Eyelid, Lacrimal & Orbital Disorders
Lids, tears, and orbit: separate the nuisances from the threats
Preseptal and orbital cellulitis
The orbital septum. This fibrous sheet runs from the orbital rim into the eyelids and separates lid (preseptal) infection from infection of the orbital fat and muscles (orbital). Pain with eye movement, ophthalmoplegia, proptosis or vision loss places the infection behind the septum.
| Feature | Preseptal | Orbital |
|---|---|---|
| Typical source | Lid trauma, insect bite, hordeolum, sinusitis | Ethmoid sinusitis through the lamina papyracea |
| Eye movements | Full and painless | Painful, restricted; diplopia |
| Globe | No proptosis; normal vision and pupils | Proptosis, chemosis, reduced acuity, possible RAPD, fever |
| Workup | Clinical; CT only if the eye cannot be examined | Contrast CT of orbits and sinuses |
| Treatment | Oral amoxicillin-clavulanate (for MRSA risk, clindamycin, or TMP-SMX plus amoxicillin because TMP-SMX alone misses streptococci); recheck in 24–48 h | Admit; IV vancomycin plus ceftriaxone; drain abscesses |
Preseptal cellulitis. Most patients are young children, and S. aureus and streptococci predominate. Admit infants, toxic-appearing children and those who fail oral treatment.
Orbital cellulitis. CT identifies subperiosteal or orbital abscesses. Add metronidazole to vancomycin and ceftriaxone when intracranial spread is suspected, and involve ophthalmology and ENT. Drain large abscesses and any abscess with worsening vision or no improvement after 24–48 hours.
Complications. Infection can progress to abscess, compressive optic neuropathy, meningitis, brain abscess, or cavernous sinus thrombosis through the valveless ophthalmic veins. Cavernous sinus thrombosis brings headache, high fever, spread of proptosis and chemosis to the other eye, and palsies of CN III, IV, V1, V2 and VI; MRI with MR venography confirms it.
A patient in diabetic ketoacidosis with orbital cellulitis and a black eschar on the palate or nasal turbinate has mucormycosis until proven otherwise: emergent surgical debridement plus amphotericin B.
Eyelid lumps and lid-margin disease
Hordeolum. A stye is an acute, painful, red abscess of an eyelid gland, usually from S. aureus: external at the lash line (glands of Zeis or Moll) or internal within a meibomian gland. Warm compresses and gentle massage several times daily let most drain within 1–2 weeks. Incise persistent lesions, give systemic antibiotics only for accompanying preseptal cellulitis, and never squeeze.
Chalazion. A chronic, painless, firm, rubbery nodule forms when a blocked meibomian gland provokes a sterile lipogranulomatous reaction to trapped sebum. It often follows an internal hordeolum and accompanies blepharitis or rosacea. Warm compresses come first; intralesional triamcinolone or incision and curettage treat persistent lesions.
Biopsy a chalazion that recurs at the same site, especially with lash loss in an older adult: sebaceous carcinoma masquerades as recurrent chalazion or chronic unilateral blepharitis. Basal cell carcinoma, typically on the lower lid or medial canthus, is the most common eyelid malignancy.
Blepharitis. Chronic bilateral lid-margin inflammation causes burning, itching, grittiness, crusting and collarettes on the lashes, with red, thickened margins worst in the morning. Anterior disease is staphylococcal, seborrheic or Demodex-related; posterior disease is meibomian gland dysfunction, linked to rosacea and seborrheic dermatitis. Warm compresses, daily lid scrubs and artificial tears control but do not cure it; antibiotic ointment treats flares, and oral doxycycline or azithromycin helps posterior disease.
Lacrimal disorders
Dacryocystitis. Infection of a lacrimal sac obstructed at the nasolacrimal duct causes a painful, red swelling just below the medial canthal tendon, tearing, and pus that can be expressed from the punctum. S. aureus and streptococci are usual. Treat with warm compresses and oral antibiotics, or IV therapy when severe or complicated by cellulitis. Avoid probing during acute infection; dacryocystorhinostomy afterward relieves the obstruction and prevents recurrence.
