Ophthalmology

THE CONCEPT

Trichiasis is a misdirection of the eyelashes so that they grow backward and rub against the cornea and conjunctiva, while the lid margin itself remains in a normal position. It must be distinguished from entropion (in which the whole lid margin is inverted) and from distichiasis (an abnormal extra row of lashes emerging from the meibomian orifices).

CAUSES & EFFECTS

It results from chronic blepharitis and, most importantly, cicatricial conditions — trachoma (a major cause worldwide and in India), Stevens–Johnson syndrome, ocular pemphigoid and chemical burns — and secondarily from entropion. The rubbing lashes cause a foreign-body sensation, watering, corneal abrasion and, if persistent, ulceration, vascularisation and scarring.

MANAGEMENT

Treatment aims to remove or destroy the offending lashes and protect the cornea: epilation (simple but temporary, as lashes regrow), electrolysis, cryotherapy or radiofrequency/argon-laser ablation of the follicles, together with treatment of any underlying entropion or cause, and lubricants or a bandage contact lens to protect the cornea.

A NOTE ON THE TRACHOMA CONNECTION

Because trachoma is the leading infectious cause of blindness worldwide and remains important in parts of India, the trichiasis it produces is a major public-health concern. Repeated chlamydial infection scars the conjunctiva and tarsus, causing entropion and trichiasis, and the constantly rubbing lashes eventually opacify the cornea. This is why the WHO 'SAFE' strategy includes Surgery for trichiasis/entropion (the 'S'), alongside Antibiotics, Facial cleanliness and Environmental improvement. Treating an individual's trichiasis therefore sits within a wider preventive effort, and recognising trachomatous trichiasis should prompt attention to the underlying disease and its transmission.

THE BOTTOM LINE

Trichiasis is misdirection of otherwise normally-sited lashes onto the cornea, most importantly from cicatricial disease such as trachoma, and is managed by destroying the offending lashes and treating the underlying entropion or scarring while protecting the cornea.

In practice, epilation gives quick relief but the lashes regrow within weeks, so definitive destruction of the follicle (by electrolysis, cryotherapy or laser) is needed for lasting cure; where trichiasis is due to entropion, correcting the lid malposition itself resolves the lash misdirection, which is why every case is examined for an underlying entropion before treating the lashes in isolation.

It is also worth distinguishing trichiasis clearly from pseudotrichiasis, in which the lashes are correctly directed but the whole margin is turned in by an entropion; the treatments differ, since true trichiasis needs lash ablation whereas pseudotrichiasis is cured by correcting the lid position, and confusing the two leads to persistent symptoms and repeated failed epilations.

• Trichiasis = misdirected lashes rubbing the cornea/conjunctiva, with a normally-positioned lid margin.
• Distinguish from entropion (whole margin inverted) and distichiasis (extra lash row from meibomian orifices).
• Causes: chronic blepharitis and cicatricial disease (trachoma — major cause; SJS, pemphigoid, burns), secondary to entropion.
• Foreign-body sensation, watering, corneal abrasion → ulceration/scarring; treat by epilation/electrolysis/cryo/laser ablation + treat cause + protect cornea.

THE CONCEPT

Blepharitis is a chronic inflammation of the eyelid margins. It is extremely common, tends to be bilateral, chronic and relapsing, and is a frequent cause of chronic ocular irritation and of recurrent styes and chalazia.

TYPES

• Anterior blepharitis — affecting the lashes: staphylococcal (crusting and 'collarettes' at the lash bases, with ulceration) or seborrhoeic (greasy scales).
• Posterior blepharitis — meibomian-gland dysfunction (inspissated oil at the gland orifices, foamy tears), strongly associated with rosacea.

FEATURES & MANAGEMENT

Symptoms are burning, itching, grittiness, redness and crusting, worse in the mornings, with red, thickened lid margins, crusts/collarettes, telangiectasia and blocked meibomian orifices; it is associated with dry eye, styes, chalazia and marginal keratitis. The mainstay of treatment is lid hygiene (warm compresses and lid scrubs), with topical antibiotics (chloramphenicol/azithromycin) for staphylococcal disease, and oral doxycycline for posterior/rosacea-related disease, plus treatment of dry eye. It is controlled rather than cured.

