notes/A K Khurana - Comprehensive Ophthalmology_18.txt

Name the bacteria which can invade the intact corneal epithelium and produce ulceration.
• Neisseria gonorrhoeae • Neisseria meningitidis
• Corynebacterium diphtheriae.
Name the layers of cornea. 1. Epithelium
2. Bowman’s membrane 3. Corneal stroma
4. Descemet’s membrane 5. Endothelium.
What are the pathological stages of corneal ulceration? 1. Stage of progressive infiltration
2. Stage of active ulceration 3. Stage of regression
4. Stage of cicatrization.

What are the characteristic features of bacterial corneal ulcer?
A clinical diagnosis of bacterial corneal ulcer is made in patients with a greyish white central or marginal ulcer associated with marked pain, photophobia, blepharospasm, lacrimation, circumcorneal congestion, purulent/mucopurulent discharge, presence or absence of hypopyon with or without vascularization.
What do you mean by hypopyon corneal ulcer?
A purulent corneal ulcer associated with collection of pus in the anterior chamber caused by Pneumococcus is called hypopyon corneal ulcer:
Name the common organisms responsible for hypopyon corneal ulceration.
1. Most fungal ulcers are associated with hypopyon. 2. Common bacteria producing hypopyon ulcer are: Pneumococcus, Pseudomonas, Gonococcus and
Staphylococcus.
What is ulcus serpens?
The characteristic hypopyon ulcer caused by Pneumococcus is called ulcus serpens.
Name the complications of corneal ulcer. 1. Toxic iridocyclitis
2. Secondary glaucoma 3. Descemetocele
4. Corneal perforation, which may be complicated by: • Iris prolapse
• Subluxation or dislocation of the lens • Anterior capsular cataract
• Purulent  iridocyclitis  often  leading  to endophthalmitis or even panophthalmitis
• Intraocular haemorrhage in the form of a vitreous haemorrhage or expulsive choroidal haemorrhage.


5. After  healing  of  corneal  ulcer  following complications may be left as sequelae:
• Keractasia
• Corneal opacity which may be nebular, macular, leucomatous or adherent leucoma
• Anterior staphyloma which usually follows a sloughing corneal ulceration.
What is a descemetocele?
When a corneal ulcer extends up to Descemet’s membrane, it herniates (bulges out) as a transparent vesicle called the descemetocele or keratocele.
What are the signs of an impending corneal perforation? Descemetocele formation associated with excessive corneal oedema are the signs of an impending corneal perforation.
What are the clinical features of perforation of corneal ulcer?
Following perforation of a corneal ulcer, immediately pain decreases and patient feels some hot fluid (aqueous) coming out of the eyes. Anterior chamber becomes shallow and iris prolapse may occur.
How will you manage a case of corneal ulcer? Management of a case of corneal ulcer is as follows:
Clinical evaluation
1.  Meticulous history should be taken and a thorough ocular  examination  including  slit-lamp biomicroscopy should be carried out to reach the clinical diagnosis for the type of corneal ulcer.
2.  Regurgitation test and syringing of lacrimal sac should be carried out to rule out associated dacryocystitis.
3.  General physical and systemic examination should be carried out to elucidate the associated malnutrition, diabetes mellitus and any other chronic debilitating disease.
Laboratory investigations
1. Routine laboratory investigations such as haemogloin, TLC, DLC, ESR, blood sugar and complete urine examination should be carried out in each case.
2. Microbiological investigations: Material is obtained by scraping the base and margins of the corneal ulcer (under topical anaesthesia) and is used for following investigations:
• Gram and Giemsa-stained smear for possible identification of infecting organisms
• 10% KOH wet preparation is made for, identification of fungal hyphae
• Culture on blood agar medium for aerobic organisms
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• Culture on Sabouraud’s dextrose agar medium for fungi.
Treatment of uncomplicated corneal ulcer
I.  Specific treatment for the cause: Bacterial corneal ulcer is treated by topical and systemic antibiotics.
1.It is preferable to start concentrated amikacin (40–100 mg/ml) eyedrops along with fortified cephazolin (33 mg/ml) eyedrops every one hourly for first 5 days and then reduced to 2 hourly, 3 hourly, 4 hourly and 6 hourly.
2.Antibiotic eye ointment should be applied at night.
3.Subconjunctival injection of gentamicin 40 mg and cephazolin 125 mg once a day for 5 days should be given in sloughing corneal ulcer.
II. Non-specific treatment includes:
1.Cycloplegic drugs, e.g. 1% atropine, 0.5% homatropine or cyclopentolate.
2.Systemic analgesics and anti-inflammatory drugs to relieve the pain and oedema.
3.Vitamins (A, B-complex and C) help in early healing of the ulcer.
III. Physical and general measures:
1.Hot fomentation gives comfort, reduces pain and causes vasodilatation.
2.Rest and good diet are useful for smooth convalescence.
What do you mean by a nonhealing corneal ulcer? Enumerate its common causes.
When a corneal ulcer does not start healing despite the best therapy for about 7 to 10 days it is labeled as a nonhealing corneal ulcer. Common causes of non-healing corneal ulcers are as follows:
Local causes
• Associated raised intraocular pressure • Multiple large concretions
• Misdirected cilia
• An impacted foreign body • Dacryocystitis
• Wrong diagnosis, e.g., fungal ulcer being treated as a bacterial ulcer
• Lagophthalmos
• Excessive vascularization of the ulcer area

Systemic causes
• Diabetes mellitus • Severe anaemia
• Malnutrition
• Chronic debilitating diseases
• Immuno-compromised patients • Patients on systemic steroids.

How will you treat a case of non-healing corneal ulcer? 1. Removal of any known cause of nonhealing: A thorough search should be made to find out any already missed cause of nonhealing and when
found it should be removed.
2. Mechanical debridement of the ulcer to remove necrosed material may hasten the healing.
3. Chemical cauterization with pure carbolic acid or 10 to 20% trichloroacetic acid may be considered in indolent cases.
4. Peritomy, i.e., severing of perilimbal conjunctival vessels may be useful in the presence of excessive corneal vascularization.
What extra measures will you take for the treatment of impending perforation?
1. Patient should be advised to avoid strain during sneezing, coughing, passing stool, etc.
2. Pressure bandage should be applied to give some external support.
3. Lowering of intraocular pressure by simultaneous use of acetazolamide 250 mg qid orally, 0.5% timolol eyedrops twice a day and intravenous mannitol (20%) drip stat. Even paracentesis with slow evacuation of the aqueous from the anterior chamber may be done, if required.
4. Tissue adhesive glue such as cyanoacrylate is helpful in preventing perforation.
5. Conjunctival flap may be used to cover and support the weak tissue.
6. Bandage soft contact lenses are also useful.
7. Therapeutic keratoplasty, when available, is considered the best mode of treatment.
How will you treat a case of perforated corneal ulcer? The best treatment is an immediate therapeutic keratoplasty. However, short of it, depending upon the size and location of the perforation measures like, use of a tissue glue (cyanoacrylate), bandage soft contact lens or conjunctival flap may be used over and above the conservative management with pressure bandage.
What is a marginal catarrhal ulcer?
Marginal catarrhal ulcer is a superficial ulcer situated near the limbus, usually seen in association with chronic staphylococcal blepharoconjunctivitis. It is thought to be caused by hypersensitivity reaction to staphylococcal toxins.
Name the common fungi associated with mycotic corneal ulceration.
The fungi most commonly responsible for mycotic corneal ulceration are: Aspergillus, Candida and Fusarium.
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What are the predisposing factors for a mycotic corneal ulcer?
1. Injury by vegetative material.
2. Immunosuppressed patients are prone to secondary fungal ulcers.
3. Excessive use of topical antibiotics and steroids predispose the cornea far fungal infections.
What are the characteristic features of a fungal corneal ulcer?
1. A typical fungal corneal ulcer is dry looking, greyish white with elevated rolled out margins and delicate feathery finger-like extensions into the surrounding stroma under the intact epithelium.
2. A sterile immune ring (yellow line of demarcation) may be present where fungal antigen and host antibodies meet.
3. Multiple, small satellite lesions may be around the ulcer.
4. Usually, a massive and thick hypopyon is present even if the ulcer is very small.
5. A history of trauma (especially by vegetative material) and clinical signs out of proportion to the symptoms, i.e., less marked photophobia and lacrimation with intense ciliary and conjunctival congestion support a fungal origin.
How will you confirm the diagnosis of a fungal corneal ulcer?
Confirmation is made by laboratory investigations, which include examination of a wet KOH, Gram’s and Giemsa-stained films for fungal hyphae and culture on Sabouraud’s dextrose agar medium.
Name the ocular antifungal drugs. I.  Polyene antifungals, e.g.,
1.Nystatin 3.5% eye ointment 2.Amphotericin-B (0.75 to 3% eyedrops) 3.Natamycin 5% suspension
II. Imidazole antifungal drugs, e.g., ketoconazole, fluconazole miconazole, clotrimazole and econazole
III. Pyrimidine, e.g. flucytosine
IV. Silver compounds, e.g., silver sulphadiazine eyedrops.
Enumerate the ocular lesions of herpes simplex. Ocular involvement by herpes simplex virus (HSV) occurs in two forms:
I.  Primary herpes: It is characterized by: 1.Vesicular lesions involving the skin of lids 2.Acute follicular conjunctivitis
3.Fine or coarse epithelial punctate keratitis II. Recurrent herpes: Its lesions are as follows:
1.Punctate epithelial keratitis


2.Dendritic ulcer
3.Geographical or amoeboid ulcer 4.Disciform keratitis.
Describe the characteristic features of recurrent herpetic keratitis.
Dendritic ulcer is a typical epithelial lesion of the recurrent herpetic keratitis. The ulcer is of an irregular zigzag linear branching shape (Fig. 6.9). The branches are generally knobbed at the ends. Floor of the ulcer stains with fluorescein and the virus laden cells at the margin take up rose bengal stain. There is an associated marked diminution of the corneal sensations.
Sometimes, the branches of the dendritic ulcer enlarge and coalesce to form a large epithelial typically known as geographical or amoeboid ulcer.

What are the features of herpes simplex virus (HSV)? Herpes simplex virus is an epitheliotropic, DNA virus. It is of two types: HSV type-1 which typically causes infection above the waist (herpes labialis) and HSV type-II which causes infection below the waist (herpes genitalis).

Name the predisposing/precipitating stress stimuli which trigger an attack of herpetic keratitis.
• Fever, especially malaria • General ill health
• Exposure to ultraviolet rays • Mild trauma
• Use of topical and systemic steroids • Immunosuppression.
What is disciform keratitis?
Disciform keratitis is stromal keratitis which occurs due to delayed hypersensitivity reaction to the HSV antigen. It is characterized by a focal disc-shaped patch of stromal oedema without necrosis. Associated diminished corneal sensations and fine keratic precipitates differentiate it from other causes of stromal oedema.
Name the antiviral drugs.
Idoxuridine (IDU), trifluorothymidine (TFT), adenine arabinoside (vidarabine) and acyclovir.
Which antiviral drug is effective for stromal viral keratitis?
• Acyclovir.
Enumerate the causes of decreased corneal sensations. • Viral keratitis, neuroparalytic keratitis, diabetic
neuropathy and leprosy.

What is herpes zoster ophthalmicus?
Herpes zoster ophthalmicus is an acute infection of the gasserian ganglion of the fifth cranial nerve by varicella zoster virus. In it, frontal nerve is more frequently affected than the lacrimal and
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nasociliary nerve. About 50% cases of herpes zoster ophthalmicus develop ocular complications.
Ocular involvement in herpes zoster ophthalmicus is associated with involvement of which nerve?
• Nasociliary nerve.
What are the characteristic features of herpes zoster? 1. Fever and malaise occur at the onset.
2. The vesicular eruptions are preceded by severe neuralgic pain along the course of the involved nerves.
3. The lesions are strictly limited to one side of the midline of head (pathognomic feature).
Enumerate the ocular lesions of herpes zoster ophthalmicus.
Conjunctivitis, keratitis, episcleritis, scleritis, iridocyclitis and secondary glaucoma.
What is Mooren’s ulcer?
Mooren’s ulcer (chronic serpiginous or rodent ulcer) is a peripheral degenerative ulcerative keratitis of unknown etiology. It is characterized by a shallow furrow-shaped ulcer having whitish overhanging margin at the advancing edge (Fig. 6.14).
What are the features of neuroparalytic keratitis? 1. No pain, no lacrimation and complete loss of
corneal sensations.
2. Marked ciliary congestion. 3. Corneal sheen is dull.
4. Corneal ulcer is usually superficial and involves the interpalpebral area.
What are the causes of exposure keratitis? 1. Extreme proptosis
2. Bell’s palsy
3. Symblepharon
4. Patients in deep coma.

What is superficial punctate keratitis? Name a few of its causes.
Superficial punctate keratitis (SPK) refers to occurrence of multiple, spotty lesions in superficial layer of cornea. Its common causes are:
1. Viral infections, e.g., adenovirus infection, epidemic keratoconjunctivitis, herpes zoster keratitis, herpes simplex keratitis, and pharyn-goconjunctival fever.
2. Chlamydial infections, e.g., trachoma.
3. Toxic, e.g., in association with blepharoconjunctivitis. 4. Trophic lesions, e.g., exposure keratitis and
neuroparalytic keratitis.
5. Allergic lesions, e.g., vernal keratitis. 6. Keratoconjunctivitis sicca.

