Chemosis

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Chemosis is edema (swelling) of the conjunctiva, causing a jelly-like protrusion of the ocular surface. Let me search the textbooks for detailed coverage.

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Chemosis

Chemosis is edema (fluid accumulation) of the bulbar conjunctiva, producing a translucent, gelatinous swelling that can protrude through the eyelids. The word comes from Greek cheme (gaping) + osis (condition).

Moderate chemosis in acute allergic conjunctivitis (Kanski's):

Moderate chemosis - bulbar conjunctiva showing translucent jelly-like swelling with visible surface vessels

Chemosis visible from below (Kanski's, Fig. 6.2C):

Chemosis seen as a translucent swelling bulging inferior to the lower lid margin

Pathophysiology

Chemosis results from increased fluid in the subconjunctival space due to one or more of the following mechanisms:

Mechanism	Example
Increased vascular permeability	Hypersensitivity (IgE-mediated), infection
Increased venous pressure	Carotid-cavernous fistula (CCF), SVC syndrome, right heart failure
Decreased plasma oncotic pressure	Nephrotic syndrome, hypoalbuminemia
Local inflammation/venous obstruction	Orbital disease, post-surgical

Causes

Acute Chemosis

Allergic (most common) - acute pollen exposure (type I hypersensitivity); hallmark of acute allergic conjunctivitis in children, frequently dramatic; resolves within hours as vascular permeability normalizes
Severe infective conjunctivitis - bacterial or viral
Angioneurotic edema (hereditary or acquired C1-esterase inhibitor deficiency)

Subacute / Chronic Chemosis

Local causes:

Thyroid eye disease (Graves' orbitopathy)
Chronic allergic conjunctivitis
Ocular or eyelid surgery (post-operative)
Trauma
Carotid-cavernous fistula (CCF) - chemosis + proptosis + red eye + pulsating exophthalmos + bruit; arterialized conjunctival vessels are the hallmark

Systemic causes:

Increased systemic vascular permeability: allergic conditions, meningitis, vasculitis
Increased venous pressure: SVC syndrome, right-sided heart failure
Decreased plasma oncotic pressure: nephrotic syndrome, hypoalbuminemia
Drugs (e.g., topical eye drops)
Venous congestion (e.g., carotid-cavernous fistula)
Myxedema

Clinical Features

Appearance: Translucent, boggy, jelly-like swelling of the bulbar conjunctiva; may herniate between the eyelids
Symptoms: Usually asymptomatic unless severe; foreign body sensation, red eye; itching and watering in allergic cases
Associated signs (depending on cause): proptosis, lid edema, conjunctival injection, restricted eye movements, bruit (CCF)

Key Associations to Remember

Cause	Key Distinguishing Feature
Acute allergy (pollen)	Children, spring/summer, dramatic chemosis, resolves in hours
Carotid-cavernous fistula	Proptosis + chemosis + arterialized (corkscrew) vessels + pulsatile exophthalmos
Thyroid eye disease	Lid lag, lid retraction, restrictive myopathy, bilateral
Nephrotic syndrome	Bilateral periorbital edema + generalized edema, low albumin
SVC syndrome	Facial/neck edema, collateral veins on chest
Gonorrheal conjunctivitis	Hyper-acute purulent discharge, preauricular lymphadenopathy

Management

Treatment is directed at the underlying cause:

Acute allergic: Cool compresses; resolves spontaneously; topical adrenaline 0.1% (a single drop) can reduce extreme chemosis; antihistamine drops for seasonal/perennial forms
Infective: Appropriate antimicrobial therapy
Post-surgical: Lubricant eye drops, time; severe cases may need temporary tarsorrhaphy
CCF: Endovascular embolization
Systemic disease: Treat the underlying condition (e.g., diuretics for heart failure, immunosuppression for nephrotic syndrome)

Sources: Kanski's Clinical Ophthalmology, 10th ed.; The Wills Eye Manual; Localization in Clinical Neurology, 8th ed.

Blepharitis

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Blepharitis

Blepharitis is chronic inflammation of the eyelid margins. It is one of the most common ocular conditions, causing persistent discomfort and irritation with a characteristic pattern of remissions and exacerbations. There is a well-known poor correlation between symptom severity and objective signs.

Classification

Blepharitis is divided into anterior and posterior forms, with considerable overlap ("mixed blepharitis"):

Feature	Anterior Blepharitis	Posterior Blepharitis
Location	Base of eyelashes, anterior lid margin	Meibomian glands, posterior lid margin
Subtypes	Staphylococcal, Seborrhoeic	Meibomian gland dysfunction (MGD)
Key deposit	Hard scales / collarettes (Staph); soft greasy scales (Seb)	Oily/turbid/toothpaste-like meibomian secretion
Lash changes	Madarosis, trichiasis, poliosis (more marked)	Mild lash changes
Cysts	Hordeolum (stye)	Chalazion (meibomian cyst)
Corneal signs	Punctate erosions, infiltrates, vascularization	More pronounced - punctate erosions, infiltrates
Tear film	Mild instability	Foamy, unstable - dry eye more marked
Associated skin disease	Staphylococcal: atopic dermatitis; Seborrhoeic: seborrhoeic dermatitis	Acne rosacea

Pathophysiology

Anterior - Staphylococcal

An abnormal cell-mediated immune response to S. aureus cell wall components produces lid inflammation. This is more common and severe in atopic dermatitis patients. Bacterial toxins directly damage the ocular surface.

