notes/A K Khurana - Comprehensive Ophthalmology_13.txt

Etiology. It is a viral infection of the lids, commonly affecting children. It is caused by a large poxvirus. Clinical features. Its typical lesions are multiple, pale, waxy, umbilicated swellings scattered over the skin near the lid margin (Fig. 15.15).
Complications include chronic follicular conjunctivitis and superficial keratitis.
Treatment. The skin lesions should be incised and the interior cauterised with tincture of iodine or pure carbolic acid.















Fig. 15.14 Hordeolum internum lower eyelid














Fig. 15.15 Molluscum contagiosum of the lids

EYELASH DISORDERS

TRICHIASIS
It refers to inward misdirection of cilia (which rub against the eyeball) with normal position of the lid margin (Fig. 15.16).
Pseudotrichiasis. The inward turning of lashes along with the lid margin (seen in entropion) is called pseudotrichiasis.
Etiology
Common causes of trichiasis are: cicatrising trachoma, ulcerative blepharitis, healed mem-branous conjunctivitis, hordeolum externum, mechanical injuries, burns, and operative scar on the lid margin.
Clinical features
Symptoms. These include foreign body sensation and photophobia. Patient may feel troublesome irritation, pain and lacrimation.
Signs. Examination reveals:
• Misdirected cilia one or more touching the cornea. • Reflex blepharospasm and photophobia occur
when cornea is abraded.
• Conjunctiva may be congested.
• Signs of causative disease viz. trachoma, blepharitis, etc. may be present.
Complications. These include recurrent corneal abrasions, superficial corneal opacities, corneal vascularisation (Fig. 15.16B) and non-healing corneal ulcer.
Treatment
A few misdirected cilia may be treated by any of the following methods:
1. Epilation (mechanical removal with forceps). It is a temporary measure, as recurrence occurs within 3–4 weeks.
2. Electrolysis. It is a method of destroying the lash follicle by electric current. In this technique,
Chapter 15	Disorders of Eyelids	371















A











B
Fig. 15.16 Trichiasis; A, diagrammatic depiction; B, clinical photograph

infiltration anaesthesia is given to the lid and a current of 2 mA is passed for 10 seconds through a fine needle inserted into the lash root. The loosened cilia with destroyed follicles are then removed with epilation forceps.
3. Cryoepilation. It is also an effective method of treating trichiasis. After infiltration anaesthesia, the cryoprobe (–20°C) is applied for 20–25 seconds to the external lid margin by double freeze-thaw technique. Its main disadvantage is depigmentation of the skin. 4. Surgical correction.When many cilia are misdirected operative treatment similar to cicatricial entropion should be employed.
DISTICHIASIS
Congenital distichiasis (Fig. 15.17) is a rare anomaly in which an extra row of cilia occupies the position of Meibomian glands which open into their follicles as ordinary sebaceous glands. These cilia are usually directed backwards and when rubbing the cornea, should be electroepilated or cryoepilated. Acquired distichiasis (metaplastic lashes) occurs when due to metaplasia and differentiation, the meibomian glands are transformed into hair follicles. The most important cause is late stage of cicatrizing


Fig. 15.17 Distichiasis

conjunctivitis associated with chemical injury, Stevens-Johnson syndrome and ocular cicatricial pemphigoid.
MADAROSIS
Madarosis refers to partial or complete loss of eyelashes.
Causes can be local or systemic.
■Local causes of madarosis include chronic blepheriris, cicatrizing conjunctivitis, and complication of cryotherapy, radiotherapy or surgery done for any eyelid lesion.
■Systemic causes of madarosis are alopecia (patchy, totalis/universalis), psoriasis, hypothyroidism and leprosy.

ANOMALIES IN THE POSITION OF LID MARGINS
ENTROPION
Entropion refers to inward rolling and rotation of the lid margin toward globe.
Etiological types
1. Congenital entropion. It is a rare condition seen since birth. Seen more commonly in lower than upper eyelid.
■Lower eyelid congenital entropion is caused by improper development of the lower lid retractors. ■Upper eyelid congenital entropion is usually secondary to mechanical effects of microphthalmos. 2. Cicatricial entropion (Fig. 15.18). It is a common variety usually involving the upper lid. It is caused by cicatricial contraction of the palpebral conjunctiva, with or without associated distortion of the tarsal plate.
Common causes are trachoma, membranous conjunctivitis, chemical burns, pemphigus and Stevens-Johnson syndrome.
372	Section II   Diseases of Eye















Fig. 15.18 Cicatricial entropion

3. Senile (involutional) entropion. It is common occurrence and affects only the lower lid in elder people (Fig. 15.19).
Etiological factors  which  contribute  for  its development are:
• Horizontal laxity of the lid due to weakening of orbicularis muscle.
• Vertical lid instability due to weakening or dehiscence of capsulopalpebral fascia (lower lid retractor).
• Over-riding of pretarsal orbicularis. Degeneration of palpebral connective tissue separates the orbicularis muscle fibres and thus allowes preseptal fibres to over-ride the pretarsal fibres and thus tipping the lid margin inwards.
• Laxity of orbital septum along with prolapse of orbital fat into the lower lid also contribute to inward rolling of lid margin.
4.Mechanical entropion.It occurs due to lack of support provided by the globe to the lids. Therefore, it may occur in patients with phthisis bulbi, enophthalmos and after enucleation or evisceration operation.
Clinical features
Symptoms occur due to rubbing of cilia against the cornea and conjunctiva and are thus similar to











Fig. 15.19 Senile entropion right lower eyelid

trichiasis. These include foreign body sensation, irritation, lacrimation and photophobia.
Signs are as follows:
1.Inturning of lid margins. On examination, lid margin is found inturned. Depending upon the degree of inturning, it can be divided into three grades:
• Grade I entropion, only the posterior lid border is inrolled,
• Grade II entropion, includes inturning up to the inter-marginal strip, and
• Grade III entropion, in which the whole lid margin including the anterior border is inturned.
2. Signs of causative disease, e.g., scarring of palpebral conjunctiva in cicatricial entropion, and horizontal lid laxity in involutional entropion may be seen.
3. Signs of complications include recurrent corneal abrasions, superficial corneal opacities, corneal vascularization and even corneal ulceration.
Treatment
1.Congenital entropionmay resolve with time without need of any intervention or may require excision of a strip of skin and muscle with plastic reconstruction of the lid crease (Hotz procedure).
2. Cicatricial entropion. It is treated by a plastic operation, which is based on any of the following basic principles:
• Altering the direction of lashes, or • Transplanting the lashes, or
• Straightening the distorted tarsus.
Surgical techniquesemployed for correcting cicatricial entropion are as follows:
i. Anterior lamellar resection. It is the simplest operation employed to correct mild degree of entropion. In this operation, an elliptical strip of skin and orbicularis muscle is resected 3 mm away from the lid margin.
ii. Tarsal wedge resection. It corrects moderate degree of entropion associated with atrophic tarsus. In this operation, in addition to the elliptical resection of skin and muscle, a wedge of tarsal plate is also removed (Fig. 15.20).
iii.Transposition oftarsoconjunctival wedge.(Modified Ketssey’s operation) (Fig. 15.21): This is indicated to treat mild to moderate amount of cicatricial entropion. It basically involves tarsal fracture and eversion of distal tarsus. A horizontal incision is made along the whole length of sulcus subtarsalis (2–3 mm above the lid margin) involving conjunctiva and tarsal plate (Fig. 15.21A). The lower piece of tarsal plate is undermined up to lid margin. Mattress sutures are then passed from the upper cut end of the tarsal plate to emerge on the skin 1 mm above
Chapter 15	Disorders of Eyelids	373


the lid margin (Fig. 15.21B). When sutures are tied the entropion is corrected by transposition of tarsoconjunctival wedge (Fig. 15.21C).
iv. Posterior lamellar graft. Indications of this operation include severe entropion with upper eyelid retraction. In this operation, the deficient or keratinized conjunctiva and the scarred and contracted tarsus are replaced by a composite posterior lamellar graft. Tarsus may be replaced by preserved sclera or ear cartilage or hard palate alongwith conjunctival or mucous membrane graph. 3. Senile entropion. Surgical techniques are as below: i. Transverse everting suture. These offer temporary cure (upto 18 months) and are thus indicated in very old patients. The transverse sutures are applied through full thickness of the lids (Fig. 15.22) to prevent over-riding of the preseptal muscles.
ii. Wies operation (Transverse lid split and everting sutures). This operation is indicated for long term cure in patients with little horizontal laxity. In this operation, an incision involving skin, orbicularis and tarsal plate is given 3 mm below the lid margin, along the whole length of the eyelid. Mattress sutures are then passed through the lower cut end of the tarsus to emerge on the skin, 1 mm below the lid margin and are tied firmly (Fig. 15.23). The entropion is corrected by prevention of over-riding of preseptal muscle by the horizontal fibrous scar tissue barrier and transferring of the pull of lid retractors to the upper border of tarsus by the everting sutures.
iii. Plication of lower lid retractors (Jones operation). It is performed in severe cases or when recurrence occurs after the above described operations. In this









A








B






C

Fig. 15.21 Transposition of tarsoconjunctival wedge



A









B

Fig. 15.22 Transverse lid everting sutures. A, diagrammatic section; and B, frontal view to show the position of sutures

operation, the lower lid retractors are exposed via horizontal skin incision at the lower border of the
Fig. 15.20 Tarsal wedge resection	tarsal plate, shortened and the sutures are used to
374	Section II   Diseases of Eye





















Fig. 15.23 Wies operation

create a barrier to prevent over-riding of the preseptal muscle. (Fig. 15.24).
iv. Quickert procedure. This is indicated in patients having associated marked horizontal lid laxity. This operation consists of transverse lid split to create barrier for over-riding of preseptal muscle, everting

