7. Specific type of idiopathic SPK, e.g., Thygeson’s SPK and superior limbic keratoconjunctivitis.
8. Photophthalmitis.

What is photophthalmia?
Photophthalmia refers to occurrence of multiple epithelial erosions due to exposure to ultraviolet rays having a wavelength of 290–311 µm. It occurs in the following conditions:
1. Exposure to naked arc light as in industrial welding. 2. Exposure to bright light of a short circuit.
3. Snow blindness due to reflected ultraviolet rays from the snow surface.
What is filamentary keratitis/keratopathy? Name its few important causes.
Filamentary keratitis is a type of superficial punctate keratitis associated with formation of corneal epithelial filaments. Its common causes are:
1. Keratoconjunctivitis sicca (KCS)
2. Recurrent corneal erosion syndrome 3. Herpes simplex keratitis
4. Thygeson’s superficial punctate keratitis
5. Prolonged patching of the eye particularly following ocular surgery like cataract
6. Trachoma.
What is interstitial keratitis? What are its common causes?
Interstitial keratitis is inflammation of the corneal stroma without primary involvement of the epithelium or endothelium. Its common causes are: congenital syphilis, tuberculosis, acquired syphilis, Cogan’s syndrome (interstitial keratitis with acute tinnitus, vertigo and deafness).
What are corneal dystrophies?
Corneal dystrophies are inherited disorders characterized by development of corneal haze in otherwise normal eyes that are free of inflammation or vascularization. These are classified as follows: 1. Anterior dystrophies which primarily affect
epithelium and Bowman’s membrane, e.g., recurrent corneal erosion syndrome.
2. Stromal dystrophies: These include—granular dystrophy, macular dystrophy and lattice dystrophy.
3. Posterior dystrophies which primarily affect the corneal endothelium and Descemet’s membrane, e.g., cornea guttata, Fuchs’ dystrophy.
4. Ectatic dystrophies e.g., keratoconus, keratoglobus.
What is Fuchs’ dystrophy?
Also called as epithelial endothelial dystrophy, affects females more than the males between 5th and 7th decade of life. It is a slowly progressive bilateral condition. Its clinical features can be divided into following four stages:
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• Stage of cornea guttata
• Oedematous stage or stage of endothelial decomp-ensation
• Stage of bullous keratopathy • Stage of scarring.

Define keratoconus and describe its treatment. Keratoconus is a noninflammatory ectatic condition of the cornea. It is usually bilateral and manifests at puberty with gradual loss of vision.
The high myopic irregular astigmatic refractive error seen in keratoconus may be treated by hard contact lens in early stages. Ultimately penetrating keratoplasty is required.

A CASE OF CORNEAL OPACITY

Case Summary
Presenting symptoms. A patient with corneal opacity usually presents with a whitish scar, causing defective vision as well as cosmetic blemish.
History may reveal a history of trauma to the eye or symptoms suggestive of healed corneal ulceration. Examination reveals an opacity on the cornea (Fig. 6.27) which may be nebular, macular or leucomatous. The location, size, shape and density of the opacity must be described.

Related Questions
What is a corneal opacity?
The term corneal opacity is used for the loss of corneal transparency due to scarring.

What are common causes of corneal opacity? 1. Congenital opacities
2. Healed corneal wounds 3. Healed corneal ulcers.

What are the types of corneal opacity?
1. Nebular corneal opacity. It is a faint opacity which results due to scars involving up to a few superficial lamellae of corneal stroma.
2. Macular opacity. It is a dense opacity produced by scars involving up to about half the thickness of the stroma.
3. Leucomatous corneal opacity (leucoma simplex). It is a very dense, white opacity, which results due to scarring of more than half thickness of corneal stroma.
4. Adherent leucoma. It results when healing occurs after perforation of cornea with incarceration of the iris.

Name the secondary changes which can occur in a long standing case of corneal opacity.
1. Hyaline degeneration
2. Calcareous degeneration 3. Pigmentation
4. Atheromatous ulceration.
How will you treat a case with corneal opacity?
1. Optical iridectomy. It may be performed in cases with central macular or leucomatous corneal opacities; provided vision improves with pupillary dilatation.
2. Keratoplasty. It provides good visual results in uncomplicated cases with corneal opacities; where optical iridectomy is not of much use.
3. Tattooing of scar. It used to be performed for cosmetic purposes. It is suitable only for firm scars in a quite eye without useful vision. Presently, it is sparingly done.
How do you perform tattooing?
First of all, the epithelium covering the opacity removed under topical anaesthesia. Then a piece of blotting paper of the same size and shape soaked in 4% gold chloride (for brown eyes) or 2% platinum chloride (for dark colour) is applied over it. After 2 to 3 minutes, the piece of blotting paper is removed and a few drops of freshly prepared hydrazine hydrate (2%) solution are poured over it. Lastly, eye is irrigated with normal saline and patched after instilling antibiotic and atropine eye ointment. Epithelium grows over the pigmented area.
What are the causes of corneal vascularization? Normal cornea is avascular. In pathological states, superficial or deep corneal vascularization may occur (Fig. 6.29).
1. Superficial corneal vascularization. In it, vessels are arranged in an arborizing pattern, present below the epithelium and their continuity can be traced with the conjunctival vessels. Its common causes are: • Trachoma
• Phlyctenular keratoconjunctivitis • Superficial corneal ulcers
• Rosacea keratitis
2. Deep corneal vascularization. In it, the vessels are generally derived from the anterior ciliary arteries and lie in the corneal stroma. These vessels are usually straight, not anastomosing and their continuity cannot be traced beyond the limbus. Its common causes are:
• Interstitial keratitis • Disciform keratitis
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• Deep corneal ulcers • Chemical burns
• Sclerosing keratitis
• Corneal graft vascularization.

What is keratoplasty?
Keratoplasty is an operation in which the patient’s diseased cornea is replaced by the donor’s healthy clear cornea. It is of two types:
1. Lamellar keratoplasty (partial thickness).
• Anterior lamellar keratoplasty (ALK), and • Deep lamellar keratoplasty (DLK)
2. Penetrating keratoplasty (full thickness).

Name the indications for keratoplasty. Anterior Lamellar keratoplasty
Indolent corneal ulcer, superficial corneal opacity and lattice dystrophy.
Penetrating keratoplasty
1. Optical, i.e., to improve vision in patient with corneal opacity, bullous keratopathy, corneal dystrophies and advanced keratoconus.
2. Therapeutic, i.e., to replace inflamed cornea not responding to treatment (indolent deep ulcer).
3. Tectonic grafts, i.e., to restore the integrity of eyeball in corneal perforation and marked corneal thinning.
4. Cosmetic, i.e., to improve appearance of the eye in deep leucomas with no vision in the eye.

What is the optimum time for the removal of donor eyes from the body of a deceased?
The donor eyes should be removed as early as possible (within 6 hours of death) and should be stored under sterile conditions.

What are the methods of corneal preservation?
1. Short-term storage (up to 48 hours): The whole globe is preserved at 4°C in a moist chamber.
2. Intermediate storage (up to 2 weeks): The donor corneal button is prepared and stored in McCareyKaufman (MK) medium and various chondroitin sulphate-enriched media such as optisol.
3. Long-term storage (up to 35 days): It is done by organ culture method or cryopreservation.

Enumerate the complications of keratoplasty operation.
I.  Early complications are: Flat anterior chamber, iris prolapse, infection, secondary glaucoma, epithelial defects, primary graft failure.
II. Late complications are: Graft rejection, recurrence of disease, marked astigmatism and cystoid macular oedema.

From which sources cornea derives its nutrition? • Perilimbal capillaries
• Aqueous humour
• Oxygen from atmosphere.

What is the nerve supply of cornea?
Cornea is supplied by the nasociliary branch of ophthalmic division of the trigeminal nerve.
What is a corneal facet?
A corneal facet is a transparent depressed scar. On slit-lamp examination light beam appears to dip in the area of a facet.
What is kerotomalacia?
Keratomalacia refers to corneal necrosis due to vitamin A deficiency. In this condition, there is no inflammatory reaction.
What is arcus senilis?
Arcus senilis is a degenerative condition of cornea characterized by an annular lipid infiltration concentric to the limbus. The ring of opacity is about 1 mm wide and is separated from the limbus by a clear zone (lucid interval of Vogt).
A CASE OF ANTERIOR STAPHYLOMA

Case Summary
Presenting symptoms. Patient presents with loss of vision, bluish discoloration and bulging of anterior part of the eyeball.
History is suggestive of symptoms of corneal ulceration (pain, redness, photophobia, watering, loss of vision and whitish discoloration) followed by bluish discoloration and bulging of anterior part of the eye. Examination reveals that cornea is replaced by a lobulated ectatic scar tissue which is blackened due to the iris plastered behind it (Fig. 6.28).

Related Questions
What is a staphyloma?
Staphyloma refers to the localized bulging of weak and thin outer tunic of the eyeball (cornea or sclera) lined by uveal tissue which shines through the thinned-out fibrous coat.
What are the types of staphyloma? 1. Anterior staphyloma
2. Ciliary staphyloma
3. Intercalary staphyloma 4. Equatorial staphyloma 5. Posterior staphyloma.
How is an anterior staphyloma formed?
In a patient with sloughing corneal ulcer when the whole cornea sloughs out, the inflamed iris is covered
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with exudates. Ultimately, these exudates organize and form a fibrous layer over which the conjunctival or corneal epithelium rapidly grows and thus a pseudocornea is formed. Since the pseudocornea is thin and cannot withstand the intraocular pressure, it usually bulges forward along with the plastered iris tissue. This ectatic cicatrix is called anterior staphyloma.
What is the treatment of anterior staphyloma?
1. Most of the times there is no chance of getting useful vision in such eyes. Therefore, treatment is carried out to improve the cosmetic appearance. Localized staphylectomy under heavy doses of steroids may be carried out. After healing, cosmetic artificial shell may be advised.
2. In patients where there is a chance of getting useful vision, keratoplasty (wherever possible) or keratoprosthesis may be performed.
What are the causes of posterior staphyloma? • Pathological myopia
• Posterior scleritis
• Perforating injuries.

What is episcleritis? Describe features of a nodule of episcleritis.
Episcleritis is a benign recurrent inflammation of episclera, involving the overlying Tenon’s capsule but not the underlying sclera.
A typical nodule of episcleritis is flat, pink or purple, surrounded by injection and is usually situated 2 to 3 mm away from the limbus.
What is the differential diagnosis of nodular episcleritis?
• Inflamed pinguecula
• Foreign body embedded in the bulbar conjunctiva • Scleritis.

DISEASES OF UVEAL TRACT A CASE OF ACUTE IRIDOCYCLITIS
Case Description
Presenting symptoms. A patient with acute iridocyclitis (anterior uveitis) presents with moderate to severe pain which radiates all over the distribution of trigeminal nerve, photophobia, watering, redness and some diminution of vision of sudden onset. History of present illness. In addition to the details about the presenting symptoms, the history of present illness should also explore the following associations:
• History of allergic conditions like bronchial asthma, hay fever, allergic rhinitis, allergic skin conditions.

• History of joint pains to rule out rheumatoid disease
• History suggestive of urethritis • History of any dental problem
• History of chronic rhinitis and/or sinusitis • History of trauma to eye
Past history should include enquiries about: • History of similar attacks in the past.
• History of chronic systemic infections such as tuberculosis, syphilis, leprosy, measles, mumps and any other infection.
• History of noninfectious systemic disorders such as diabetes, gout, rheumatoid arthritis and collagen disorder.
• History of allergic and autoimmune disorders. General physical and systemic examination should be conducted to rule out systemic diseases enumerated in the history. Special care should be given to dental, ENT, lymph nodes and joint examinations.
Ocular examination may reveal following signs (Fig. 8.8):
• Visual acuity is diminished.
• Lids may show slight oedema.
• Circumcorneal congestion is marked.
• Cornea may be slightly hazy due to oedema and KPs at the back of cornea which are seen on slit-lamp examination.
• Anterior chamber shows aqueous cells and aqueous flare, hypopyon may also be present.
• Iris may show loss of normal pattern, muddy colour, posterior synechiae, iris nodules and patches of atrophy.
• Pupil is narrow, irregular and sluggishly reacting. Exudates may be present in pupillary area, occlusio pupillae and seclusio pupillae may be seen in some cases.
• Lens. Pigment dispersal, exudates and iris adhesion may be seen on anterior capsule. Complicated cataract may also occur.
• lOP may be normal, low or raised. It is raised firstly in hypertensive uveitis and secondly in pupillary block secondary glaucoma.
A CASE OF CHRONIC IRIDOCYCLITIS

Case Description
Presenting symptoms are mild to moderate dull ache in the eye, mild photophobia and diminution of vision. History of present illness and past history should explore the diseases mentioned in a case of acute iridocyclitis. Ocular examination may reveal mild circumcorneal flush, keratic precipitates, aqueous flare, aqueous cells, iris atrophic patches, iris nodules, posterior synechial neovascularization and irregular pupil.
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Related Questions
Define uveitis
Uveitis refers to inflammation of any part or whole of the uveal tract. Uveal tract includes iris, ciliary body and choroid.
How do you classify uveitis? I.  Anatomical classification
1.Anterior uveitis (iridocyclitis) 2.Intermediate uveitis (pars planitis) 3.Posterior uveitis (choroiditis) 4.Panuveitis
II. Clinical classification 1.Acute uveitis 2.Chronic uveitis
III. Pathological classification 1.Suppurative or purulent uveitis
2.Non-suppurative uveitis, which may be: i. Non-granulomatous uveitis ii.Granulomatous uveitis
IV.Etiological classification (Duke-Elder’s) 1.Infective uveitis
2.Allergic uveitis 3.Toxic uveitis 4.Traumatic uveitis
5.Uveitis associated with non-infective systemic diseases
6.Idiopathic uveitis.

What is the differential diagnosis of acute iridocyclitis? Acute iridocyclitis must be differentiated from other causes of acute red eye; especially acute congestive glaucoma and acute conjunctivitis. The differentiating features are shown in Table 8.1.
What are the differences between granulomatous and non-granulomatous uveitis?
These are shown in Table 8.2.
What are the common causes of acute anterior uveitis?
1. Microbial allergy, e.g., allergy to tubercular proteins, streptococcal proteins, spirochaetal proteins, etc.
2. Atopic uveitis
3. HLA associated uveitis, e.g., HLA-B27: Anterior uveitis is associated with ankylosing spondylitis and Reiter’s syndrome.
4. Idiopathic.
What are the causes of granulomatous uveitis? • Tuberculosis
• Syphilis
• Sarcoidosis • Leprosy


• Vogt-Koyanagi-Harada’s disease • Sympathetic ophthalmia.
Whatarethecommoncausesofunilateral iridocyclitis? • Traumatic uveitis
• Herpes zoster uveitis
• Fuchs’ heterochromic cyclitis • Retinal detachment
• Haemophthalmitis
• Iridocyclitis secondary to intraocular tumours.

