Lecture Notes

Question 1

What can be used to measure degree of proptosis?

Answer 1

exophthalmometer

A simple clinical test to detect unilateral proptosis is to stand behind the seated patient and tilt his head back slowly, observing as the eyes appear beyond the brow - if there is proptosis, the proptosed eye will appear before the normal eye.

Question 2

What is the definition of unilateral proptosis?

Answer 2

Difference of more than 2 mm between the two eyes.

Question 3

What is a carotid-cavernous sinus fistula?

Answer 3

An arteriovenous fistula may develop between the internal carotid artery or a dural artery in the cavernous sinus, and the cavernous sinus itself.

As a result, the orbital veins are exposed to high intravascular pressure, the ey eis proptosed and the conjunctival veins are dilated/engorged.

Question 4

Which types of tumours may produce signs of orbital disease?

Answer 4

lacrimal gland tumours
optic nerve gliomas
meningiomas
lymphomas
rhabdomyosarcomas
mets from other systemic cancers

Question 5

What is a dermoid cyst?

Answer 5

These congenital cystic lesions are caused by the continued growth of ectodermal tissue beneath the surface, which may present in the medial or lateral aspect of the superior orbit.

Question 6

What are the possible mechanical causes of ptosis?

Answer 6

A large lid lump pulling the lid down.

Lid oedema, increasing the volume and weight of the lid.

Downward tethering of the lid by conjunctival scarring.

Structural abnormalities, including a disinsertion of the aponeurosis of the levator muscle, usually in elderly patients.

Question 7

What are the possible neurological causes of ptosis?

Answer 7

Third nerve palsy.

Horner syndrome, due to a sympathetic nerve lesion.

Marcus Gunn jaw-winking syndrome. Here, congenital ptosis is due to a developmental miswiring of the nerve supply to the pterygoid muscle of the jaw (cranial nerve V) and the levator of the eyelid (cranial nerve III) so that the eyelid moves in conjunction with chewing movements.

Question 8

What are the possible myogenic causes of ptosis?

Answer 8

Myasthenia gravis

Some forms of muscular dystrophy.

Chronic progressive external ophthalmoplegia.

Question 9

What are four diagnostic tests that may assist in the diagnosis of ocular myasthenia?

Answer 9

Repeated upgaze and downgaze movements result in fatigue and increased ptosis.

Ask the patient to look down for 15 seconds and then look up at an elevated target. The lid overshoots and then falls slightly after the period of rest (Cogan twitch test).

Ice applied to the lid for 2 minutes, through a rubber glove, significantly reduces a myasthenic posis.

Weakness of eyelid closure (orbicularis weakness).

Question 10

What is involutional entropion?

Answer 10

orbicularis muscle overrides the tarsal plate due to weak lower lid retractors

Question 11

What is cicatricial entropion?

Answer 11

caused by conjunctival scarring, which draws the lid margin inwards

Question 12

What are some of the common causes of ectropion?

Answer 12

• age-related orbicularis muscle laxity
• scarring of the periorbital skin
• seventh nerve palsy

Question 13

What forms around lashes in blepharitis?

Answer 13

Collarette

Question 14

What is the most common cause of posterior blepharitis?

Answer 14

Meibomian gland dysfunction

Question 15

What happens in meibomian gland dysfunction?

Answer 15

The terminal ducts of the meibomian glands are obstructed by squamous debris and the lipid product of the glands, usually a clear oil, becomes viscous.

It appears cloudy and opaque when expressed from the glands by pressure applied through the lid, and this is a simple and excellent diagnostic test for the condition.

Posterior blepharitis is usually caused by meibomian gland dysfunction, often referred to as MGD.

Question 16

In anterior blepharitis, what might collarettes indicate?

Answer 16

may indicate infestation by Demodex folliculorum

Question 17

What is blepharitis associated with?

Answer 17

seborrhoeic dermatitis, atopic eczema, rosacea

Question 18

How is anterior blepharitis treated?

Answer 18

• Remove squamous debris: lid scrubs with bicarbonate solution
• Reduce inflammation: topical steroids
• Treat staph lid disease: topical antibiotics e.g. Fusidic acid
• Treat demodex infestation: tea tree oil

Question 19

What is a chalazion?

Answer 19

obstructed meibomian gland causes a granuloma within the tarsal plate

Painless!

Question 20

What is a cyst of Moll?

Answer 20

Small translucent cyst on the lid margin caused by obstruction of a sweat gland

Question 21

What is a cyst of Zeis?

Answer 21

Opaque cyst on the eyelid margin caused by blockage of an accessory sebaceous gland

Question 22

What is a squamous cell papilloma?

Answer 22

This is a common, frond-like lid lesion with a fibrovascular core and thickened squamous epithelium.

It is usually asymptomatic but can be excised for cosmetic reasons with cautery to the base.

Question 23

What is a keratoacanthoma?

Answer 23

This is a brownish pink, fast-growing lesion with a central crater filled with keratin.

Treatment is by excision. Careful histology must be performed as some may have the malignant features of a squamous cell carcinoma (see below).

Question 24

How is entropion different from trichiasis?

Answer 24

In entropion, the lid margin is affected.

In trichiasis, the eyelashes are directed back towards the globe but the lid margin remains normally apposed.

Question 25

What is dry eye disease (DED) caused by?

Answer 25

caused by either a deficiency of tear secretion or excessive evaporation

results in tear hyperosmolarity = ocular surface damage and inflammation and chronic symptoms of ocular discomfort with visual loss

NOTE: also known as keratoconjunctivitis sicca (KCS)

Question 26

What are the two major forms of dry eye disease?

Answer 26

1. Aqueous-deficient dry eye
2. Evaporative dry eye

Question 27

What is the pathophysiology of aqueous-deficient dry eye (ADDE)?

Answer 27

1. Inflammatory damage to lacrimal glands by invading lymphocytes
2. Less commonly, congenital lacrimal deficiency, from lymphomatous or sarcoid infiltration of lacrimal gland or secretion by conjunctival scarring in trachoa, Sjogren’s or mucous membrane pemphigoid

Question 28

Which cells are implicated in inflammatory damage in Sjogrens?

Answer 28

T-cells

Question 29

What are the commonest causes of secondary Sjogrens?

Answer 29

1. Rheumaroid arthritis
2. SLE
3. PBC
4. Scleroderma

Question 30

What other conditions is Meibomian gland dysfunction a feature of?

Answer 30

rosacea, seborrheic and atopic dermatitis

also: toxic response to the use of 13 cis-retinoic acid in treatment of acne

Disorders of lid congruity, aperture and dynamics can also cause EDE, so that it is a possible complication of proptosis, ectropion and Parkinson disease – where blink rate is reduced.

Question 31

What is Meibomian gland dysfunction?

Answer 31

A condition in which delivery of Meibomian oil to the tear film is obstructed by changes in the terminal ducts of the glands and by an increase in viscosity of the delivered lipid.

This leads to tear film instability and increased water loss

Question 32

What is the commonest cause of evaporative dry eye (EDE) disease?

Answer 32

Meibomian gland dysfunction

Question 33

How is Sjogren’s diagnosed?

Answer 33

1. Clinical findings (reduced lacrimal and salivary function)
2. Presence of raised titres of anti-Rho and anti-La antibodies
3. Demonstration of T-cell infiltration in minor salivary gland biopsy

Question 34

How does the tear film appear in dry eye disease?

Answer 34

shows dark spots of early tear film break‐up occur during blink suppression, diagnostically, <5 seconds after the last blink

In normal subjects, the stained tear film can remain intact for an extended period in the absence of blinking,

Question 35

Why is evaporative dry eye seen in Parkinson’s disease?

Answer 35

Blink rate is reduced

Question 36

What is a feature of both aqueous-deficient and evarpoative dry eye?

Answer 36

Tear film instability

Question 37

What is seen on fluorescein staining in dry eye disease?

Answer 37

characteristic pattern of fluorescent dots over the exposed corneal and conjunctival surface

Question 38

What is the grading scale used for dry eye disease?

Answer 38

Oxford grading scale

Question 39

Where does vision loss start in glaucoma?

Answer 39

Peripheral

Question 40

How many gangion cells are lost before any noticable visual field loss is realised in glaucma?

Answer 40

40%

Question 41

What proportion of blindness worldwide is due to glaucoma?

Answer 41

Responsible for 8% of global blindness & is the no. 1 cause of irreversible blindness in Western society.

Glaucoma is the 2nd most common cause of registration of visual impairment in the over 65s (1 st AMD & macular degeneration, 3rd DR).

Question 42

What proportion of visits to ophthamic units are due to glacuoma?

Answer 42

1 in 4

Question 43

What is the retinal nerve fibre layer (RNFL) made up of?

Answer 43

Made up of retinal ganglion cell axons and follow a specific pattern:
Fibres ‘close’ to fovea & disc (papillomacular bundle) = linear route
Fibres everywhere else (nasal, superior temporal, inferior temporal) = bypass the papillomacular bundle = arcuate path

Question 44

What is the optic cup?

Answer 44

Anatomical depression in optic nerve head that is not occupied by axons (importance = cup/disc ratio).

Question 45

What is the neuroretinal rim?

Answer 45

The tissue between the border of the cup and the disc

Made up of retinal ganglion cells

Question 46

What is aqueous humour?

Answer 46

Colourless, clear fluid for nutrition, structural support & removal of waste products (RE: avascular cornea).

Produced by ciliary body (2-3 L/min) through an active process (Na/K ATPase moving ions between pigmented & non-pigmented cells).

Question 47

What are the main locations of resistance to outflow of aaqueous humour?

Answer 47

Endothelium, which uses transcytosis to transport material across cells.

Juxtacanalicular, which uses collagen beams & GAG proteins to slow water.

Question 48

What is the definition of glaucoma?

Answer 48

Glaucoma is a collection of diseases that cause optic neuropathy (damage to the optic nerve head specifically) and produce visual field loss.

The condition is often associated with a raised intraocular pressure (IOP > 21), which ranges between 10 - 21 mmHg. However, not always the case (25% of patients will have normal tension glaucoma).

Question 49

What is the term ‘glaucoma suspect’ used for?

Answer 49

Used when there is at least 1 x clinical feature of the disease, including an elevated lOP, a suspicious optic nerve (“cupping”), abnormal visual field, or a strong family history.

Question 50

What are some of the common risk factors for glaucoma?

Answer 50

Question 51

What is filamentary keratitis?

Answer 51

Tags of abnormal mucus that attach to the corneal surface, causing pain due to tugging during blinking.

Question 52

What is diagnostic of aqueous-deficient dry eye on Schirmer test?

Answer 52

< 10mm wetting in 5 minutes

Occasionally, reflex overproduction of tears due to ocular irritation may confuse the diagnosis.

Question 53

How is ADDE treated?

Answer 53

1. Low-viscosity cellulose polymers (prolong the residence time of moisturizing drop and allow inflammatory mediators to be flushed from the ocular surface)
2. Mild steroids (suppress inflammation, but must monitor for raised IOP)
   3.** Hyaluronic acid** (where inflammation in limited)

Other agents are available which are directed towards lubrication, water retention, protection from hyperosmolar damage (osmoprotection), stabilization of the tear film lipid layer and promotion of epithelial cell viability.

Question 54

How should tear substitutes been used in ADDE?

Answer 54

• Use regularly throughout the day (not PRN)
• Avoid substitutes that contain preservatives (can exacernate the condition)

Question 55

What is unique about preparations containig hyaluronic acid for ADDE?

Answer 55

Their non‐Newtonian property (less viscous when moving, more viscous when stationary) allows them to be formulated at relatively high viscosity, which extends their retention time, while they ‘shear thin’ during the blink or saccade, avoiding intolerance due to frictional drag.

Question 56

Which agents are used longer term for anti-inflammatory purposes in ADDE?

Answer 56

topical cyclosporin A, tacrolimus and lifitegrast, which inhibit the migration of activated lymphocytes to the ocular surface

Question 57

What might be done in ADDE when tear flow becomes greatly reduced?

Answer 57

It may be necessary to occlude the puncta with plugs, or more permanently with surgery, to conserve the tears

Question 58

Where MGD contributes to dry eye disease, how is management different?

Answer 58

the main goal should be to reduce lid margin inflammation and restore the Meibomian contribution to the tear film lipid layer.

Treatment is designed to achieve a more efficient control of the tear film stability, applying heat and massage to the lids, antibiotic drops or ointment and systemic antibiotics where necessary

Question 59

How is ectropion managed?

Answer 59

Correction of lid deformity is required

Question 60

If lid closure is inadequate, how is this treated?

Answer 60

A temporary ptosis can be induced with a local injection of botulinum toxin into the levator muscle to effect a short‐term paralysis and lowering of the upper lid.