Fig. 15.24 Plication of lower lid retractors: A, front view; B, cut section

sutures to transfer pull of lower lid retractors to upper border of tarsus and horizontal lid shortening to correct the laxity (Fig. 15.25). Thus Quickert procedure basically combines horizontal lid shortening with Weis procedure.
ECTROPION
Out rolling or outward turning of the lid margin is called ectropion.
Etiological types
1. Congenital ectropion. This is very rare, but may be seen in Down syndrome and blepharophimosis syndrome. It may occur in both the upper and lower lids and is due to a congenital shortage of the skin.
2. Involutional ectropion. It is the commonest variety and involves only the lower lids (Fig. 15.26A). It occurs due to following age-related changes:
• Horizontal laxity of eyelid,
• Medial canthal tendon laxity,
• Lateral canthal tendon laxity, and • Disinsertion of lower lid retractors.
3. Cicatricial ectropion. It occurs due to scarring of the skin and can involve both the lids (Fig. 15.26B). Common causes of skin scarring are: thermal burns, chemical burns, lacerating injuries and skin ulcers.
4. Paralytic ectropion. It results due to paralysis of the seventh nerve. It mainly occurs in the lower lids. Common causes of facial nerve palsy are: Bell’s palsy, head injury, infections of the middle ear and operations on parotid gland.
5.Mechanical ectropion. It occurs in conditions where either the lower lid is pulled down (as in tumours) or pushed out and down (as in proptosis and marked chemosis of the conjunctiva).
Clinical features
Symptoms
• Epiphora is the main symptom in ectropion of the lower lid.
• Symptoms due to associated chronic conjunct-ivitis include: irritation, discomfort and mild photophobia.
Signs
1.Lid margin is outrolled. Depending upon the degree of outrolling, ectropion can be divided into three grades:
• Grade I: In it only punctum is everted.
• Grade II: Lid margin is everted and palpebral conjunctiva is visible.
• Grade III: The fornix is also visible.
2. Signs of the etiological condition such as:
Chapter 15	Disorders of Eyelids	375










A

A












B











C
Fig. 15.25   Quickert procedure: A, two vertical incisions for horizontal lid shortening and horizontal slit incision; B, passage of lid everting suture after completion of horizontal lid resection and C, final position of the sutures

• Skin scars in cicatricial ectropion and
• Seventh nerve palsy in paralytic ectropion may also be seen.
3. In involutional ectropion one or more of the following signs can be elicited:
• Horizontal lid laxity can be demonstrated by positive snap test, i.e., lid can be easily pulled away from the globe but fails to snap back to the normal position on release.
• Medial canthal tendon laxity. Normally on pulling the lid laterally the inferior punctum moves by 1–2 mm only; while it can the moved upto limbus

B
Fig. 15.26 A. Involutional ectropion, B. Cicatricial ectropion lower eyelid

in mild and upto pupil in severe degree of medial tendon laxity.
• Lateral canthal tendon laxity is evidenced by rounded appearance of the lateral canthus and its more than 2 mm movement on pulling the lid medially.
Complications
• Dryness and thickening of conjunctiva and corneal ulceration (exposure keratitis) may occur due to prolonged exposure.
• Eczema and dermatitis of the lower lid skin may occur due to prolonged epiphora.
Treatment
1.Congenital ectropion. Mild ectropion often requires no treatment. Moderate or severe ectropion is treated like cicatricial ectropion with horizontal lid tightening and full thickness skin graft to vertically lengthen anterior lamella.
2. Involutional ectropion. Depending upon the severity, following three operations are commonly performed:
i.  Medial conjunctivoplasty. It is useful in mild cases of ectropion involving punctal area. It consists of excising a spindle-shaped piece of conjunctiva and subconjunctival tissue from below the punctal area (Fig. 15.27).
376	Section II   Diseases of Eye


















Fig. 15.27 Medial conjunctivoplasty

ii. Horizontal lid shortening. It is performed by a full thickness pentagonal excision in patients with moderate degree of ectropion (Fig. 15.28).
iii.Byron Smith’s modified Kuhnt-Szymanowski operation. It is performed for severe degree of ectropion which is more marked over the lateral half of the lid. In it, a base up pentagonal full thickness excision from the lateral third of the eyelid is combined with triangular excision of the skin from the area just lateral to lateral canthus to elevate the lid (Fig. 15.29).
iv. Lateral tarsal strip technique is very useful for generalized ectropion associated with horizontal lid laxity.
3. Paralytic ectropion. Paralytic ectropion often resolves spontaneously within 6 months especially when due to Bells palsy. Therefore, temporary measures are taken initially. Permanent surgical treatment is required only in non-resolving cases.
Temporary measures include: • Topical lubricants,













Fig. 15.28 Horizontal lid shortening

Fig. 15.29 Modified Kuhnt-Szymanowski operation

• Taping temporal side of eyelid, and • Suture tarsorrhaphy.
Permanent measures include:
• Horizontal lid tightening with or without middle lamellar buttress such as ear cartilage or
• Palpebral sling operation, in which a fascia lata sling is passed in the subcutaneous layer all around the lid margins.
4. Cicatricial ectropion. Depending upon the degree it can be corrected by any of the following  plastic operations:
i.  V-Y operation. It is indicated in mild degree ectropion. In it a V-shaped incision is given, skin is undermined and sutured in a Y-shaped pattern (Fig. 15.30).
ii. Z-plasty (Elschnig’s operation). It is useful in mild to moderate degree of ectropion.
iii.Excision of scar tissue and full thickness skin grafting. It is performed in severe cases. Skin graft may be taken from the upper lid, behind the ear, or inner side of upper arm.
5. Mechanical ectropion. It is corrected by treating underlying mechanical force causing ectropion.
SYMBLEPHARON
In this condition, lids become adherent with the eyeball as a result of adhesions between the palpebral and bulbar conjunctiva.










Fig. 15.30 V-Y operation
Chapter 15	Disorders of Eyelids	377


Etiology
It results from healing of the kissing raw surfaces upon the palpebral and bulbar conjunctiva. Common causes are thermal or chemical burns, membranous conjunctivitis, injuries, conjunctival ulcerations, ocular pemphigus and Stevens-Johnson syndrome.
Clinical features
Clinical features of symblepharon are:
• Ocular movements become restricted,
• Diplopia may be experienced due to restricted ocular motility,
• Lagophthalmos, i.e., inability to close the lids may occur due to adhesions.
• Cosmetic disfigurement is a common complaint. Types of symblepharon, depending upon the extent of adhesions, are as below:
• Anterior symblepharon—adhesions present only in the anterior part (Fig. 15.31A and D).
• Posterior symblepharon—adhesions presentin the fornices (Fig. 15.31B and E).
• Total symblepharon—adhesions involving whole of the lid (Fig. 15.31C).
Complications
These include dryness, thickening and keratinisation of conjunctiva due to prolonged exposure and corneal ulceration (exposure keratitis).

Treatment
1. Prophylaxis. During the stage of raw surfaces, the adhesions may be prevented by: .
• Sweeping a glass rod coated with lubricant around the fornices several times a day.
• Therapeutic soft contact lens of large size, also helps in preventing the adhesions.
2. Curative treatment consists of symblepharectomy. The raw area created may be covered by:
• Mobilising the surrounding conjunctiva in mild cases.
• Conjunctival or buccal mucosal graft is required in severe cases.
• Amniotic membrane transplantation (AMT), also gives good results.

ANKYLOBLEPHARON
It refers to the adhesions between margins of the upper and lower lids.
Etiology. Ankyloblepharon may occur as: • Congenital anomaly and
• Acquired adhesions after healing of chemical burns, thermal burns, ulcers and traumatic wounds of the lid margins.
Clinically ankyloblepharon may be complete or incomplete. It is usually associated with symblepharon.











A	B	C












D	E
Fig. 15.31 Symblepharon: Diagrammatic depiction of anterior (A), posterior (B) and total symblepharon (C), clinical photographs of anterior (D) and posterior (E) symblepharon
378	Section II   Diseases of Eye


Treatment. Lids should be separated by excision of adhesions between the lid margins and kept apart during healing process. When adhesions extend to the angles, epithelial grafts should be given to prevent recurrences.
BLEPHAROPHIMOSIS
In this condition the extent of the palpebral fissure is decreased. It appears contracted at the outer canthus.
Etiology. It may be congenital (see page 379) or acquired, due to formation of a vertical skin fold at the lateral canthus (epicanthus lateralis) following eczematous contractions.
Treatment. Usually no treatment is required. In marked cases, canthoplasty operation is performed.
LAGOPHTHALMOS
This condition is characterised by inability to close the eyelids voluntarily.
Etiology. It occurs in patients with paralysis of orbicularis oculi muscle, cicatricial contraction of the lids, symblepharon, severe ectropion, proptosis, following over-resection of the levator muscle for ptosis, and in comatosed patients. Physiologically some people sleep with their eyes open (nocturnal lagophthalmos).
Clinical features. It is characterised by incomplete closure of the palpebral aperture associated with features of the causative disease.
Complications include conjunctival and corneal xerosis and exposure keratitis.
Treatment is as below:
1. Measures to prevent exposure keratitis
• Artificial tear drops should be instilled frequently and the open palpebral fissure should be filled with an antibiotic eye ointment during sleep and in comatosed patients.
• Soft bandage contact lens may be used to prevent exposure keratitis.
• Tarsorrhaphy may be performed to cover the exposed cornea when indicated.
2. Measures to treat the cause of lagophthalmos, wherever possible should be taken.