What are the keratic precipitates; what are their types and significance?
Keratic precipitates are proteinaceous cellular deposits occurring at the back of cornea (Fig. 8.9). These are of the following types:
1. Fine KPs are characteristic of Fuchs’ cyclitis and herpes zoster uveitis.
2. Small and medium size KPs are seen in acute and chronic non-granulomatous uveitis. These are composed of lymphocytes and may number in hundreds (usually 40–60).
3. Mutton fat KPs. These typically occur in granulomatous iridocyclitis and are composed of epithelioid cells and macrophages. They are large, thick, fluffy, lardaceous KPs, having a greasy or waxy appearance. They are usually few (10–15) in number.
What are iris nodules?
Iris nodules typically occur in granulomatous uveitis.Nodules situated at pupillary border are known as Koeppe’s nodules, while those seen near the collarette are called Busacca’s nodules (Fig. 8.12).
What are synechiae? Describe their types. Synechiae are adhesions of the iris with other intraocular structures. These can be divided into following types:
1. Anterior synechiae: These include anterior peripheral synechiae seen in the angle of anterior chamber and anterior central synechiae seen in adherent leucoma.
2. Posterior synechiae: These refer to adhesions of posterior surface of iris to the anterior surface of crystalline lens or intraocular lens implant or posterior capsule or anterior phase of the vitreous. These are of the following types:
• Posterior segmental synechiae (Figs. 8.9 and 8.15) • Annular synechiae (Fig. 8.13), and
• Total posterior synechiae (Fig. 8.14).

What is seclusio pupillae and iris bombe?
Annular or ring synechiae are 360° adhesions of pupillary margin to anterior capsule of the lens.
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These prevent the circulation of aqueous humour from posterior to anterior chamber (seclusio pupillae). Thus, the aqueous collects behind the iris and pushes it anteriorly (leading to iris bombe formation).
What is occlusio pupillae?
Occlusio pupillae refers to occlusion of pupil by the exudates.
What is festooned pupil?
When atropine is instilled in the presence of segmental posterior synechiae, the pupil does not dilate in the areas of synechiae, but dilates in the areas without synechiae. This results in an irregular and dilated pupil known as festooned pupil.
Name the various types of HLA associated uveitis. HLA-B27:	Anterior uveitis seen with ankylosing
spondylitis and Reiter’s syndrome HLA-B5:	Behcet’s disease
HLA-BW54:   Glaucomatocyclitic crisis
HLA-BW22:   Vogt-Koyanagi-Harada’s syndrome.

What are the causes of diminution of vision in a patient with iridocyclitis?
Oneormore ofthefollowingfactors causediminution of vision:
• Corneal oedema • Aqueous haze
• Exudates in the pupillary area • Complicated cataract
• Cyclitic membrane • Vitreous haze
• Papillitis
• Macular oedema.
What are the complications of iridocyclitis? • Complicated cataract (Fig. 8.15)
• Secondary glaucoma • Cyclitic membrane
• Cystoid macular oedema
• Secondary periphlebitis retinae • Band-shaped keratopathy
• Phthisis bulbi.

What is the treatment of iridocyclitis? I.  Nonspecific treatment
a. Local therapy
1.Mydriatic cycloplegic drugs, e.g., 1% atropine, eyedrops or ointment; or 2% homatropine eyedrops.
2.Corticosteroid eyedrops such as dexa-methasone eyedrops 4 times a day.
b. Systemic therapy
1.Corticosteroids are quite useful in severe cases.

2.Nonsteroidal  anti-inflammatory  drugs (NSAIDs) such as aspirin and phenylbutazone are used when steroids are contraindicated.
3.Immunosuppressive drugs are used in desperate and extremely serious cases.
4.Adrenocorticotropic hormone (ACTH) may be required in recalcitrant cases.
c. Physical measures
1.Hot fomentation. It is very soothing, diminishes pain and increases circulation.
2.Dark goggles give feeling of comfort by reducing photophobia.
II. Specific treatment
It consists of treatment of the cause when discovered, e.g., antitubercular drugs for the underlying Koch’s disease, adequate treatment of associated syphilis, toxoplasmosis, etc.
What are the features of Fuchs’ uveitis?
Fuchs’ uveitis is a chronic non-granulomatous type of low-grade anterior uveitis. It is unilateral and affects middle-aged persons. The disease is characterized by:
• Heterochromia of iris
• Fine KPs at the back of cornea • Faint aqueous flare
• Absence of posterior synechiae • A fairly common rubeosis iridis
• Comparatively early development of complicated cataract and secondary glaucoma.
What are the features of glaucomatocyclitic crisis (Posner Schlossman syndrome)?
It typically affects young adults and is characterized by:
• Recurrent attacks of acute rise of IOP (40-50 mm of Hg) without shallowing of anterior chamber
• Fine KPs at the back of cornea without any posterior synechiae
• Epithelial corneal oedema • A dilated pupil
• A white eye (no congestion).
What is sympathetic ophthalmitis?
Sympathetic  ophthalmitis  is  rare  bilateral granulomatous panuveitis which occurs following penetrating ocular trauma usually associated with incarceration of uveal tissue in the wound. The injured eye is called exciting eye and the fellow eye which also develops uveitis is called sympathizing eye.
What are Dalen-Fuchs’ nodules?
Dalen-Fuchs’ nodules are proliferation of the pigment epithelium of iris and ciliary body to form nodular aggregations in sympathetic ophthalmitis.
Chapter 24	Clinical Ophthalmic Cases	541


What is Behcet’s disease?
Behcet’s disease is an idiopathic multisystem disease associated with HLA-B5. It is characterized by:
• Recurrent acute iridocyclitis associated with, hypopyon
• Aphthous ulceration • Genital ulceration
• Erythema multiforme.

What are ocular lesions of sarcoidosis?
1. Sarcoid plaque on the skin of the eyelids
2. Granulomatous infiltration of the lacrimal gland with xerosis
3. Conjunctival sarcoid nodules 4. Episcleritis
5. Iridocyclitis may occur as: • Acute iridocyclitis
• Chronic granulomatous iridocyclitis (more common) with Koeppe’s and Busacca’s nodules on the iris and mutton fat KPs
• Uveoparotid fever (Heerfordt’s syndrome) 6. Vitritis with snowball opacities
7. Choroidal and retinal granulomas
8. Secondary periphlebitis retinae with candle wax droppings.

What is VKH syndrome?
Vogt-Koyanagi-Harada’s (VKH) syndrome is an idiopathic multisystem disorder associated with HLA-BW22. It is characterized by:
• Cutaneous lesions such as: alopecia, poliosis and vitiligo
• Neurological  lesions  include meningism, encephalopathy, tinnitus, vertigo and deafness
• Ocular, features are: chronic granulomatous anterior uveitis, posterior uveitis and exudative retinal detachment.

What is endophthalmitis? Enumerate common causes of purulent endophthalmitis. Endophthalmitis is inflammation of the inner structures of the eyeball which include uveal tissue, retina and vitreous. Purulent endophthalmitis is a dreaded complication. Its common causes are:
1. Exogenous infections following: • Perforating injuries
• Perforation of corneal ulcer
• Intraocular operations such as cataract surgery and glaucoma surgery
2. Endogenous or metastatic endophthalmitis may occur rarely through blood stream from some septic focus in the body such as caries teeth, puerperal sepsis and generalized septicaemia.

What is panophthalmitis? Describe its treatment. Panophthalmitis is an intense purulent inflammation of the whole eyeball including the Tenon’s capsule.
Since, there is little hope of saving such an eye, evisceration operation should be performed to remove the pus and infected intraocular contents leaving behind the sclera.
Which is the most common presenting symptom in a patient with choroiditis?
Floaters, i.e., moving small black spots in front of the eyes is the most common presenting symptom in a patient with choroiditis. Floaters occur due to pouring of exudates in the vitreous.
What are the symptoms of central choroiditis? • Defective vision
• Floaters
• Micropsia (patient complains of seeing the objects smaller than normal due to separation of cones of macula due to oedema)
• Metamorphopsia (patient perceives distorted imagesof the objects) results due to alteration in the retinal contour caused by a raised patch of choroiditis
• Macropsia, i.e., perception of the objects larger than they are, may occur due to crowding together of cones
• Photopsia, i.e., a subjective sensation of flashes of light may result due to irritation of cones by inflammatory oedema.
What is the most common cause of central choroiditis? • Toxoplasmosis.
What is pathognomic feature of fungal endop-hthalmitis?
Fluffy ball opacities in the vitreous are pathognomic of fungal endophthalmitis.
At what stage vitrectomy operation should be performed in a patient with endophthalmitis? Vitrectomy is the treatment of choice for fungal endophthalmitis. In bacterial endophthalmitis it should be performed when the condition does not improve with intensive conservative therapy for 48 hours.
What is Reiter’s syndrome?
Reiter’s syndrome is characterized by a triad of urethritis, arthritis and conjunctivitis. In 20 to 30% cases, acute non-granulomatous uveitis is also associated.
What are the causes of a patch of iris atrophy? • Senile
• Post-inflammatory • Glaucomatous
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• Neurogenic, in lesions of ciliary ganglion • Essential iris atrophy.

DISEASES OF LENS

A CASE OF SENILE CATARACT

Case Description
Age and sex. It is seen equally in persons of either sex, usually above the age of 45 years (average 50–60 years).
Presenting symptoms. Patient usually presents with a gradual, painless and progressive loss of vision. In the early stages, there may or may not be associated history of coloured haloes, uniocular polyopia, glare and misty vision.
History of present illness. In addition to the details about the presenting symptoms, the history of present illness should be taken:
• To rule out other cause of acquired cataract, e.g., history of exposure to radiations (radiation cataract) excessive heat in industrial workers especially in glass workers and iron workers (heat cataract), history of injury to the affected eye (traumatic cataract), history of diabetes mellitus (diabetic cataract), history of atopic diseases (atopic cataract), history of steroid intake (steroid cataract), history suggestive of anterior uveitis (complicated cataract), etc.
• To rule out diseases affecting surgical treatment such as history of hypertension, diabetes mellitus, bronchial asthma.
Ocular signs observed in different types of senile cataract are shown in Table 9.1, page 191
General physical and systemic examination (see page 195).
Ocular examination. In addition to ocular examination to note signs of different types of cataract, the following useful information is essential before the patient is considered for surgery (see page 196):
• Retinal function tests,
• Search for local source of infection,
• Slit-lamp examination for anterior segment status, and
• IOP measurement.

Related Questions
What is your diagnosis?
Senile cataract (immature, mature, hypermature or nuclear, depending upon the type of cataract).
Define cataract.
Normal crystalline lens is a transparent structure. Any opacity in the lens or its capsule is called a cataract.

How do you classify cataracts? A.Etiological classification
I.  Congenital and developmental cataract II.Acquired cataract
1.Senile cataract 2.Traumatic cataract 3.Complicated cataract 4.Metabolic cataract 5.Electric cataract 6.Radiational cataract 7.Toxic cataract, e.g.,
a.Corticosteroid-induced cataract b.Miotics-induced cataract
c. Copper-induced and iron-induced cataracts (in chalcosis and siderosis respectively).
8.   Cataract associated with skin diseases (dermatogenic cataract).
9.   Cataract associated with osseous diseases. 10. Cataract associated with miscellaneous
syndromes e.g.,
• Dystrophic myotonica • Down’s syndrome.
B.  Morphological classification (Fig. 9.5)
1. Capsular cataract: It involves the capsule and may be:
a.Anterior capsular cataract b.Posterior capsular cataract
2. Cortical cataract: It involves the cortex of the lens. 3. Nuclear cataract: It involves the nucleus of the
crystalline lens.
4. Polar cataract: It involves the capsule and superficial part of the cortex in the polar region and may be:
a.Anterior polar cataract b.Posterior polar cataract.
What are the types of senile cataract? • Cortical cataract
• Nuclear cataract.

Name the stages of maturation of senile cortical cataract.
• Stage of lamellar separation • Stage of incipient cataract
• Stage of immature senile cataract (cuneiform or cupuliform)
• Stage of mature senile cataract
• Stage of hypermature senile cataract (Morgagnian or sclerotic type).

What do you mean by nuclear sclerosis?
Nuclear sclerosis is an aging process in which lens nucleus becomes inelastic and hard. Refractive index of the lens is increased resulting in myopia. These
Chapter 24	Clinical Ophthalmic Cases	543


changes begin centrally and spread peripherally. On oblique illumination pupillary area looks greyish.

How will you differentiate immature senile cataract (ISC) from nuclear sclerosis without cataract changes? See Table 9.3, Page 192.

Name the complications which can occur during maturation of cortical cataract.
a. Lens-induced glaucoma, which may be:
1. Phacomorphic glaucoma (secondary narrow-angle glaucoma). It occurs due to intumescent (swollen) lens causing blockage of the angle of anterior chamber and pupil.
2. Phacolytic glaucoma (secondary open-angle glaucoma). It occurs due to blockage of trabecular meshwork by macrophages laden with lens proteins leaked from the Morgagnian hypermature cataract.
b.  Phacoanaphylaxis
c.  Subluxation or dislocation of the lens.

What are the characteristics of diabetic cataract?
A true diabetic cataract is characterized by appearance of bilateral snowflake-like opacities hence the name ‘snowflake cataract’ or ‘snow-storm cataract.’

What are the characteristics of a complicated cataract?
A typical complicated cataract is characterized by ‘bread-crumb’ appearance of the opacities situated in the posterior subcapsular area, which exhibit ‘polychromatic lustre’ on slit-lamp examination.

Enumerate the indications for extraction of a catara-ctous lens.
1. Grossly diminished vision hampering easy living 2. Medical indications, e.g.,
• Lens-induced glaucoma • Phacoanaphylaxis
• Patient having diabetic retinopathy or retinal detachment, treatment of which is hampered by the presence of lens opacities
3. Cosmetic indication. Some patients may insist for cataract extraction (even with no hope of getting useful vision) in order to obtain a black pupil.