A more permanent result can be obtained by suturing together part of the apposed margins of the upper and lower lids to reduce the palpebral aperture (e.g. lateral tarsorrhaphy), or the use of gold/platinum weights inserted into the lids to assist closure.

Question 61

Which cells are lost in most forms of dry eye, but particularly in cicatricial conjunctival disorders?

Answer 61

Goblet cells

Question 62

What is symblepharon?

Answer 62

A symblepharon is a partial or complete adhesion of the palpebral conjunctiva of the eyelid to the bulbar conjunctiva of the eyeball.

Question 63

How does vitamin A deficiency cause blindness?

Answer 63

Vitamin A deficiency (xerophthalmia) is a condition causing childhood blindness on a worldwide scale. It is associated with generalized malnutrition in countries such as India and Pakistan.

**Goblet cells are lost from the conjunctiva and the ocular surface becomes keratinized (xerosis). **An aqueous deficiency may also occur.

A characteristic corneal melting and perforation which occurs in this condition (keratomalacia) may be prevented by early treatment with vitamin A.

Question 64

What is epiphora?

Answer 64

excessive tearing caused by excessive tear production or secondary to poor drainage

Question 66

Where is the tear drainage system most likely to become blocked in adults?

Answer 66

The tear drainage system may become blocked at any point, such as the puncta or canaliculi, but the most common site is the nasolacrimal duct.

Causes include infections or direct trauma to the nasolacrimal system and, occasionally, topically applied drugs.

Question 68

What is a dacryocystogram used for?

Answer 68

special radiographic test to see if there is blockage of the tear canals

A more physiological test follows the passage of a drop of technetium isotope instilled into the lateral conjunctival sac, through the drainage system, using a gamma camera (dacryoscintigram)

Question 69

What is dacryocystorhinostomy (DCR)?

Answer 69

describes the creation of a functional pathway from the canaliculi into the nose by means of creating an osteotomy and opening the nasolacrimal sac into the nose.

Question 70

What procedure is being done in this image?

Answer 70

DCR (dacryocystorhinostomy)

Question 71

What should be considered if there is a ciliary flush present?

Ciliary flush = redness localised to the episclera (near the limbus)

Answer 71

Keratitis
Uveitis
Acute glaucoma

Question 72

What are papillae (in the conjunctiva)?

Answer 72

Question 73

What do follicles in the conjunctival represent?

Answer 73

Lymphoid collection with its own germinal centre

Implies viral or chlamydial infections, or sometimes toxic reaction to topical medication.

Question 74

What are keratic precipitates?

Answer 74

Deposits of inflammatory cells on the corneal endothelium. Neutrophils are responsible for fine KPs and lymphocytes or macrophages for coarse, or ‘mutton fat’ KPs.

Question 75

What is pannus?

Answer 75

Chronic keratitis may stimulate the peripheral ingrowth of subepithelial blood vessels = pannus

Question 76

Which organism causes the most severe form of ophthalmia neonatorum?

Answer 76

Neisseria gonorrhoae

Systemic complications include rhinitis, stomatitis, arthritis, meningitis and septicaemia. Patients should be managed with the help of a paediatrician. Due to increasing resistance to penicillin, a systemic, third‐generation cephalosporin (ceftriaxone (or cefotaxime) given im or iv) is used to treat the condition. The eye must be kept clean with 0.9% saline irrigation. Topical bacitracin ointment can also be given but systemic treatment is the most important. Parents should be referred to a sexually transmitted diseases (STD) clinic.

Question 77

Which organism causes adult inclusion keratoconjunctivitis?

Answer 77

chlamydial serotypes D-K

Question 78

How does adult inclusion keratoconjunctivitis present?

Answer 78

Patients present with a mucopurulent follicular conjunctivitis and develop a micropannus (superficial peripheral corneal vascularization) associated with subepithelial scarring. Urethritis or cervicitis is common.

Question 79

How is adult inclusion keratoconjunctivitis treated?

Answer 79

Inclusion conjunctivitis is treated with systemic tetracycline because of the likelihood of genital tract infection. Other systemic agents in use include doxycycline and erythromycin, and azithromycin may be given as a single dose. The patient should be referred to an STD clinic.

Question 80

What is the cause of trachoma?

Answer 80

chlamydial serotypes A-C

Question 81

What is the hallmark of trachoma?

Answer 81

Subconjunctival fibrosis caused by frequent re-infections associated with the unhygienic conditions

Blindness may occur due to corneal scarring from recurrent keratitis and trichiasis

Question 82

How is trachoma treated?

Answer 82

Trachoma is treated with oral or topical tetracycline or erythromycin. Azithromycin, an alternative, requires only a single oral dose. Entropion and trichiasis require surgical correction.

Question 83

What is vernal keratoconjunctivitis (VKC or spring catarrh)?

Answer 83

recurrent, bilateral allergic inflammation of the conjunctiva

Question 84

How is vernal keratoconjunctivitis treated?

Answer 84

Initial therapy is with mast cell stabilizers (e.g. sodium cromoglycate, nedocromil, lodoxamide) and antihistamines (e.g. levocabastine), or with agents combining mast cell stabilizing and antihistamine properties (e.g. olopatidine).

Topical steroids are required in severe cases but long-term use is avoided if possible because of the risks of steroid-induced glaucoma or cataract.

In such cases, topical cyclosporine or tacrolimus may be used.

Mucolytics (acetylcysteine) may be required to help dissolve the corneal plaque but surgical removal may be necessary.

Question 85

What is giant papillary conjunctivitis?

Answer 85

inflammatory condition of the upper tarsal conjunctiva, presenting with hyperaemia and roughness of the conjunctival surface in response to contact lens use

Question 86

What are pingueculae?

Answer 86

small, yellowish, paralimbal lesions in the horizontal meridian that are unassociated with irritation and never impinge on the cornea.

Question 87

What are pterygia?

Answer 87

Pterygia are wing-shaped elevations of the interpalpebral conjunctiva, usually bilateral, and located nasally. The apex of the pterygium is directed towards the cornea, onto which it progressively extends with time.

Question 88

Why must you avoid topical steroids in patients with HSV dendritic ulcers?

Answer 88

Topical steroids must not be given to patients with a dendritic ulcer, since they may exacerbate the disease and cause extensive corneal ulceration.

Question 89

What is sisciform keratitis?

Answer 89

a deeper, disc-shaped, localized area of secondary corneal stromal edema and haze accompanied by anterior uveitis

immunogenic reaction to herpes (HSV) antigen in the strome

Question 90

How is herpes zoster ophthalmicus treated?

Answer 90

Oral antiviral treatment given for seven days (e.g. aciclovir, famciclovir) is effective in reducing post‐infective neuralgia (a severe chronic pain in the area of the rash) if given within 3 days of the eruption of skin vesicles. Ocular disease may require antibacterials to prevent secondary infection. Steroid use is controversial.

Question 91

What tissue adhesive may be used in patients with corneal perforations?

Answer 91

Cyanoacrylate glue

Question 92

How is acanthamoeba keratitis treated?

Answer 92

Topical chlorhexidine, polyhexamethylene biguanide (PHMB) and propamidine are used to treat the condition.

Prolonged treatment over a period of several months is often needed.

Question 93

What type of medium is used to grow organisms in suspected fungal keratitis?

Answer 93

Liquid and solid Sabouraud media are used to grow the fungi, often requiring prolonged incubation.

Question 94

How do you distinguish between fungal and bacterial keratitis?

Answer 94

The whitish inflammatory stromal infiltrate of fungal keratitis may be difficult to distinguish from that of bacterial keratitis, but the presence of satellite lesions outside the main lesion may be an important clue to diagnosis.

Question 95

What is interstitial keratitis?

Answer 95

This term is used for any vascular keratitis that affects the corneal stroma without epithelial involvement. In the past, the most common cause was congenital syphilis, leaving a midstromal scar interlaced with the empty (‘ghost’) blood vessels. Corneal grafting may be required when the opacity is marked and visual acuity reduced.

Question 96

What are the 3 types of corneal dystrophies?

Answer 96

Anterior
Stromal
Posterior

Question 97

What are anterior corneal dystrophies?

Answer 97

Anterior dystrophies involving the epithelium. These may present with painful attacks as in inherited recurrent corneal erosion. In Meesmann dystrophy, tiny microcysts are scattered throughout the epithelium. Both are dominantly inherited.

Question 98

What are stromal (corneal) dystrophies?

Answer 98

Stromal dystrophies presenting with visual loss. If very anterior, they may also cause corneal erosion and pain. Examples are granular corneal dystrophy (dominant trait) and macular dystrophy (recessive trait).

Question 99

What are posterior (corneal) dystrophies?

Answer 99

Posterior dystrophies which affect the endothelium occur in congenital and adult forms. Loss of endothelial pumping results in corneal oedema which leads to a gradual loss of vision.

An example is Fuchs dystrophy, which may present in middle to late adult life. It may be a sporadic condition or be inherited as a dominant trait. An X-linked form of endothelial dystrophy exists. The clinical features of Fuchs dystrophy are identical to those seen in other forms of endothelial failure.

Question 100

What is keratoconus?

Answer 100

a painless disorder, usually sporadic but sometimes inherited, in which progressive central corneal thinning leads to an ectatic conical shape and marked myopia and astigmatism.

Question 101

What is the pathophysiology of keratoconus?

Answer 101

The condition is due to a failure of cohesion between the stromal collagen fibrils and lamellae of unknown cause, causing them to slip over one another and unravel. This leads to stromal thinning and ectasia. Thinning may be pronounced, but rarely leads to perforation.

Question 102

How is the optical impact of keratoconus treated?

Answer 102

Early stages = rigid contact lenses that arch over the irregularly shaped cornea

Late/Advanced stages = surgical intervention (penetrating keratoplasty - replacement of the central cornea with a full thickness corneal allograft)

More recently, using lamellar techniques, it has been possible to replace the corneal stroma alone, leaving the healthy endothelium intact.

Question 103

What is the function of the corneal endothelium?

Answer 103

to transfer water from the corneal stroma to the anterior chamber and thus maintain a miminum corneal thickness

This ensures the regular order and separation of the stromal collagen fibrils that is necessary for corneal transparency

Question 104

How is endothelial cell loss repaired?

Answer 104

By cell spreading (which entails an enlargement of cells and fall in cell density)

Question 105

What happens when the corneal cell density drops below a certain critical level?

Answer 105

Loss of barrier and pumping functions occurs -> stromal oedema and clouding as the regular packing of the collagen fibres is disrupted

This may be detected at an early stage as an increase in corneal thickness or inferred by the presence of punctate excrescences in Descemet layer of the cornea (corneal guttae).

Question 106

What are corneal guttae?

Answer 106

Collections of abnormal basil laminar material synthesized by the sick endothelial cells

Question 107

What are the causes of endothelial cell damage?

Answer 107

Causes of endothelial cell damage include uveitis, cataract surgery, corneal graft failure and, as noted earlier, inherited endothelial disease (Fuchs dystrophy).

Question 108

What is the commonest indication for corneal graft surgery?

Answer 108

Endothelial failure

Treatment = endothelial keratoplasty

Question 109

What is band-shaped keratopathy?

Answer 109

Subepithelial deposition of calcium phosphate in the exposed part of the cornea where CO2 loss and the consequent raised pH favour its deposition

Seen in patients with chronic uveitis or glaucoma

Question 110

How is band-shaped keratopathy treated?

Answer 110

If symptomatic, it can be scraped off surgically, aided by a chelating agent such as sodium edetate to remove the calcium at the time of surgery.

Question 111

What might band keratopathy be a sign of?

Answer 111

Systemic hypercalcaemia (as in hyperparathyroidism or renal failure)

The lesion is then more likely to occupy the 3 o’clock and 9 o’clock positions of the paralimbal cornea.

James, Bruce; Bron, Anthony; Parulekar, Manoj V.. Ophthalmology: Lecture Notes (p. 296). Wiley. Kindle Edition.

Question 112

What is a Mooren ulcer?

Answer 112

Rare cause of painful peripheral corneal thinning - it is a condition of progressive corneal melting with an immune basis, which starts near the limbus and spreads relentlessly across the cornea.

Question 113

What is anterior chamber-associated immune deviation (ACAID)?

Answer 113

ACAID provides a distinct immunological privilege to the eye. The regulation of inflammatory processes by ACAID leads to protection from potentially blinding inflammatory processes. ACAID suppresses CD4, Th1/2, and B cells

Question 114

What is unique about corneal transplants compared to other types of transplants?

Answer 114

Up to 90% of such first‐time keratoplasties in avascular corneas succeed without HLA cross‐matching and with only the use of topical corticosteroid drops to prevent rejection.