Anterior - Seborrhoeic

Strongly associated with generalized seborrhoeic dermatitis (scalp, nasolabial folds, retroauricular skin, sternum).

Posterior - Meibomian Gland Dysfunction (MGD)

Bacterial lipases (from S. aureus and others) break down meibum triglycerides into free fatty acids (FFAs). FFAs:

Raise the melting point of meibum → inspissation, gland plugging
Promote S. aureus growth
Disrupt the lipid layer of the tear film → increased tear evaporation and osmolarity → unstable tear film and dry eye

Demodex

Demodex folliculorum longus - anterior blepharitis
Demodex folliculorum brevis - posterior blepharitis

Collarettes (cylindrical collections of keratin, waste, mite eggs around lash bases) are considered pathognomonic of Demodex infestation.

Clinical Features

Symptoms

Burning, grittiness, mild photophobia, crusting of lid margins
Symptoms worse in the morning (vs. dry eye alone which worsens through the day)
Stinging may be more prominent in posterior disease
Contact lens intolerance
Usually bilateral and symmetrical, no visual disturbance

Signs - Anterior (Staphylococcal)

Blepharitis with lash collarettes (Wills Eye Fig. 5.8.1):

Anterior blepharitis showing crusting and collarettes around the eyelash bases

Hard scales and crusting at the base of lashes
Collarettes (cylindrical collections around lash bases) - pathognomonic
Mild papillary conjunctivitis, chronic conjunctival hyperaemia
Long-standing: scarring/notching of lid margin, madarosis (lash loss), trichiasis, poliosis (white lashes)

Signs - Anterior (Seborrhoeic)

Hyperaemic, greasy anterior lid margins
Soft scales; lashes stuck together

Signs - Posterior (MGD)

Meibomitis with inspissated meibomian glands (Wills Eye Fig. 5.8.2):

Posterior blepharitis showing inspissated meibomian glands visible through the tarsal conjunctiva

Capping of meibomian gland orifices with oil globules
Pouting, recession, or plugging of gland orifices
Hyperaemia and telangiectasis of the posterior lid margin
Expression of turbid or toothpaste-like meibomian secretion on pressure
Lid transillumination: gland loss and cystic ductal dilatation
Oily, foamy, unstable tear film; froth at lid margins and inner canthi

Complications / Associated Conditions

Dry eye syndrome (all types, most severe in posterior)
Corneal changes: superficial punctate keratopathy (SPK), peripheral infiltrates, vascularization (pannus), phlyctenules
Chalazion / hordeolum
Atopic keratoconjunctivitis (in patients with atopic dermatitis)
Acne rosacea (posterior)
Blepharokeratoconjunctivitis (chronic progression)

Red flag: Intractable, unilateral, or asymmetric blepharitis (especially upper vs. lower eyelid asymmetry) is a rare but important presentation of sebaceous cell carcinoma of the eyelid - requires appropriate clinical workup. - Wills Eye Manual

Angular Blepharitis

Involves the canthal area (medial or lateral angle)
Caused by Moraxella lacunata (most common) or S. aureus
Associated with angular conjunctivitis
Treatment: topical tetracycline or chloramphenicol

Treatment

Step-by-step (Wills Eye Manual)

Eyelid hygiene (cornerstone) - lid margin scrubs twice daily with commercial eyelid scrub or dilute baby shampoo on a washcloth
Warm compresses - 5-10 minutes, 2-4 times daily (softens inspissated meibum)
Artificial tears - preservative-free, 4-8 times/day if dry eye component
Topical antibiotics - erythromycin ointment or azithromycin gel-drop to lid margins at bedtime (moderately severe disease)
Oral tetracyclines - doxycycline 100 mg twice daily (unresponsive cases, rosacea); azithromycin 500 mg/day x 3 days for 3 cycles with 7-day intervals is an alternative
Omega-3 supplementation - improves meibomian gland function
Cyclosporine 0.05%/0.09% or lifitegrast 5% drops twice daily for the inflammatory/dry eye component
Demodex-directed therapy - tea-tree oil lid scrubs or hypochlorous acid lid cleansing agent for minimum 6 weeks if collarettes present and prior treatment failed
Advanced meibomian gland treatments - thermal pulsation + expression, intense pulsed light (IPL), microblepharoexfoliation, meibomian gland probing

Note: Tetracycline derivatives (doxycycline) are contraindicated in pregnancy, breastfeeding, and children ≤8 years. Use erythromycin 200 mg twice daily as an alternative. - Wills Eye Manual

Follow-up

Review at 2-4 weeks. Lid hygiene and warm compresses may be reduced to once daily as the condition improves but are typically needed indefinitely - blepharitis is rarely cured, only controlled.

Sources: Kanski's Clinical Ophthalmology, 10th ed.; The Wills Eye Manual, 8th ed.

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