What preoperative evaluation would you like to carry out before cataract surgery?
1. General physical and systemic examination to rule out: diabetes mellitus, hypertension, obstructive lung disorders and any potential source of infection in the body such as septic gums, urinary tract infection, etc.

2. Ocular examination with special reference to: 1.Retinal function tests
2.Search for local source of infection, i.e. conjunctivitis, dacryocystitis, blepharitis, etc.
3.Intraocular pressure measurement.

Name the retinal function tests that you would like to carry out before planning cataract surgery?
1. Light perception (PL)
2. Projection of light rays (PR)
3. A test for Marcus Gunn pupillary response 4. Two-light discrimination test.
What is the most accurate method of predicting the macular potential for visual acuity in the presence of advanced cataract?
• Laser interferometry.
Name the objective tests for evaluating posterior segment of eye in a cataract patient.
1. Ultrasonography (A and B scan) 2. Electroretinography
3. Electro-oculography
4. Visually-evoked response.
Surgical management of adulthood cataracts
For questions related to surgical management of cataract, see page 605.
A CASE OF CONGENITAL/DEVELOPMENTAL CATARACT

Case Description
Age and sex. Congenital cataract is present since birth. Developmental cataract may occur any time from infancy to adolescence. It is equally common in both sexes.
Presenting symptoms. Parents may bring the child with one or more of the following complaints:
• White reflex in the pupillary area (leukocoria)
• Inability of the child to see well which may be noticed by the parents
• Wandering movements of the eyes • Deviation (squint) in one eye
• Nystagmus.
History of present illness should include:
• Details about the time of appearance and progress of the above symptoms.
• Obstetrical history to explore occurrence of rubella, malnutrition, diabetes mellitus, exposure to radiations and drug intake during pregnancy.
• Birth history should include information about: home or hospital delivery; full-term or premature birth; normal or low birth weight (LBW) for age; history of birth trauma; and history of ocular infections after birth.
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• Family history should include history of similar complaints in the family, history of any other ocular or systemic defects in the family, history of diabetes mellitus and history of consanguinous marriage.
General physical and systemic examination should be carried out thoroughly with special attention for any associated mental retardation, cerebral palsies, features of rubella, features of galactosaemia, hepatosplenomegaly and cardiovascular anomalies such as patent ductus arteriosus (PDA), ventricular septal defect (VSD) and pulmonary stenosis (PS). Ocular examination. Conspicuous sign is leukocoria (white reflex in pupillary area). Make special note of visual acuity (if possible), any associated squint, nystagmus and other congenital anomalies such as microphthalmos, microcornea, aniridia, iris coloboma, and persistent pupillary membrane. Lens should be examined in detail after dilation of the pupil. If possible fundus should be examined to know the status of the posterior segment.

Related Questions
Name the types of congenital cataract.
• Cataracta centralis pulverulenta (embryonic nuclear cataract)
• Lamellar (zonular) cataract • Sutural cataract
• Anterior polar cataract • Posterior polar cataract • Coronary cataract
• Blue dot punctate cataract • Total congenital cataract.
Enumerate the etiological factors associated with congenital cataract.
1. Heredity (about 3% cases) 2. Maternal factors, e.g.,
• Malnutrition during pregnancy • Rubella infection
• Toxoplasmosis
• Cytomegalo inclusion disease
• Drug ingestion during pregnancy, e.g., thalidomide, corticosteroids
3. Fetal or infantile factors, e.g.,
• Anoxia due to placental haemorrhage
• Metabolic disorders, e.g., galactosaemia, neonatal hypoglycaemia
• Lowe’s syndrome
• Myotonia dystrophica • Birth trauma
• Malnutrition in early infancy 4. Idiopathic (about 50% cases).

What are the features of zonular (lamellar) cataract? Zonular cataract typically occurs in a zone of fetal nucleus surrounding the embryonic nucleus (Fig. 9.7). The area of the lens internal and external to the zone of cataract is clear, except for small linear opacities like spokes of a wheel (riders) which run outwards towards the equator. It is usually bilateral and frequently causes severe visual defect.
What is the differential diagnosis of a white pupillary reflex?
1. Congenital cataract 2. Retinoblastoma
3. Retinopathy of prematurity (retrolental fibroplasia) 4. Persistent hyperplastic primary vitreous
5. Parasitic endophthalmitis
6. Exudative retinopathy of Coats.

How will you manage a case of congenital cataract? 1. Small stationary lens opacities which do not
interfere with vision can safely be ignored.
2. Incomplete central stationary cataracts may be treated by optical iridectomy or use of mydriatics to improve the vision considerably.
3. Complete cataracts should be removed surgically as early as possible.

Name the surgical procedures in vogue for mana-gement of childhood cataracts.
1. Discission (needling) operation (almost obsolete) 2. Anterior capsulotomy and irrigation aspiration of
the lens matter. 3. Lensectomy.

How should paediatric aphakia be corrected?
1. Children above the age of 5 years can be corrected by implantation of posterior chamber intraocular lens during surgery.
2. Those below the age of 5 years should preferably be treated by extended wear contact lens. Spectacles can be prescribed in bilateral cases. At a later stage secondary IOL implantation may be considered.
3. Epikeratophakia and keratophakia are still under trial.
A CASE OF APHAKIA
Case Description
Presenting symptoms. Patient usually gives history of cataract extraction operation (postoperative aphakia). Sometimes, patient may present with such a situation following trauma to the eye (aphakia due to traumatic posterior dislocation of lens) and rarely without any cause (aphakia due to spontaneous posterior dislocation of lens).
Chapter 24	Clinical Ophthalmic Cases	545


• Patient usually has marked loss of vision both for distance and near due to high hypermetropia and absence of accommodation, respectively.
• Patient may complain of seeing red (erythropsia) and blue (cyanopsia) images. This occurs due to excessive entering of ultraviolet and infrared rays in the absence of crystalline lens.
Signs of aphakia seen on ocular examination: • Limbal scar may be seen in surgical aphakia • Anterior chamber is deeper than normal
• Iridodonesis, i.e., tremulousness of the iris can be demonstrated
• Pupil is jet black in colour
• Purkinje image test shows only two images (normally four images are seen)
• Fundus examination shows hypermetropic small disc • Retinoscopy reveals high hypermetropia.
A CASE OF PSEUDOPHAKIA

Case Description
Presenting symptoms
• Patient usually gives a history of cataract operation and may also be aware of the intraocular lens (IOL) implantation.
• Patient may give history of normal far vision (emmetropia produced by IOL) but defective near vision due to loss of accommodation.
• Some patients may give history of normal near vision but defective far vision (due to 2–3 D myopia produced by a high power IOL).
• Some patients are uncomfortable due to defective vision both for distance and near. This occurs due to hypermetropia produced by a low power IOL and loss of accommodation.
Signs of pseudophakia
• Surgical limbal scar may be seen.
• Anterior chamber is slightly deeper than normal. • When implanted, the angle supported anterior
chamber IOL (Fig. 9.30) and iris claw IOL(Fig. 9.31) are seen in the anterior chamber.
• Mild iridodonesis (tremulousness of iris) may be demonstrated.
• Purkinje image test shows four images.
• Pupil is blackish in colour. When light is thrown in pupillary area, shining reflexes are observed. When examined under magnification after dilating the pupil, the presence of posterior chamber IOL when implanted is confirmed (Fig. 9.32).
• Visual status and refraction of the patient will vary depending upon the power of IOL implanted as described above.

Related Questions
Define aphakia.
Aphakia literally means absence of the crystalline lens from the eye. However, from the optical point of view, it may be considered as a condition in which the lens is absent from the pupillary area and does not take part in refraction. Optically aphakia may be: • Complete aphakia, i.e., whole of the lens is absent
from its normal position.
• Partial aphakia, i.e., part of the lens is present in the pupillary area. In this situation aphakic and phakic portions are seen simultaneously in pupillary area.
Enumerate the refractive changes which occur in an aphakic eye.
1. Eye becomes highly hypermetropic.
2. Total power of the eye is reduced to +44 DS from +60 DS.
3. Anterior focal distance becomes 23 mm (from 15 mm in normal phakic eye).
4. Posterior focal distance becomes 31 mm (from 24 mm in normal phakic eye).
5. There is anterior shift of nodal point and principal focus.
6. There is complete loss of accommodation due to absence of lens.
7. Astigmatism is induced due to corneal/limbal scar.
Name the various modalities for correction of aphakia and enumerate advantages and disadvantages of each.
1. Spectacles
Advantages: It is cheap, easy and safe method of correcting aphakia.
Disadvantages: (i) Image is magnified by 30 per cent, so not useful in unilateral aphakia (produces diplopia), (ii) problems of spherical and chromatic aberrations may be troublesome, (iii) field of vision is limited, (iv) prismatic effect of thick glasses causes, ‘roving ring scotoma’ (v) cosmetic blemish, especially in young aphakics.
2. Contact lenses
Advantages: (i)Less magnification (5%) of the image, (ii) elimination of aberrations and prismatic effect of thick glasses, (iii) wider and better field of vision, (iv) cosmetically better accepted by young persons. Disadvantages: (i) more cost, (ii) cumbersome to wear, especially in old age and in childhood, (iii) corneal complications may occur.
3. Intraocular lens implantation
It is the best available method of treatment. Advantages: It offers all the advantages which the contact lenses offer over the spectacles. In addition, the
546	Section Vi   Practical Ophthalmology


disadvantages of contact lenses are also taken care of. Disadvantage: It requires more skilled surgeons and costly equipment.
4. Refractive corneal surgery
It is still under trial and includes keratophakia and epikeratophakia.
What are fundus findings in a patient with high hypermetropia?
Fundus examination in a patient with high hyper-metropia may show:
• Pseudopapillitis
• Shot silk appearance of the retina
Enumerate the signs of aphakia. • Deep anterior chamber
• Iridodonesis
• Jet black pupil
• Purkinje’s image test shows only two images (normally four)
• Fundus examination shows small optic disc • Retinoscopy, reveals high hypermetropia.
What is the average standard power of the lenses required for spectacle correction of aphakia?
In preoperative emmetropic patient, the standard power of the lenses required for spectacle correction of aphakia for distance vision is + 10DS with an additional cylindrical lens for acquired astigmatism. For near vision correction an additional +3 DS is required as the accommodation is absent in an aphakic eye.
What is pseudophakia?
Pseudophakia refers to presence of an intraocular lens in the papillary area.
What is the refractive position of the pseudophakic eye?
A pseudophakic eye may be emmetropic, myopic or hypermetropic depending upon the power of the IOL implanted.
What is the average standard power of the posterior chamber IOL?
Exact power of an IOL to be implanted varies from individual to individual and is calculated by biometry using keratometer and A-scan ultrasound.
What is the average weight of an IOL?
Average weight of an IOL in air is 15 mg and in aqueous humour is about 5 mg.
What is the power of the IOL in air vis-a-vis in the aqueous humour?
Power of an IOL in air is much more (about +60D) than that in the aqueous humour (about + 20D).

What is the difference in the power of an anterior chamber IOL versus posterior chamber IOL? Equivalent power of an anterior chamber IOL is less (say about +18D) than that of posterior chamber IOL (+20D).
Surgical management of cataract
For questions related to surgical management of a cataract patient, see page 605.

GLAUCOMA
A CASE OF PRIMARY ANGLE-CLOSURE GLAUCOMA

Case Description
Age and sex. Primary narrow-angle glaucoma usually presents between 50 and 60 years of age. It occurs more commonly in females than males in a ratio of 4:1.
Presenting symptoms depend upon the stage of the disease as follows:
1. Primary angle-closure suspect (PACS). Patient does not present in this stage as there are no symptoms. It is diagnosed:
• On routine slit-lamp examination in patients presenting with some other eye disease, and
• In fellow eye of the patients presenting with subacute or acute angle-closure glaucoma.
• On glaucoma screening.
2. Primary angle-closure (PAC). Patient presents with transient blurring of vision, coloured haloes around the light due to corneal oedema and mild headache. These symptoms are due to transient rise in intraocular pressure (IOP) and occur in intermittent attacks at irregular intervals. The attacks are usually precipitated by overwork in the evening, anxiety and fatigue.
Acute primary angle-closure (Acute PAC). Patient presents with an attack of sudden onset of very severe pain in the eye which radiates along the branches of fifth nerve. Frequently, there is history of associated nausea, vomiting and prostrations. There is history of rapidly progressive loss of vision, redness, photophobia and watering. About 5% patients give history of typical previous intermittent attacks.
3. Primary angle-closure glaucoma (PACG). Patients may have dull pain and discomfort in the eye along with marked diminution of vision. Patients may or may not give history of preceding attack of acute PAC. 4. Absolute glaucoma. Such patients present with:
• Pain in the eye which is severe and irritating, • Constant headache,
• Watering and redness of the eye, and
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• Complete loss of vision (no perception of light) This stage results if PACG is left untreated.
Ocular examination. The signs observed on ocular examination depend upon the stage of glaucoma (See page 239–247):
1. Primary angle-closure suspect (PACS). The eye is white and quiet. Anterior chamber is shallow. Gonioscopy reveals narrow angle. IOP is usually normal.
2. Primary angle-closure (PAC). Usually, the eye looks normal except for a shallow anterior chamber and narrow angle (on gonioscopy).
Acute primary angle-closure. Signs areas follows: • Lids may be oedematous.
• Conjunctiva is chemosed, and congested, (both conjunctival and ciliary vessels are congested).
• Cornea becomes oedematous and insensitive.
• Anterior chamber isvery shallow. Aqueous flare or cells may be seen in anterior chamber.
• Angle of anterior chamber is completely closed as seen on gonioscopy.
• Iris may be discolored.
• Pupil is semidilated, vertically oval and fixed. It is non-reactive to both light and accommodation.
• lOP is markedly elevated, usually between 40 and 70 mm of Hg.
• Optic disc is oedematous and hyperaemic.
• Fellow eye shows shallow anterior chamber and a narrow angle.
3. Primary angle-closure glaucoma (PACG). Signs are as follows:
• The IOP remains constantly raised.
• Eye is painless and white like primary open angle glaucoma.
• Visual field defects appear which are similar to those in POAG.
• Optic disc may show glaucomatous cupping. • Visual acuity is decreased.
• Gonioscopy reveals angle closed by peripheral anterior synechiae.
4. Absolute glaucoma. Signs are as follows: • Lids show mild oedema.
• Palpebral aperture is slightly narrow.
• The anterior ciliary veins are dilated with a slight ciliary flush around the cornea (perilimbal reddish blue zone).
• In long-standing cases, few prominent and enlarged vessels are seen in the form of ‘caput medusae.’
• Cornea in early cases is clear but insensitive. Slowly it becomes hazy and may develop epithelial bullae (bullous keratopathy) or filaments (filamentary keratitis).