A NOTE ON THE ASSOCIATED OCULAR SURFACE DISEASE

A practical point is that blepharitis rarely occurs in isolation — it drives, and coexists with, evaporative dry eye and a whole spectrum of lid-related disease. The unhealthy meibomian secretions destabilise the tear film, so patients have both the irritation of blepharitis and the grittiness of dry eye, and they are prone to recurrent styes, chalazia and marginal (catarrhal) keratitis from staphylococcal hypersensitivity. This is why management addresses the whole ocular surface — lid hygiene, tear supplements and sometimes anti-inflammatory treatment — rather than the lid margin alone, and why patients are counselled that it is a chronic condition needing ongoing maintenance.

THE BOTTOM LINE

Blepharitis is a common, chronic, relapsing lid-margin inflammation (anterior staphylococcal/seborrhoeic or posterior meibomian) controlled — not cured — by lifelong lid hygiene, with antibiotics for staphylococcal or rosacea-related disease.

A useful practical tip is that improvement in blepharitis is gradual and depends heavily on the patient persisting with daily lid hygiene, so counselling about the chronic nature of the condition and demonstrating the compress-and-scrub routine matters as much as any prescription; abrupt discontinuation typically leads to relapse within weeks.

A further useful point is that staphylococcal blepharitis is associated with a type-IV hypersensitivity to staphylococcal exotoxin, which explains the marginal (catarrhal) infiltrates and phlyctenules some patients develop; recognising this immune component clarifies why lid hygiene and controlling the lid bacteria, rather than antibiotics alone, form the basis of long-term management.

• Blepharitis = chronic, bilateral, relapsing inflammation of the lid margins.
• Anterior (staphylococcal — collarettes/ulceration; or seborrhoeic — greasy scales) vs posterior (meibomian-gland dysfunction, linked to rosacea).
• Burning, itching, grittiness, crusting worse in mornings; red margins, telangiectasia, blocked meibomian orifices; associated dry eye, styes, chalazia, marginal keratitis.
• Mainstay lid hygiene (warm compresses, scrubs); topical antibiotic (staph), oral doxycycline (posterior/rosacea); controlled not cured.

THE CONCEPT

Lagophthalmos is the inability to close the eyelids completely, so that part of the cornea remains exposed. It matters because the exposed cornea dries out and is at risk of breakdown.

CAUSES

The commonest cause is a facial (VII) nerve palsy (weakness of the orbicularis oculi that closes the lids); others are proptosis (thyroid eye disease), severe ectropion or cicatricial lid disease, and reduced consciousness/sedation. Loss of the protective Bell's phenomenon (upward rolling of the eye on lid closure) further increases the risk.

EFFECT & MANAGEMENT

The result is exposure keratopathy — drying of the lower cornea with punctate erosions, progressing to ulceration and infection. Management is to lubricate and protect the cornea (drops by day, ointment at night, taping, a moisture chamber) and treat the cause; for severe or persistent exposure, a tarsorrhaphy or gold-weight lid loading (in VII palsy) is used, and any proptosis or ectropion is corrected.

A NOTE ON THE FACIAL-PALSY EYE

The commonest and most instructive scenario is the eye in a facial (VII) nerve palsy, where several protective mechanisms fail together: the orbicularis cannot close the lids (lagophthalmos), the blink is lost, and the lower lid may sag into a paralytic ectropion, sometimes compounded by reduced tear production. Such an eye can break down quickly and silently, especially if corneal sensation is also impaired. It therefore needs immediate and generous protection — lubricant ointment and taping at night, with early consideration of a temporary tarsorrhaphy or gold-weight upper-lid loading — while facial function is awaited, so that a recoverable nerve palsy does not leave a permanently scarred cornea.

THE BOTTOM LINE

Lagophthalmos is incomplete lid closure (commonest cause a VII palsy) that exposes and dries the cornea, demanding prompt lubrication and protection, with tarsorrhaphy or lid loading for severe cases.

Assessing the eye also involves testing corneal sensation and the Bell's phenomenon, because an anaesthetic cornea or an absent Bell's greatly increases the risk of silent breakdown; these findings raise the urgency of protective measures and lower the threshold for surgical lid closure, so they are specifically checked in every patient with lagophthalmos.