The reason for this difference is that the cornea is the site of an immune privilege which protects the graft from rejection.

Question 115

When is graft survival lower in corneal transplants?

Answer 115

Graft survival is much lower when the host cornea is heavily vascularized, probably in part because the cornea is also richly provided with lymphatics which undermine the graft’s immune privilege. Although tissue can be HLA‐matched for the grafting of vascularized corneas at high risk of rejection, the value of this is still uncertain.

Question 116

What are the types of endothelial-layer corneal transplants?

Answer 116

DSEK (Descemet stripping endothelial keratoplasty)

DMEK (Descemet Membrane Endothelial Keratoplasty).

The graft used in DSEK incorporates a thin layer of the donor stroma, DMEK allows an even thinner graft to be used with no stroma. DALK (Deep Anterior Lamellar Keratoplasty) involves replacing the corneal epithelium and stroma without disturbance of the endothelium, minimizing the risk of rejection.

Question 116

What are the clinical features of graft rejection?

Answer 116

Redness, pain or visual loss = must be seen urgently by an eye specialist, as this may indicate graft rejection.

Examination shows graft oedema, iritis and a line of activated T-cells attacking the graft endothelium.

Intensive topical steroid application in the early stages can restore graft clarity.

Question 117

Is episcleritis or scleritis more worrying?

Answer 117

SCLERITIS

It is an emergency (sight-threatening condition).

Question 118

What is scleromalacia perforans?

Answer 118

Anterior necrotizing scleritis without inflammation, so called scleromalacia perforans, is a rare, severe eye disorder developing an autoimmune damage of episcleral and scleral performing vessels (hypersensitivity type III)

Associated with rheumatoid arthritis.

Question 119

Scleritis affecting the posterior part of the globe may cause/stimulate what?

Answer 119

choroidal effusions, or may simulate a tumour

Question 120

What is the collective name for any light-scattering opacity in the lens?

Answer 120

Cataract

Question 121

What are some ocular causes of cataracts?

Answer 121

Question 122

What are some systemic causes of cataract?

Answer 122

Question 123

What are the different locations of cataracts?

Answer 123

Nuclear, cortical or subcapsular

Question 124

Which protein type is implicated in nuclear cataracts?

Answer 124

Crystallins - the major lens proteins, undergo cross‐linking and the formation of molecular aggregates of sufficient size to scatter light.

Results in brown products.

Colour perception and contrast sensitivity may be altered but, initially, visual acuity may not be greatly affected. The hardness conferred to the lens nucleus by protein cross‐linking may create problems when performing lens fragmentation during phacoemulsification surgery.

Question 125

What is the pathophysiology of a cortical cataract?

Answer 125

This form of cataract is due to a breakdown of groups of fibres in the lens cortex. Because these fibres are radially arranged in a pattern that relates to depth and clock position, the affected zones have a radial, spoke-like appearance and may be peripheral or extend more centrally. Peripheral spoke opacities have no effect on vision but those that encroach upon the visual axis will do so and may require action if symptomatic.

Question 126

What can cause posterior subcapsular cataracts?

Answer 126

Posterior subcapsular cataract may arise acutely following blunt injury to the eye or after vitreous surgery (vitrectomy), or it may evolve slowly after X-radiation to the orbit and with steroid treatment.

Question 127

What is the name of an eye with a lens impant?

Answer 127

Pseudophakic

Question 128

After cataract surgery, what is the patient given?

Answer 128

Short course of steroid and antibiotic drops

Can get new glasses (if needed) after a few weeks

Question 129

What are the 6 major complications of cataract surgery?

Answer 129

1. Vitreous loss
2. Iris prolapse
3. Endophthalmitis
4. Cystoid macular oedema
5. Retinal detachment
6. Opacification of the posterior capsule

Question 130

How can cataract surgery cause vitreous loss?

Answer 130

If the posterior capsule is accidentally torn during the operation, the vitreous gel may prolapse forward into the anterior chamber, where it represents a risk for glaucoma by obstructing aqueous outflow via the trabecular meshwork.

Prolapsed gel may also cause retinal traction and increase the risk of retinal detachment, and may interfere with placement of the lens implant.

The gel requires careful aspiration and excision (vitrectomy) at the time of surgery.

Placement of the intraocular lens usually follows during the same procedure, but may need to be deferred to a secondary procedure.

Question 131

How can cataract surgery cause iris prolapse?

Answer 131

The iris may protrude through the surgical incision in the immediate postoperative period, appearing as a dark elevation at the incision site accompanied by pupil distortion. This requires prompt surgical repair.

Question 132

How do patients with endophthalmitis (following cataract surgery) present?

Answer 132

Painful red eye
Reduced visual acuity
Collection of white cells int eh anterior chamber (hypopyon)

Question 133

What should be done if a patient presents with endophthalmitis?

Answer 133

This is an extreme ophthalmic emergency. The patient requires urgent sampling of the aqueous and vitreous for microbiological analysis and intravitreal injection of a broad-spectrum antibiotic at the time of sampling (e.g. vancomycin and ceftazidime) to provide immediate cover. Further management is dependent on the microbiological report and clinical response. The use of intravitreal corticosteroids in conjunction with the antimicrobials is debated.

Question 134

How can cataract surgery cause cystoid macular oedema?

Answer 134

The macula may become oedematous following routine uncomplicated surgery. The risk is greater if surgery was accompanied by vitreous loss or inflammation. It may settle with time but can produce a severe and permanent reduction in acuity. The release of prostaglandin from inflamed intraocular tissues plays an important role and prompt treatment with topical NSAIDs and steroid can alleviate the oedema in a proportion of patients. It may be necessary to inject steroids into or around the eye in resistant cases.

Question 135

How might cataract surgery cause opacification of the posterior capsule?

Answer 135

Normally, the thin capsular layer that lies behind the implant is crystal clear. However, in approximately 20% of patients, clarity of the posterior capsule decreases in the months following surgery, when residual epithelial cells migrate across its surface to form an opaque scar. Vision then becomes blurred and there may be problems with glare. This is often referred to as an ‘aftercataract’.

Question 136

How is opacification of the posterior capsule after cataract surgery treated?

Answer 136

The treatment is YAG laser capsulotomy, using a neodymium yttrium garnet (Nd‐YAG) laser to create a small central opening in the capsule as an outpatient procedure. There is a small risk of cystoid macular oedema or retinal detachment following YAG capsulotomy.

Research aimed at reducing capsule opacification has shown that the lens implant material, the shape of the lens edge and overlap of the intraocular lens by a small rim of anterior capsule are important factors in preventing this complication.

Question 137

How is the lens affected in Alport syndrome?

Characteristics: deafness and nephropathy

Answer 137

bilateral, conical anterior protrusion of the anterior lens surface (anterior lenticonus)

It is caused by mutations influencing the structure of type IV collagen, a key component of basal laminae within the glomerulus, the Organ of Corti and the lens capsule.

Question 138

Which inherited disorders are assoociated with disorders of lens position?

Answer 138

Homocystinuria - displaced downwards
Marfan syndrome - displaced upwards

Question 139

What is intermediate uvevitis?

Answer 139

Inflammation of the ciliary body is termed cyclitis, of the pars plana is pars planitis and of the vitreous is vitritis. As a group, these are termed intermediate uveitis.

Question 140

What is posterior uveitis?

Answer 140

Inflammation of the posterior uvea is termed posterior uveitis and may involve the choroid (choroiditis), the retina (retinitis) or both (chorioretinitis).

Question 141

Which type of uveitis is painful?

Answer 141

Anterior

Question 142

What is the mainstay of treatment in uveitis?

Answer 142

Steroids

Anterior = eye drops
Posterior = systemic

Question 143

Why should you dilate the pupil in anterior uveitis?

Answer 143

relieves the pain from ciliary spasm + prevents the formation of posterior synechiae

Question 144

What causes visual loss in posterior uveitis/retinitis?

Answer 144

occur either from direct destruction to the retina and choroid (e.g. in toxoplasmosis or CMV infection) or from fluid accumulation in the layers of the macula (macular oedema)

Question 145

Where is a sub-tenon injetion done?

Answer 145

The principle of a sub-Tenon injection. A cannula is placed in the potential space between the sclera and Tenon capsule. Injection of steroid separates the two layers and the steroid spreads to surround the eye.

Question 146

What are some causes of uveitis?

Infectious, non-infectious ocular disease + systemic disease-associated

Answer 146

Question 147

What does Reiter disease encompass?

Answer 147

Urethritis
Arthritis
Conjunctivitis

Question 148

What is Fuchs heterochromic uveitis?

Answer 148

This is a rare, unilateral, chronic uveitis usually presenting in young adults. The cause is uncertain, it may be immunemediated and there are no systemic associations.

A mild anterior uveitis is present, but without signs of conjunctival or ciliary injection, and there are no posterior synechiae. There are KPs distributed diffusely over the cornea and there is iris heterochromia, the iris colour of the affected eye being different from that of the fellow eye, due to a loss of epithelial pigment cells. The vitreous may be inflamed and condensations (the cause of the floaters) may be present. About 70% of patients develop cataract. Glaucoma occurs to a lesser extent.

Question 149

How is ocular toxoplasmosis diagnosed?

Answer 149

The clinical appearance is usually diagnostic, but a positive anti-toxoplasma antibody test is suggestive. However, a high percentage of the population have positive IgG titres due to prior infection.

Question 150

What is Vogt-Koyanagi-Harada (VKH) disease?

Answer 150

a multisystem disorder presenting with a bilateral panuveitis with exudative retinal detachments and followed by neurological and cutaneous manifestations such as alopecia (focal baldness) and loss of lash and skin pigments (poliosis and vitiligo).

It is a cell‐mediated autoimmune disease probably directed against tyrosinase‐related proteins, TRP1 and TRP2 contained in melanocytes.

Question 151

What are the possible ocular manifestations of AIDS?

Answer 151

Question 152

What is the treatment for CMV retinitis?

Answer 152

Chronic antiviral therapy with ganciclovir and/or foscarnet

Question 153

What is sympathetic ophthalmitis?

Answer 153

A penetrating or surgical injury to one eye involving the retina may rarely excite a peculiar form of uveitis which involves not only the injured eye but also the fellow eye.

Question 154

Which ocular disease is uveitis associated?

Answer 154

Posterior scleritis
Retinal detachment
Angle closure glaucoma

Question 155

What causes visual symptoms in glaucoma?

Answer 155

Axon loss results in visual field defects and a loss of visual acuity if the central visual field is involved.

Question 156

Where and how is aqueous humour secreted?

Answer 156

into the posterior chamber by the ciliary processes

combination of active transport and ultrafiltration

Question 157

Where the increased resistance occurs within the meshwork itself and the angle is not obstructed by peripheral iris, this is termed what?

Answer 157

Open-angle glaucoma

Question 158

Where the increased resistance is due to the peripheral iris blocking the trabecular meshwork, this is termed what?

Answer 158

angle-closure glaucoma

Question 159

What are the 3 causes of outflow obstruction?

Answer 159

1. thickening of the trabecular lamellae, which reduces pore size
2. reduction in the number of lining trabecular cells
3. increased extracellular material in the trabecular meshwork spaces.

Question 160

What is ocular HTN?

Answer 160

raised IOP without evidence of visual damage or pathological optic disc cupping

Question 161

In which lighting are acute attacks of acute angle-closure glaucoma more common?

Answer 161

Dim light (pupil more dilated)

Question 162

When does chronic angle-closure glaucoma?

Answer 162

Chronic angle-closure glaucoma may also occur, when extensive PAS causes a gradual elevation of intraocular pressure associated with glaucomatous optic nerve head damage, pathological cupping and visual field loss. It may be asymptomatic until significant changes have occurred.

Question 163

What type of glaucoma may be seen in carotid-cavernous sinus fistula?

Answer 163

Raised episcleral venous pressure as a cause

Question 164

Mutations in which gene can cause a juvenile form of open-angle glaucoma?

Answer 164

myocilin gene (GLC1A) on Chr 1

Question 165

What is a pachymeter used for?

Answer 165

Measuring the thickness of the cornea

Question 166

What is the first line medical treatment for chronic open-angle glaucoma?

Answer 166

Prostaglandin analogues

MoA = increase the passage of aqueous through the uveoscleral pathway

Question 167

What is a common preservative used in eye drops?

Answer 167

Benzalkonium Chloride (BAK)

Acts as a detergent lysing cell membranes and killing bacteria

Question 168

What is a trabeculectomy?

Answer 168

Fistula created between the anterior chamber and subconjunctival space

Question 169

What are 6 complications of a trabeculectomy?