• Anterior chamber is very shallow. • Iris becomes atrophic.
• Pupil becomes fixed and dilated and gives a greenish hue.
• Optic disc shows glaucomatous optic atrophy.
• Intraocular pressure is high; eyeball becomes stony hard.
A CASE OF PRIMARY OPEN-ANGLE GLAUCOMA

Case Description
An early case of primary open-angle glaucoma (POAG) is usually not given in undergraduate examinations. However, an advanced or a case of POAG which has been operated for trabeculectomy may be kept as short or long case.
Age and sex. POAG usually affects about 1 in 100 of the general population (of either sex) above the age of 40 years. The disease is essentially bilateral. Presenting symptoms. The disease is insidious and usually asymptomatic. Mild symptoms experienced by the patients include:
• Mild headache and eyeache.
• Difficulty in reading (patients usually give history of frequent change in near vision glasses).
• Occasionally, an observant patient may notice a defect in the visual field (scotoma).
• In late stages patient may complain of delayed dark adaptation.
Ocular examination. Anterior segment is usually normal. In advanced cases, the pupils are sluggishly reacting. Fixed and dilated pupils are seen in absolute glaucoma. Diagnosis is usually made from triad of raised intraocular pressure (IOP), glaucomatous optic disc changes and visual field changes (see pages 239-247). In a case of POAG operated for trabeculectomy, a filteration conjunctival bleb is seen at the site of operation near the limbus.
A CASE OF PHACOMORPHIC GLAUCOMA Presenting symptoms. Patient presents with a sudden onset of severe pain, redness, watering from the eyes and marked loss of vision. Usually, there is associated nausea, vomiting, headache and prostration. Patient always gives history of preceding gradual painless loss of vision.
Ocular examinationreveals following signs (Fig. 10.21): • Lids may be oedematous.
• Conjunctiva is chemosed and congested (both conjunctival and ciliary vessels are congested).
• Cornea becomes oedematous and insensitive.
• Anterior chamber is very shallow (opposite eye normal). Aqueous flare and cells may be seen in the anterior chamber.
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• Pupil is semidilated, vertically oval and fixed.
• Lens is cataractous, swollen and bulging forward (intumescent cataract).
• IOP is markedly elevated.

A CASE OF PHACOLYTIC GLAUCOMA

Case Description
The presenting symptoms and signs are similar to phacomorphic glaucoma except for following differences:
• Anterior chamber is not shallow. It is normal or slightly deep. Aqueous is turbid.
• Lens shows hypermature Morgagnian senile cataract.
RELATED QUESTIONS
What are normal values of intraocular pressure? • Range: 10 to 21 mm of Hg
• Mean: 16 ± 2.5 mm of Hg

What is the normal amount of aqueous humour present in the eye?
Normal amount of aqueous humour present in the anterior chamber is about 0.25 ml and in posterior chamber is 0.06 ml.
What is the normal rate of aqueous production? • 2.3 ml/minute.

What is the site of aqueous production? • Ciliary processes.
Name the mechanisms concerned with aqueous production.
• Diffusion
• Ultrafiltration
• Active secretion.
Define glaucoma.
Glaucoma is not a single disease but a group of disorders in which intraocular pressure is sufficiently raised (above the tolerance limit of the affected eye) to impair normal functioning of the optic nerve.
How do you classify glaucoma? I.  Congenital/developmental
1.Primary congenital glaucoma (without associated anomalies)
2.Developmental glaucoma with other associated anomalies
II. Primary glaucomas
1.Primary open-angle glaucoma (POAG) 2.Primary angle-closure glaucoma (PACG) 3.Primary mixed mechanism glaucoma
III. Secondary glaucomas.

What is the incidence of primary angle-closure glaucoma?
• 1 in 1000 people over 40 years • Male to female ratio is 1:4.
Name the predisposing factors for PACG. • Hypermetropic eyes
• Small corneal diameter
• Relative large size of the crystalline lens • Short axial length of eyeball
• Shallow anterior chamber • Plateau iris configuration.
Name the precipitating factors for an attack of acute congestive glaucoma.
• Dim illumination
• Emotional stress, anxiety and excitement • Use of mydriatics.
Describe the mechanism of rise in IOP in acute narrow-angle glaucoma.
Mid-dilated pupil—increased contact between the lens and relative iris pupil block—physiological iris bombe formation—appositional angle closure (causing transient rise in IOP)— synechial angle closure—prolonged rise in IOP.
Name the clinical stages of primary angle-closure glaucoma.
1. Primary angle-closure suspect (PACS) 2. Primary angle-closure (PAC)
• Acute primary angle-closure
3. Primary angle-closure glaucoma (PACG) 4. Absolute glaucoma.
Name the provocative tests used in primary angle-closure suspect (PACS) and primary angle closure (PAC) stage to confirm the diagnosis.
1. Darkroom test 2. Prone test
3. Prone darkroom test
4. Mydriatic test (10% phenylephrine test)
5. Mydriatic-miotic test (10% phenylephrine and 2% pilocarpine test).
Enumerate the sequelae of an attack of acute primary angle closure (Acute PAC).
• Sectoral iris atrophy
• Spiralling of iris fibres
• Iris hole (pseudopolycoria) • Large irregular pupil
• Glaucomflecken
• Peripheral anterior synechiae • Chronic corneal oedema.
Chapter 24	Clinical Ophthalmic Cases	549


How will you treat a case of acute primary angle-closure?
I.  Immediate medical treatment to control pain and lower the intraocular pressure
1.Injectable analgesic to relieve the severe pain 2.Acetazolamide 500 mg stat and then 250 mg
qid orally.
3.Hyperosmotic agents, e.g., glycerol 1 to 2 g per kg body weight orally in lemon juice and/ or mannitol 1 to 2 g per kg body weight (20% solution) IV over 30 minutes.
4.Pilocarpine eyedrops 2 to 4% every 15 minutes for one hour and then qid.
5.Timolol maleate eyedrops 0.5% bd.
6.Topical steroid 3 to 4 times a day to control the inflammation.
II. Surgical treatment
1.Peripheral iridectomy/laser iridotomy is sufficient when peripheral anterior synechiae (PAS) are formed in less than 50% of the angle.
2.Filtration surgery (e.g., trabeculectomy) is performed when PAS are formed in more than 50% of the angle.
3.Peripheral iridectomy/laser iridotomy should also be considered as prophylaxis for the fellow eye.

Name the structures forming angle of the anterior chamber.
1. Root of the iris
2. Anterior most part of the ciliary body 3. Scleral spur
4. Trabecular meshwork
5. Schwalbe’s line (prominent end of Descemet’s membrane of cornea).

How will you grade the angle width gonioscopically? Shaffer’s grading system is as follows:
Grade 4 (Wide open angle) • Angle width is 35°–45°
• Structures seen are from Schwalbe’s line to ciliary body
• Closure impossible Grade 3 (Open angle)
• Angle width is 20°–35°
• Structures seen are from Schwalbe’s line to scleral spur
• Closure impossible
Grade 2 (Moderately narrow angle) • Angle width is about 20°.
• Structures seen are from Schwalbe’s line to trabecular meshwork
• Angle closure is possible but unlikely


Grade 1 (Very narrow angle) • Angle width is about 10°
• Structure seen is Schwalbe’s line only • High-angle closure risk
Grade 0 (Closed angle) • Angle width is 0°
• None of the angle structures are seen (iridocorneal contact)
• Completely closed angle.

Name the structures forming aqueous outflow system.
• Trabecular meshwork • Schlemm’s canal
• Collector channels.
What is the incidence of primary congenital/ developmental glaucoma?
• Affects 1 in 10,000 live births • Male to female ratio is 3:1.
What  is  the  pathogenesis  of  developmental glaucoma?
Failure in the absorption of mesodermal tissue resulting in failure of development of the angle structures.
What are gonioscopic findings of developmental glaucoma?
• Barkan’s membrane may be present • Thickening of trabecular meshwork
• Insertion of iris above the scleral spur • Peripheral iris stroma hypoplasia.
What is buphthalmos?
This term is used when eyeball enlarges (corneal diameter becomes more than 13 mm) in children developing congenital glaucoma at an early age (before the age of 3 years).
What is the treatment of primary congenital glaucoma?
• Goniotomy
• Trabeculotomy
• Trabeculectomy (with antifibrosis treatment).
What are the causes of secondary congenital glaucoma?
I.  Glaucoma associated with mesodermal dysgenesis of the anterior ocular segment, e.g.:
1.Posterior embryotoxon 2.Axenfeld’s anomaly 3.Rieger’s syndrome 4.Peter’s anomaly
II. Glaucoma associated with aniridia (50%)
III. Glaucoma associated with ectopia lentis syndrome 1.Marfan’s syndrome
550	Section Vi   Practical Ophthalmology


2.Weill-Marchesani’s syndrome 3.Homocystinuria
IV.Glaucoma associated with phacomatoses: 1.Sturge-Weber syndrome (50% cases)
2.Von Recklinghausen’s neurofibromatosis (25% cases)
V. Miscellaneous conditions 1.Lowe’s syndrome (50% cases) 2.Naevus of Ota 3.Nanophthalmos
4.Congenital microcornea (60%) 5.Congenital rubella syndrome (10% cases).
What is the incidence of primary open-angle glaucoma?
• It affects 1 in 100 population (of either sex) above the age of 40 years.
• It forms about one-third cases of all glaucomas.
What are the features of glaucomatous cupping of the disc?
These include (Fig. 10.10 and 10.11) the following: 1. Cup/disc ratio is increased (normal 0.3 to 0.4),
asymmetry of more than 0.2 is suspicious. 2. Notching of the rim.
3. Nasal shift of the vessels at disc. 4. Pallor area on the disc.
5. Presence of splinter haemorrhages on or near the disc margin.
Name the predisposing factors for POAG. 1. Heredity (positive family history)
2. Age (between 5th and 7th decade) 3. High myopia
4. Diabetes mellitus.

What is the characteristic triad of POAG?
1. Intraocular pressure more than 21 mm of Hg 2. Glaucomatous cupping of the disc
3. Glaucomatous field defects.

What is ocular hypertension?
Ocular hypertension or glaucoma suspect is the term used when a patient has an IOP constantly more than 23 mm of Hg but no optic disc or visual field changes.
What is low tension glaucoma (LTG)?
This term is used when typical glaucomatous disc cupping with or without visual field changes is associated with an IOP constantly below 21 mm of Hg.
What are the other ocular associations of POAG? 1. High myopia
2. Fuchs’ dystrophy
3. Retinitis pigmentosa

4. Central retinal vein occlusion (CRVO) 5. Primary retinal detachment.
What are glaucomatous field defects? 1. Baring of the blind spot
2. Paracentral scotoma in Bjerrum’s area (an arcuate area extending above and below the blind spot upto between 10° and 20° of fixation point)
3. Seidel scotoma
4. Arcuate or Bjerrum’s scotoma 5. Double arcuate scotoma
6. Roenne’s central nasal step
7. Advanced field defects with tubular vision.

What is the treatment for primary open-angle glaucoma?
1. Medical treatment: It is still the initial therapy. Topical timolol maleate 0.25% BD which may be increased to 0.5% BD Pilocarpine TDS 2% which may be increased to 4% BD was previously used as drug of second choice. Recently latanoprost (0.005%, OD) is being considered the drug of first choice (provided patients can afford to buy it. Dorzolamide (2%, 2–3 times/day) has replaced pilocarpine as the second drug of choice and even as adjunct drug. If the patient does not respond to a single drug the two drugs can be combined. If still the IOP is not controlled, tablet acetazolamide 250 mg TDS may be added.
2. Argon laser trabeculoplasty:It may be considered as an alternative to medical therapy or as an additional measure in patients not responding to medical therapy alone.
3. Surgical therapy: It is usually undertaken when patient does not respond to maximal medical therapy alone or in combination with laser trabeculoplasty. Recently, it is also being considered as the primary line of treatment. Surgical treatment mainly consists of filtration surgery trabeculectomy.
What are secondary glaucomas?
In secondary glaucomas, intraocular pressure is raised due to some other primary ocular or systemic disease. Depending upon the causative primary disease,secondary glaucomas are classified as follows:
1. Lens-induced glaucomas
2. Glaucomas associated with uveitis 3. Pigmentary glaucoma
4. Neovascular glaucoma
5. Pseudoexfoliative glaucoma (glaucoma capsulare) 6. Glaucomas associated with intraocular haemor-
rhages
7. Steroid-induced glaucoma
Chapter 24	Clinical Ophthalmic Cases	551


8. Traumatic glaucoma 9. Glaucoma in aphakia
10. Glaucoma associated with intraocular tumours 11. Glaucomas associated with iridocorneal
endothelial (ICE) syndromes
12. Ciliary block glaucoma (malignant glaucoma).

