Also read anatomy of the lacrimal system and cornea and diseases

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Anatomy of the Lacrimal System, Cornea, and Corneal Diseases

PART 1: LACRIMAL DRAINAGE SYSTEM

Source: Kanski's Clinical Ophthalmology, 10th Edition

Anatomy

The lacrimal drainage system consists of five key structures:

1. The Puncta

Located at the posterior edge of the lid margin, at the junction of the lash-bearing lateral five-sixths (pars ciliaris) and the medial non-ciliated one-sixth (pars lacrimalis).
The punctum and vertical canaliculus are part of the tarsal plate.
Normally the puncta face slightly posteriorly and can be inspected by everting the medial lids.

2. The Canaliculi

Each canaliculus passes vertically from the lid margin for about 2 mm (the ampulla), then turns medially and runs horizontally for ~8 mm to reach the lacrimal sac.
The horizontal canaliculus is surrounded by the palpebral part of the orbicularis oculi muscle (Horner muscle).
The superior and inferior canaliculi usually unite (>90% of cases) to form the common canaliculus, which opens into the lateral wall of the lacrimal sac.
A small mucosal flap - the Rosenmüller valve - overhangs the junction of the common canaliculus and the lacrimal sac (the internal punctum), preventing reflux of tears into the canaliculi.

3. The Lacrimal Sac

10-12 mm long, lying in the lacrimal fossa between the anterior and posterior lacrimal crests.
The lacrimal bone and the frontal process of the maxilla separate the lacrimal sac from the middle meatus of the nasal cavity.
In a dacryocystorhinostomy (DCR), an anastomosis is created between the sac and the nasal mucosa to bypass nasolacrimal duct obstruction.

4. The Nasolacrimal Duct

12-18 mm long, the inferior continuation of the lacrimal sac.
Descends, angling slightly laterally and posteriorly, to open into the inferior nasal meatus, lateral to and below the inferior turbinate.
The opening is partially covered by a mucosal fold - the valve of Hasner.

Physiology of Tear Drainage

Tears secreted by the main and accessory lacrimal glands flow across the ocular surface. Drainage proceeds as follows:

Tears flow along the upper and lower marginal strips, pooling in the lacus lacrimalis medial to the lower puncta, then entering the canaliculi by capillarity and suction.
With each blink, the pretarsal orbicularis oculi muscle compresses the ampullae, shortens and compresses the horizontal canaliculi, and moves the puncta medially - resisting reflux. Simultaneously, contraction of the lacrimal part of the orbicularis creates positive pressure that forces tears down the nasolacrimal duct into the nose (mediated by helically arranged connective tissue fibres around the lacrimal sac).
When the eyes open, the canaliculi and sac expand, creating negative pressure that draws tears from the canaliculi into the sac.

Common Lacrimal Diseases

Condition	Key Features
Conjunctivochalasis	Redundant conjunctival folds occlude the puncta
Punctal stenosis	Primary (idiopathic) or secondary (drug-induced, infection, inflammation)
Canalicular obstruction	May require complex surgical repair; caused by trauma, infection, drugs
Nasolacrimal duct obstruction	Most common cause of epiphora; treated by DCR
Dacryolithiasis	Calcified concretions within the lacrimal sac
Chronic canaliculitis	Often caused by Actinomyces israelii; presents with red, swollen punctum
Acute dacryocystitis	Painful swelling over the lacrimal sac; usually S. aureus or Streptococcus
Chronic dacryocystitis	Mucoid/mucopurulent reflux on pressure over sac; treated by DCR
Congenital NLD obstruction	Failure of valve of Hasner to open; resolves spontaneously in 90% by 1 year
Congenital dacryocele	Distended lacrimal sac at birth from obstruction at both ends

PART 2: CORNEA - ANATOMY

Sources: Kanski's Clinical Ophthalmology, 10th Ed.; Robbins & Kumar Basic Pathology

Structure and Layers

The cornea and its overlying tear film make up the major refractive surface of the eye. Its shape significantly influences refractive power (the basis of LASIK surgery for myopia and hyperopia).

The cornea has 5 layers (from anterior to posterior):

Layer	Key Features
Epithelium	5-6 cell layers of non-keratinized stratified squamous epithelium; rests on a basement membrane; regenerates rapidly
Bowman layer	Acellular condensed collagen just beneath the epithelial basement membrane; does not regenerate if damaged
Stroma	~90% of corneal thickness; collagen lamellae arranged in precise orthogonal pattern for transparency; avascular; contains keratocytes (fibroblasts)
Descemet membrane	Specialized basement membrane of the endothelium; thickens with age
Endothelium	Single layer of cells derived from neural crest; lines the posterior surface; pumps fluid out of stroma to maintain clarity; does not regenerate in humans

Key properties:

The stroma lacks blood vessels and lymphatics - this contributes to corneal transparency and the high success rate of corneal transplantation (immune privilege).
The corneal endothelium is derived from neural crest and is not related to vascular endothelium.