Tarsorrhaphy
In this operation, adhesions are created between a part of the lid margins with the aim to narrow down or almost close the palpebral aperture. It is of two types: temporary and permanent.
1. Temporary tarsorrhaphy
Indications. (i) To protect the cornea when seventh nerve palsy is expected to recover. (ii) To assist healing of an indolent corneal ulcer. (iii) To assist

in healing of skin-grafts of the lids in the correct position.
Surgical technique. This can be carried out as median or paramedian tarsorrhaphy (Fig. 15.32).
i. Incision. For paramedian tarsorrhaphy, about 5 mm long incision site is marked on the corresponding parts of the upper and lower lid margins, 3 mm on either side of the midline. An incision 2 mm deep is made in the grey line on the marked site and the marginal epithelium is then excised taking care not to damage the ciliary line anteriorly and the sharp lid border posteriorly.
ii. Suturing. The raw surfaces thus created on the opposing parts of the lid margins are then sutured with double-armed 6–0 silk sutures passed through a rubber bolster.
2. Permanent tarsorrhaphy
Indications. (i) Established cases of VII nerve palsy where there is no chance of recovery; and (ii) established cases of neuroparalytic keratitis with severe loss of corneal sensations.
Technique. It is performed at the lateral canthus to create permanent adhesions. The eyelids are overlapped after excising a triangular flap of skin and orbicularis from the lower lid and corre-sponding triangular tarsoconjunctival flap from the upper lid.
BLEPHAROSPASM
It refers to the involuntary, sustained and forceful closure of the eyelids.
Etiology
Blepharospasm occurs in two forms:
1. Essential (spontaneous) blepharospasm. It is a rare idiopathic condition involving patients between 45 and 65 years of age.
2. Reflex blepharospasm. It usually occurs due to reflex sensory stimulation through branches of fifth nerve, in














Fig. 15.32 Surgical technique of paramedian tarsorrhaphy
Chapter 15	Disorders of Eyelids	379


conditions such as: phlyctenular keratitis, interstitial keratitis, corneal foreign body, corneal ulcers and iridocyclitis. It is also seen in excessive stimulation of retina by dazzling light, stimulation of facial nerve due to central causes and in some hysterical patients.
Clinical features
• Persistent epiphora may occur due to spasmodic closure of the canaliculi which may lead to eczema of the lower lid.
• Oedema of the lids is of frequent occurrence.
• Spastic entropion (in elderly people) and spastic ectropion (in children and young adults) may develop in long-standing cases.
• Blepharophimosis may result due to contraction of the skin folds following eczema.

Treatment
Treatment of essential blepharospasm:
• Botulinum toxin, injected subcutaneously over the orbicularis muscle, blocks the neuromuscular junction and relieves the spasm.
• Facial denervation mayberequiredinseverecases.
Treatment of reflex blepharospasm:
• Causative disease should be treated to prevent recurrences.
• Associated complications should also be treated.

PTOSIS
Abnormal drooping of the upper eyelid is called ptosis. Normally, upper lid covers about upper one-sixth of the cornea, i.e., about 2 mm. Therefore, in ptosis it covers more than 2 mm.

Clinic-etiological Types I. Congenital ptosis
Etiology. It is associated with congenital weakness (maldevelopment) of the levator palpebrae superioris (LPS).
Characteristic features of congenital ptosis are:
• Drooping of one or both upper lids  more often since birth of variable severity (mild, moderate or severe).
• Lid crease is either diminished or absent.
• Lid lag on downgaze (i.e., ptotic lid is higher than the  normal) due to tethering effect of abnormal LPS muscle. This is in contrast to acquired ptosis in which ptotic lid is lower than the normal in downgaze also.
• LPS function may be poor, fair or good depending upon the degree of weakness.

1. Simple congenital ptosis (not associated with any other anomaly) (Fig. 15.33A).
2. Congenital ptosis with associated weakness of superior rectus muscle.
3. Blepharophimosis syndrome, which comprises congenital ptosis, blepharophimosis, telecanthus and epicanthus inversus (Fig. 15.33B).
4. Congenital synkinetic ptosis (Marcus Gunn jaw-winking ptosis). In this condition, there occurs retraction of the ptotic lid with jaw movements, i.e., with stimulation of ipsilateral pterygoid muscle.
II. Acquired ptosis
Depending upon the cause it can be neurogenic. myogenic, aponeurotic or mechanical.
1. Neurogenic ptosis. It is caused by innervational defects such as:
• Third nerve palsy (see page 355), • Horner’s syndrome,
• Ophthalmoplegic migraine, and • Multiple sclerosis.
Horner’s syndrome, occurring due to oculo-symp-athetic paresis, is characterised by classic triad of:
• Mild ptosis (due to paralysis of Muller’s muscles), • Miosis (due to paralysis of dilator pupillae), and • Reduced ipsilateral sweating (anhydrosis),













A



Associated features. Based on the absence or presence	B of other associated features, the congenital ptosis
may occur in following forms:


Fig. 15.33 Congenital ptosis: A, simple: B, blepharophimosis syndrome
380	Section II   Diseases of Eye


• Other features include mild enophthalmos , loss of cilio-spinal reflex, heterochromia, i.e., ipsilateral iris is lighter in color, pupil is slow to dilate, and there occurs slight elevation of the lower eyelid.
Note. Also see page 317
2. Acquired myogenic ptosis. It occurs due to acquired disorders of the LPS muscle or of the myoneural junction. It may be seen in patients with myasthenia gravis, dystrophia myotonica, ocular myopathy, oculopharyngeal muscular dystrophy and following trauma to the LPS, muscle thyrotoxicosis, and Lambert-Eaton myasthenia syndrome.
3. Aponeurotic ptosis. It develops due to defects of the levator aponeurosis in the presence of a normal functioning muscle. It includes:
• Involutional (senile) ptosis,
• Postoperative ptosis (which is rarely observed after cataract and retinal detachment surgery),
• Ptosis due to aponeurotic weakness associated with blepharochalasis, and
• Traumatic dehiscence or disinsertion of the aponeurosis.
4. Mechanical ptosis. It may result due to excessive weight on the upper lid as seen in patients with lid tumours, multiple chalazia and lid oedema. It may also occur due to scarring (cicatricial ptosis) as seen in patients with ocular pemphigoid and trachoma.

Clinical evaluation
Following scheme may be adopted for work up of a ptosis patient:
I. History
It should include age of onset, family history, history of trauma, eye surgery and variability in degree of the ptosis.
II. Examination
1.  Exclude pseudoptosis (simulated ptosis) on inspection. Its common causes are:
• Ipsilateral conditions such a microphthalmos, phthisis bulbi, enophthalmos, prosthesis, brow ptosis, dermatochalasis, and hypotropia.
• Contralateral conditions include: eyelid retraction, high myopia, and proptosis.
2.  Observe the following points in each case:
• Whether ptosis is unilateral or bilateral. Causes of bilateral ptosis include congenital ptosis, myasthenia gravis, myotonic dystrophy, Kearns-Sayre syndrome, Lambert-Eaton myasthenic syndrome, and chronic progressive external ophthalmoplegia.
• Function of orbicularis oculi muscle. • Eyelid crease is present or absent.

• Jaw-winking phenomenon is present or not.
• Associated weakness of any extraocular muscle. • Bell’s phenomenon (up and outrolling of the
eyeball during forceful closure) is present or absent.
3.  Measurement of amount (degree) of ptosis.
• In unilateral cases, difference between the vertical height of the palpebral fissures of the two sides indicates the degree of ptosis (Fig. 15.34).
• In bilateral cases it can be determined by measuring the amount of cornea covered by the upper lid and then subtracting 2 mm.Ptosis is graded depending upon its amount as:
• Mild ptosis	:	2 mm • Moderate ptosis  :	3 mm • Severe ptosis	:	4 mm
4. Margin reflex distance (MRD) refers to the distance between the upper lid margins and corneal light reflex (of a pen torch held in front, on which patient is looking). Normal value of MRD is 4–5 mm.
5. Assessment of levator function. It is determined by the lid excursion caused by LPS muscle (Burke’s method). Patient is asked to look down, and thumb of one hand is placed firmly against the eyebrow of the patient (to block the action of frontalis muscle) by the examiner. Then the patient is asked to look up and the amount of upper lid excursion is measured with a ruler (Fig. 15.35) held in the other hand by the examiner. Levator function is graded as follows:
• Normal	:   15 mm
• Good	:   8 mm or more • Fair:	:   5–7 mm
• Poor	:   4 mm or less
6. Special investigations. Those required in patients with acquired ptosis are as follows:















Fig. 15.34 Measurement of degree of ptosis in millimeters
Chapter 15	Disorders of Eyelids	381














A












B
Fig. 15.35 Assessment of levator function: A, looking down: B, looking up

i.  Tensilon test is performed when myasthenia is suspected. There occurs improvement of ptosis with intravenous injection of edrophonium (Tensilon) in myasthenia.
ii. Phenylephrine test is carried out in patients suspected of Horner’s syndrome.
iii.Neurological investigations may be required to find out the cause in patient with neurogenic ptosis.
7. Photographic record of the patient should be maintained for comparison. Photographs should be taken in primary position as well as in up and down gazes.

Treatment
I. Treatment of Congenital ptosis
It almost always needs surgical correction. In severe ptosis, surgery should be performed at the earliest to prevent stimulus deprivation amblyopia. However, in mild and moderate ptosis, surgery should be delayed until the age of 34 years, when accurate measurements are possible. Congenital ptosis can be treated by any of the following operations:
1. Tarso-conjunctivo-Mullerectomy (Fasanella-Servat operation).It is performed in cases having mild ptosis (1.5–2 mm) and good levator function. In it, upper

lid is everted and the upper tarsal border along with its attached Muller’s muscle and conjunctiva are resected (Fig. 15.36).
2. Levator resection. It is a very commonly performed operation for moderate and severe grades of ptosis. It is contraindicated in patients having severe ptosis with poor levator function.
Amount of levator resection required: Most of the surgeons find it out by adjusting the lid margin in relation to cornea during operation on the table in individual case. However, a rough estimate in different grades of ptosis can be made:
■Moderate ptosis. Depending on the level of LPS function the amount of LPS to be resected is as below:
• Good function	:   16–17 mm (minimal) • Fair function	:   18–22 mm (moderate)
• Poor function	:   23–24 mm (maximum) ■Severe ptosis. Fair levator function: 23–24 mm
(maximum LPS resection).
Techniques. Levator muscle may be resected by either conjunctival or skin approach.
i.  Conjunctival approach (Blaskowics’ operation): This technique is comparatively easy but not suitable for large amount of resection. In it LPS muscle is exposed by an incision made through the conjunctiva near the upper tarsal border, after the upper lid is doubly everted over a Desmarre’s lid retractor (Fig. 15.37).
ii. Skin approach (Everbusch’s operation): It is a more frequently employed technique. It allows comparatively better exposure of the LPS muscle through a skin incision along the line of future lid crease (Fig. 15.38).
3. Frontalis sling operation (Brow suspension). This is performed in patients having severe ptosis with no levator function. In this operation, lid is anchored to the frontalis muscle via a sling (Fig. 15.39). Fascia lata (best material) or some non-absorbable material