Answer 169

1. shallowing of the anterior chamber in the immediate postoperative period risking damage to the lens and cornea
2. intraocular infection
3. possibly accelerated cataract development
4. failure to reduce intraocular pressure adequately
5. scarring causing a longer term rise in IOP
6. an excessively low pressure (hypotony) which may cause macular oedema.

Question 170

What agents can be used to prevent subconjunctival fibrosis following trabeculectomy?

Answer 170

antimetabolite drugs (5-fluorouracil and mitomycin)

Question 171

What is microinvasive glaucoma surgery (MIGS)?

Answer 171

Question 172

How is primary angle-closure glaucoma treated?

Answer 172

IV acetazolamide + topical acetazolamide

+ topical pilocarpine
+ beta-blockers

Question 173

How is an iridotomy performed?

Answer 173

With a Nd-YAG laser or surgically

Question 174

Which genes have been linked to primary congenital glaucoma?

Answer 174

CYP1BI and LTBP2 genes

Autosomal recessive

Question 175

What is buphthalmos?

Answer 175

Enlargement of the globe

Question 176

How is glaucomatous optic neuropathy distinguished from other causes of raised IOP?

Answer 176

enlarged optic CUP

Question 177

What is the pathogenesis of AMD?

Answer 177

The RPE removes and processes the used discs of the photoreceptor outer segments. Over time, undigested lipid products, such as the age pigment lipofuscin, accumulate in the RPE and the excess material is transferred to Bruch membrane, impairing its diffusional properties. Extracellular deposits form between the RPE and Bruch membrane which can be seen with the ophthalmoscope as discrete, sub-retinal yellow lesions called drüsen.

Question 178

Which condition are angioid streaks associated with?

Answer 178

These are seen classically in the rare recessive disorder pseudoxanthoma elasticum, and uncommonly, in systemic diseases such as Paget disease and sickle cell disease.

Again, there may be a profound reduction in central vision. Vision is also reduced if the crack itself passes through the fovea.

Question 179

What is central serous retinopathy?

Answer 179

a localized accumulation of fluid between the neuroretina and the RPE separates the two layers and disturbs the photoreceptor layer

It results from a localized breakdown in the normal barrier function of the RPE.

Question 180

How is macular oedema treated?

Answer 180

Steroids in high doses (oral or periocular injection) are helpful in macular oedema caused by uveitis; acetazolamide may be helpful in treating patients with macular oedema accompanying retinitis pigmentosa or occurring following intraocular surgery. Non-steroidal anti-inflammatory drops may also have a role in preventing and treating cystoid macular oedema associated with intraocular surgery.

Question 181

What is chloroquine associated with?

Answer 181

Toxic maculpathy

The maculopathy is initially only detected by accurate assessment of macular function. At this early stage, discontinuation of the drug reverses the maculopathy. Later, a pigmentary, ‘target lesion’ is seen ophthalmoscopically, associated with metamorphopsia and an appreciable and irreversible loss of central vision.

Question 182

What dose of chloroquine and hydroxychloroquine is associated with ocular toxicity?

Answer 182

Ocular toxicity is unlikely with a dose of less than 4 mg (chloroquine phosphate) per kg lean body weight per day or a total cumulative dose of less than 300 g.

The screening of patients on hydroxychloroquine at the recommended dose is also advised annually after 5 years of treatment or sooner if higher doses (>5 mg/kg/day) of the drug are used.

Question 183

How does the vitreous gel change with age?

Answer 183

With ageing, the vitreous gel undergoes degenerative changes (earlier in myopes) with liquefaction and the formation of fragments of condensed vitreous. These cast shadows on the retina, giving rise to the common symptom of vitreous ‘floaters’.

Subjectively, these take the form of spots or cobwebs which obscure vision only slightly and move when the eyes move, reflecting the fluid nature of the vitreous. Symptoms are most marked on bright days, when the small pupil throws a sharper image on the retina.

Question 184

Which two layers are separated in a retinal detachment?

Answer 184

Neuroretina + pigment epithelium (there is a potential space between them)

Question 185

What are the three types of retinal detachments?

Answer 185

1. rhegmatogenous (due to tear or hole)
2. tractional (due to contracting fibrous tissue)
3. exudative (fluid accumulates due to exudative precess e.g. in pregnancy-induced HTN or retinal tumours)

Question 186

What are tears in the retina associated with?

Answer 186

The onset of a posterior vitreous detachment

An underlying peripheral weakness of the retina e.g. lattice degeneration increases tear probability

Question 187

What is an operculated tear?

Answer 187

An operculated tear results from vitreous traction that pulls a plug of sensory retina out into the vitreous cavity.

Question 188

How are retinal tears unassociated with sub-retinal fluid treated?

Answer 188

Retinal tears unassociated with sub-retinal fluid are treated prophylactically with a laser or cryoprobe to induce inflammation and increase the adhesion between the neuroretina surrounding the tear and the pigment epithelium, thus preventing a retinal detachment. It is always important to check the peripheral retina in the fellow eye, as tears or an asymptomatic retinal detachment may be present here too.

Question 189

Which systemic diseases are associated with retinitis pigmentosa?

Answer 189

Usher syndrome, abetalipoproteinaemia and Laurence-Moon syndrome.

Question 190

What is retinoschisis?

Answer 190

In retinoschisis, the retina splits into an inner and outer leaf at the outer plexiform and inner nuclear junction. It is usually seen in the lower temporal quadrant of the retina and is often bilateral. The appearance is not dissimilar to a retinal detachment. Rarely, it may cause a retinal detachment when there are holes in both the inner and outer retinal leaves. These patients may require surgery.

Question 191

What are the 3 signs of typical retinitis pigmentosa?

Answer 191

1. peripheral clumps of retinal pigmentation (termed ‘bone spicule’ pigmentation);
2. attenuation of the retinal arterioles;
3. disc pallor - optic atrophy.

Patients may also have cataracts at an early age and may develop macular oedema.

Question 192

What is cone dystrophy?

Answer 192

This is less common than retinitis pigmentosa. It is usually autosomal dominant, but many cases are sporadic. Patients present in the first decade of life with poor vision. Examination reveals an abnormal, banded macular appearance which has been likened to a bull’seye target. No treatment is possible but it is important to provide appropriate help, not only to maximize vision but also to help with educational problems. Genetic counselling should be offered.

Question 193

What is the Rb1 gene responsible for?

Answer 193

a tumour suppressor gene whose product (pRB) plays a key role in the cell cycle as a negative regulator of cell proliferation. Mutations remove this anti-proliferative action, and predispose to cancer formation.

In somatic cases (60% of all cases), a single retinal cell loses one normal allele of the Rb1 gene during retinal development. Loss of the second normal allele results in disease which is always unilateral. Somatic cases cannot transmit disease to offspring.

In germline cases (40% of all cases), one copy of the Rb1 gene is defective (mutated) at the time of conception from a defective sperm or ovum, and every cell in the body has the defective gene. This can occur as a random event with unaffected parents (sporadic), or either parent might have undergone treatment for retinoblastoma and carry the defective gene, which is passed on to the offspring (inherited) in 50% of cases (autosomal dominant inheritance - see Chapter 2). Such cases can have unilateral or bilateral disease often with multiple tumours. They can genetically transmit the disease to their offspring and are also at risk of developing non-ocular second cancers (50% lifetime risk).

Question 194

Which patients develop astrocytomas of the retina and optic nerve?

Answer 194

patients with certain dominantly inherited systemic disorders:
* tuberous sclerosis
* neurofibromatosis (less commonly).

Question 195

How do astrocytomas of the retina and optic nerve present?

Answer 195

They appear as white mulberry-like lesions, are seldom symptomatic and require no treatment. However, their identification may assist in the diagnosis of these important systemic diseases.

Question 196

What is a sign of macular disease?

Answer 196

Distorsion of vision

Question 197

How does AMD affect vision?

Answer 197

AMD results in loss of acuity but never total loss of vision.

Question 198

What may be a sign of retinitis pigmentosa?

Answer 198

Poor night vision

Question 199

Where do cotton-wool spots occur and why?

Answer 199

They occur at the margins of an ischaemic retinal infarct due to obstruction of axoplasmic flow and a build-up of axonal debris in the nerve fibre layer of the retina.

Their visibility depends on nerve fibre layer thickness at that site, so that they are readily seen close to the optic disc, where the nerve fibre layer is thick but not in the periphery, where the nerve fibre layer is thin. They are white in colour because the accumulated axoplasmic particles scatter light, whereas the normal nerve fibre is transparent.

Question 200

Outline the classification of diabetic retinopathy

Answer 200

Question 201

How is diabetic retinopathy graded?

Answer 201

Question 202

What are the 3 types of emboli involved in retinal artery occlusions?

Answer 202

1. fibrin-platelet emboli (from carotids)
2. cholesterol emboli (from carotids)
3. calcific emboli (from heart valves)

Question 203

What type of symptoms do fibrin-platelet emboli cause?

Answer 203

Fibrin–platelet emboli typically cause a fleeting loss of vision as the emboli pass through the retinal circulation (amaurosis fugax).

Question 204

What is the acute treatment of central and branch artery occlusions?

Answer 204

Aimed at dilating the arteriole to allow the embolus to pass more distally and limit the damage (usually not very successful)

Question 205

Central retinal vein occlusion (CRVO) and branch retinal vein occlusion (BRVO) may result from what?

Answer 205

• abnormality of the blood itself (the hyperviscosity syndromes and abnormalities in coagulation);
• an abnormality of the venous wall (inflammation);
• an increased ocular pressure;

Question 206

Is retinal neovascularisation higher in CRVO or CRAO? Why?

Answer 206

Paradoxically, the incidence of retinal neovascularization is greater in CRVO than CRAO, even though the ischaemia is partial in CRVO and more complete in CRAO. This is because the partially ischaemic, functioning retina following CRVO produces more angiogenic factors such as VEGF than a completely ischaemic retina seen in CRAO.

Question 207

How is venous occlusion treated?

Answer 207

If the retinal is ischaemia - retinal laster treatment

If macular oedema present - anti-VEGF agents

Question 208

What is the pathogenesis of retinopathy of prematurity?

Answer 208

There is an initial failure of normal retinal vascularization, followed by a phase of aggressive new vessel formation extending forward into the vitreous and causing traction detachment.

Question 209

What are the risk factors for retinopathy of prematurity?

Answer 209

Question 210

Which types of sickle cell patients develop severe retinopathy?

Answer 210

Patients with sickle-cell haemoglobin C disease (SC disease) and sickle-cell haemoglobin with thalassaemia (SThal) develop a severe form of retinopathy.

Question 211

Draw the pathway of parasympathetic control to the eyes.

Answer 211

Question 212

What is the pathway of sympathetic pupillary control?

Answer 212

Question 213

What is a relative afferent pupillary defect (RAPD)?

Answer 213

A lesion of the optic nerve on one side blocks the afferent limb of the pupillary light reflex. The pupils are equal and of normal size, but the pupillary response to light directed to the affected side is reduced, while the near reflex is intact. Testing for an RAPD is critical in a patient suspected of having an optic nerve lesion, such as optic neuritis. An RAPD may be seen with extensive retinal disease but not with opacities of the cornea or lens.

Question 214

What is light-near dissociation?

Answer 214

The key feature is an impaired reaction of the pupils to light, while the near response to accommodation is retained. It is seen with Adie tonic pupil, the Argyll Robertson pupil and with periaqueductal brainstem lesions such as Parinaud syndrome. Other causes include diabetes and multiple sclerosis. There is no condition in which the light reflex is intact but the near reflex is defective.

Question 215

What causes an adie tonic pupil?

Answer 215

It is due to a ciliary ganglionitis which denervates the parasympathetic supply to the iris and ciliary body. On recovery from the ganglionitis, reinnervation is incomplete and the partially denervated receptors of the iris and ciliary body become supersensitive to muscarinic stimulation.

Question 216

What is an Argyll Robertson pupil?

Answer 216

The pupils are bilaterally small and irregular. They do not react to light but respond to accommodation. The iris stroma has a typical feathery appearance and loses its architectural detail. Classically, it is seen in neurosyphilis. It is suggested that a periaqueductal lesion on the dorsal aspect of the Edinger Westphäl nucleus involves fibres associated with the response to light, but spares those associated with the near response.

Question 217

What causes a midbrain pupil?

Answer 217

Lesions affecting the pretectal nuclear complex in the dorsal region of the midbrain can disrupt retinotectal fibres while preserving the supranuclear accommodative pathway. This produces mydriasis and a light-near dissociation. Causes include demyelination, infarction, enlargement of the third ventricle and space-occupying tumours such as pinealoma, as part of a dorsal midbrain (Parinaud) syndrome.

Question 218

In coma with pontine lesion, what happens to the pupils?