What are lens-induced glaucomas?
1. Phacomorphic glaucoma: Here in IOP is raised due to secondary angle closure and/orpupil block by:
i. Intumescent (swollen) cataractous lens (Fig. 10.21)
ii. Anterior subluxated lens iii.Spherophakia
2. Phacolytic glaucoma: Here in IOP is raised due to clogging of trabecular meshwork by the macrophages laden with the leaked lens proteins, usually in hypermature cataract.
3. Lens particle glaucoma: It occurs due to blockage of trabeculae by the lens particles following rupture of the lens or after ECCE.
4. Phacoanaphylactic glaucoma: Sensitization of eye or its fellow to lens proteins. Inflammatory material clogs trabecular meshwork.
5. Phacotoxic glaucoma: Herein IOP is raised due to lens matter induced uveitis.
What is malignant glaucoma?
Malignant or ciliary block glaucoma occurs rarely as a complication of any intraocular operation. Classically, it occurs following peripheral iridectomy or filtration operation for primary narrow angle glaucoma. Its pathogenesis includes cilio-lenticular or ciliovitreal block.
It is characterized by a markedly raised intraocular pressure, persistent flat anterior chamber and a negative Seidel’s test.
What is differential diagnosis of acute congestive glaucoma?
• Acute conjunctivitis • Acute iridocyclitis
• Secondary acute congestive glaucomas – Phacomorphic glaucoma
– Phacolytic glaucoma
– Glaucomatocyclitic crisis.
What is postinflammatory glaucoma? Postinflammatory glaucoma refers to rise in intraocular pressure due to following complications of anterior uveitis:
• Annular synechiae • Occlusio pupillae
• Angle closure following iris bombe formation

• Angle-closure due to organization of the inflammatory debris.
What is pigmentary glaucoma?
Pigmentary glaucoma refers to raised IOP in patients with pigment dispersion syndrome. It typically affects young myopic males. Its features are similar to POAG with associated pigment deposition on corneal endothelium (Krukenberg’s spindle) trabecular meshwork, iris, lens and zonules.
What is neovascular glaucoma?
Neovascular glaucoma refers to raised IOP occurring due to formation of a neovascular membrane involving angle of the anterior chamber. Usually, stimulus to new vessel formation is retinal ischaemia as seen in diabetic retinopathy, CRVO, Eales’ disease. Other rare causes are chronic uveitis, intraocular tumours, old retinal detachment, CRAO and retinopathy of prematurity.
What is pseudoexfoliation glaucoma? Pseudoexfoliation  glaucoma  is  a  type  of secondary open-angle glaucoma associated with pseudoexfoliation (PEX) syndrome. PES refers to amyloid like deposits on pupillary border, anterior lens surface, posterior surface of iris, zonules and ciliary processes.
What is steroid-induced glaucoma?
Steroid-induced glaucoma is secondary open-angle glaucoma having features similar to POAG. It probably occurs due to deposition of mucopolysaccharides in the trabecular meshwork in patients using topical steroid eyedrops. Roughly 5% of general population is high steroid responder (develop marked rise of IOP after about 6 weeks of steroid therapy), 35% are moderate and 60% are nonresponders.
Enumerate the causes of glaucoma in aphakia.
• Raised IOP due to postoperative hyphaema, inflammation, vitreous filling the anterior chamber.
• Angle closure due to flat anterior chamber • Pupil block with or without angle closure • Undiagnosed pre-existing POAG
• Steroid-induced glaucoma • Epithelial in growth
• Aphakic malignant glaucoma.

DISEASES OF EYELIDS

A CASE OF BLEPHARITIS
Case Description
Age and sex. Though more common in children, blepharitis may occur at any age equally in both sexes.
552	Section Vi   Practical Ophthalmology


Presenting symptoms. Patients usually complain of deposits at the lid margin, associated with irritation, discomfort, occasional watering and history of falling of cilia or gluing of cilia.
Ocular examination may reveal signs of either seborrhoeic or ulcerative (Fig. 15.7 and 15.8) or mixed blepharitis.
• Signs of seborrhoeic blepharitis are: accummulation of white dandruff-like scales on the lid margin. On removing these scales underlying surface is found to be hyperaemic (no ulcers). Lashes fall out easily. In long standing cases lid margin is thickened and the sharp posterior lid border tends to be rounded leading to epiphora.
• Signs of ulcerative blepharitis. Yellow crusts are seen at the root of cilia which glue them together. Small ulcers, which bleed easily, are seen on removing the crusts. In between the crusts, the anterior lid margin may show dilated blood vessels (rosettes).

Related Questions
What is blepharitis and how do you classify it? Blepharitis is a chronic inflammation of the lid margins. It can be divided into four classical types: 1. Seborrhoeic or squamous blepharitis
2. Ulcerative blepharitis
3. Mixed ulcerative with seborrhoeic blepharitis 4. Posterior blepharitis or meibomitis.
How will you differentiate squamous blepharitis from ulcerative blepharitis?
1. In squamous blepharitis white dandruff-like scales are seen at the lid margin while in ulcerative blepharitis yellow crusts are seen.
2. On removing the white scales underlying surface is found to be hyperaemic in squamous blepharitis. While in ulcerative blepharitis, small ulcers which bleed easily are seen on removing the crusts.
3. Cilia may be glued together in ulcerative blepharitis, but not so in squamous belpharitis.
What are the complications of ulcerative blepharitis? When not treated for a long time, the following complications may occur:
1. Chronic conjunctivitis 2. Trichiasis
3. Madarosis (sparseness or absence of lashes) 4. Poliosis (greying of cilia)
5. Tylosis (thickening of lid margin)
6. Eversion of punctum leading to epiphora 7. Recurrent styes.


How will you treat a case of squamous blepharitis? 1. Scales should be removed from the lid margin
with the help of lukewarm solution of 3% soda-bicarb or some baby shampoo.
2. Combined steroid and broad spectrum eye ointment should be rubbed at the lid margin twice daily.
3. Associated seborrhoea should be treated adequately.
How will you treat a case of ulcerative blepharitis? 1. Hot compresses.
2. Crusts should be removed after softening with 3% soda-bicarb.
3. Antibiotic ointment should be applied at lid margin immediately after removal of crusts.
4. Antibiotic eyedrops should be instilled 3 to 4 times a day.
5. Oral antibiotics such as amoxycillin, cloxacillin, erythromycin or tetracycline may be useful.
A CASE OF CHALAZION (MEIBOMIAN CYST)

Case Description
Presenting symptoms. Patient usually presents with a painless swelling near the lid margin. Patient may be concerned about the cosmetic disfigurement caused and may also feel mild heaviness in the lids. Sometimes, mild defective vision may occur due to astigmatism caused by pressure of chalazion on the cornea.
Ocular examinations reveal a small, firm to hard, nontender swelling present slightly away from the lid margin (Fig. 15.12). Overlying skin is normal and mobile. The swelling usually points on the conjunctival side as red, purple or grey area seen on everting the lid. Sometimes, the main bulk of swelling may project on the skin side and occasionaly on the lid margin.
Differential diagnosis. Chalazion needs to be differentiated from meibomian gland carcinoma, tuberculomata and tarsitis.
A CASE OF STYE
Presenting symptoms include acute pain and swelling in the lid. Patient also experiences heaviness in the eyelid, mild photophobia and watering.
Ocular examination during stage of cellulitis reveals tender swelling, redness and oedema of the affected lid margins (Fig. 15.11). During stage of abscess formation a visible plus point on the lid margin in relation to the roof of affected cilia is formed. Differential diagnosis. Stye (hordeolum externum) should be differentiated from hordeolum internum.
Chapter 24	Clinical Ophthalmic Cases	553


Related Questions
What is a chalazion?
Chalazion is also known as tarsal or meibomian cyst. It is a chronic noninfective granulomatous inflammation of the meibomian gland.
What is hordeolum externum (stye)?
Hordeolum externum is an acute suppurative inflammation of one of the Zeis’ glands.
It is characterized by a localized, hard, red, tender swelling at the lid margin (PI.IV.I). In advanced stage, a pus point is visible at the lid margin.
What  is  hordeolum  internum?  How  will  you differentiate it from hordeolum externum? Hordeolum internum is a suppurative inflammation of the meibomian gland associated with blockage of the duct. It may occur as primary staphylococcal infection of the meibomian gland or due to secondary infection in a chalazion (infected chalazion).
Its symptoms are similar to hordeolum externum except that pain is more intense due to the swelling being deeply embedded in the dense fibrous tissue. On examination it can be differentiated from hordeolum externum by the facts that in it, the point of maximum tenderness and swelling is away from the lid margin and that pus usually points on the tarsal conjunctiva (seen as a yellowish area on everting the lid) and not on the root of cilia.
When not treated, what complications can occur in a case of chalazion?
1. A large chalazion of the upper lid may press on the cornea and may cause blurred vision due to induced astigmatism.
2. A large chalazion of the lower lid may rarely cause eversion of the punctum or even ectropion and epiphora.
3. Occasionally, a chalazion may burst on the conjunctival side forming a fungating mass of granulation tissue.
4. Due to secondary infection the chalazion may be converted into hordeolum internum.
5. Calcification may occur, though very rarely.
6. Malignant change into meibomian gland carcinoma may be seen occasionally in elderly people.
How do you treat a case of chalazion?
1. Conservative treatment in the form of hot fomentation, topical antibiotic eyedrops and oral anti-inflammatory drugs may lead to self-resolution in a small, soft and recent chalazion.


2. Intralesional injection of long acting steroid (triamcinolone) is reported to cause resolution in about 50% cases.
3. Incision and curettage is the conventional and effective treatment for chalazion.
Describe the steps of incision and curettage of a chalazion.
1. Local anaesthesia is obtained by topical instillation of 4% Xylocaine drops in the conjunctival sac and infiltration of the lid in the region of chalazion with 2% Xylocaine.
2. A chalazion clamp is applied with its fenestrated side on the conjunctival side and the lid is everted.
3. A vertical incision is made to avoid injury to the other meibomian glands.
4. The contents are curetted out with the help of a chalazion scoop.
5. To avoid recurrence its cavity should be cauterized with carbolic acid.
6. An antibiotic eye ointment is instilled and eye is padded.
What is the treatment of a marginal chalazion? Destruction by diathermy is the treatment of choice for a marginal chalazion.
A CASE OF TRICHIASIS AND ENTROPION

Description of a Case of Trichiasis
Presenting symptoms. Patients may present with a foreign body sensation, photophobia, irritation and lacrimation. Sometimes, patient may experience troublesome pain.
Past history of the disease causative of trichiasis such as cicatrizing trachoma, ulcerative blepharitis, membranous conjunctivitis, mechanical injuries, burns and operation of the lid margin may be explored.
Ocular examination reveals one or more misdirected cilia touching the eyeball (Fig. 15.16). There may or may not be signs of the causative disease.

Description of a Case of Entropion
Presenting symptoms and past history exploration are similar to a case of trichiasis.
Ocular examination reveals inturned lid margin (Fig. 15.18 and 15.19). Depending upon the degree of inturning the entropion can be divided into three grades. In grade I entopion, only the posterior lid border is inrolled. Grade II entropion includes inturning up to the intermarginal strip, while in grade III, the whole lid margin including the anterior lid border is inturned.
Examination may also reveal signs of the causative disease.
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Related Questions
Define trichiasis
Trichiasis refers to inward misdirection of cilia which rub against the eyeball.
What are the common causes of trichiasis? 1. Cicatrizing trachoma
2. Ulcerative blepharitis
3. Healed membranous conjunctivitis 4. Healed hordeolum externum
5. Mechanical injuries
6. Burns and operative scars on the lid margin.

When not treated in time, what complications can occur in a case of trichiasis?
1. Corneal abrasions
2. Superficial corneal opacities 3. Corneal vascularization
4. Non-healing corneal ulceration.
What is distichiasis?
Distichiasis is condition of an extra posterior row of cilia which occupy the position of meibomian glands.
How will you treat a case of trichiasis? 1. Epilation: It is a temporary measure.
2. Electrolysis: After local infiltration of anaesthesia, a current of 2 milliampere is passed for about 10 seconds through a fine needle inserted into the lash root. The loosened cilia with destroyed follicles are then removed with the help of an epilation forceps.
3. Cryoepilation: After infiltration anaesthesia, the cryoprobe (– 20°C) is applied for 20 to 25 seconds to the external lid margin. The loosened lash is pulled with an epilation forceps.
4. Surgical correction: It is similar to cicatricial entropion and should be employed when many cilia are misdirected.
Define entropion.
Entropion refers to turning in of the lid margin.

What are the types of entropion?
Depending upon the cause, entropion may be of the following types:
1. Congenital entropion 2. Cicatricial entropion 3. Spastic entropion
4. Mechanical entropion.

What are the causes of cicatricial entropion? 1. Trachoma
2. Membranous conjunctivitis 3. Chemical burns
4. Pemphigus
5. Stevens-Johnson syndrome.


Name  the  surgical  techniques  employed  for correcting cicatricial entropion.
1. Resection of skin and muscle
2. Resection of skin, muscle and tarsus 3. Modified Burow’s operation
4. Jaesche-Arlt’s operation
5. Modified Ketssey’s operation.
Name the surgical techniques used to correct a senile (involutional) entropion.
1. Modified Wheeler’s operation
2. Bick’s procedure with Reeh’s modification 3. Weiss operation
4. Tucking of inferior lid retractors (Jones, Reeh and Webing operation).
A CASE OF ECTROPION
CASE DESCRIPTION
Presenting symptoms include watering (epiphora) and cosmetic disfigurement. Patients may also have symptoms of associated chronic conjunctivitis which include irritation, discomfort and mild photophobia. Ocular examination. The lid margin is outrolled (Fig. 15.25). Depending upon the degree of outrolling, ectropion can be divided into three grades. In grade I ectropion, only the punctum is everted. In grade II ectropion lid margin is everted and palpebral conjunctiva is visible while in grade III the fornix is also visible.
Examination may also reveal signs of etiological condition such as scar in cicatricial ectropion (Fig. 15.26B) and seventh nerve palsy in paralytic ectropion.
RELATED QUESTIONS
What is ectropion?
Outrolling or outward turning of the lid margin is called ectropion.
What are the types of ectropion? 1. Senile ectropion
2. Paralytic ectropion 3. Cicatricial ectropion 4. Spastic ectropion.
What is the treatment of senile ectropion? Depending upon the severity of the ectropion, following three operations are commonly performed: 1. Medial conjunctivoplasty
2. Horizontal shortening
3. Byron-Smith’s modified Kuhnt-Szymanowski operation.
What is a symblepharon?
Symblepharon is a condition in which lids become adherent with the eyeball. It results from healing of
Chapter 24	Clinical Ophthalmic Cases	555


the kissing raw surfaces of the palpebral and bulbar conjunctiva.
What are the common causes of symblepharon? 1. Chemical burns
2. Thermal burns
3. Membranous conjunctivitis 4. Conjunctival injuries
5. Ocular pemphigus
6. Stevens-Johnson syndrome.