Finally, the amount of cornea exposed and whether it lies in the interpalpebral zone determine the urgency: a small, well-lubricated gap may be managed conservatively, whereas exposure of the visual axis or a frankly staining cornea calls for prompt surgical protection, so the degree of lagophthalmos is quantified and the cornea examined with fluorescein at each review.

• Lagophthalmos = incomplete lid closure leaving the cornea exposed.
• Causes: facial (VII) nerve palsy (commonest), proptosis (thyroid eye disease), severe ectropion/cicatricial disease, reduced consciousness; worse if Bell's phenomenon lost.
• Leads to exposure keratopathy — drying, punctate erosions, ulceration, infection.
• Treat with lubrication (drops/ointment), taping, moisture chamber, treat cause; tarsorrhaphy or gold-weight loading (VII palsy) if severe.

THE CONCEPT

The eyelids are a common site for skin tumours, and malignant lid tumours occur mostly on the lower lid (the most sun-exposed area). The commonest by far is basal cell carcinoma (BCC), which accounts for about 90% of malignant lid tumours.

BASAL CELL CARCINOMA & OTHERS

BCC is slow-growing and locally invasive but rarely metastasises. The classic appearance is a pearly nodule with a rolled edge and central ulceration (a 'rodent ulcer'), surface telangiectasia and loss of lashes (madarosis). Other lid malignancies are squamous cell carcinoma (more aggressive, can metastasise), sebaceous gland carcinoma (dangerous — it arises from the meibomian glands and masquerades as a recurrent chalazion or chronic blepharitis), and melanoma.

WARNING SIGNS & MANAGEMENT

Features that should raise suspicion of malignancy are ulceration, induration, loss of lashes (madarosis), an irregular or pearly margin, telangiectasia and a 'recurrent chalazion'. Any suspicious lesion should be biopsied; treatment is surgical excision with margin control (Mohs) and lid reconstruction (radiotherapy in selected cases).

A NOTE ON RECONSTRUCTION & THE 'LID-SPARING' AIM

An important principle in treating lid malignancies is balancing complete tumour removal against preserving lid function. The lid must both cover and protect the eye, so after excising a tumour with clear margins (ideally confirmed by Mohs micrographic surgery or frozen-section margin control), the surgeon reconstructs the lid to restore a smooth margin, adequate closure and a functioning tear drainage. Incomplete excision risks recurrence, while over-aggressive removal risks exposure keratopathy from a poorly-closing lid — so oculoplastic reconstruction is an integral part of management, and any suspicious lid lesion is referred rather than simply shaved off.

THE BOTTOM LINE

Basal cell carcinoma is the commonest lid malignancy — a slowly invasive 'rodent ulcer' on the lower lid — while sebaceous gland carcinoma dangerously mimics a recurrent chalazion; any suspicious lid lesion needs biopsy and margin-controlled excision.

Because these tumours are slow but relentless, early referral of any non-healing, ulcerating or pearly lid lesion — or a 'chalazion' behaving atypically — gives the best outcome, allowing smaller excisions and simpler reconstruction; delay allows local spread that can eventually involve the orbit and require far more extensive surgery.

For completeness, prevention matters too, since most lid malignancies are sun-related; advising sun protection and prompt attention to non-healing lid lesions, especially in fair-skinned and older patients, reduces both the incidence and the eventual extent of surgery required, and periodic self-examination of the lids is a simple safeguard.

• Eyelids are a common site for skin cancer; most malignant lid tumours are on the lower lid (sun-exposed).
• Basal cell carcinoma = commonest (~90%): slow, locally invasive, rarely metastasises; pearly rolled edge with central ulcer ('rodent ulcer'), telangiectasia, madarosis.
• Others: squamous cell carcinoma (aggressive), sebaceous gland carcinoma (masquerades as recurrent chalazion/blepharitis — can metastasise), melanoma.
• Warning signs: ulceration, induration, lash loss (madarosis), pearly/irregular margin, recurrent 'chalazion'; biopsy + excision with margin control (Mohs) + reconstruction.