Fig. 15.36 Fasanella-Servat operation
382	Section II   Diseases of Eye



















Fig. 15.37 Conjunctival approach for levator resection
















Fig. 15.38 Skin approach for levator resection


















Fig. 15.39 Frontalis sling operation

(e.g., supramide suture, silicon rod) may be used as sling.
II. Treatment of acquired ptosis
• Treat the underlying cause wherever possible.
• Conservative treatment should be carried out and surgery deferred at least for 6 months in neurogenic ptosis.
• Surgical procedures (when required) for acquired ptosis are essentially the same as described for congenital ptosis. However, the amount of levator resection required is always less than the congenital ptosis of the same degree. Further, in most cases the simple Fasanella-Servat procedure is adequate.
LID RETRACTION
Normally, the upper eyelid covers 1/6th of the cornea (about 2 mm). Lid retraction is labelled when the lid margin is either at or above the level of superior limbus. Causes of lid retraction are as below:
1. Congenital. The lid retraction may occur isolated or in association with Duane’s retraction syndrome and Down’s syndrome.
2. Thyroid eye disease is the more common cause. 3. Mechanical causes of lid retraction are:
• Surgical overcorrection of ptosis, and
• Scarring of the upper eyelid skin after burns, trauma or infection.
4. Neurogenic causes include:
• Facial palsy (due to unopposed levator action), • Third nerve misdirection,
• Marcus-Gunn jaw winking syndrome • Parinaud syndrome, and
• Effect of sympathomimetic eyedrops 5. Systemic causes:
• Uraemia.

TUMOURS OF EYELIDS

Almost all types of tumours arising from the skin, connective tissue, glandular tissue, blood vessels, nerves and muscles can involve the eyelids. A few common tumours are listed and only the important ones are described here.
Classification
1. Benign tumours. These include; simple papilloma, naevus, angioma, haemangioma, neurofibroma and sebaceous adenoma.
2. Pre-cancerous conditions. These are solar keratosis, carcinoma in situ and xeroderma pigmentosa.
3. Malignant tumours. Commonly observed tumours include squamous cell carcinoma, basal cell carcinoma, malignant melanoma and sebaceous gland adenocarcinoma.
Chapter 15	Disorders of Eyelids	383


BENIGN TUMOURS 1. Papillomas
Papillomas are the most common benign tumours arising from the surface epithelium. These occur in two forms: squamous papillomas and seborrhoeic keratosis.
i.  Squamous papillomas derived from squamous cells occur in adults, as very slow growing or stationary, raspberry-like growths or as a pedunculated lesion, usually involving the lid margin. These may be nonspecific or related to human papilloma virus (viral wart or verruca vulgaris). Its treatment consists of simple excision.
ii. Seborrhoeic keratosis (basal cell papilloma), derived from basal cells occurs in middle-aged and older persons. Their surface is friable, verrucous and slightly pigmented.
2. Xanthelasma
These are creamy-yellow plaque-like lesions which frequently involve the skin of upper and lower lids near the inner canthus (Fig. 15.40). Xanthelasma occurs more commonly in middle-aged women. Xanthelasma represents lipid deposits in histiocytes in the dermis of the lid. These may be associated with diabetes mellitus or high cholesterol levels. ■Treatment: Excision may be advised for cosmetic reasons; but recurrences are common.

3. Haemangioma
Haemangiomas of the lids are common tumours. These occur in three forms:
i. Capillary haemangioma (Fig. 15.41) is the most common variety which occurs at or shortly after birth, often grows rapidly and in many cases resolves spontaneously by the age of 7 years. These may be superficial and bright red in colour (strawberry naevus) or deep bluish or violet in colour. They consist of proliferating capillaries and endothelial cells. ■Treatment. Unless the tumour is very large it may be left untouched until the age of 7 years (as in many












Fig. 15.40 Xanthelasma












Fig. 15.41 Capillary haemangioma

cases it resolves spontaneously). The treatment modalities include:
• Excision: It is performed in small tumours.
• Intralesional steroid (triamcinolone) injection is effective in small to medium size tumours.
• High dose oral steroid therapy, alternate day regimen is recommended for large diffuse tumours.
• Superficial radiotherapy may also be given for large tumours.
ii. Naevus flammeus (port wine stain). It may occur pari passu or more commonly as a part of Sturge-Weber syndrome. It consists of dilated vascular channels and does not grow or regress like the capillary haemangioma.
iii. Cavernous haemangiomas are developmental venous anomaly and usually occur after first decade of life. It consists of large endothelium-lined vascular channels and usually does not show any regression. Treatment is similar to capillary haemangiomas.
4. Neurofibroma
Lids  and  orbits  are  commonly  affected  in neurofibromatosis (von Recklinghausen’s disease). The tumour is usually of plexiform type (Fig. 15.42).
5. Keratoacanthomas
Keratoacanthomas occur as nonpigmented protrusions with a keratin filled central crater.












Fig. 15.42 Neurofibroma upper eyelid
384	Section II   Diseases of Eye


These are comparatively uncommon tumours that grow rapidly for 2 to 6 weeks and then spontaneously involute over a few months.
■Differential diagnosis need to be made sometimes from the squamous cell carcinoma.
■Treatment consists of complete excision and biopsy. Incomplete specimen may be indistinguishable from a squamous cell carcinoma on histopathological examination.
6. Naevi
Naevi are common cutaneous lesions that arise from the arrested epidermal melanocytes .
Types. Depending upon the depth of involvement, naevi are of three types:
• Junctional naevi,located at the epidermis/dermis. • Junctional naevi, are flat, brown in appearance
(Fig. 15.43).
• Dermal naevi, located within the dermis, are elevated lesions which may not be visibly pigmented.
• Compound naevi, are slightly elevated and share features of junctional and dermal naevi.

PREMALIGNANT TUMOURS Actinic (solar) keratosis
Actinic keratosis, though a common lesion of sun exposed skin is relatively uncommon on the eyelids. ■Clinical features include a flat, scaly lesion with
hyperkeratosis with or without keratin horn. ■Histologically, it is characterized by parakeratosis
and cellular atypia but no invasion.

Xeroderma pigmentosa
Characteristic features of this autosomal recessive (AR) disease are:
• Progressive cutaneous pigmentation resulting from damage on exposure to natural sunlight.
• Bird-like facies is typical of this condition.
• Predisposition to develop lid tumours (basal














Fig. 15.43 Divided naevi of eyelids


cell carcinoma, squamous cell carcinoma and melanoma) and conjunctival malignancies.
MALIGNANT TUMOURS
1. Basal cell carcinoma
As per western literature it is the commonest malignant tumour of the lids (90%) usually seen in elderly people. It is locally malignant and involves most commonly lower lid (50%) followed by medial canthus (25%), upper lid (10–15%) and outer canthus (5–10%). Predisposing factors include increasing age, white skin, sun exposure, xeroderma pigmentosa and basal cell naevus syndrome.
Clinical features. It may present in four forms: • Non-ulcerated nodular form
}
• Sclerosing or morphea type	rare presentation, • Pigmented basal cell carcinoma.
• Noduloulcerative basal cell carcinoma is the most common presentation. It starts as a small nodule which undergoes central ulceration with pearly rolled margins. The tumour grows by burrowing and destroying the tissues locally like a rodent and hence the name rodent ulcer (Fig. 15.44).
Histological features. The most common pattern is solid basal cell carcinoma in which the dermis is invaded by irregular masses of basaloid cells with characteristic peripheral palisading appearance.
Treatment includes:
• Surgery. Local surgical excision of the tumour along with a 3 mm surrounding area of normal skin with primary repair is the treatment of choice. Mohs’ microsurgical technique or frozen section biopsy should be adopted for complete removal.
• Radiotherapy and cryotherapy should be given only in inoperable cases for palliation.
2. Squamous cell carcinoma
It forms the second commonest malignant tumour of the lid. Its incidence (5%) is much less than the














Fig. 15.44 Basal cell carcinoma lower eyelid
Chapter 15	Disorders of Eyelids	385

basal cell carcinoma. It commonly arises from the lid margin (mucocutaneous junction) in elderly patients de novo or from pre-existing lesion such as actinic keratosis, Bowen’s disease and radiation dermatosis. It affects lower lids more frequently.
Risk factors include sun exposure, radiation, fair skin, injury or other irritative insults. There is a male predilection.
Clinical features. It may present in two forms:
• Ulcerated, scaly, erythematous plaque like growth with elevated and indurated margins is the common presentation (Fig. 15.45).
• Fungating or polypoid verrucous lesion without
ulceration, is a rare presentation.	Fig. 15.46 Meibomian gland carcinoma lower eyelid

4. Malignant melanoma (Melanocarcinoma) Malignant melanoma (Fig. 15.47) is a rare tumour of the lid (less than 1% of all eyelid lesions). It may arise from a pre-existing naevus, but usually arises de novo from the melanocytes present in the skin.







Fig. 15.45 Squamous cell carcinoma of upper lid


Metastasis. It is metastasized in preauricular and submandibular lymph nodes.
Histological features. It is characterised by an irregular downward proliferation of epidermal cells into the dermis. In well-differentiated form, the malignant cells have a whorled arrangement forming epithelial pearls which may contain laminated keratin material in the centre.
Treatment is on the lines of basal cell carcinoma.
3. Sebaceous gland carcinoma
It is a rare tumour arising from the meibomian glands (western literature). However, Indian literature reports the sebaceous gland carcinoma being the commonest malignancy of eyelid followed by basal cell and squamous cell carcinoma.
Clinical features. It usually presents initially as a nodule (which may be mistaken for a chalazion), more frequently on the upper eyelid. Which then grows to form a big growth (Fig. 15.46). Rarely, a diffuse tumour along the lid margin may be mistaken as chronic blepharitis.
Treatment. Surgical excision with reconstruction of the lids is the treatment of choice. Recurrences are common.






