Ординатура / Офтальмология / Английские материалы / Comprehensive Ophthalmology_Khurana_2007

Preparations

1.Methylcellulose. It is the most commonly used substance. It is only a viscous and not a viscoelastic substance. Its active ingredient is highly purified 2% hydroxypropyl methylcellulose.

2.Sodium hyaluronate (1%) (Healon). Being extremely viscoelastic and non-inflammatory, it is thebestavailableviscoelasticsubstance.However, being expensive, it is less popular than methylcellulose.

3.Hypromellose (2%). It is a viscous substance similar to methylcellulose.

4.Chondroitin sulfate (20% and 50%). It is a viscoelastic substance similar to sodium hyaluronate. It is also available as 1:3 mixture of 4% chondroitin sulfate and 3% sodium hyaluronate (Viscoat) and in combination with methylcellulose (Ocugel).

Alternatives to viscoelastic substances

Substances used as alternative to viscoelastics for maintenance of anterior chamber are air, serum and other blood products and balanced salt solution. However, none of these match the properties of viscoelastic substances.

Clinical uses

1.Cataract surgery with or without IOL implantation. It is the most important indication. Here the viscoelastic substance is used for:

i.Maintenance of anterior chamber;

ii.Protection of corneal endothelium;

iii.Coating the IOL

iv.Preventing the entry of blood and fluid in the anterior chamber.

2.Other uses. Viscoelastic substances are also useful in glaucoma surgery, keratoplasty, retinal detachment surgery and repair of the globe in perforating injuries.

Side-effects

Post-operative rise in intraocular pressure may occur if a considerable amount of viscoelastic substance is left inside the anterior chamber; so it must be washed off after surgery.

VITREOUS SUBSTITUTES

See page 247.

LASERS IN OPHTHALMOLOGY

The word LASER is an acronym for ‘Light Amplification by Stimulated Emission of Radiation’. Laser light is characterised by monochromaticity, coherence and collimation. These properties make it the brightest existing light.

PRODUCTION OF LASER BEAM

In the laser system atomic environments of various types are stimulated to produce laser light. A laser system consists of a transparent crystal rod or a gas or liquid filled cavity constructed with a fully reflective mirror at one end and a partially reflective mirror at the other. Surrounding the rod or cavity is an optical or electrical source of energy that will raise the energy level of the atoms within the cavity or rod to a high and unstable level. This phenomenon is called population inversion. From this level, the atoms spontaneously decay back to a lower energy level, releasing the excess energy in the form of light which is amplified to an appropriate wavelength. Thus, laser is created mainly by two means: population inversion in active medium and amplification of appropriate wavelength of light.

TYPES OF LASERS

There are various types of lasers depending upon the type of atomic environment stimulated to produce the laser beam. Common types of lasers are depicted in Table 18.3.

Table 18.3. Lasers used in ophthalmology

MECHANISMS OF LASER EFFECTS AND THEIR THERAPEUTIC APPLICATIONS

1. Photocoagulation. The principal lasers used in ophthalmic therapy are the thermal lasers, which depend upon absorption of the laser light by tissue pigments. The absorbed light is converted into heat, thus raising the temperature of the target tissue high enough to coagulate and denature cellular elements. Argon, diode, krypton and diode pump frequency doubled Nd-YAG lasers are based on this mechanism.

Modes of action. Photocoagulation is effective in treating ocular diseases by production of a scar, occlusion of vessels, tissue atrophy, and tissue contraction.

Therapeutic applications based on photocoagulation are as follows:

1.Eyelid lesions such as haemangioma.

2.Corneal conditions e.g., reduction of postoperative astigmatism from cataract sutures— by Argon laser suturotomy and treatment of corneal neovascularisation.

3.Laser for glaucoma. Procedures employed include laser iridotomy for narrow-angle glaucoma, argon laser trabeculoplasty (ALT) for open-angle glaucoma, laser goniopunctures for developmental glaucoma, prophylactic pan-retinal photocoagulation to prevent neovascular glaucoma in patients with retinal hypoxic states (e.g., central retinal vein occlusion) and cyclophotocoagulation for absolute or near absolute glaucoma.