THE CONCEPT

Dacryocystorhinostomy (DCR) is the standard surgical treatment for nasolacrimal-duct obstruction and chronic dacryocystitis. It relieves the watering and eliminates the infected sac by creating a new drainage route that bypasses the blocked duct.

THE PRINCIPLE

The operation makes a bony opening (ostium) between the lacrimal-sac fossa and the nasal cavity and anastomoses the lining of the sac to the nasal mucosa (at the middle meatus), so tears drain directly from the sac into the nose. It may be done as an external DCR (through a small skin incision — high success) or an endoscopic/endonasal DCR (through the nose, leaving no scar), often with temporary silicone intubation.

INDICATIONS & OUTCOME

It is indicated for chronic dacryocystitis, symptomatic NLD obstruction and a mucocele, and is performed once any acute infection has settled. Success rates are high (~90%); complications include bleeding, scarring, failure (re-obstruction) and infection.

A NOTE ON EXTERNAL VERSUS ENDOSCOPIC DCR

A commonly-discussed point is the choice between the two DCR approaches. External DCR, through a small skin incision at the side of the nose, has the highest and most reliable success rate and allows direct suturing of the mucosal flaps, at the cost of a small (usually inconspicuous) scar. Endoscopic (endonasal) DCR is performed entirely through the nose, leaving no external scar and allowing simultaneous treatment of nasal pathology, with success rates now approaching those of the external route in experienced hands. The choice depends on the surgeon's expertise, the anatomy and any associated nasal disease — but the underlying principle, creating a sac-to-nose bypass, is the same for both.

THE BOTTOM LINE

DCR cures nasolacrimal-duct obstruction and chronic dacryocystitis by creating a sac-to-nose bypass, performed externally or endoscopically with high success once the acute infection has settled.

It is also worth remembering that DCR is deferred until any acute dacryocystitis has been controlled with antibiotics, since operating on an acutely infected, inflamed sac increases bleeding and failure; once the eye is quiet, the bypass can be created electively with a high chance of relieving the watering permanently.

A practical adjunct worth noting is that a temporary silicone stent is often left through the new passage for a few weeks to months to keep it open while it heals, and its later removal in clinic is straightforward; the underlying aim throughout is a permanently patent, epithelialised channel from sac to nose.

• DCR = surgery for nasolacrimal-duct obstruction/chronic dacryocystitis; bypasses the blocked duct.
• Creates a bony ostium between the lacrimal sac and the nose and anastomoses sac to nasal mucosa (middle meatus).
• External DCR (skin incision, high success) or endoscopic/endonasal DCR (no scar); often with silicone intubation.
• Indications: chronic dacryocystitis, NLD obstruction, mucocele (after acute infection settles); success ~90%; complications — bleeding, scar, failure, infection.

THE CONCEPT

Xanthelasma are soft, yellowish, flat plaques of lipid-laden macrophages deposited in the skin of the eyelids, typically at the medial (inner) canthus and often bilateral and symmetrical. They are the commonest cutaneous xanthoma.

SIGNIFICANCE

Although many patients are normolipaemic, xanthelasma can be a marker of dyslipidaemia (hypercholesterolaemia) — so serum lipids should be checked, especially in a younger patient — and it is associated with an increased risk of atherosclerotic cardiovascular disease. They are not sight-threatening and are usually a cosmetic concern.

MANAGEMENT

Management is reassurance plus lipid assessment and treatment where a dyslipidaemia is found. For cosmesis they can be removed by surgical excision, laser, trichloroacetic-acid application or cryotherapy, though recurrence is common.

A NOTE ON THE SYSTEMIC IMPLICATIONS

The main clinical value of recognising xanthelasma is as a potential window onto the patient's lipid status and cardiovascular risk. While plenty of people with xanthelasma have normal lipids, its presence — particularly in a younger patient or with other signs such as a premature corneal arcus or tendon xanthomata — should prompt a fasting lipid profile and assessment of cardiovascular risk factors, since it may signal familial or acquired hypercholesterolaemia. Managing the lipids not only addresses the underlying disorder but may slow the appearance of new lesions, which is why the eyelid finding is treated as a cue for a wider systemic assessment rather than a purely cosmetic issue.