Fig. 15.47 Malignant melanoma

Clinical features. It may present in three forms:
• Lentigo maligna type is characterized initially by a flat, pigmented, well-defined lesion which later on becomes elevated as it invades the dermis.
• Superficial spreading type is characterized by mildly elevated, pigmented lesion with irregular margins.
• Nodular type is characterized by a rapidly growing lesion (may not be visibly pigmented), which ulcerates and bleeds frequently.
Metastasis. The tumour spreads locally as well as to distant sites by lymphatics and bloodstream. Treatment. It is a radio-resistant tumour. Therefore, surgical excision with 10 mm margins (confirmed on frozen section) with reconstruction of the lid is the treatment of choice.
16
Diseases of Lacrimal Apparatus



Chapter Outline

APPLIED ANATOMY Main lacrimal gland
Accessory lacrimal glands Lacrimal passages
•
•
•
TEAR FILM Structure Functions Secretion of tears Elimination of tears
•
•
•
•
THE DRY EYE Sjogren’s syndrome
•
THE WATERING EYE Etiology
•



Applied AnAtomy

The lacrimal apparatus comprises • Lacrimal glands, and
• Lacrimal passages, which include: puncta, canaliculi, lacrimal sac and nasolacrimal duct (NLD) (Fig. 16.1)

Lacrimal glands
Lacrimal glands includes main and accessory.

Main lacrimal gland
It consists of an upper orbital and a lower palpebral part.

1. Orbital part
Orbital part is larger, about the size and shape of a small almond, and is situated in the fossa for lacrimal gland at the outer part of the orbital plate of frontal bone. It has got two surfaces—superior and inferior. The superior surface is convex and lies in contact with the bone. The inferior surface is concave and lies on the levator palpebrae superioris muscle.

2. Palpebral part
Palpebral part is small and consists of only one or two lobules. It is situated upon the course of the

• Clinical evaluation
DACRYOCYSTITIS
• Congenital dacryocystitis Adult dacryocystitis
•
•
Surgical technique of DCR and DCT
SWELLINGS OF LACRIMAL GLAND
• Dacryoadenitis Mikulicz’s syndrome Dacryopes
•
•
•
Tumours














Fig. 16.1 The lacrimal apparatus
ducts of orbital part from which it is separated by LPS muscle. Posteriorly, it is continuous with the orbital part.
Ducts of lacrimal gland
Approximately 10–12 ducts pass downward from the main gland to open in the lateral part of superior fornix. One or two ducts also open in the lateral part of inferior fornix.
Accessory lacrimal glands
1. Glands of Krause. These are microscopic glands lying beneath the palpebral conjunctiva between fornix and the edge of tarsus. These are about 42 in the upper fornix and 6–8 in the lower fornix (see Fig. 15.4).
Chapter 16	Diseases of Lacrimal Apparatus	387


2. Glands of Wolfring. These are present near the upper border, of the superior tarsal plate and along the lower border of inferior tarsus (see Fig. 15.4).
Structure, blood supply and nerve supply Structure.All lacrimal glands are serous acini, similar in structure to the salivary glands. Microscopically these consist of glandular tissue (acini and ducts), connective tissue and puncta.
Blood supply. Main lacrimal gland is supplied by lacrimal artery which is a branch of ophthalmic artery.
Nerve supply includes:
1. Sensory supply comes from lacrimal nerve, a branch of the ophthalmic division of the fifth nerve.
2. Sympathetic supplycomes from the carotid plexus of the cervical sympathetic chain.
3. Secretomotor fibres are derived from the superior salivary nucleus (pons)       greater petrosal nerve
synapse at pterygopalatine ganglion zygomatic nerve	lacrimal nerve	lacrimal gland.

Lacrimal passages
1. Lacrimal puncta
These are two small, rounded or oval openings on upper and lower lids, about 6 and 6.5 mm, respectively, temporal to the inner canthus. Each punctum is situated upon a slight elevation called lacrimal papilla which becomes prominent in old age. Normally, the puncta dip into the lacus lacrimalis (collection of tear fluid in the inner canthus).
2. Lacrimal canaliculi
Superior and inferior canaliculi join the puncta to the lacrimal sac. Each canaliculus has two parts: vertical (1–2 mm) and horizontal (6–8mm) which lie at right angle to each other. The horizontal part converges towards inner canthus to open in the sac. The two canaliculi may open separately or may join to form common canaliculus which opens immediately into the outer wall of lacrimal sac. Afold of mucosa at this point forms the valve of Rosenmuller which prevents reflux of tears.
3. Lacrimal sac
Location: It lies in the lacrimal fossa located in the anterior part of medial orbital wall. The lacrimal fossa is formed by lacrimal bone and frontal process of maxilla. It is bounded by anterior and posterior lacrimal crests. Lacrimal fascia, which encloses the lacimal sac, is formed by periorbita. The periorbita splits at the posterior lacrimal crest into two layers

which enclose the sac and again fuse at the anterior lacrimal crest. Between the lacrimal sac and the fascia lies alveolar tissue and venous plexus which becomes continuous around the nasolacrimal duct. Size: When distended, lacrimal sac is about 12–15 mm in length and 5–6 mm in breadth with a volume of about 2 cc.
Parts: It has got three parts: fundus (portion above the opening of canaliculi), body (middle part) and the neck (lower small part which is narrow and continuous with the nasolacrimal duct).
4. Nasolacrimal duct (NLD)
Dimensions and location. It extends from neck of the lacrimal sac to inferior meatus of the nose. It is about 15–18 mm long and lies in a bony canal formed by the maxilla and the inferior turbinate.
Direction of the NLD is downwards, backwards and laterally. Externally, its location is represented by a line joining inner canthus to the ala of nose. The upper end of the NLD is the narrowest part. Numerous membranousvalves are present in the NLD, the most important is the valve of Hasner, which is present at the lower end of the duct and prevents reflux from the nose.

teAR Film
Structure of tear film
Wolff was the first to describe the detailed structure of the fluid covering the cornea and called it precorneal film. He described this film to consist of three layers, which from posterior to anterior are mucus layer, aqueous layer and lipid or oily layer (Fig. 16.2).
1. Mucus layer. It is the innermost and about 0.2 mm thick stratum of the tear film. It consists of mucin secreted by conjunctival goblet cells and glands of Manz. It converts the hydrophobic corneal surface into hydrophilic one.
2. Aqueous layer. The bulk of tear film (7.0 mm) is formed by this intermediate layer which consists of
tears secreted by the main and accessory lacrimal glands. The tears mainly comprise of water and small quantities of solutes such as sodium chloride, sugar, urea and proteins. Therefore, it is alkaline and salty in taste. It also contains antibacterial substances like lysozyme, betalysin and lactoferrin.
3. Lipid or oily layer. This is the outermost  and thinnest (0.1mm) layer of tear film formed at air-tear interface from the secretions of meibomian, zeis, and moll glands. This layer prevents the overflow of tears, retards their evaporation and lubricates the eyelids as they slide over the surface of the globe.
388	Section iii   Diseases of Eye


















Fig. 16.2 Structure of the tear film


Functions of tear film
1. Keeps moist the cornea and conjunctiva. 2. Provides oxygen to the corneal epithelium. 3. Washes away debris and noxious irritants.
4. Prevents infection due to presence of anti-bacterial substances.
5. Facilitates movements of the lids over the globe.

Secretion of tears
Tears are continuously secreted throughout the day by accessory (basal secretion) and main (reflex secretion) lacrimal glands. Reflex secretion is in response to sensations from the cornea and conjunctiva, probably produced by evaporation and breakup of tear film. Hyperlacrimation occurs due to irritative sensations from the cornea and conjunctiva. Afferent pathway of this secretion is formed by fifth nerve and efferent by parasympathetic (secretomotor) supply of lacrimal gland.

Elimination of tears
From the lacrimal gland, the tears flow downwards and laterally across the ocular surface. A variable

amount of tears is lost by evaporation from the ocular surface. The remainder of tears flow along the superior and inferior marginal strips and collects as lacus lacrimalis in the inner canthus (Fig. 16.3A), from where it is drained by the lacrimal passage into the nasal cavity. About 70% tears is drained via inferior canaliculus and 30% via the superior canaliculus by an active lacrimal pump mechanism constituted by the fibres of orbicularis as below: When the eyelids close with each blink there occurs: • Contraction of pretarsal orbicularis oculi which
compresses the ampulla and shortens the canaliculi. This movement propels the tear fluid present in the ampulla and horizontal part of canaliculi towards the lacrimal sac.
• Contraction of preseptal fibers of orbicularis distends the lacrimal sac and creates therein a negative pressure which draws the tear fluid from canaliculi into the lacrimal sac (Fig. 16.3B).
When the eyelids open following events occur:
• Relaxation of pretarsal orbicularis allows the canaliculi and ampulla to expand and reopen, and












A	B	C
Fig. 16.3 Elimination of tears by lacrimal pump mechanism
Chapter 16	Diseases of Lacrimal Apparatus	389


to draw the tear fluid from the lacus lacrimalis and marginal tear strips.
• Relaxation of preseptal fibres (Horner’s muscle) results in collapse of sac, as a consequence a positive pressure is created which forces the tears down the nasolacrimal duct (NLD) into the nose (Fig. 16.3C). Gravity also helps in downward flow of tears along the NLD.
Note. In atonia of sac, tears are not drained through the lacrimal passages, in spite of anatomical patency; resulting in epiphora.

tHe dRy eye

The dry eye per se is not a disease entity, but a symptom complex occurring as a sequelae to deficiency or abnormalities of the tear film.
Etiology
According to International Dry Eye Workshop report (DEWS report 2007), the causes of dry eye can be classified as below:
I. Aqueous deficiency dry eye
Aqueous deficiency dry eye also known as keratoconjunctivitis sicca (KCS). Its causes include: a. Sjogren’s syndrome (Primary keratoconjunctivitis sicca).
b. Non-Sjogren’s keratoconjunctivitis sicca. Causes can be grouped as below:
1. Primary age-related hyposecretion is the most common cause.
2. Lacrimal gland deficiencies as seen in congenital alacrima, infiltrations of lacrimal gland, e.g., in sarcoidosis, tumours, post-radiation fibrosis of lacrimal gland and surgical removal.
3. Lacrimal gland duct obstruction as seen in old trachoma, chemical burns, cicatricial pemphigoid and Stevens-Johnson syndrome.
4. Reflex hyposecretion (neurogenic causes) as seen in Familial dysautonomia (Riley-Day syndrome), Parkinson disease, reflex sensory block, reflex motor blade, 7th cranial nerve damage, reduced corneal sensations after refractive surgery and corneal lens wear.
II. Evaporative dry eye
It is caused by the conditions which decrease tear film stability and thus increase evaporation.
Causes can be grouped as:
1. Meibomian gland dysfunction as seen in chronic posterior blepharitis, rosacea, and congenital absence of meibomian glands.
2. Lagophthalmos as seen in facial nerve palsy, severe proptosis, symblepharon and eyelid scarring.