Answer 218

In coma, both pupils may become miosed if a pontine lesion is present. The light reflex is preserved but difficult to demonstrate with a small pupil. Remember that patients taking pilocarpine for glaucoma or receiving morphine also show bilateral miosis.

Question 219

In coma associated with unilateral expanding supratentorial mass, what happens to the eyes?

Answer 219

Coma associated with a unilateral expanding supratentorial mass, for example a haematoma, results in pressure on the third nerve and dilation of the pupil. Intrinsic third nerve lesions also cause a dilated pupil

Question 220

What drugs have a pharmacological effect on the pupil?

Answer 220

Question 221

How does myelination of the optic nerve develop?

Answer 221

During development, myelination of the optic nerve begins proximally and spreads centrifugally, to be completed at the lamina cribrosa at term.

Question 222

How can optic disc drüsen affect papilloedema examination?

Answer 222

Optic disc drüsen, which are accumulations of proteinaceous amyloid material within the optic nerve head, can also result in a swollen‐looking optic disc.

Question 223

How does the optic disc appear in myopia?

Answer 223

In myopia, it is common to see a pale ‘myopic crescent’ of peripapillary choroidal atrophy at the temporal margin of the optic disc, allowing the overlying, white sclera to show through.

In high myopia, the optic disc may be surrounded by such an atrophic area (peripapillary atrophy), which may be confused with disc swelling.

Question 224

What is the crucial feature of disc swelling due to raised ICP?

Answer 224

In the short term there is no visual loss.

However, in some patients with advanced papilloedema, a fleeting visual loss may occur, lasting seconds, when posture is altered from lying to standing (transient visual obscurations).

Visual loss (reduced acuity and significant contraction of the visual fields) can occur with chronic papilloedema.

Question 225

What are some causes of a swollen optic disc?

Answer 225

Question 226

When the optic disc is swollen, why is there no spontaneous venous pulsation?

Answer 226

The central retinal vein is exposed to cerebrospinal fluid (CSF) in the subarachnoid space of the optic nerve as it leaves to join the veins of the orbit. Normally, venous pressure in the retinal veins at the nerve head is just above ocular pressure.

Venous pulsation occurs because the vein collapses briefly with each rise in ocular pressure caused by arterial inflow during systole. When the CSF pressure is higher than the ocular pressure, as occurs in papilloedema due to raised ICP, the pressure in the veins at the disc rises above the ocular pressure and spontaneous venous pulsation is lost.

Absence of spontaneous venous pulsation is seen in 5–20% of those with normal nerve heads, but in this case, venous collapse at the nerve head can be induced by light pressure on the globe through the lids.

Question 227

What causes optic neuritis and what are the two subtypes?

Answer 227

Inflammation or demyelination of the optic nerve results in optic neuritis.

This is termed papillitis if the optic nerve head is visibly affected and retrobulbar neuritis if the optic nerve is affected more posteriorly, with no visible disc swelling.

Question 228

What should be considered aside from MS in patients with optic neuritis?

Answer 228

Neuromyelitis optica (NMO)

This is an AI condition where the spinal cord and optic nerves become inflammed

Question 229

What antibiodies can be tested for to diagnose neuromyelitis optica (NMO)?

Answer 229

anti MOG antibodies and aquaporin 4 antibodies

Question 230

What is the pathogenesis of ischaemic optic neuropathy?

Answer 230

The anterior optic nerve may become ischaemic if the posterior ciliary vessels are compromised as a result of degenerative vaso-occlusive or vasculitic disease of the arterioles. The resulting disc swelling is due to an anterior ischaemic optic neuropathy.

Question 231

What are the symptoms in ischaemic optic neuropathy?

Answer 231

The patient complains of a sudden loss of vision or visual field, often on waking, since the blood pressure falls and vascular perfusion of the eye decreases during sleep. If accompanied by pain or scalp tenderness, the diagnosis of giant cell arteritis must carefully be considered. Ischaemic optic neuropathy is the usual cause of blindness in that disease.

Question 232

What are the causes and distinguishing features of optic atrophy?

Answer 232

Question 233

Which muscles are responsible for moving the eyes through the cardinal positions of gaze?

Answer 233

Question 234

Outline the connections of the nuclei and higher centres controlling horizontal eye movements?

Answer 234

Vestibular, Saccade and smooth pursuit pathways shown for the right eye only.

Question 235

What is a concomitant squint?

Answer 235

where the angle of deviation remains constant in all directions of gaze and the range of eye movements of both eyes are full. This is the common squint seen in childhood.

Question 236

What is an incomitant squint?

Answer 236

Where the angle of deviation changes with gaze. This could be due to:
* underaction of one or more of the eye muscles due to a nerve palsy (paralytic or paretic squint) or muscular weakness (myogenic squint) as in myasthenia gravis;
* mechanical restriction of the muscles ‐ resulting from entrapment of muscles (after orbital fracture), muscle infiltration or scarring (in thyroid eye disease) or an orbital mass. For a nerve palsy, the squint is greatest in the field

Question 237

In which direction is a squint largest in a nerve vs. mechanical palsy?

Answer 237

For a nerve palsy, the squint is greatest in the field of action of the affected muscle (i.e. the direction in which that muscle would normally take the globe), while with mechanical restriction, the squint is greatest in the direction away from the affected muscle.

Question 238

Describe a gaze palsy.

Answer 238

In gaze palsies, there is a disturbance of the supranuclear coordination of eye movements. Pursuit and saccadic eye movements may also be affected if the cortical pathways to the nuclei controlling eye movements are interrupted.

Question 239

What is epicanthus vs telecanthus?

Answer 239

Epicanthus (a crescentic fold of skin on the side of the nose that incompletely covers the inner canthus) or telecanthus (increased distance between the inner canthi), which may simulate a convergent squint.

Question 240

What is a latent squint (phoria)?

Answer 240

A latent squint (phoria) is a tendency of the eyes to lose binocular fixation, so that they drift apart when they are visually dissociated e.g. in the absence of bifoveal visual stimulation by the same object of regard. It is not necessarily an abnormal condition and small phorias can be demonstrated in most people who otherwise have normal binocular single vision. In general, an esophoria (a tendency of the eyes to drift inwards) is most common in people with hypermetropia and an exophoria (a tendency of the eyes to drift outwards) in those with myopia.

Question 241

What is a manifest squint (tropia)?

Answer 241

A manifest squint (tropia) on the other hand occurs even when both eyes are open and being simultaneously stimulated. One eye is fixing, and the other eye deviating. Tropias appear spontaneously without the need to dissociate the two eyes. Tropias can be constant, or intermittent with variable control.

Question 242

What drops are used before measuring refractive error?

Answer 242

Refractive error is measured following topical administration of cyclopentolate eye drops to paralyse accommodation and dilate the pupil. The eye is then examined to exclude opacities of the cornea, lens or vitreous and abnormalities of the retina or optic disc.

Question 243

How does a convergent squint develop?

Answer 243

A convergent squint develops because of the increased accommodative effort required to focus, particularly on near objects. The link (synkinesis) between the accommodative and convergence mechanisms leads to an excessive convergence and ultimately to a convergent squint of one eye. Where the squint only occurs on attempted focusing on near objects (an accommodative squint), amblyopia does not develop since binocular visual alignment remains normal for part of the time, during distant viewing.

Question 244

Outline the principles of squint surgery

Answer 244

F(a) Recession. The conjunctiva has been incised to expose the medial rectus muscle. The muscle is then disinserted and moved backwards on the globe. (b) Resection. Following exposure of the muscle, the anterior tendon and muscle are resected, thus shortening them; the muscle is then reattached to its original position.

Question 245

What are the two types of incomitant squints?

Answer 245

Incomitant squints can be paralytic (due to nerve palsy) or myogenic (due to muscle weakness, or tight or trapped muscles which restrict eye movement).

Question 246

What causes proptosis in thyroid eye disease?

Answer 246

infiltration of the extraocular muscles with lymphocytes and the deposition of glycosaminoglycans in the tissues, leading to proptosis, exposure of the globes and limitation of eye movements

Question 247

What are some causes of an isolated nerve palsy?

Answer 247

Question 248

What is the most commonly affected muscle in thyroid eye disease?

Answer 248

Inferior rectusThe inferior rectus is the most commonly affected muscle. Its movement becomes restricted and there is mechanical limitation of the eye in upgaze, which also aggravates the upper lid retraction. Involvement of the medial rectus causes mechanical limitation of abduction, thereby mimicking a sixth nerve palsy. A CT or an MRI scan shows enlargement of the rectus muscles.

Question 249

What two serious acute complications are associated with thyroid eye disease?

Answer 249

1. Excessive exposure of the conjunctiva and cornea with the formation of chemosis (oedematous swelling of the conjunctiva), and corneal ulcers due to exposure and failure of the lids to protect the cornea. The condition may lead to corneal perforation.
2. Compressive optic neuropathy due to compression and ischaemia of the optic nerve by the thickened muscles. This leads to field loss and may cause blindness.

Question 250

How is myasthenia gravis treated?

Answer 250

Patients are treated, in collaboration with a neurologist, with oral pyridostigmine.

Systemic steroids, other immunosuppressive agents, and surgical removal of the thymus also have a role in treatment.

Question 251

What is orbital myositis?

Answer 251

This inflammation of the extraocular muscles is associated with pain and diplopia, leading to a restriction in the movement of the involved muscle (similar to that seen in dysthyroid eye disease). It is not usually associated with systemic disease, but thyroid abnormalities should be excluded. The conjunctiva over the involved muscle is inflamed. CT or MRI scanning shows thickening of the muscle. If symptoms are troublesome, it responds to a short course of steroids.

Question 252

What is chronic progressive external ophthalmoplegia (CPEO)?

Answer 252

CPEO is a rare condition where the movement of the eyes is slowly reduced bilaterally, often symmetrically.

It is caused by a mitochondrial DNA mutation affecting muscle function. There is an associated ptosis.

Ultimately, eye movement may be lost completely. There may be accompanying retinal dystrophy and heart block.

Question 253

What is brown syndrome?

Answer 253

In this condition, elevation of the eye in adduction is restricted due to restriction of the superior oblique muscle. The superior oblique muscle tendon fails to pass smoothly through its trochlear pulley or there is a stiff, inelastic tendon-muscle complex. The exact cause remains unknown. The condition may be congenital or result from orbital trauma or inflammation.

Question 254

What is Duane syndrome?

Answer 254

This is due to a ‘congenital miswiring’ or faulty innervation of the medial and lateral rectus muscles. The sixth nerve and/or nucleus may rarely be absent. The lateral rectus receives reduced or absent innervation from the sixth nerve. This is often accompanied by aberrant innervation of the lateral rectus by the third nerve. There is therefore reduced activity of the lateral rectus during attempted abduction, and co-contraction of the medial and lateral rectus during adduction. This results in narrowing of the palpebral aperture on adduction, with retraction of the eye into the orbit (due to simultaneous contraction of medial and lateral rectus muscles). The condition may be unilateral or, more rarely, bilateral.

Children do not usually develop amblyopia, because the eyes are aligned in the straight ahead (primary) position, or with a small abnormal head posture (face turn away from the affected lateral rectus). Rarely, surgical intervention is needed if there is a squint or if there is a significant abnormal head posture.

Question 255

What is the definition of gaze? What controls gaze?

Answer 255

Gaze is the coordinated movement of the two eyes together, in a given direction, as in right, left, up or downgaze. It is under the control of supranuclear pathways.

Question 256

What is the role of the paramedian pontine reticular formation (PPRF)?

Answer 256

Controls horizontal movements of the eyes

Lesions affecting the PPRF are usually associated with other brainstem disease. It may be seen in patients with vascular disease and tumours.

James, Bruce; Bron, Anthony; Parulekar, Manoj V.. Ophthalmology: Lecture Notes (p. 559). Wiley. Kindle Edition.

Question 257

What are lesions of the paramedian pontine reticular formation (PPRF) often caused by?

Answer 257

Other brainstem disease

It may be seen in patients with vascular disease and tumours.

There is a failure of horizontal movements of both eyes to the side of the lesion (a horizontal gaze palsy), and deviation of the eyes to the contralateral side in acute cases.

Question 258

Where is the lesion in internuclear ophthalmoplegia?

Answer 258

medial longitudinal fasciculus (MLF)

Question 259

What is the role of the medial longitudinal fasciculus (MLF)?

Answer 259

The MLF connects the sixth nerve nucleus to the third nerve nucleus on the opposite side and coordinates their activity in horizontal gaze movements.

Question 260

What can cause internuclear ophthalmoplegia?

Answer 260

It may be affected by demyelination (e.g. multiple sclerosis - usually bilateral) and vascular disease (unilateral).