PART 3: CORNEAL DISEASES

1. Keratitis and Corneal Ulceration

Kanski's + Robbins & Kumar

Pathogens causing keratitis include: bacterial, fungal, viral (especially HSV and VZV), and protozoal (Acanthamoeba).

Pathophysiology: Dissolution of the corneal stroma is accelerated by activation of collagenases within corneal epithelium and stromal fibroblasts (keratocytes). Exudate from iris and ciliary body vessels leaking into the anterior chamber may form a hypopyon (visible pus level) - though the hypopyon seldom contains organisms and represents a vascular response to acute inflammation.

Herpes simplex keratitis (chronic form): May be associated with a granulomatous reaction involving the Descemet membrane.

Signs of active keratitis:

Epithelial defect with fluorescein staining
Stromal infiltrate/opacity
Hypopyon
Ciliary injection

2. Keratoconus

Kanski's Clinical Ophthalmology, 10th Ed.; Robbins & Kumar Basic Pathology

Definition: A progressive disorder in which central or paracentral corneal stromal thinning occurs, accompanied by apical protrusion and irregular astigmatism.

Epidemiology:

Prevalence: 0.1-0.2% (incidence ~1 in 2000)
Men slightly more affected than women
Presentation commonly in the teens or twenties
~50% of normal fellow eyes progress to KC within 16 years
Eventually bilateral in almost all cases

Risk factors and associations:

Allergy, asthma, eczema, persistent eye rubbing
Systemic: Down syndrome, Ehlers-Danlos syndrome, Marfan syndrome, osteogenesis imperfecta
Ocular: vernal keratoconjunctivitis, Leber congenital amaurosis, retinitis pigmentosa

Grading (by keratometry):

Mild: <48 D
Moderate: 48-54 D
Severe: >54 D

Clinical Signs:

"Oil droplet" red reflex on direct ophthalmoscopy at 0.5 m distance
Irregular "scissoring" reflex on retinoscopy
Vogt striae - fine vertical lines in the deep stroma
Fleischer ring - iron deposits at the base of the cone (visible with cobalt blue light)
Munson sign - V-shaped distortion of the lower lid on downgaze
Rizzuti sign - conical reflection on the nasal cornea when light is directed from the temporal side

Histology (Robbins): Thinning of the cornea with breaks in the Bowman layer are the hallmarks.

Complication - Acute Hydrops:

Descemet membrane ruptures, allowing aqueous humor to flood the corneal stroma
Sudden severe vision loss
May be followed by corneal scarring

Treatment:

Spectacles or rigid contact lenses (RGP) for mild-moderate
Corneal collagen cross-linking (CXL) to halt progression
Intrastromal corneal ring segments (ICRS) for moderate disease
Penetrating keratoplasty (PKP) or deep anterior lamellar keratoplasty (DALK) for advanced/contact-lens-intolerant cases

3. Fuchs Endothelial Dystrophy

Robbins & Kumar Basic Pathology

Results from loss of corneal endothelial cells, leading to edema and thickening of the stroma.
One of the principal indications for corneal transplantation in the United States.
Major manifestations: stromal edema and bullous keratopathy (blistering of the epithelium).
Treated by Descemet membrane endothelial keratoplasty (DMEK) or DSAEK.

4. Xerophthalmia (Vitamin A Deficiency)

Kanski's Clinical Ophthalmology

WHO Grading:

XN = night blindness
X1A = conjunctival xerosis; X1B = Bitot spots
X2 = corneal xerosis
X3A/X3B = corneal ulceration (<1/3 or >1/3 of cornea)
XS = corneal scar; XF = xerophthalmic fundus

Keratomalacia (sterile corneal melting by liquefactive necrosis) is an indicator of very severe vitamin A deficiency - treated as a medical emergency due to risk of death in infants. Treatment: oral vitamin A 200,000 IU (oil-based) or IM 100,000 IU (aqueous-based).

5. Dry Eye / Keratoconjunctivitis Sicca

Kanski's Clinical Ophthalmology

Corneal complications of severe dry eye include:

Punctate epithelial erosions (stain with fluorescein)
Filamentary keratitis - strands of mucus/debris attached to corneal surface (stain with rose Bengal)
Mucous plaques
In severe cases: epithelial breakdown, corneal melting, perforation, bacterial keratitis

Investigations measure:

Tear film break-up time (BUT) - stability
Schirmer test - aqueous production
Rose Bengal / lissamine green staining - epithelial surface damage

Key Sources:

Kanski's Clinical Ophthalmology: A Systematic Approach, 10th Edition - Chapters 3 (Lacrimal drainage), 5 (Dry eye / cornea), 7 (Corneal ectasia/diseases)
Robbins & Kumar Basic Pathology - Chapter on Eye Pathology (Cornea section)

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