3. Defective blinking such as low blink rate as seen in prolonged computer users and other causes.
4. Vitamin A deficiency and other factors affecting ocular surface, e.g., topical drugs, preservatives, contact lens wear, ocular surface allergic disease and scarring disorders.
Clinical features
Symptoms suggestive of dry eye include irritation, foreign body (sandy) sensation, feeling of dryness, itching, nonspecific ocular discomfort and chronically sore eyes not responding to a variety of drops instilled earlier.
Signs of dry eye are as below:
• Tear film signs. It may show presence of stingy mucous and particulate matter. Marginal tear strip is reduced or absent (normal height is 1 mm). Froth in the tears along the lid margin is a sign of meibomian gland dysfunction.
• Conjunctival signs. It becomes lustureless, mildly congested, conjunctival xerosis and keratinization may occur. Rose Bengal or Lisamin green staining may be positive (details given in tear film tests).
• Corneal signs. It may show punctate epithelial erosions, filaments and mucus plaques. Cornea may loose lusture. Vital stains, fluorescein, Rose Bengal or Lisamin green may delineate the above lesions.
• Signs of causative disease such as posterior blepharitis, conjunctival scarring diseases (trachoma, Stevens-Johnson syndrome, chemical burns, ocular pemphigoid) and lagophthalmos may be depicted.
Tear film tests
These include tear film break-up time (BUT), Schirmer-I test, vital staining with Rose Bengal, tear levels of lysozyme and lactoferrin, tear osmolarity and conjunctival impression cytology. Out of these BUT, Schirmer-I test and Rose Bengal staining are most important and when any two of these are positive, diagnosis of dry eye syndrome is confirmed. 1. Tear film break-up (BUT). It is the interval between a complete blink and appearance of first randomly distributed dry spot on the cornea. It is noted after instilling a drop of fluorescein and examining in a cobalt-blue light of a slit-lamp. BUT is an indicator of adequacy of mucin component of tears. Its normal values range from 15 to 35 seconds. Values less than 10 seconds imply an unstable tear film.
2. Schirmer-I test. It measures total tear secretions. It is performed with the help of a 5 × 35 mm strip of Whatman-41 filter paper which is folded 5 mm from one end and kept in the lower fornix at the junction of lateral one-third and medial two-thirds. The patient is asked to look up and not to blink or
390	Section iii   Diseases of Eye


close the eyes (Fig. 16.4). After 5 minutes wetting of the filter paper strip from the bent end is measured. Normal values of Schirmer-I test are more than 15 mm. Values of 5–10 mm are suggestive of moderate to mild keratoconjunctivitis sicca (KCS) and less than 5 mm of severe KCS.
3. Rose Bengal staining. It is a very useful test for detecting even mild cases of KCS. Depending upon the severity of KCS three staining patterns A, B and C have been described: ‘C’ pattern represents mild or early cases with fine punctate stains in the interpalpebral area; ‘B’ the moderate cases with extensive staining; and ‘A’ the severe cases with confluent staining of conjunctiva and cornea.
Grading of dry eye severity
Various criteria have been proposed to grade severity of dry eye. Recently accepted system based on severity of signs and tear film tests recommended by Dry Eye Workshop (DEWS) Report (2007) grades the severity of dry eye into 4 levels:
• Level 1 (mild dry eye),
• Level 2 (moderate dry eye), • Level 3 (severe dry eye), and • Level 4 (very severe dry eye).
Treatment
At present, there is no cure for dry eye. The following treatment modalities have been tried with variable results:
1. Supplementation with tear substitutes. Artificial tears remains the mainstay in the treatment of dry eye. These are available as drops, ointments and slow-release inserts. Mostly available artificial tear drops contain either cellulose derivatives (e.g., 0.25 to 0.7% methyl cellulose and 0.3% hypromellose) or polyvinyl alcohol (1.4%).
2. Topical cyclosporine (0.05%, 0.1%) is reported to be very effective drug for dry eye in many recent studies.















Fig. 16.4 Schirmer test


It helps by reducing the cell-mediated inflammation of the lacrimal tissue.
3. Mucolytics, such as 5% acetylcystine used 4 times a day helps by dispersing the mucus threads and decreasing tear viscosity.
4.Preservation of existing tears by reducing evaporation and decreasing drainage.
• Evaporation can be reduced by decreasing room temperature, use of moist chambers and protective glasses.
• Punctal occlusion to decrease drainage can be carried out by collagen implants, cynoacrylate tissue adhesives, electrocauterisation, argon laser occlusion and surgical occlusion to decrease the drainage of tears in patients with very severe dry eye.
• Permanent lateral tarsorrhaphy may be required in very severe cases.
5. Treatment of the causative disease of dry eye when discovered is very useful e.g.:
• Systemic tetracyclines and lid hygiene in patients with chronic posterior blepharitis
• Vitamin A supplement for the deficiency • Treat the cause of lagophthalmos.
SjOGrEN’S SyNDrOME
Etiology: It is an autoimmune chronic inflammatory disease with multisystem involvement. It typically occurs in women between 40 and 50 years of age. Characteristic feature is an aqueous deficiency dry eye—the keratoconjunctivitis sicca (KCS).
• In primary Sjogren’s syndrome patients present with sicca complex—a combination of KCS and xerostomia (dryness of mouth).
• In secondary Sjogren’s syndrome dry eye and/or dry mouth are associated with an autoimmune disease, commonly rheumatoid arthritis.
Pathological features include focal accumulation and infiltration by lymphocytes and plasma cells with destruction of lacrimal and salivary glandular tissue.

tHe WAteRinG eye

It is characterised by overflow of tears from the conjunctival sac. The condition may occur either due to excessive secretion of tears (hyperlacrimation) or may result from inadequate drainage (outflow) of normally secreted tears (epiphora).
Etiology
A. Causes of hyperlacrimation
1. Primary hyperlacrimation. It is a rare condition which occurs due to direct stimulation of the lacrimal gland. It may occur in early stages of lacrimal gland
Chapter 16	Diseases of Lacrimal Apparatus	391


tumours and cysts and due to the effect of strong parasympathomimetic drugs.
2. Reflex hyperlacrimation. It results from stimulation of sensory branches of fifth nerve due to irritation of cornea or conjunctiva. It may occur in multitude of conditions which include:
• Affections of the lids: Stye, hordeolum internum, acute meibomitis, trichiasis, concretions and entropion.
• Affections of the conjunctiva: Conjunctivitis which may be infective, allergic, toxic, irritative or traumatic.
• Affections of the cornea: These include, corneal abrasions, corneal ulcers and non-ulcerative keratitis.
• Affections of the sclera: Episcleritis and scleritis.
• Affections of uveal tissue: Iritis, cyclitis, iridocyclitis. • Acute glaucomas.
• Endophthalmitis and panophthalmitis. • Orbital cellulitis.
3. Central lacrimation (psychical lacrimation). The exact area concerned with central lacrimation is still not known. It is seen in emotional states, voluntary lacrimation and hysterical lacrimation.
B. Causes of epiphora
Inadequate drainage of tears may occur due to physiological or anatomical (mechanical) causes.
I. Physiological cause is ‘lacrimal pump’ failure due to lower lid laxity or weakness of orbicularis muscle. II. Mechanical obstruction in lacrimal passages may lie at the level of punctum, canaliculus, lacrimal sac or nasolacrimal duct.
1.  Punctal causes include:
• Eversion of lower punctum: It is commonly seen in old age due to laxity of the lids. It may also occur following chronic conjunctivitis, chronic blepharitis and due to any cause of ectropion.
• Punctal obstruction: There may be congenital absence of puncta or cicatricial closure following injuries, burns or infections. Rarely, a small foreign body, concretion or cilia may also block the punctum. Prolonged use of drugs like idoxuridine and pilocarpine is also associated with punctal stenosis.
2. Causes in the canaliculi. Canalicular obstruction may be congenital or acquired due to foreign body, trauma, idiopathic fibrosis and canaliculitis. Commonest cause of canaliculitis is actinomyces. 3. Causes in the lacrimal sac. These include congenital mucous membrane folds, traumatic strictures, dacryocystitis, specific infections like tuberculosis and syphilis, dacryolithiasis and tumours (Atonia of the sac is a physiological cause).

4. Causes in the nasolacrimal duct. Congenital lesions include noncanalization, partial canalization or imperforated membranous valves. Acquired causes of obstruction are traumatic strictures, inflammatory strictures, idiopathic stenosis, tumours and diseases of the surrounding bones.
Clinical evaluation of a case of `watering eye’
1. Ocular examination with diffuse illumination using magnificationshould be carried to rule out any cause of reflex hypersecretion located in lids, conjunctiva, cornea, sclera, anterior chamber, uveal tract and so on. This examination should also exclude punctal causes of epiphora and any swelling in the sac area. 2. Regurgitation test. A steady pressure with index finger is applied over the lacrimal sac area above the medial palpebral ligament. Reflux of mucopurulent discharge indicates chronic dacryocystitis with obstruction at lower end of the sac or the nasolacrimal duct.
3. Fluorescein dye disappearance test (FDDT). In this test 2 drops of fluorescein dye are instilled in both the conjunctival sacs and observations are made after 2 minutes. Normally, no dye is seen in the conjunctival sac. A prolonged retention of dye in conjunctival sac indicates inadequate drainage which may be due to atonia of sac or mechanical obstruction.
4. Lacrimal syringing test.It is performed after topical anaesthesia with 4% xylocaine (Fig. 16.5). Normal saline is pushed into the lacrimal sac from lower punctum with the help of a syringe and lacrimal cannula.
• A free passage of saline through lacrimal passages into the nose rules out any mechanical obstruction.



