4.Lesions of iris. These include laser coreoplasty for updrawn pupil, photomydriasis for pathologic miotic pupil, laser sphincterotomy and laser shrinkage of iris cyst.

5.Lesions of retina and choroid. These form the most important indications. Common conditions are:

Diabetic retinopathy in which pan-retinal photocoagulation (PRP) is carried out for proliferative retinopathy and focal or gridphotocoagulation for exudative maculopathy.

Peripheral retinal vascular abnormalities such as Eales’ disease, proliferative sickle cell disease, Coats’ disease and retinopathy of prematurity.

Intraocular tumours such as retinoblastoma, malignant melanoma and choroidal haemangioma.

Macular diseases, such as central serous retinopathy, and age-related macular degeneration (ARMD).

For sealing of holes in retinal detachment.

Complications of laser photocoagulation. These include: accidental foveal burns, macular oedema and macular pucker, pre-retinal fibrosis, haemorrhage from retina and choroid, retinal hole formation, ischaemic papillitis, localised opacification of lens and accidental corneal burns.

2. Photodisruption. Laser based on this mechanism ionize the electrons of the target tissue producing a physical state called plasma. This plasma expands with momentary pressures as high as 10 kilobars, exerting a cutting/incising effect upon the tissues. Nd:YAG laser is based on this mechanism.

Therapeutic applications of Nd:YAG laser include capsulotomy for thickened posterior capsule and membranectomy for pupillary membranes. Recently it has also been tried for phacolysis (laser phaco surgery) in phacoemulsification technique of cataract extraction.

3. Photoablation. Lasers based on this mechanism produce UV light of very short wavelength which breaks chemical bonds of biologic materials, converting them into small molecules that diffuse away. These lasers are collectively called excimer (excited dimer) lasers. These act by tissue modelling.

Therapeutic applications of excimer lasers are: photorefractive keratectomy (PRK), laser assisted insitu keratomileusis (LASIK) for correction of refractive errors and phototherapeutic keratectomy (PTK) for corneal diseases such as band-shaped keratopathy.

CRYOTHERAPY IN

OPHTHALMOLOGY

Cryopexy means to produce tissue injury by application of intense cold (–40o C to –100o C). This is achieved by a cryoprobe from a cryo-unit (Fig. 18.1).

Principle.Working of cryoprobes is based on the Joule Thompson principle of cooling.

Cryounit and probe. The cryounit uses freon, nitrous oxide or carbon dioxide gas as cooling agent. Cryoprobes are available in different sizes such as, 1

Fig. 18.1. Cryoprobes : A and B, for cataract extractionstraight and curved, respeativaly; C, for cyclocryopexy; and D, internal structure

mm for intravitreal use, 1.5 mm straight or curved probe for cataract extraction, 2.5 mm for retina and 4 mm for cyclocryopexy (Fig. 18.2). Temperature produced depends upon the size of the cryoprobe tip, duration of freezing process and the gas used.

Modes of action

Cryopexy produces the required therapeutic effect by different modes which include tissue necrosis (as in cyclocryopexy and cryopexy for tumours), production of adhesions between tissues (e.g. between retina, pigment epithelium and choroid in retinal detachment), vascular occlusions (as in Coats’ disease) and adherence of the cryoprobe to the iceball in the tissue (as in cataract extraction).

Fig. 18.2. Ophthalmic cryo unit.

Uses

1.Lids. Cryosurgery may be used for following lesions: (i) Cryolysis for trichiasis, (ii) Cryotherapy for warts and molluscum contagiosum, (iii) Cryotherapy for basal cell carcinoma and haemangioma.

2.Conjunctiva. Cryotherapy is used for hypertrophied papillae of vernal catarrh.

3.Cornea. Herpes simplex keratitis may be treated by cryotherapy.

4.Lens. Cryoextraction of the lens used to be the best intracapsular technique. However, now-a- days intracapsular cataract extraction (ICCE) is no more performed.