What do you mean by ankyloblepharon? Ankyloblepharon refers to the adhesions between margins of the upper and lower lids. It may be congenital or may result after healing of chemical or thermal burns.
What is blepharophimosis?
In blepharophimosis vertical as well as horizontal extent of the palpebral fissure is decreased.
What is lagophthalmos? Enumerate its common causes.
Lagophthalmos refers to the inability to voluntarily close the eyelids. Its common causes are:
1. Paralysis of seventh nerve 2. Marked proptosis
3. Cicatricial contraction of the lids
4. Following over-resection of the levator palpebrae superioris
5. Symblepharon
6. Comatosed patient.
What is belpharospasm?
Belpharospasm refers to the involuntary, sustained and forceful closure of the eyelids. It is of two types: essential belpharospasm and reflex blepharospasm.
A CASE OF PTOSIS

Case Description
Age and sex. Ptosis may be congenital or acquired. Acquired ptosis may occur at any age in either sex. History. It should include age of onset, family history, history of trauma, eye surgery, and variability in degree of ptosis.
Examination should include: 1. Inspection to note:
• True ptosis or pseudoptosis • Unilateral or bilateral ptosis
• Eyelid crease and function of orbicularis • Presence of Jaw winking phenomenon
• Associated weakness of extraocular muscles • Bell’s phenomenon
2. Measurement of degree of ptosis 3. Assessment of levator function

4. Special investigations for acquired ptosis (For details see page 380).
RELATED QUESTIONS
What is ptosis?
Abnormal drooping of the upper eyelids is called ptosis. Normally, upper lid covers about upper one sixth (2 mm) of the cornea. Therefore, in ptosis it covers more than 2 mm.
What are the types of ptosis?
I.  Congenital ptosis which may be:
1.Simple congenital ptosis (not associated with any other anomaly) (Fig. 15.33A).
2.Congenital ptosis with associated weakness of the superior rectus muscle.
3.As a part of blepharophimosis syndrome (Fig. 15.33B).
4.Congenital synkinetic ptosis (Marcus Gunn jaw winking ptosis).
II. Acquired ptosis includes: 1.Neurogenic ptosis 2.Myogenic ptosis 3.Aponeurotic ptosis 4.Mechanical ptosis.
How do you grade ptosis?
Depending upon the amount of ptosis in mm, it is graded as follows:
1. Mild ptosis (2 mm)
2. Moderate ptosis (3 mm) 3. Severe ptosis (4 mm).
How do you grade levator function?
Depending upon the amount of lid excursion caused by levator muscle (Burke’s method), its function is graded as follows:
Normal	:	15 mm
Good	:	8 mm or more Fair	:	5–7 mm
Poor	:	4 mm or less

Which test is carried out to confirm the diagnosis in a patient with ptosis suspected of myasthenia gravis? • Tensilon or edrophonium test.
Which test is carried out in a patient suspected of Horner’s syndrome?
• Phenylephrine test.
Name the three basic surgical procedures for ptosis correction.
1. Fasanella – Servat operation 2. Levator resection operation 3. Frontalis sling operation
556	Section Vi   Practical Ophthalmology


Name the common lid tumours. I.  Benign tumours
1.Simple papilloma 2.Naevus 3.Haemangioma 4.Neurofibroma
II. Precancerous conditions 1.Solar keratosis 2.Carcinoma in-situ 3.Xeroderma pigmentosa
III. Malignant tumours 1.Squamous-cell carcinoma 2.Basal-cell carcinoma 3.Malignant melanoma 4.Sebaceous gland carcinoma.
Which is the most common malignant tumour of the lids?
• Basal-cell carcinoma.
Which is the most common site for occurrence of basal-cell carcinoma?
• Medial canthus.
What is the structure of an eyelid?
Each eyelid from anterior to posterior consists of the following layers:
1. Skin
2. Subcutaneous areolar tissue
3. Layer of striated muscle (orbicularis oculi and levator palpebrae superioris in upper lid only)
4. Submuscular areolar tissue
5. Fibrous layer (tarsal) plate and septum orbitale 6. Layer of non-striated muscle fibres (Muller’s
muscle)
7. Conjunctiva.
Name the glands of the eyelids. 1. Meibomian glands
2. Glands of Zeis 3. Glands of Moll
4. Accessory lacrimal glands of Wolfring.
What are the causes of pseudoproptosis? • Anophthalmos
• Enophthalmos • Phthisis bulbi • Atrophic bulbi
• Trachoma (stage of sequelae)
• Any tumour or nodule of upper lid.

DISEASES OF LACRIMALAPPARATUS

A CASE OF CHRONIC DACRYOCYSTITIS Case Description
Age and sex. The disease may occur at any age and in any sex. However, in general, females are much


more commonly affected than males and the disease is more common between 40 and 60 years of age. Presenting symptoms. A patient presents with a long standing history of watering from the eyes which may or may not be associated with a swelling at the inner canthus.
Ocular examination may reveal any of the following signs:
• No swelling is seen at the medial canthus but regurgitation test is positive, i.e., a reflux of mucopurulent discharge from the puncta when pressure is applied over the lacrimal sac area.
• A swelling may be seen at the medial canthus (Fig. 16.8). Milky or gelatinous mucoid fluid regurgitates from the lower punctum on pressing the swelling (lacrimal mucocele).
• Sometimes on pressing the swelling, a frank purulent discharge flows from the lower punctum (lacrimal pyocele).
• Sometimes, a swelling is seen at the inner canthus with a negative regurgitation test (encysted mucocele).

Related Questions
What are the causes of a watering eye?
Watering from the eyes may occur either due to excessive lacrimation or may result from obstruction to the outflow of normally secreted tears (epiphora). The common causes of watering eye are listed at page 390.
Name the tests which you would like to carry out to evaluate a case of watering eye.
1. Examination with diffuse illumination under magnification to rule out causes of hyperl-acrimation and punctal causes of epiphora
2. Regurgitation test for chronic dacryocystitis 3. Fluorescein dye disappearance test (FDDT) 4. Lacrimal syringing test
5. Jone’s dye test I and II 6. Dacryocystography
7. Lacrimal scintillography.
What is regurgitation test?
In regurgitation test a steady pressure with index finger is applied over the lacrimal sac area above the medial palpebral ligament. Reflux of mucopurulent discharge (a positive regurgitation test) indicates chronic dacryocystitis with obstruction at the lower end of sac or nasolacrimal duct.
What are the causes of a negative regurgitation test? Causes of a negative regurgitation test are:
• Normal sac (no dacryocystitis) • Wrong site of pressure
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• Patient might have emptied the sac just before coming to the examiner’s chamber
• Encysted mucocele • Internal fistula.
Name the indications of lacrimal syringing. 1. Diagnostic indications:
• Epiphora
• For dacryocystography 2. Therapeutic indications:
• Congenital dacryocystitis
• Early cases of chronic catarrhal dacryocystitis 3. Prognostic:
After DCR operation.

Describe the procedure and interpretations of the results of lacrimal syringing.
1. Topical anaesthesia is obtained by instilling 4% Xylocaine in the conjunctival sac.
2. Lower punctum is dilated with a punctum dilator. 3. Normal saline is pushed into the lacrimal sac through the lower punctum with the help of a syringe and lacrimal cannula (Fig. 16.5) and
results are interpreted as follows:
• A free passage of saline through lacrimal passages into the nose indicates either no obstruction or partial obstruction.
• In the presence of obstruction no fluid passes into the nose. When obstruction is in the nasolacrimal duct, the sac fills with the normal saline which refluxes from the upper punctum.
• In case of lower canalicular obstruction, there will be immediate reflux of the saline through the lower punctum. Under these circumstances, the procedure should be repeated through the upper punctum. A free passage of saline into the nose will confirm the blockage in the lower canaliculus while regurgitation back through the same punctum will indicate block at the level of common canaliculus.
What is dacryocystitis, how will you classify it? Dacryocystitis is inflammation of the lacrimal sac. It can be classified as follows:
1. Congenital dacryocystitis
2. Adult dacryocystitis which may occur as: • Chronic dacryocystitis, and
• Acute dacryocystitis.

What is the etiology of congenital dacryocystitis? How will you treat it?
Congenital dacryocystitis follows stasis of secretions in the lacrimal sac due to congenital blockage in the nasolacrimal duct (usually a membranous occlusion at the lower end of NLD).

Its treatment, depends upon the age at which child is brought (see page 393).
What is the treatment of choice in adulthood chronic dacryocystitis?
Dacryocystorhinostomy (DCR) operation is the operation of choice since it re-establishes the lacrimal drainage. When DCR is contraindictated, dacryocystectomy may be performed.
What is dacryocystectomy? Enumerate its indications. Dacryocystectomy is the excision of the lacrimal sac. It should be performed only when DCR is contraindicated as in following conditions:
1. Too young (less than 4 years) or too old (more than 60 years) a patient.
2. Markedly shrunken and fibrosed sac.
3. Tuberculosis, syphilis, leprosy or mycotic infection of the sac.
4. Tumours of the sac.
5. Gross nasal diseases like atrophic rhinitis.
6. Anunskilledsurgeon,becauseitissaidthatagood ‘DCT’ is always better than a badly done ‘DCR’.
What are tears?
Tears form the aqueous layer of tear film and are secreted by the accessory and main lacrimal glands. Tears mainly comprise water and small quantities of salts such as sodium chloride, sugar, urea and proteins. Therefore, it is alkaline and saltish in taste. It also contains antibacterial substances like lysozyme, betalysin and lactoferrin.
What are the layers of tear film?
Wolf described the following three layers of tear film: 1. Mucous layer: It is the innermost and thinnest
layer of tear film. It consists of mucin secreted by the conjunctival goblet cells. It converts the hydrophobic corneal surface into a hydrophilic one.
2. Aqueous layer: It consists of tears secreted by the main and accessory lacrimal glands and forms the main bulk of the tear film.
3. Lipid or oily layer: It consists of secretions of the meibomian, Zeis and Moll’s glands. It prevents the overflow of tears and retards their evaporation.
What are the functions of tear film?
1. It keeps the cornea and conjunctiva moist. 2. Provides oxygen to the corneal epithelium. 3. It washes away debris and noxious irritants.
4. It prevents infection due to presence of anti-bacterial substances.
5. It facilitates movement of the lids over the globe.
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What is dry eye?
Dry eye per se is not a disease entity but a symptom complex occurring as a sequela to deficiency or abnormalities of the tear film.
What are the causes of dry eye?
1. Aqueous deficiency dry eye (keratoconjunctivitis sicca—KCS)
• Congenital alacrimia • Sjogren’s syndrome • Riley-Day syndrome
• Idiopathic hyposecretion 2. Mucin deficiency dry eye
• Hypovitaminosis A (xerophthalmia) • Stevens-Johnson syndrome
• Trachoma
• Chemical burns 3. Lipid abnormalities
• Chronic blepharitis • Chronic meibomitis
4. Impaired eyelid function • Bell’s palsy
• Exposure keratitis • Ectropion
5. Epitheliopathies of corneal surface.

Name the important tear film tests performed to diagnose the dry eye.
• Tear film break-up-time (BUT) • Schirmer I test
• Rose bengal staining.
What is tear film break-up time?
Tear film break-up time is the interval between a complete blink and appearance of the first randomly distributed dry spot on the corneal surface. Its normal values range between 15 and 35 seconds. Values less than 10 seconds employ an unstable tear film.
What is Schirmer I Test?
Schirmer test measures the total tear secretions with the help of 5 × 35 mm strip of Whatman No. 42 filter paper. Its normal values are more than 15 mm of wetting of the filter paper strip in 5 minutes. Values between 5 and 10 mm are suggestive of mild to moderate keratoconjunctivitis sicca (KCS) and less than 5 mm of severe KCS.
What is Sjogren’s syndrome?
Sjogren’s syndrome is an autoimmune disease usually occurring in women between 40 and 50 years of age. Its main feature is an aqueous deficiency dry eye (KCS). It occurs in two forms:
1. Primary Sjogren’s syndrome: In it, KCS is combined with xerostomia (dry mouth).


2. Secondary Sjogren’s syndrome: In it dry eye and/ or dry mouth is associated with an autoimmune disease, commonly rheumatoid arthritis.
What is the treatment of dry eye?
1. Supplementation by artificial tear solution such as: 0.7% methylcellulose, 0.3% hypromellose or 1.4% polyvinyl alcohol.
2. Preservation of existing tears by punctal occlusions with collagen implants or electrocauterization.
3. Mucolytics such as 5% acetylcysteine help by dispersing the mucous threads.

DISEASES OF ORBIT A CASE OF PROPTOSIS
Case Description
Presenting symptoms. A patient presents with a history of the bulging of the eyeball which may be gradually or rapidly progressive. It may or may not be associated with visual loss, diplopia, pain or other symptoms. Ocular examination reveals outward protusion of the eyeball which may be:
• Unilateral (Fig. 17.7) or bilateral (Fig. 17.11) • Axial or eccentric
• Pulsatile or non-pulsatile
• Reducible or non-reducible
• May or may not be associated with lagophthalmos.