Fig. 16.5 Technique of lacrimal syringing
392	Section iii   Diseases of Eye


• In the presence of partial obstruction, saline passes with considerable pressure on the syringe.
• In the presence of obstruction no fluid passes into nose and it may reflux through same punctum (indicating obstruction in the same or common canaliculus) or through opposite punctum (indicating obstruction in the lower sac or nasolacrimal duct).
5. Jones dye tests. These are performed when partial obstruction is suspected. Jones dye tests are of no value in the presence of total obstruction.
i. Jones primary test (Jones test I). It is performed to differentiate between watering due to partial obstruction of the lacrimal passages from that due to primary hypersecretion of tears. Two drops of 2% fluorescein dye are instilled in the conjunctival sac and a cotton bud dipped in 1% xylocaine is placed in the inferior meatus at the opening of nasolacrimal duct. After 5 minutes the cotton bud is removed and inspected. A dye-stained cotton bud indicates adequate drainage through the lacrimal passages and the cause of watering is primary hypersecretion (further investigations should aim at finding the cause of primary hypersecretion). While the unstained cotton bud (negative test) indicates either a partial obstruction or failure of lacrimal pump mechanism. To differentiate between these conditions, Jones dye test-II is performed.
ii. Jones secondary test (Jones test II). When primary test is negative, the cotton bud is again placed in the inferior meatus and lacrimal syringing is performed. A positive test suggests that dye was present in the sac but could not reach the nose due to partial obstruction. A negative test indicates presence of lacrimal pump failure.
6. Dacryocystography. It is valuable in patients with mechanical obstruction. It tells the exact site, nature and extent of block (Fig. 16.6). In addition, it also gives


information about mucosa of the sac, presence of any fistulae, diverticulae, stone, or tumour in the sac. To perform it a radiopaque material such as lipiodol, pentopaque, dianosil or condray-280 is pushed in the sac with the help of a lacrimal cannula and X-rays are taken after 5 minutes and 30 minutes to visualize the entire passage. For better anatomical visualization the modified technique known as subtraction macrodacryocystography with
canalicular catheterisation should be preferred.
7. Radionucleotide dacryocystography (lacrimal scintillography). It is a noninvasive technique to assess the functional efficiency of lacrimal drainage apparatus. A radioactive tracer (sulphur colloid or technetium) is instilled into the conjunctival sac and its passage through the lacrimal drainage system is visualised with an Anger gamma camera (Fig. 16.7).

dACRyoCyStitiS

Inflammation of the lacrimal sac is not an uncommon condition. It may occur in two forms: congenital and adult dacryocystitis.
CONGENITAL DACryOCySTITIS
It is an inflammation of the lacrimal sac occurring in newborn infants; and thus also known as dacryocystitis neonatorum.
Etiology
It follows stasis of secretions in the lacrimal sac due to congenital blockage in the nasolacrimal duct. It is of very common occurrence. As many as 30% of newborn infants are believed to have closure of nasolacrimal duct at birth.
• Membranous occlusion’ at its lower end, near the valve of Hasner is the commonest cause.
• Other causes of congenital NLD block are: presence of epithelial debris, membranous occlusion at its upper end near lacrimal sac, complete noncanalisation and rarely bony occlusion.
• Common bacteria associated with congenital dacryocystitis areStaphylococci, Pneumococci and Streptococci.








A	B
Fig. 16.7  Lacrimal scintillography showing: A, normal lacrimal excretory system on right side; B, obstruction at
Fig. 16.6 Normal dacryocystogram	the junction of lacrimal sac and nasolacrimal on left side
Chapter 16	Diseases of Lacrimal Apparatus	393


Clinical features
Congenital dacryocystitis usually presents as a mild grade chronic inflammation. It is characterised by: 1. Epiphora, usually developing after seven days of birth. It is followed by copious mucopurulent discharge from the eyes.
2. Regurgitation test is usually positive, i.e., when pressure is applied over the lacrimal sac area, purulent discharge regurgitates from the lower punctum.
3. Swelling on the sac area may appear eventually.

Differential diagnosis
Congenital dacryocystitis needs to be differentiated from other causes of watering in early childhood especially:
■Ophthalmia neonatorum and ■Congenital glaucoma.
Complications
When not treated in time it may be complicated by recurrent conjunctivitis, acute or chronic dacryocystitis, lacrimal abscess and fistulae formation.
Treatment
It depends upon the age at which the child is brought. The treatment modalities employed are as follows: 1. Massage over the lacrimal sac area and topical antibiotics constitute the  mainstay of treatment of congenital NLD block. Massage increases the hydrostatic pressure in the sac and helps to open up the membranous occlusions. It should be carried out at least 4 times a day to be followed by instillation of antibiotic drops. This conservative treatment coupled with spontaneous recanalization cure obstruction in about 90% of the infants upto 6-9 months.
2. Lacrimal syringing (irrigation) with normal saline and antibiotic solution. It should be added to the conservative treatment if the condition is not cured up to the age of 3 months. Lacrimal irrigation helps to open the membranous occlusion by exerting hydraulic pressure. Syringing may be carried out once a week or once in two weeks.
3. Probing of NLD with Bowman’s probe. It should be performed in case the condition is not cured by the age of 6 months. Some surgeons prefer to wait till the age of 9–12 months. It is usually performed under general anaesthesia. While performing probing, care must be taken not to injure the canaliculus. In most instances, a single probing will relieve the obstruction. In case of failure, it may be repeated after an interval of 3–4 weeks.

4. Balloon catheter dilation, with the help of a probe carrying inflatable balloon, may be carried out in children where repeated probing is failure or directly in cases where the obstruction seems to be due to scarring or constriction rather than merely by a distal membrane.
5. Intubation with silicone tube may be performed if repeated probings and balloon catheter dilation are failure. The silicone tube should be kept in the NLD for about six months.
6. Dacryocystorhinostomy (DCR) operation: When the child is brought very late or repeated probing, balloon catheter dilation and intubation are a failure, then conservative treatment by massaging, topical antibiotics and intermittent lacrimal syringing should be continued till the age of 4 years. After this, DCR operation should be performed.

ADuLT DACryOCySTITIS
Adult dacryocystitis may occur in an acute or a chronic form.

Chronic Dacryocystitis
Chronic dacryocystitis is more common than the acute dacryocystitis.

Etiology
The etiology of chronic dacryocystitis is multifactorial. The well-established fact is a vicious cycle of stasis and mild infection of long duration. The etiological factors can be grouped as under:
A. Predisposing factors
1. Age. It is more common between 40 and 60 years of age.
2. Sex.The disease is predominantly seen in females (80%) probably due to comparatively narrow lumen of the bony canal.
3. Race. It is rarer among Negroes than in Whites; as in the former NLD is shorter, wider and less sinuous.
4. Heredity. It plays an indirect role. It affects the facial configuration and so also the length and width of the bony canal.
5. Socio-economic status. It is more common in low socio-economic group.
6. Poor personal hygiene. It is also an important predisposing factor.
B. Factors responsible for stasis of tears in lacrimal sac 1. Anatomical factors,which retard drainage of tears
include: comparatively narrow bony canal, partial canalization of membranous NLD and excessive membranous folds in NLD.
394	Section iii   Diseases of Eye


2. Foreign bodies in the sac may block opening of NLD.
3. Excessive lacrimation, primary or reflex, causes stagnation of tears in the sac.
4. Mild grade inflammation of lacrimal sac due to associated recurrent conjunctivitis may block the NLD by epithelial debris and mucus plugs.
5. Obstruction of lower end of the NLD by nasal diseases such as polyps, hypertrophied inferior concha, marked degree of deviated nasal septum, tumours and atrophic rhinitis causing stenosis may also cause stagnation of tears in the lacrimal sac.
C. Source of infection
Lacrimal sac may get infected from the conjunctiva, nasal cavity (retrograde spread), or paranasal sinuses.
D. Causative organisms
These include: Staphylococci, Pneumococci, Streptococci and Pseudomonas pyocyanea. Rarely chronic granulomatous infections like tuberculosis, syphilis, leprosy and occasionally rhinosporiodosis may also cause dacryocystitis.
Clinical features
Clinical features of chronic dacryocystitis may be divided into four stages:
1. Stage of chronic catarrhal dacryocystitis. It is characterised by mild inflammation of the lacrimal sac associated with blockage of NLD.
• Watering eye is the only symptom in this stage and sometimes mild redness in the inner canthus.
• On syringing the lacrimal sac, either clear fluid or few fibrinous mucoid flakes regurgitate.
• Dacryocystography reveals block in NLD, a normal-sized lacrimal sac with healthy mucosa.
2. Stage of lacrimal mucocele. It follows chronic stagnation causing distension of lacrimal sac.
• Characteristic features include constant epiphora associated with a swelling just below the inner canthus (Fig. 16.8).