Dacryoadenitis. Lacrimal gland inflammation instead swells the upper outer lid into an S-shaped contour (mumps or EBV in children, sarcoidosis in adults).
Congenital nasolacrimal duct obstruction. An imperforate membrane at the valve of Hasner causes tearing, mucoid discharge and crusted lashes from the first weeks of life, while the conjunctiva stays white. About 90% open by 12 months. Lacrimal sac (Crigler) massage and cleaning are first-line, topical antibiotics are reserved for purulent flares, and obstruction persisting near 1 year is treated with nasolacrimal duct probing.
Tearing with photophobia, blepharospasm and a cloudy or enlarged cornea is congenital glaucoma, not a blocked duct, and needs urgent ophthalmology referral.
Thyroid eye disease
Mechanism. TSH-receptor autoantibodies, acting with IGF-1 receptor signaling, activate orbital fibroblasts to deposit glycosaminoglycans and expand fat, while extraocular muscles enlarge in a fusiform, tendon-sparing pattern on CT. It is the most common cause of unilateral or bilateral proptosis in adults and usually accompanies Graves hyperthyroidism, but it can occur in euthyroid or hypothyroid patients. An active inflammatory phase of about 6–24 months precedes fibrosis.
Findings. Upper lid retraction with scleral show is the most common sign; others are lid lag on downgaze, proptosis, periorbital edema, chemosis and exposure keratopathy. Restrictive myopathy causes diplopia, classically limited upgaze from a tight inferior rectus; muscles are involved in the order inferior, medial, superior, lateral, then obliques ("I'M SLOw"). Compressive optic neuropathy at the orbital apex (reduced acuity, color desaturation, RAPD) is the emergency.
Management. Smoking raises risk and severity and blunts treatment response. Radioactive iodine can worsen active disease: give prednisone prophylaxis with mild active disease, and prefer methimazole or thyroidectomy when disease is moderate to severe. All patients need euthyroidism and lubricants, with selenium for mild active disease. Moderate to severe active disease is treated with IV methylprednisolone or teprotumumab, an IGF-1 receptor antibody whose adverse effects include hyperglycemia and hearing loss. Optic neuropathy calls for high-dose IV steroids and urgent orbital decompression; inactive disease is rehabilitated surgically.
Ptosis and lid malposition
| Cause | Ptosis | Pupil | Other clues |
|---|---|---|---|
| Aponeurotic | Mild–moderate; high lid crease | Normal | Age, contact lenses, eye surgery; good levator function |
| Horner syndrome | Mild (Müller muscle) | Miosis; anisocoria worse in dim light | ± Anhidrosis; carotid dissection, Pancoast tumor |
| CN III palsy | Severe (levator) | Dilated if compressive | Eye down and out; PCom aneurysm vs microvascular |
| Myasthenia gravis | Fatigable, variable | Always normal | Worse late in day; ice-pack test; AChR antibodies |
Aponeurotic ptosis. The most common acquired ptosis: the levator aponeurosis stretches or detaches with age, contact lens wear or eye surgery. Surgery is offered when the lid blocks vision. Dermatochalasis, excess upper-lid skin draping over the lashes, mimics ptosis while the lid margin sits normally.
Neurogenic ptosis. A painful new Horner syndrome needs urgent neck vascular imaging for carotid dissection. A pupil-involving third nerve palsy needs emergent CTA or MRA for a posterior communicating artery aneurysm, whereas a pupil-sparing palsy in a patient with diabetes or hypertension is usually microvascular. Myasthenic ptosis worsens with sustained upgaze and often comes with diplopia.
Entropion and ectropion. In entropion the lid margin rolls inward so lashes abrade the cornea, causing irritation, tearing, abrasions and ulcers; involutional disease of the aging lower lid is most common, and cicatricial forms follow trachoma, chemical burns, ocular pemphigoid or Stevens-Johnson syndrome. In ectropion the lid turns outward, exposing the eye and everting the punctum so that tears spill; causes are involutional, paralytic (facial nerve palsy) or cicatricial. Lubrication and taping help temporarily, and surgery corrects both.