Question 261

How do patients with internuclear ophthalmoplegia present?

Answer 261

The patient complains of horizontal diplopia. There is reduction of adduction on the same side as the lesion, and nystagmus of the contralateral, abducting eye (abducting nystagmus).

Question 262

What is Parinaud syndrome?

Answer 262

In Parinaud syndrome, a lesion in the dorsal midbrain affects the centre for vertical gaze. It may be seen in patients with demyelination, space-occupying lesions such as a pinealoma which presses on the tectum, infarction of the dorsal midbrain or an enlarged third ventricle from hydrocephalus.

Also known as dorsal midbrain syndrome.

Question 263

How do patients with parinaud syndrome (dorsal midbrain syndrome) present?

Answer 263

The disorder causes deficient (and often painful or uncomfortable) elevation of both eyes, convergence of the eyes and retraction into the orbit associated with nystagmus on attempted elevation (convergence-retraction nystagmus) and lightnear dissociation of the pupil (the pupil reacts poorly to a light stimulus but constricts normally on accommodation).

Question 264

What is an upbeat nystagmus often associated with?

Answer 264

Brainstem disease

It may also be seen in toxic states, for example following excess alcohol intake.

Question 265

What is a downbeat nystagmus often associated with?

Answer 265

Posterior fossa lesion near the cervicomedullary junction (e.g. a Chiari malformation, where cerebellar tissue is dragged through the foramen magnum).

It may also be seen in patients with demyelination, and again may be present in toxic states.

Question 266

What are the 3 main causes of congenital nystagmus?

Answer 266

a defect in the central control mechanisms of eye movements (congenital idiopathic motor nystagmus)

conditions that interfere with visual development within the first few months of life (when steady fixation develops) - for example, bilateral congenital cataracts or glaucoma

albinism - the exact mechanism is not understood but may relate to a failure of visual development.

Question 267

What is the extent of possible traumatic damage to the eye?

Answer 267

Question 268

When should you suspect a blow-out fracture?

Answer 268

If the orbital rim is intact and the following signs are present:
* emphysema
* patch of paraesthesia below the rim (infraorbital nerve damage)
* limitation of eye movement (esp upgaze and downgaze
* eye may become recessed into the orbit (enophthalmos)
* lid margin cut at the medial canthus - epiphora

Question 269

What is siderosis oculi?

Answer 269

a complication due to a magnetic intraocular or intraorbital foreign body

Retained, iron-containing foreign bodies may have an insidious and particularly devastating effect on the eye (siderosis oculi). A tiny, high-velocity metal fragment, penetrating the ocular coats and retained in the peripheral vitreous cavity, can, with time, lead to a progressive, pigmentary degeneration of the retina. The mechanism of damage is by the diffusion of ferrous ions throughout the globe and the generation of free radicals in affected tissues, via the Fenton reaction. A discolouration of the iris (heterochromia), a dilated and unresponsive pupil (fixed mydriasis) and cataract are late clues to the diagnosis. Failure to detect and remove such a foreign body at the time of injury results in irreversible blindness.

Question 270

What can be seen following a chemical injury?

Answer 270

After chemical injury, the conjunctiva may appear white and ischaemic. Extensive changes to the corneal limbus, the site of the epithelial corneal stem cells, grossly impair corneal healing by retarding epithelial resurfacing.

Additional complications such as uveitis, secondary glaucoma and cataract contribute to the overall burden of disease.

Question 271

How can electromagnetic radiation affect the eye?

Answer 271

Electromagnetic radiation may injure the conjunctiva and the cornea. Unprotected exposure to ultraviolet radiation from an artificial source (such as an arc lamp (arc eye) or sunlamp), or a natural source (reflected from snow (snow blindness) or water), is the commonest cause of this painful condition. Typically, severe ocular pain starts acutely, 6 hours after exposure to the radiation, and the cornea shows diffuse epithelial oedema and punctate keratitis which resolve within 24-48 hours.

Question 272

What causes a hyphaema?

Answer 272

Rupture of blood vessels at the root of the iris

Question 273

What is iridonesis?

Answer 273

fluttering of the iris diaphragm on eye movement - may suggest dislocation of the lens following blunt trauma

Question 274

What develops quickly after penetrating trauma?

Answer 274

Cataracts

Question 275

What is commotio retinae?

Answer 275

traumatic retinopathy secondary to direct or indirect trauma to the globe.

Question 276

What is retinal dialysis?

Answer 276

a separation of the peripheral retina from its junction with the pars plana of the ciliary body

Question 277

What is a cyclodialysis cleft?

Answer 277

A cyclodialysis cleft is a separation of the ciliary body from the scleral spur, creating a direct connection between the anterior chamber and the suprachoroidal space.

Many will spontaneously close, but those that do not can cause chronic hypotony, resulting in hypotony maculopathy, optic disc edema, and decreased visual acuity. Treatment begins with conservative medical therapy, but when this fails, a wide range of laser and surgical procedures have been reported to be effective.

Question 278

How is a corneal abrasion?

Answer 278

This results from a glancing blunt injury which shears a patch of corneal epithelium from the basal lamina. It is extremely painful, but normally heals in a few days, depending on its size of the epithelial defect. It is treated with antibiotic ointment, with or without an eye pad. Dilatation of the pupil with cyclopentolate 1% can help to relieve pain caused by spasm of the ciliary muscle.

Question 279

What is recurrent corneal erosion?

Answer 279

Recurrent corneal erosion is a condition of repeated painful attacks of corneal epithelial detachment, following a non-lacerating corneal injury. Recurrent attacks of extreme, debilitating pain cause marked epiphora and temporary visual loss. The detached epithelium may remain intact, but loose, or be sheared by an extensive erosion. Painful symptoms, persisting for days or weeks, are followed by periods of quiescence.

Despite adequate epithelial resurfacing and an absence of corneal scarring, epithelial adhesion remains impaired, so that the cornea remains vulnerable to further epithelial detachments at the site of injury. Typically, a patient experiences an episode of severe pain on opening the eyes after a night’s sleep, as the opening upper lid pulls on the poorly adherent epithelium and triggers an attack. The history alone should suggest the likely diagnosis. Between attacks, the cornea may look normal on biomicroscopy but a few, tiny epithelial microcysts, which take up fluorescein in a brilliant and distinctive manner, often mark the affected zone and can direct the clinician’s attention to the region requiring treatment.

Question 280

What is a common cause of recurrent erosion?

Answer 280

A common cause of recurrent erosion is glancing trauma with a flexible object such as a baby’s fingernail, twig or a plastic implement. This scuffs off the corneal epithelium at the site of contact, probably taking with it a layer of the underlying epithelial basement membrane critical for epithelial reattachment once epithelial resurfacing has taken place.

Occasionally, recurrent erosion may occur as a complication of bilateral epithelial basement membrane, or map-dot-fingerprint disorder. Here, there is an intrinsic, sometimes inherited, defect in epithelial adhesion which gives rise recurrent erosion attacks after minimal trauma or arising spontaneously; the risk of attacks is bilateral and the disorder is characterized by clusters of epithelial dots or of subepithelial map or fingerprint-like patterns detected by retro-illumination at the slit lamp.

Question 281

What is the management for recurrent corneal erosion?

Answer 281

In the first instance, attacks are treated with a simple lubricating ointment at night to reduce friction between the upper lid and the globe. Nightly use of hypertonic agents to draw water from the cornea, such as 5% sodium chloride drops or corn syrup, is also advised. Other conservative measures include the use therapeutic hydrogel contact lenses or gas-permeable scleral lenses. Doxycycline prescribed with steroid eye drops may also be effective.

Where such measures fail, a surgical approach using corneal micropuncture or phototherapeutic (laser) keratoplasty (PTK), to create a subepithelial scar at the site of the original injury, may give long-lasting relief or a permanent cure.

Question 282

How is UV injury to the cornea managed?

Answer 282

This responds quickly to topical steroids. Dilation of the pupil with cyclopentolate 1% to overcome the associated spasm of the ciliary muscle and application of a lubricant gel is the standard treatment. Although often given, there is no evidence for the application of topical antibiotics.

Question 283

How should corneal foreign bodies be removed?

Answer 283

with a needle under topical anaesthesia

Where the foreign body contains iron, a rust ring may remain which can be removed with a small, rotating burr. Subtarsal objects can often be swept away with a cotton wool bud from the everted lid. The patient is then treated as for an abrasion. If there is any suggestion that a foreign body may have penetrated the globe, the eye must be carefully examined with dilation of the pupil to allow a good view of the lens and retina. A radiograph of the orbits, with the eyes looking up and then down, or a CT scan, may also be indicated if an intraocular foreign body is suspected. Microsurgical techniques can be used to remove foreign bodies from the eye under direct view.

Question 284

How should a corneal and scleral penetrating trauma be managed?

Answer 284

Once identified, no further examination of the globe should be performed but a shield should be gently placed over the eye and the patient referred for urgent ophthalmic assessment and treatment. It should be assumed that the patient will need surgery under general anaesthesia and the patient prepared appropriately and kept nil by mouth. These serious injuries, often with grave implications for sight, require careful microsurgical suturing to restore the integrity of the globe.

Question 285

How is uveitis managed?

Answer 285

This responds to treatment with steroids and dilating drops. It may be accompanied by elevated intraocular pressure requiring additional medical treatment.

Question 286

How is a hyphaema treated?

Answer 286

This usually settles with rest, but a re‐bleed may occur in the first 5–6 days after injury. Children may sometimes require admission to hospital for a few days, while adults can be treated at home, provided they can rest and no complications develop. Steroid eye drops are given for a short time, together with dilation of the pupil. Steroids may reduce the risk of re‐bleeds.

Question 287

What is the commonest complication of hyphaema?

Answer 287

The commonest complication is a raised ocular pressure, particularly if there is a secondary bleed, which tends to be more severe than the first. It is for this reason that rest is important, although the patient can be ambulant. Raised pressure is due to the accumulation of empty, red cell ‘ghosts’ in the trabecular meshwork or damage to the drainage angle itself (e.g. angle recession). It usually responds to medical treatment, but occasionally surgical intervention is required. When the hyphaema has settled, it is important that the eye is carefully checked for other complications of blunt trauma. A hyphaema clears more slowly after trauma in patients with sickle cell disease because the hypoxic and acidic environment within the anterior chamber precipitates sickling, and the rigid sickle cells are more difficult to remove via the trabecular meshwork.

Question 288

How is commotio retinae treated?

Answer 288

In commotio retinae, the affected zone of retina opacifies and obscures the underlying choroidal detail. It usually resolves, but requires careful observation, since retinal holes may develop in affected areas and may lead to subsequent retinal detachment.

Question 289

How is retinal dialysis managed?

Answer 289

Retinal dialysis, a separation of the retina from the ora serrata, requires surgical intervention to repair any detached retina.

Question 290

How is a vitreous haemorrhage managed?

Answer 290

A vitreous haemorrhage although it may absorb over several weeks may require earlier removal by vitrectomy. An ultrasound scan is useful in detecting associated retinal detachments when the retina cannot be viewed directly.

Question 291

What may prevent resurfacing of the cornea with epithelium in chemical injury? How is this managed?

Answer 291

Extensive damage to the limbus may prevent resurfacing of the cornea with epithelium. A prolonged epithelial defect may lead to a corneal ‘melt’ (keratolysis).

Stem cell deficiency is treated later, by limbal stem cell transplantation, for instance from the normal, fellow eye or from a donor source. Alternatively or additionally, an overlay of amniotic membrane can be applied to the damaged surface, which protects and maintains the underlying tissue and promotes epithelial resurfacing. It is also possible to resurface the cornea by transplanting expanded sheets of corneal limbal or even oral mucosal cells, grown in culture.

Question 292

What should be done in a patient with a eye suspected of having a penetrating injury?

Answer 292

Place an eyeshield over an eye suspected of having a penetrating injury.

Question 293

How many people worldwide have some form of visual impairment? (WHO)

Answer 293

2.2 billion

Defined as: distance acuity worse than 6/12 or N6 for near)

Question 294

How many people worldwide are blind?

Answer 294

43 million people are blind

Visual acuity less than 3/60.

90% of the blind live in the poorest parts of the developing world.

Question 295

Which gender is more affected by blindness?

Answer 295

The prevalence of blindness is greater in women in all regions. Nearly, two-thirds of the world’s blind are women. In the developed world, this is partly because women live longer than men, but in the developing world, cultural factors can mean that women are less informed about opportunities for treatment and have fewer resources to pay for and access care. In sub-Saharan Africa and south Asia, the proportion of eligible women who receive cataract surgery may be half that for men.

Question 296

What are the reasons for the greater prevalence of blindness in the developing world?