THE BOTTOM LINE

Xanthelasma are benign eyelid lipid plaques that are chiefly important as a possible marker of dyslipidaemia and cardiovascular risk, warranting a lipid check and treated cosmetically if desired.

For completeness, when xanthelasmata are removed cosmetically the patient is warned that recurrence is common, particularly if an underlying dyslipidaemia is left untreated, so lipid control is emphasised alongside any procedure; the lesions themselves never threaten vision and treatment is entirely elective.

It is also useful to remember that xanthelasma may recur after removal and can be multiple and progressive, so patients are counselled realistically about outcomes; the eyelid deposits themselves are entirely benign, and the clinical priority remains identifying and treating any underlying lipid disorder rather than the plaques.

• Xanthelasma = soft, yellow, flat lipid plaques in the eyelid skin, typically at the medial canthus, often bilateral; commonest cutaneous xanthoma.
• May be normolipaemic but can indicate dyslipidaemia (hypercholesterolaemia) — check lipids (especially if young); associated with cardiovascular risk.
• Not sight-threatening; mainly a cosmetic concern.
• Reassure + treat any dyslipidaemia; remove for cosmesis (excision, laser, TCA, cryotherapy) — recurrence common.

THE CONCEPT

Infections around the eye are divided by their relation to the orbital septum (a fibrous sheet from the orbital rim to the lids) into preseptal (in front of the septum) and orbital (behind the septum) cellulitis. The distinction is critical because orbital cellulitis is a sight- and life-threatening emergency while preseptal cellulitis is usually not.

THE COMPARISON

MANAGEMENT

Preseptal cellulitis is treated with oral (or intravenous) antibiotics and close monitoring. Orbital cellulitis requires emergency admission, intravenous antibiotics, urgent CT of the sinuses/orbit, and ENT involvement, with surgical drainage of any abscess, because it can progress to a subperiosteal/orbital abscess, cavernous-sinus thrombosis, meningitis and blindness.

A NOTE ON WHY THE DISTINCTION IS URGENT

The reason the preseptal/orbital distinction is drilled so hard is that orbital cellulitis can blind or kill within hours to days, whereas preseptal cellulitis usually settles on oral antibiotics. Behind the septum, infection (typically spreading from ethmoid sinusitis in a child) can form a subperiosteal or orbital abscess, compress the optic nerve, or propagate backward to cause cavernous-sinus thrombosis, meningitis or a brain abscess. The examiner therefore expects the clinician to check the three cardinal discriminators — vision, proptosis and eye movements — in any child with a swollen red eye, and to treat any suggestion of orbital involvement as an emergency with imaging, intravenous antibiotics and ENT/ophthalmology input.

THE BOTTOM LINE

Preseptal and orbital cellulitis are separated by the orbital septum and, crucially, by vision, proptosis and eye movements — preseptal is usually managed with antibiotics, while orbital cellulitis is a sight- and life-threatening emergency.

A final practical point is that in children a swollen, red eye with even subtle proptosis, painful eye movements or any change in vision must be assumed to be orbital cellulitis until imaging proves otherwise, because the ethmoid sinus is thin-walled and infection crosses into the orbit easily at this age; a low threshold for admission and CT is therefore the safe approach.

As a final safeguard, any deterioration in a patient treated for presumed preseptal cellulitis — new proptosis, restricted or painful movements, or falling vision — must trigger immediate reassessment for orbital involvement, since preseptal infection can occasionally progress posteriorly and the window to prevent optic-nerve damage or intracranial spread is short.

• Cellulitis around the eye is classified by the orbital septum: preseptal (anterior) vs orbital (posterior).
• Preseptal: lid swelling/redness but NORMAL vision, NO proptosis, FULL painless eye movements; usually from skin/lid infection or trauma.
• Orbital: proptosis, painful restricted eye movements, reduced vision/RAPD, chemosis, systemic upset; usually from ethmoid sinusitis (esp children) — EMERGENCY.
• Preseptal → oral/IV antibiotics + monitor; orbital → emergency admission, IV antibiotics, CT sinuses/orbit, ENT, drain abscess; risks orbital abscess, cavernous-sinus thrombosis, meningitis, blindness.