Related Questions
What is proptosis and exophthalmos?
Proptosis refers to forward displacement of the eyeball beyond the orbital margin. Though the word exophthalmos (out eye) is synonymous with proptosis; somehow it has become customary to use the term exophthalmos for the displacement associated with thyroid eye disease.
What are the causes of unilateral proptosis? 1. Congenital conditions
• Dermoid cyst
• Congenital cystic eyeball • Teratoma
2. Traumatic lesions
• Orbital haemorrhage
• Retained intraorbital foreign body • Traumatic aneurysm
3. Inflammatory lesions
• Orbital cellulitis or abscess • Panophthalmitis
• Cavernous sinus thrombosis • Pseudotumour
4. Circulatory disturbances and vascular lesions
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• Orbital varix • Aneurysm
5. Cysts of the orbit
• Implantation cyst • Hydatid cyst
• Cysticercus cellulosae
6. Tumours of the orbit, which may be
• Primary tumours (arising from the various intraorbital structures)
• Secondary tumours (invading from the surrounding structures)
• Metastatic tumours from the distant primary tumours.
Enumerate the causes of bilateral proptosis. 1. Developmental anomalies of the skull
• Oxycephaly
2. Inflammatory conditions • Mikulicz’s syndrome
• Late stage of cavernous sinus thrombosis
3. Endocrine exophthalmos (most common cause) (Fig. 17.11)
4. Orbital tumours, e.g.:
• Lymphoma or lymphosarcoma. • Secondaries from:
– Neuroblastoma – Nephroblastoma – Ewing’s sarcoma
– Leukaemic infiltration 5. Systemic diseases, e.g:
• Histiocytosis-X
• Systemic amyloidosis • Xanthomatosis
• Wegener’s granulomatosis.

What are the causes of acute proptosis?
1. Orbital emphysema following fracture of medial orbital wall
2. Orbital haemorrhage
3. Rupture of ethmoidal mucocele.

What are the causes of intermittent proptosis? 1. Orbital varix (most common cause)
2. Periodic orbital oedema 3. Highly vascular tumour.
What are the causes of pulsatile proptosis?
1. Caroticocavernous fistula (most common cause) 2. Saccular aneurysm of ophthalmic artery
3. Congenital orbital encephalocele
4. Hiatus in the orbital roof due to trauma, operation or that associated with neurofibromatosis.
How will you investigate a case of proptosis? Evaluation of a case of proptosis includes the following:

I. Clinical evaluation a) History
b) Local examination
(1) Inspection; (2) palpation; (3) auscultation; (4) transillumination; (5) visual acuity; (6) papillary reactions; (7) fundoscopy; (8) ocular motility; (9) exophthalmometry
c) Systemic examination II. Laboratory investigations
• Thyroid function tests • Haematological tests
• Stool examination for cysts and ova • Urine analysis
III. Roentgen examination
1. Plain radiograph of orbit 2. CT Scanning
3. Ultrasonography
4. Magnetic resonance imaging (MRI) 5. Carotid angiography
IV. Histopathological studies
1. Fine-needle aspiration biopsy (FNAB) 2. Incisional biopsy
3. Excisional biopsy.

What is enophthalmos? Enumerate its causes. Enophthalmos is the inward displacement of the eyeball. Its common causes are:
1. Congenital microphthalmos
2. Congenital maxillary hypoplasia
3. Traumatic blow-out fractures of the orbital floor. 4. Post-inflammatory cicatrization of the extraocular
muscles as in pseudotumour syndromes.
5. Paralytic enophthalmos as seen in Horner’s syndrome.
6. Atrophy of the orbital contents, e.g., senile atrophy of orbital fat, atrophy following irradiation of malignant tumours.
What is Graves’ ophthalmopathy?
This is a term coined to denote typical ocular changes which include: lid retraction, lid lag and proptosis (Fig. 17.11). These changes are also known as endocrine exophthalmos, dysthyroid ophthalmopathy, thyroid ophthalmopathy and ocular Graves’ disease (OGD).
Name the extraocular muscle most frequently affected in Graves’ ophthalmopathy.
• Inferior rectus.
What is American Thyroid Association classification of Graves’ ophthalmopathy?
American Thyroid Association (ATA) has classified Graves’ ophthalmopathy irrespective of the hormonal status into the following classes; characterized by the acronym ‘NOSPECS’:
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Class 0	:   No signs and symptoms.
Class 1	:   Only signs, no symptoms. Signs are limited to lid retraction with or without lid lag and mild proptosis.
Class 2	:   Soft tissue involvement with signs of class I and symptoms including lacrim-ation, photophobia, lid or conjunctival swelling.
Class 3	:   Proptosis is well established.
Class 4    :   Extraocular muscle  involvement (limitation of movements and diplopia).
Class 5    :   Corneal involvement (exposure keratitis) Class 6    :   Sight loss due to optic nerve involvement
with disc pallor or papilloedema.

What are the two clinical types of Graves’ ophthal-mopathy?
1. Thyrotoxic exophthalmos (exophthalmic goitre): In this form, a mild exophthalmos is associated with lid signs and all signs of thyrotoxicosis which include: tachycardia, muscle tremors and raised basal metabolism.
2. Thyrotropic exophthalmos (exophthalmic ophthalmoplegia): In this marked exophthalmos and an infiltrative ophthalmoplegia is associated with euthyroidism or hypothyroidism.
What are the causes of pseudoproptosis? 1. Buphthalmos
2. Lid retraction
3. High-axial myopia 4. Staphyloma
5. Enophthalmos of the opposite eye.

What are the causes of reducible proptosis? • Early stages of ocular Graves’ disease
• Haemangioma • Orbital varix
• Caroticocavernous fistula.

Which is the most common primary tumour of the orbit presenting as proptosis?
• Cavernous haemangioma.
Name the most common primary orbital tumour of childhood.
• Rhabdomyosarcoma.

DISORDERS OF OCULAR MOTILITY A CASE OF SQUINT
Case Description
Presenting symptoms. Patient presents with deviation of one eye which may be on medial side (convergent squint) or lateral side (divergent squint).

History of present illness must include following important points:
• Age of onset
• Mode of onset, sudden or gradual
• Precipitating factors such as, systemic illness ocular cause, emotional breakdown, trauma
• History of diplopia
• Birth history is important in early childhood onset deviation
• History of use of glasses.
Family history is also important in a case of strabismus. Ocular examination should reveal:
• Whether the manifest squint is convergent (Fig. 14.14) or divergent (Fig. 14.16).
• Abnormal head posture associated or not.
• Whether the squint is unilateral or alternating.
• Ocular movements are normal (concomitant squint) or limited (paralytic or nonconcomitant squint).
• Angle of squint on corneal reflex test (Hirschberg’s test).
Note. Detailed orthoptic examination is not expected from an undergraduate student.

Related Questions
Name the various extraocular muscles. • Superior rectus
• Inferior rectus • Medial rectus • Lateral rectus
• Superior oblique • Inferior oblique.
What is the origin of rectus muscles?
The rectus muscles originate from a common tendinous ring (annulus of Zinn), which is attached at the apex of the orbit.
Where are the rectus muscles inserted?
The rectus muscles are inserted into the sclera by flat tendons at different distances from the limbus as under:
• Medial rectus	—	5.5 mm • Inferior rectus	—	6.5 mm • Lateral rectus	—	6.9 mm • Superior rectus	—	7.7 mm
What is the nerve supply of extraocular muscles? The extraocular muscles are supplied by third, fourth and sixth cranial nerves. The third cranial nerve (oculomotor) supplies the superior, medial and inferior recti and inferior oblique muscles. The fourth cranial nerve (trochlear) supplies the superior oblique muscle, and sixth cranial nerve supplies the lateral rectus muscle.
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What are the actions of extraocular muscles? Action of each extraocular muscle is as below:

Muscle	Primary	Secondary	Tertiary action	action	action
Medial	Adduction	-	-rectus
Lateral	Abduction	-	-rectus
Superior	Elevation	Intorsion	Adduction rectus
Inferior	Depression	Extorsion	Adduction rectus
Superior	Intorsion	Depression	Abduction oblique
Inferior	Extorsion	Elevation	Abduction oblique

Describe uniocular movements of the eyeball. Uniocular movements of the eyeball are called ductions. These are as follows:
1. Adduction. It is medial rotation along the vertical axis.
2. Abduction. It is lateral rotation along the vertical axis.
3. Infraduction.  It  is  downward  movement (depression) alone the horizontal axis.
4. Supraduction. It is upward movement (elevation) along the horizontal axis.
5. Incycloduction (Intorsion). It is rotatory movement along the anteroposterior axis in which superior pole of cornea (12 O’clock point) moves medially.
6. Excycloduction (Extorsion). It is rotatory movement along the anteroposterior axis in which superior pole of cornea (12 O’clock point) moves laterally.
What are version movements of the eyeball? Versions also known as conjugate movements, are synchronous (simultaneous) symmetric movements of both the eyes in the same direction. For example: • Dextroversion is the movement of both eyes to
the right.
• Levoversion is the movernent of both eyes to the left.

What are vergence movements of the eyeball? Vergences, also called as disjugate movements, are synchronous and symmetric movements of both eyes in opposite directions, e.g.:
• Convergence is simultaneous inward movement of both the eyes.
• Divergence is simultaneous outward movement of both the eyes.

Define synergists, antagonists and yoke muscles. 1. Synergists are the muscles which have a similar primary action in the same eye, e.g., superior rectus and inferior oblique of the same eye act as synergistic elevators.
2. Antagonists are the muscles which have opposite actions in the same eye, e.g., superior and inferior recti are the antagonists to each other in the same eye.
3. Yoke muscles (contralateral synergists) are a pair of muscles (one from each eye) which contract simultaneously during version movements. Different pairs of yoke muscles are as follows:
• Right medial rectus and left lateral rectus • Right lateral rectus and left medial rectus
• Right superior rectus and left inferior oblique • Right inferior rectus and left superior oblique • Right superior oblique and left inferior rectus • Right inferior oblique and left superior rectus.
What is Hering’s law of equal innervation? According to it, an equal and simultaneous innervation flows from the brain to a pair of muscles which contract simultaneously (yoke muscles) in different binocular movements, e.g., during dextroversion, right lateral rectus muscles and left medial rectus muscle, receiving an equal and simultaneous flow of innervation.
What is Sherrington’s law of reciprocal innervation? According to it, during ocular movements an increased flow of innervation to the contracting muscles is accompanied by a simultaneous decreased flow of innervation to the relaxing antagonists. For example, during dextroversion an increased innervational flow to the right lateral rectus and left medial rectus is accompanied by a decreased flow to the right medial rectus and left lateral rectus muscles.
What is the primary position of gaze?
It is the position assumed by the eyes when fixing a distant object (straight ahead) with the erect position of head.
What are the secondary positions of gaze?
These are the positions assumed by the eyes while looking straight up, and down to the right and to the left.
What are the cardinal positions of gaze?
These are the positions which allow examination of each of the 12 extraocular muscles in their main field of action. There are six cardinal positions of gaze, viz. dextroversion, levoversion, dextroelevation, levoelevation, dextrodepression and levodepression.
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What are the three grades of binocular single vision? Grade I. Simultaneous macular perception (SMP): It is the power to see two dissimilar objects which can be superimposed to form a joint picture. For example, when the picture of a lion is projected onto the right eye and that of a cage to the left eye, an individual with presence of SMP will see the lion in the cage. Grade II. Fusion: It consists of the power to superimpose two incomplete but similar images to form one complete image.
Grade III. Stereopsis: It consists of the ability to perceive the third dimension (depth perception).
What is squint; how do you classify it?
Normally, visual axes of the two eyes are parallel to each other in the primary position of gaze and this alignment is maintained in all positions.
A misalignment of the visual axes of the two eyes is called squint or strabismus. Broadly, it can be classified as:
1. Apparent squint or pseudostrabismus 2. Latent squint (heterophoria)
3. Manifest squint (heterotropia), which includes: i. Concomitant squint
ii.Incomitant squint.

What is heterophoria? and what are its types?
Also known as latent squint, it is a condition in which the tendency of the eyes to deviate is kept latent by fusion. Therefore, when the influence of fusion is removed the visual axis of one eye deviates. Common types of heterophoria are:
1. Esophoria: It is a tendency to converge when binocularity is broken by any means.
2. Exophoria: It is a tendency to diverge.
3. Hyperphoria: It is a tendency to deviate upwards, while hypophoria is a tendency to deviate downwards. However, in practice it is customary to use the term right or left hyperphoria, depending on the eye which remains up as compared to the other.
Name a few tests by which heterophoria can be diagnosed.
1. Cover-uncover test 2. Maddox rod test
3. Maddox wing test.
What is suppression?
Suppression is a temporary active cortical inhibition of the image of an object formed on the retina of the squinting eye. This phenomenon occurs only during binocular vision (with both eyes open). It can be tested by Worth’s four-dot test.

What is abnormal retinal correspondence? Normally, fovea of the two eyes act as corresponding points and have the same visual direction (normal retinal correspondence). Sometimes in a patient with squint, fovea of the normal eye and an extra foveal point on the retina of the squinting eye acquire a common visual direction, i.e., become the corresponding points. This adjustment is called abnormal retinal correspondence (ARC).
Name a few methods by which angle of squint can be measured.
1. Hirschberg’s corneal reflex test. 2. Prism bar cover test (PBCT).
3. By synoptophore (major amblyoscope). 4. Krimsky’s corneal reflex test.
5. Perimeter method.
Describe Hirschberg’s corneal reflex test. Hirschberg’s corneal reflex test is a rough but hand method to estimate the angle of manifest squint. In this, the patient is asked to fixate at a light point held at a distance of 33 cm and the deviation of the corneal light reflex from the centre of pupil is noted in the squinting eye. Roughly, the angle of squint is 15° and 45° when the corneal light reflex falls on the border of pupil and limbus, respectively.
What is a concomitant squint?
Concomitant squint is a type of manifest squint in which the angle of deviation remains constant in all the directions of gaze; and there is no associated limitation of ocular movements.
How do you classify concomitant esotropia? 1. Infantile esotropia.
2. Accommodative esotropia.
3. Non-accommodative esotropia.

What is accommodative esotropia? Accommodative esotropia occurs due to overaction of convergence associated with accommodation reflex. Refractive type of accommodative esotropia is associated with high hypermetropia (+4 to +7D).
How do you classify concomitant exotropia (divergent squint)?
1. Congenital exotropia 2. Primary exotropia
a. Intermittent b. Constant
– Unilateral – Alternating
3. Secondary (sensory deprivation) exotropia 4. Consecutive exotropia.
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What is paralytic squint?
Paralytic squint is a type of incomitant squint in which ocular deviation results from complete or incomplete paralysis of one or more extraocular muscles.