Answer 296

Question 297

What is the method of choice of cataract treatment in the developing world?

Answer 297

Of the surgical methods available for treatment, extracapsular cataract extraction has been the method of choice in the developing world, since it is cheaper than phacoemulsification and not dependent on expensive, high‐tech equipment and support costs.

However, increasingly, small incision cataract surgery (SICS) is being adopted, which is a low‐cost and faster procedure permitting the use of intraocular lens implants. Since sutures are not used, rehabilitation is faster.

Question 299

Outline cataract treatment in India

Answer 299

In India, where cataract blindness remains a significant problem, the Aravind Eye Care system has created a highly efficient, high-volume, low-cost, self-financing system for performing cataract surgery. The system uses income from patients who can afford to pay for private surgery, to pay for the poor, who receive free surgery. Patients are screened in eye camps and those in need of surgery or other treatment are referred to hospital.

Question 300

Outline the epidemiology of trachoma.

Answer 300

Trachoma is endemic in 48 countries, in Latin America, Africa, the Middle East, Asia and Australasia. Some 157.7 million people living in endemic areas require prophylactic treatment.

In 2019, there were 2.5 million people with trachomatous trichiasis, falling from 7.6 million in 2002. Ten percent of the world population are potentially at risk, mostly in dry, hot parts of the developing world.

Question 301

How is trachoma transmitted?

Answer 301

Transmission is by the transfer of the elementary bodies of the bacteria from one person to another, usually from the nasal and ocular secretions of an infected child. This may involve eye-to-eye transmission with the fingers, the sharing of towels, handkerchiefs and bedclothes, coughing and sneezing. In addition, eyeseeking flies (e.g. Musca sorbens) act as important vectors, carrying the infective particles from eye or nose, to other individuals.

Question 302

Outline the natural history of trachoma.

Answer 302

Initially, follicles (collections of lymphocytes) appear in the superior tarsal conjunctiva, followed by papillae. Then, the limbal cornea is invaded by superficial vessels (pannus), with the development of peripheral scarring. The first infection with C. trachomatis does not cause serious disease. Repeated episodes lead to extensive upper tarsal conjunctival scarring in children and young adults, and lid deformity and trichiasis, usually in middle-aged adults, which together exacerbate the corneal changes. Continued re-infection leads to chronic corneal scarring and blindness.

Question 303

What strategy was developed to tackle trachoma worldwide?

Answer 303

SAFE strategy = Surgery, Antibiotics, Face washing, Environmental change

Question 304

What antibiotic is used in trachoma?

Answer 304

A single dose of oral azithromycin (20 mg/kg up to 1 g) is effective in treating infected individuals, but the disease must be eradicated from all individuals in a community to prevent re-infection, and treatment must be repeated yearly.

This is expensive, and the disease will recur unless changes are made to the environment in which the organism prospers. This is much harder to achieve.

Question 305

Which organism is responsible for onchocerciasis (river blindness)?

Answer 305

The filarial nematode, onchocerca volvulus

Question 306

Outline the epidemiology of onchocerciasis (river blindness)

Answer 306

In 2017, 220 million people required preventative anti-helminthic and it was estimated that 1.15 million people had sight loss due to onchocerciasis.

Question 307

Outline the life cycle of onchocerca volvulus

Responsible for onchocerciasis (river blindness)

Answer 307

Microfilariae in the skin of an affected patient are ingested when the female blackfly (e.g. Simulium damnosum) bites a human for a blood meal. The microfilariae develop into infective larvae in the fly, pass to its mouth and are then transmitted to a human with the next bite. Following moulting, the larvae develop into adult worms in the body. They are found in subcutaneous skin nodules (onchocercomata). A female worm may produce 1600 microfilariae a day and generate a body load of 150 million. These migrate in the dermis and its lymphatics and die after a couple of years if they are not taken up into a blackfly.

Question 308

How long is the onchocerca volvulus nematode and what is their lifespan?

Answer 308

The adult female worm is 30-80 cm long and the male 3-5 cm long.

In the human body they have a lifespan of 9-14 years.

A female worm may produce 1600 microfilariae a day and generate a body load of 150 million. These migrate in the dermis and its lymphatics and die after a couple of years if they are not taken up into a blackfly.

Question 309

What is a characteristic early sign of eye disease?

Answer 309

Fluffy, punctate stromal keratitis.

Each opacity representing an inflammatory reaction around a dead microfilarium.

Question 310

What is being done to prevent the incidence of river blindness?

Answer 310

Water courses provide the breeding grounds for the blackfly, which is why those whose work or daily life takes them to the banks of rivers are most at risk of infection - hence the name river blindness. Control programmes are aimed at the blackfly vector, by spraying its habitat with larvicides, trapping methods and the removal of vegetation from breeding sites. The onchocerciasis control programme has been successful in the endemic West African region and South America. A low population density in affected areas (principally farming and fishing communities) increases the likelihood of multiple blackfly bites. Protective clothing reduces the possibility of bites but may not always be practical. Vector control programmes are a long-term proposition because the female worm lives for 9-14 years, which perpetuates microfilarial infiltration of the skin.

Question 311

Which medication can be used in the treatment of onchocerciasis?

Answer 311

Ivermectin (given once a year)

Question 312

What programme was developed to tachle onchocerciasis?

Answer 312

The African programme for onchocerciasis control (APOC) had developed a system whereby the local community is responsible for the delivery of ivermectin treatment. This has now closed but the work continues with the Expanded Special Project for the Elimination of Neglected Tropical Diseases in Africa (ESPEN).

Question 313

What are sources of vitamin A?

Answer 313

Dietary carotenoids from dark, leafy green vegetables, carrots, red palm oil, mangoes and papayas, and so on are absorbed and broken down to release vitamin A (roughly 12 molecules of carotene for every molecule of vitamin A). Preformed vitamin A is available in breast milk, liver, fish oils, eggs and dairy products.

Question 314

What is the name for blindness due to vitamin A deficiency?

Answer 314

Xerophthalmia

Question 315

How is vitamin A blindness related to morbidity?

Answer 315

In countries where vitamin A deficiency is prevalent, 50% of those affected die within 2 years of becoming blind.

Question 316

Outline the epidemiology of vitamin A deficiency

Answer 316

About 190 million children under 5 years of age suffer from vitamin A deficiency and some 5-10 million develop xerophthalmia each year, with loss of sight in half a million. The peak incidence occurs between 3 and 5 years of age.

Question 317

What is the sequence of clinical features of xerophthalmia?

Answer 317

1. Night blindness
2. Ocular surface xerosis (conjunctival or corneal)
3. Corneal ulceration or focal melting (keratomalacia)

Question 318

What causes night blindness in xerophthalmia?

Answer 318

Due to lack of the visual pigment rhodopsin

Question 319

Why does vitamin A deficiency cause ocular surface xerosis?

Answer 319

Vitamin A deficiency causes a loss of ocular surface wettability due to a reduced expression of epithelial glycocalyx mucins and a loss of goblet cells and their secreted gel mucin. Tear production may also be reduced. This results in:
* Conjunctival xerosis: involving keratinization, thickening and non-wetting of the conjunctiva, frequently with Bitot spots near each limbus (foamy triangular surface plaques containing keratinized cells and saprophytic bacteria)
* Corneal xerosis: involving punctate keratiopathy or diffuse drying of the cornea, usually with stromal oedema. it imarsnusmunan ine

Question 320

What is phthisis bulbi?

Answer 320

Phthisis bulbi is an clinical condition representing an end-stage ocular response to severe eye injury or disease damage.

Question 321

What is being done to tackle xerophthalmia?

Answer 321

Treatment with vitamin A supplementation, fortification of food or increasing the natural dietary intake is highly cost-effective (the WHO recommends the provision of two doses of vitamin A annually to children between the ages of 6 and 59 months). A protein-rich diet is also advised. Delivery of supplements is often combined with immunization programmes. Education about breastfeeding, diet and food availability and preparation is also important. Care should be taken in women of childbearing age, as vitamin A in large doses may have teratogenic effects; lower doses are therefore recommended.

Question 322

How is measles related to vitamin A deficiency blindness?

Answer 322

Measles is an important cause of corneal scarring and childhood blindness and its severity is exacerbated by vitamin A deficiency.

During infection with measles, vitamin A stores are significantly depleted, which can result in severe corneal disease.

Vitamin A deficiency also increases mortality from this disease.

Associated exposure keratopathy, herpes simplex keratitis and other secondary infections may also cause corneal opacification. This may be compounded by treatment with local remedies that traumatize the eye, or cause infection or chemical burns.

Question 323

In which region is CMV retinitis most common?

Answer 323

Southeast Asia

Question 324

Outline the presentation of ophthalmia neonatorum.

Answer 324

Gonorrhoeal keratitis may progress rapidly to corneal perforation and endophthalmitis. Chlamydial infection is the commonest cause and the associated keratitis, if untreated, may progress to corneal scarring. It can also be associated with a pneumonitis. Because of the systemic implications of these eye infections, both are treated with systemic and topical antibiotics.

Topical instillation of povidone-iodine eye drops into the eyes of neonates, at the time of delivery, is a simple and cost-effective means to prevent either disease.

Question 325

When does development of the eye begin in utero?

Answer 325

Development of the eye begins early in utero, with the optic grooves appearing at 3 weeks, and is largely completed at 7 months of gestation. The visual pathways continue to mature over the next few months in and ex utero. The globe continues to grow post-natally.

Question 326

When in utero is the eye most susceptible to disease?

Answer 326

Teratogenic events in the first 3-8 weeks can result in severe eye abnormalities. The choroidal fissure closes at 7 weeks, and incomplete closure can result in chorio-retinal and/or optic nerve colobomas.

Question 327

Why are the first few years of life crucial for visual development?

Answer 327

Adequate stimulation of both retinas in the first 6-8 years of life is essential to achieve normal visual acuity in adult life.
Visual deprivation of one or both eyes from any cause can result in amblyopia (a ‘lazy eye’).

Question 328

When is there no need for action in delayed visual maturation (DVM)?

Answer 328

1. Eyes are structurally normal
2. No abnormal eye movements
3. No other developmental concerns

Such babies can be observed until & months age, by which time most cases improve spontaneously. If there is no improvement after this time, a brain scan and electro-diagnostic testing (ERG and VEP) are indicated.

Question 329

Visual development: 0-3 months

Answer 329

Briefly holds gaze on an object
Takes interest in (stares at) surroundings, blinks at bright lights
Tracks vertically and horizontally
Makes eye contact at 6-8 weeks; fixes on mother’s face

Question 330

Visual development: 3-6 months

Answer 330

Follows adults or moving objects with eyes across midline
Displays interest in human faces
Observes own hands
Briefly fixes on and reaches for small objects

Question 331

Visual development: 7-12 months

Answer 331

Recognizes objects at home, tracks across the room
Interested in pictures, inspects toys, enjoys hide-andseek
Responds to smiles and voices, develops stranger anxiety

Question 332

Visual development: 1 - 1.5 years

Answer 332

Enjoys picture books and points to pictures
Holds objects close to eyes to inspect

Question 333

Visual development: 2-3 years

Answer 333

Recognizes faces in photographs
Begins to inspect objects without touching them
Likes to watch moving objects, such as wheels on a toy vehicle
Watches and imitates other children
‘Reads’ pictures in books

Question 334

Visual development: 3-4 years

Answer 334

• Copies patterns
• Recognizes colours
• Can close eyes on request and may be able to wink

Question 335

Visual development: 4-5 years

Answer 335

• Draws a recognizable person and house and names pictures
• Uses eyes and hands together with increasing skill * Moves and rolls eyes expressively
• Can place small objects into small openings * Demonstrates visual interest in new objects

Question 336

What is telecanthus?

Answer 336

Wide set eyes

Question 337

What are some formal tests of visual fields in older children?

Answer 337

Humphrey instrument or manual perimetry with the Goldmann instrument.

For the younger child, tests are more observational, where the clinician places objects (typically bright toys) randomly in various positions in the visual field, and observes the child’s response - normally a rapid head and eye movement in the direction of the toy.

Question 338

What are the possible visual acuity tests for children?

Answer 338

Question 339

What is binocular vision?

Answer 339

Binocular vision is the ability of the higher visual centres of the brain to process the visual signals from both eyes simultaneously, to produce a single, three-dimensional visual percept.

It is a function in higher evolved species where the location of the eyes in the head permits an overlap of the visual fields when the eyes are directed at an object of regard. This condition is maximized in humans and in sub-human primates where the eyes are frontally disposed, thus achieving a large binocular visual field. Since each eye views the visual scene from a slightly different angle, the images on each retina have slight horizontal disparity and it is this which creates the three-dimensional percept, carrying depth and distance information, which is the basis of stereopsis.

