative DED causes: thyroid eye disease (with lid retraction, proptosis, infrequent blinking, lagophthalmos), eyelid inflammation (blepharitis), infrequent blinking from screen staring (now the most frequent contributor), environmental factors (dusty, windy, hot/dry conditions), neurologic conditions (stroke, Bell's palsy, Parkinsonism), exposure keratitis (lagophthalmos), and mask-associated dry eye (MADE, more prevalent since COVID-19). Mixed etiology (both aqueous-deficient and evaporative) is common.

What are the symptoms and signs of Dry Eye Disease, and how is it treated?

Symptoms: foreign body sensation/grittiness, burning/stinging/itching, redness, reflex tearing, mucous discharge, blurry/fluctuating vision (worse with reading, screens, driving), light sensitivity, heavy eyelids, and eye fatigue. Signs: decreased tear film breakup time (TBUT, normally >10 seconds), punctate epithelial erosions on fluorescein staining (superficial punctate keratopathy) in severe cases, and possible corneal erosions/scarring. Treatment: medical — artificial tears (avoid long-term preserved drops), longer-acting gels/ointments at bedtime, cyclosporine A 0.05% drops, short-term topical steroids; interventional — punctal plugs, lid taping overnight or tarsorrhaphy in severe lagophthalmos; plus treating the underlying cause (e.g., blepharitis).

What is Epiphora, what causes it, and how is it diagnosed and treated?

Epiphora is excessive watering of the eye with tear overflow at the lid margin due to insufficient drainage. Causes include overproduction of tears (secondary to emotions/pain, dry eye reflex lacrimation, ocular surface inflammation like conjunctivitis/keratitis/foreign body, or irritation like entropion/trichiasis) and decreased drainage (malposition of puncta as in ectropion, obstruction anywhere along the drainage system, or lacrimal pump failure from lower lid laxity or orbicularis weakness/facial palsy). Diagnosis: check for punctal occlusion/stenosis via slit lamp, anterior segment inflammation, lid/punctal/lash malposition, and fluorescein dye evaluation of drainage patency. Treatment: address the underlying cause; for congenital nasolacrimal duct obstruction in infants, escalate stepwise from digital massage + topical antibiotics (85% resolve within the first year), to nasolacrimal duct probing after age 1, repeat probing, silastic intubation, and finally dacryocystorhinostomy (DCR) if all else fails — note that probing is not curative in adults.

Compare acute and chronic Dacryocystitis, and describe Dacryoadenitis (definition, etiology, features, treatment).

Dacryocystitis is acute or chronic infection of the lacrimal sac, usually secondary to nasolacrimal duct obstruction (commonly staphylococci/streptococci). Acute: pain, redness, swelling below the medial canthus, epiphora, possible fever, very tender/tense swelling with erythema, can progress to abscess or preseptal cellulitis; treated with warm compresses, decongestants, and systemic/topical antibiotics, followed by DCR once resolved. Chronic: chronic epiphora, recurrent unilateral conjunctivitis, painless lacrimal sac swelling (mucocele), positive regurgitation test on sac pressure; treated with DCR. Dacryoadenitis is acute or chronic inflammation of the lacrimal gland (outer 1/3 of upper lid), caused most commonly by viral infection (Epstein-Barr virus) or less commonly bacterial/fungal/parasitic infection, autoimmune disease (thyroid eye disease, Sjögren's), or other inflammatory/neoplastic causes. Acute form presents with pain aggravated by eye movement, ptosis with S-shaped lid deformity, red eye, diplopia, tenderness/oedema/erythema of the outer upper lid, proptosis, and possible fever; chronic form is more common and presents as painless lacrimal gland enlargement. Treatment: symptomatic for viral cases, systemic antibiotics for bacterial cases, oral corticosteroids for idiopathic cases, and treatment of the underlying disorder if chron