Fig. 16.8 Lacrimal mucocele

• Regurgitation test.Milky or gelatinous mucoid fluid regurgitates from the lower punctum on pressing the swelling.
• Dacryocystography at this stage reveals a distended sac with blockage somewhere in the NLD.
• Encysted mucocele. Sometimes due to continued chronic infection, opening of both the canaliculi into the sac are blocked and a large fluctuant swelling is seen at the inner canthus with a negative regurgitation test. This is called encysted mucocele.
3. Stage of chronic suppurative dacryocystitis. Due to pyogenic infection, the mucoid discharge becomes purulent, converting the mucocele into ‘pyocoele’. • The condition is characterised by epiphora,
associated recurrent conjunctivitis and swelling at the inner canthus with mild erythema of the overlying skin.
• On regurgitation a frank purulent discharge flows from the lower punctum.
• If openings of canaliculi are blocked at this stage the so called encysted pyocoele results.
4. Stage of chronic fibrotic sac. Low grade repeated infections for a prolonged period ultimately result in a small fibrotic sac due to thickening of mucosa, which is often associated with persistent epiphora and discharge.
• Dacryocystography at this stage reveals a very small sac with irregular folds in the mucosa.
Complications
• Chronic intractable conjunctivitis, acute or chronic dacryocystitis.
• Ectropion of lower lid, maceration and eczema of lower lid skin due to prolonged watering.
• Chances of corneal ulceration are those as simple corneal abrasions may become infected.
• High risk of developing endophthalmitis is always there if  an intraocular surgery is performed in the presence of dacryocystitis.  Because of this, syringing of lacrimal sac is always done in suspected cases before attempting any intraocular surgery.
Treatment
1. Conservative treatment by probing and  lacrimal syringing may be useful in recent cases only. Long-standing cases are almost always associated with blockage of NLD which usually does not open up with probing.
2. Balloon catheter dilation also known as balloon dacryocystoplasty can be tried in patient with partial nasolacrimal duct obstruction. Success rate reported in adults is about 50%.
Chapter 16	Diseases of Lacrimal Apparatus	395


3. Dacryocystorhinostomy (DCR). It should be the operation of choice as it re-establishes the lacrimal drainage. However, before performing surgery, the infection especially in pyocoele should be controlled by topical antibiotics and repeated lacrimal syringings.
4. Dacryocystectomy (DCT). It should be performed only when DCR is contraindicated. Indications of DCT include: (i) Too young (less than 4 years) or too old (more than 60 years) patient. (ii) Markedly shrunken and fibrosed sac. (iii) Tuberculosis, syphilis, leprosy or mycotic infections of sac. (iv) Tumours of sac. (v) Gross nasal diseases like atrophic rhinitis. (vi) An unskilled surgeon, because it is said that, a good ‘DCT’ is always better than a badly done ‘DCR’. (for surgical procedure see page 396).
5. Conjunctivodacryocystorhinostomy (CDCR). It is performed in the presence of blocked canaliculi.

Acute Dacryocystitis
Acute dacryocystitis is an acute suppurative inflammation of the lacrimal sac, characterised by presence of a painful swelling in the region of sac.
Etiology
It may develop in two ways:
1. As an acute exacerbation of chronic dacryocystitis. 2. As an acute peridacryocystitis due to direct involv-ement from the neighbouring infected structuressuch as: paranasal sinuses, surrounding bones and dental abscess or caries teeth in the upper jaw. ■Causative organisms. Commonly involved are Streptococcus haemolyticus, Pneumococcus and Staphylococcus.
Clinical features
Clinical features of acute dacryocystitis can be divided into 3 stages:
1. Stage of cellulitis. It is characterised by a painful swelling in the region of lacrimal sac associated with epiphora and constitutional symptoms such as fever and malaise. The swelling is red, hot, firm and tender. Redness and oedema also spread to the lids and cheek. When treated resolution may occur at this stage. However, if untreated, self-resolution is rare. 2. Stage of lacrimal abscess. Continued inflammation causes occlusion of the canaliculi due to oedema. The sac is filled with pus, distends and its anterior wall ruptures forming a pericystic swelling. In this way, a large fluctuant swelling the lacrimal abscess is formed. It usually points below and to the outer side of the sac, owing to gravitation of pus and presence of medial palpebral ligament in the upper part (Fig. 16.9). 3. Stage of fistula formation.When the lacrimal abscess is left unattended, it discharges spontaneously,














Fig. 16.9 Acute dacryocystitis: Stage of lacrimal abscess













Fig. 16.10 Acute dacryocystitis: Stage of external lacrimal fistula

leaving an external fistula below the medial palpebral ligament (Fig. 16.10). Rarely, the abscess may open up into the nasal cavity forming an internal fistula.
Complications These include:
• Acute conjunctivitis,
• Corneal abrasion which may be converted to corneal ulceration,
• Lid abscess,
• Osteomyelitis of lacrimal bone, • Orbital cellulitis,
• Facial cellulitis and acute ethmoiditis.
• Rarely cavernous sinus thrombosis and very rarely generalized septicaemia may also develop.
Treatment
1. During cellulitis stage. It consists of systemic and topical antibiotics to control infection; and systemic anti-inflammatory analgesic drugs and hot fomentation to relieve pain and swelling.
2. During stage of lacrimal abscess. In addition to the above treatment when pus starts pointing on the skin, it should be drained with a small incision.
396	Section iii   Diseases of Eye


The pus should be gently squeezed out, the dressing done with betadine soaked roll gauze.
Later on depending upon condition of the lacrimal sac either DCT or DCR operation should be carried out, otherwise recurrence will occur.
3. Treatment of external lacrimal fistula. After controlling the acute infection with systemic antibiotics, fistulectomy along with DCT or DCR operation should be performed.

SurGICAL TEChNIquE OF DACryOCySTOrhINOSTOMy
Dacryocystorhinostomy (DCR) operation can be performed by following techniques:
• Conventional external approach, DCR and • Endonasal (surgical or laser)DCR
• Endocanalicular laser DCR.

Conventional external approach DCr (Fig. 16.11)
1. Anaesthesia. General anaesthesia is preferred, however, it may be performed with local infiltration anaesthesia in adults.
2. Skin incision. Either a curved incision along the anterior lacrimal crest or a straight incision 8 mm medial to the medial canthus is made.


3. Exposure of medial palpebral ligament (MPL) and anterior lacrimal crest. MPL is exposed by blunt dissection and cut with scissors to expose the anterior lacrimal crest.
4. Dissection of lacrimal sac. Periosteum is separated from the anterior lacrimal crest and alongwith the lacrimal sac is reflected laterally with blunt dissection exposing the lacrimal fossa.
5. Exposure of nasal mucosa. A 15 mm × 10 mm bony osteum is made by removing the anterior lacrimal crest and the bones forming lacrimal fossa, exposing the thick pinkish white nasal mucosa.
6. Preparation of flaps of sac. A probe is introduced into the sac through lower canaliculus and the sac is incised vertically. To prepare anterior and posterior flaps, this incision is converted into H shape.
7. Fashioning of nasal mucosal flaps is also done by vertical incision converted into H shape.
8. Suturing of flaps. Posterior flap of the nasal mucosa is sutured with posterior flap of the sac using 6–0 vicryl or chromic cat gut sutures. It is followed by suturing of the anterior flaps.
9. Closure. MPL is sutured to periosteum, orbicularis muscle is sutured with 6–0 vicryl and skin is closed with 6–0 silk sutures.













A	B	C











d	e	F

Fig. 16.11 Surgical steps of external dacryocystorhinostomy: A, skin incision; B, exposure of bony lacrimal fossa; C, preparation of bony osteum and exposure of nasal mucosa; D, preparation of flaps of the nasal mucosa and lacrimal sac; E, suturing of posterior flaps: F, suturing of anterior flaps
Chapter 16	Diseases of Lacrimal Apparatus	397


Endonasal DCr
Presently  many  eye  surgeons,  alone  or  in collaboration with the ENT surgeons, are preferring endonasal DCR over conventional external approach DCR because of its advantages (described below).
Surgical steps of endonasal DCR are (Fig. 16.12): 1. Preparation and anaesthesia. Nasal mucosa is prepared for 15–30 minutes before operation with nasal decongestant drops and local anaesthetic agent. Conjunctival sac is anaesthetised with topically instilled 2% lignocaine. Then 3 ml of lignocaine 2% with 1 in 2 lac adrenaline is injected into the medial parts of upper and lower eyelids and



















A

















C


via subcaruncular injection to the lacrimal fossa region.
2. Identification of sac area. A 20-gauge light pipe is inserted via the upper canaliculi into the sac. With the help of endoscope, the sac area which is transilluminated by the light pipe is identified (Fig. 16.12A) and a further injection of lignocaine with adrenaline is made below the nasal mucosa in this area. 3. Creation of opening in the nasal mucosa, bones
forming the lacrimal fossa and posteromedial wall of sac can be accomplished by two techniques:
i.  By cutting the tissues with appropriate instruments or



















B

















d

Fig. 16.12 Surgical steps of endonasal DCR: A. endoscopic identification of sac area in the middle meatus; B,C, opening created in the middle meatus; D, stenting of rhinostomy opening with fine silicone tubes
398	Section iii   Diseases of Eye


ii. By ablating with Holmium YAG laser (endoscopic laser-assisted DCR).
Note. The size of opening is about 12 mm × 10 mm (Fig. 16.12B).
4. Stenting of rhinostomy opening. The outflow system is then stinted using fine silicone tubes passed via the superior and inferior canaliculi into the rhinostomy and secured with a process of knotting (Fig. 16.12C). Nasal packing and dressing is done.
5. Postoperative care and removal of sialistic lacrimal stents. After 24 hours of operation nasal packs are removed and patient is advised to use decongestent, antibiotic and steroid nasal drops for 3–4 weeks. The sialistic lacrimal stents are removed 8–12 weeks after surgery and the nasal drops are continued further for 2–3 weeks.
Advantages and disadvantages of endonasal DCr vis-a-vis external DCr
Advantages and disadvantages of endoscopic DCR vis-a-vis external DCR are summerized in Table 16.1.
Table 16.1 Advantages and disadvantages of endonasal DCR vis-a-vis external DCR

Endonasal DCR	External DCR

Endocanalicular Laser DCr
In this technique, laser probe is passed through a canaliculus upto the medial wall of sac. An opening is created by ablating the posteriomedial wall of the sac, bone forming the lacrimal fossa and adjacent nasal mucosa. It is performed with a Holmium YAG or KTP laser. This is a quick procedure and can be carried out under local anaesthesia. It is particularly useful for the elderly patients. Success rate is only 70%. Failure can be tackled by endonasal DCR or conventional external DCR.
SurGICAL TEChNIquE OF DACryOCySTECTOMy (DCT)
1 to 4 steps are same as for external DCR operation. 5. Removal of lacrimal sac. After exposing the sac, it is separated from the surrounding structures by blunt dissection followed by cutting its connections from the lacrimal canaliculi. It is then held with artery forceps and twisted 3-4 times to tear it away from the nasolacrimal duct (NLD).