Question 340

What are some age-appropriate tests to detect the presence and level of binocular vision?

Answer 340

Lang, TNO and Titmus tests, the Wirt Fly test and the synoptophore - often referred to by children as ‘putting the lion in the cage test’.

Question 341

When might it be more difficult to see a bright red reflex?

Answer 341

It is important to remember that it may be more difficult to see a bright red reflex in heavily pigmented fundi (e.g. Asian or Afro-Caribbean eyes) as more light is absorbed and less reflected back. This apparent absence of a red reflex is a common cause of referral to the ophthalmologist. Examining the fundus in a child takes considerable patience and skill. It is easier after pupillary dilatation with eye drops, usually cyclopentolate.

Question 342

Which children may high a higher change of having refractive errors?

Answer 342

Those born prematurely, or showing developmental delay, including that resulting from birth hypoxia.
Those with multisystem disorders or genetic syndromes such as Trisomy 21.

Question 343

What is the incidence of clinically significant refractive errors requiring the use of spectacle correction in childhood?

Answer 343

5% (the Baltimore Pediatric Eye Disease Study).

Question 344

How dangerous is proprosis in childhood?

Answer 344

EMERGENCY

Question 345

What are the 3 main causes of proptosis in childhood?

Answer 345

1. Rhabdomyosarcoma
2. Bleeding into vascular malformation
3. Infection e.g. orbital cellulitis

Question 346

When to infantile (capillary) haemangiomas develop and how are they treated?

Answer 346

These lesions, extending into the lids, typically present within a few weeks of birth. They can grow rapidly and induce astigmatism or ptosis, with resultant amblyopia.

Timely treatment with topical (Timolol) or systemic beta-blockers (Propranolol) is essential.

Question 347

Where do dermoid cysts often occur in children?

Answer 347

These present in infancy and early childhood as well-defined lesions along the supero-temporal, or less commonly, supero-nasal orbital rim. Treatment is with surgical excision.

Question 348

What is the treatment for ptosis in children?

Answer 348

The treatment is surgical and involves shortening of the levator muscle (resection) or suspending the eyelid from the brow (brow suspension) using material such as silicone or fascia lata harvested from the leg.

Question 350

How is congenital epiphora treated?

Answer 350

Congenital epiphora - specifically refers to watery eyes resulting from congenital obstruction of the nasolacrimal duct. Spontaneous resolution is seen in many cases within the first year of life. Persistent cases can be treated with syringing and probing, with a high success rate.

Question 351

What is the commonest cause of uveitis in children?

Answer 351

Juvenile idiopathic Arthritis (JIA)-related uveitis

The presentation of uveitis in children differs from that in adults as it does not cause redness or pain. Consequently, it may be overlooked and children with uveitis or diseases that may cause uveitis need regular screening.

Question 352

How does a congenital glaucoma present?

Answer 352

an enlarged eye (bupthalmos);

photophobia

epiphora (beware of diagnosing an obstructed nasolacrimal duct in these children).

Question 353

Which two childhood conditions may result in a white pupillary reflex?

Answer 353

Coats disease and retinoblastoma

Question 354

What is Coats disease?

Answer 354

This is a form of exudative vascular retinopathy, characterized by abnormally dilated vessels in the peripheral retina that leak blood and blood products. Yellow, cholesterol-rich fluid forms under the retina, resulting in an exudative detachment. It can be difficult to distinguish from retinoblastoma, but an ultrasound B-scan can be used to exclude a mass lesion.

Question 355

What are the important retinal causes of reduced vision in childhood?

Answer 355

1. Retinal dystrophies (retinoschisis and rod cone dystrophies).
2. Albanism
3. Coats disease
4. Astrocytomas are hamartomatous lesions of the retina.
5. Retinoblastoma

Question 356

What is retinopathy of prematurity (ROP)?

Answer 356

Retinal development continues through gestation, and vascularization is completed near term. Premature birth interferes with normal retinal vascularization, with a risk of abnormal retinal vascular proliferation that can cause retinal scarring and/or detachment (ROP). Babies born before 32 weeks gestation or of birthweight ≤1500 g are at risk of ROP and undergo regular screening eye examinations in the first few weeks of life. Most cases do not require treatment, but ROP beyond a certain threshold will require prompt laser treatment of the avascular retina to reduce risk of visual loss.

Question 357

Which eye problems are seen in premature children?

Answer 357

1. Retinopathy of prematurity (ROP)
2. Strabismus
3. Refractive error
4. Cortical visual impairment and developmental delay

Question 358

Children can develop tumours of the anterior visual pathway - which ones?

Answer 358

• Optic pathway gliomas, some of which are related to neurofibromatosis (type 1).
• Extrinsic compression of the optic pathway from supra-sellar tumours (craniopharyngiomas).

These children often present with visual loss or nystagmus.

Question 359

When do squints often develop?

Answer 359

It is not uncommon for the eyes to converge or diverge randomly during the first 2-3 months while the fixation system is still developing. This is referred to as neonatal ocular misalignment, and can be kept under observation unless there are concerns about the child’s vision. Persistence of ocular misalignment beyond 3 months warrants referral to an ophthalmologist.

Question 360

What are the 6 causes of childhood squint?

Answer 360

1. Refractive
2. Non-refractive
3. Mixed
4. Neurogenic
5. Myogenic
6. Obstruction of the optical media (e.g. cataract)

Question 361

In children with suspected NAI, which ophthalmic examinations should be done?

Answer 361

Dilated fundoscopy (for external evidence of trauma + retinal haemorrhage)

Question 362

How does the International Classification of Diseases (2018) used by the World Health Organisation (WHO) classifiy distance visual impairment?

Answer 362

Mild: visual acuity worse than 6/12 to 6/18.
Moderate: visual acuity worse than 6/18 to 6/60.
Severe: visual acuity worse than 6/60 to 3/60.
Blindness: visual acuity worse than 3/60.

The definition of blindness, a visual acuity of < 3/60 with the best possible refractive correction, can also be met if there is a visual field loss to less than 10°, in the better eye.

Question 363

What is near vision impairment?

Answer 363

Near vision impairment is defined as an acuity worse than N6 at 40 cm.

Question 364

An estimate in 2010, of the age-standardized prevalence of blindness in adults ≥50 years, was X% in high-income regions compared to levels of up to Y%, in western sub-Saharan Africa?

Answer 364

An estimate in 2010, of the age-standardized prevalence of blindness in adults ≥50 years, was ≤0.4% in high-income regions compared to levels of up to 6%, in western sub-Saharan Africa.

Question 365

What are the leading causes of visual impairment worldwide?

Answer 365

Globally, uncorrected refractive errors are the main cause of moderate and severe distance visual impairment that can be corrected and near visual impairment; cataracts remain the leading cause of blindness in middle- and low-income countries.

Question 366

What is protanomaly color blindness?

Answer 366

Protanomaly makes certain shades of red look more green and less bright.

Question 367

What is a Deuteranomaly?

Answer 367

Deuteranomaly is the most common type of red-green color vision deficiency

Question 368

What is tritanomaly?

Answer 368

Tritanomaly makes it hard to tell the difference between blue and green and between yellow and red

Tritanopia (absence of function) makes someone unable to tell the difference between blue and green, purple and red, and yellow and pink. It also makes colors look less bright.

Question 369

What is the inheritance of deuteranopia and protanopia?

Answer 369

X-linked recessive

Deuteranopia or more commonly deuteranomaly is the usual cause of red-green colour blindness. Protanopia or protonomaly is more unusual. Both are inherited in an X-linked recssive manner. Thus, males (1 in 12) are more commonly affected than females (1 : 200). It affects the ability to detect long and middle wavelengths of the optical spectrum and hence to sense the colours green or red and to discriminate their admixtures. Red and green are colours used in traffic lights and signalling systems.

Question 370

What is done in the UK for those with visual impairment?

Answer 370

In the United Kingdom, a Certificate of Visual Impairment is completed for a child. This is also useful nationally in planning visual services for children. It is important to provide resources for the whole family of a child with visual impairment. Financial assistance may also be available for those with severe visual impairment. Every local authority in the United Kingdom will have a qualified teacher of the visually impaired (QTVI) and other educational and social care staff trained to provide for the special educational needs of children with visual impairment. The local authority will also provide an education health and care (EHC) plan for young people up to 25 years of age.

Question 371

In the UK, what registration do adults with visual impairment get?

Answer 371

In the United Kingdom, people with visual impairment are eligible to be registered as sightimpaired (partially sighted) or severely sight-impaired (blind) (Table 20.1). This is a process initiated by the consultant ophthalmologist, by completing a Certificate of Visual Impairment (CVI). The process of registration enables the affected individual to access support from social services and entitles them to certain concessions. People who are registered as severely sight-impaired/blind or sight-impaired/partially sighted are not automatically entitled to any welfare benefits; this is subject to age and other circumstances.

Question 372

What are some useful contacts and agencies for those with visual impairment?

Answer 372

• RNIB (Royal National Institute of Blind People www.rnib.org.uk
• The Royal College of Ophthalmologists www.rcophth.ac.uk
• VIScotland www.ssc.education.ed.ac.uk
• CAF - Contact a Family - for families with disabled children www.cafamily.org.uk

Question 373

Which aminoglycosides are used in opthalmology?

Answer 373

Gentamicin (broad spectrum including pseudomonas).
Neomycin (in combination with steroid drops).
Tobramycin.

Question 374

Treatment of chlamydial infections?

Answer 374

Azithromycin (trachoma).

Question 375

Treatment of Acanthamoeba infections?

Answer 375

Propamidine isethionate.
Chlorhexidine (specialist formulation).
Polyhexamethylene biguanide (PHMB) (specialist formulation).

Question 376

Treatment of viral infections?

Answer 376

Aciclovir.
Ganciclovir (topical and slow release implants available to treat CMV retinitis).
Trifluorothymidine (specialist formulation).

Question 377

Treatment of fungal infections?

Answer 377

(Specialist formulation of drops is required.)

Pimaricin (natamycin) 5%.

Question 378

Non-steroidal anti-inflammatory preparations?

Answer 378

Bromfenac.
Diclofenac.
Flurbiprofen sodium.
Ketorolac trometamol.

Question 379

Steroid preparations?

Answer 379

Betamethasone (also available combined with an antibiotic).
Dexamethasone (also available combined with an antibiotic).
Fluorometholone.
Loteprednol etabonate.
Prednisolone.
Rimexolone.

Intravitreal preparations (dexamethasone, fluocinolone acetonide) are available to treat macular oedema associated with diabetes and retinal vein occlusion.

Question 380

Mast cell stabilizers?

Answer 380

Lodoxamide.
Nedocromil.
Olopatadine (also antihistamine).
Sodium cromoglycate.

Question 381

Antihistamines?

Answer 381

Antazoline.
Azelastine.
Epinastine.
Ketotifen.
Levocabastine.
Olopatadine (also mast cell stabilizer).

Question 382

Mucolytics?

Answer 382

Acetlycysteine.

Question 383

Antimuscarinics?

Answer 383

Atropine.
Cyclopentolate hydrochloride (routinely used for therapeutic pupillary dilation). Homatropine hydrobromide.
Tropicamide (routinely used for diagnostic pupillary dilation).

Question 384

Sympathomimetics

Answer 384

Phenylephrine hydrochloride.

Question 385

Beta receptor antagonists?

Answer 385

Betaxolol.
Carteolol.
Levobunolol.
Timolol.

Question 386

Prostaglandin analogues?

Answer 386

Bimatoprost (synthetic prostamide).
Latanoprost.
Tafluprost.
Travoprost.

Question 387

Sympathomimetics?

Answer 387

Brimonidine tartrate.
Apraclonidine.

Question 388

Carbonic anhydrase inhibitors?

Answer 388

Brinzolamide.
Dorzolamide.
(Systemically, acetazolamide is used to treat acute elevation of intraocular pressure.)

Question 389

Miotics?

Answer 389

Pilocarpine.

Question 390

Local anaesthetics?

Answer 390

Lidocaine hydrochloride.
Oxybuprocaine hydrochloride.
Proxymetacaine hydrochloride (causes less stinging on initial application).
Tetracaine hydrochloride.

Question 391

Ocular lubricants?

Answer 391

Carbomers (polyacrylic acid).
Carmellose sodium.
Hypromellose.
Macrogols (polyethylene glycols).
Polyvinyl alcohol.
Sodium chloride 0.9%.
Sodium hyaluronate.
Eye ointments containing paraffin.

Question 392

Vascular endothelial growth factor inhibitors?

Answer 392

For the treatment of wet age-related macular degeneration, retinal vein occlusion and diabetic macular oedema.

Aflibercept.
Pegaptanib.
Ranibizumab.