5.Ciliary body. Cyclocryopexy for absolute glaucoma and neovascular glaucoma.

6.Retina. (i) Cryopexy is widely used for sealing retinal holes in retinal detachment. (ii) Prophylactic cryopexy to prevent retinal detachment in certain prone cases. (iii) Anterior retinal cryopexy (ARC) in retinal ischaemic disease e.g., retinopathy of primaturty to prevent neovascularization. (iv) Cryotreatment of retinoblastoma and angioma.

OCULAR MANIFESTATIONS OF SYSTEMIC DISEASES

Introduction

Nutritional deficiences

– Xerophthalmia

Systemic infections

Metabolic disorders

Disorders of skin and mucous membranes

Haematological diseases

OCULAR ABNORMALITIES IN TRISOMIES

ADVERSE OCULAR EFFECTS OF COMMON SYSTEMIC DRUGS

OCULAR MANIFESTATIONS OF

SYSTEMIC DISEASES

INTRODUCTION

Ocular involvement in systemic disorders is quite frequent. It is imperative for the ophthalmologists as well as physicians to be well conversant with these. Many a time, the ocular manifestations may be the presenting signs and the ophthalmologist will refer the patient to the concerned specialist for diagnosis and/or management of the systemic disease. While, in other cases the opinion for ocular involvement may be sought for by the physician who knows to look for it.

Ocular lesions of the common systemic disorders are enumerated and a few important ones are described here.

OCULAR MANIFESTATIONS OF NUTRITIONAL DEFICIENCES

1.Deficiency of vitamin A. Ocular manifestations of vitamin A deficiency are referred to as xerophthalmia.

2.Deficiency of vitamin B1 (thiamine). It can cause corneal anaesthesia, conjunctival and corneal dystrophy and acute retrobulbar neuritis.

3.Deficiency of vitamin B2 (riboflavin). It can produce photophobia and burning sensation in

the eyes due to conjunctival irritation and vascularisation of the cornea.

4.Deficiency of vitamin C. It may be associated with haemorrhages in the conjunctiva, lids, anterior chamber, retina and orbit. It also delays wound healing.

5.Deficiency of vitamin D. It may be associated with zonular cataract, papilloedema and increased lacrimation.

XEROPHTHALMIA

They term xerophthalmia is now reserved (by a joint WHO and USAID Committee, 1976) to cover all the ocular manifestations of vitamin A deficiency, including not only the structural changes affecting the conjunctiva, cornea and occasionally retina, but also the biophysical disorders of retinal rods and cones functions.

Etiology

It occurs either due to dietary deficiency of vitamin A or its defective absorption from the gut. It has long been recognised that vitamin A deficiency does not occur as an isolated problem but is almost invariably accompanied by protein-energy malnutrition (PEM) and infections.

WHO classification (1982)

The new xerophthalmia classification (modification of original 1976 classification) is as follows:

Clinical features

1.X N (night blindness). It is the earliest symptom of xerophthalmia in children. It has to be elicited by taking detailed history from the guardian or relative.

2.X1A (conjunctival xerosis). It consists of one or more patches of dry, lustreless, nonwettable conjunctiva (Fig. 19.1), which has been well described as ‘emerging like sand banks at receding tide’ when the child ceases to cry. These patches almost always involve the inter-palpebral area of the temporal quadrants and often the nasal quadrants as well. In more advanced cases, the entire bulbar conjunctiva may be affected. Typical xerosis may be associated with conjunctival thickening, wrinkling and pigmentation.

Fig. 19.2. Xerophthalmia, stage XIB: Bitot spots.

4.X2 (corneal xerosis). The earliest change in the cornea is punctate keratopathy which begins in the lower nasal quadrant, followed by haziness and/or granular pebbly dryness (Fig. 19.3). Involved cornea lacks lustre.

5.X3A and X3B (corneal ulceration/keratomalacia), Stromal defects occur in the late stage due to colliquative necrosis and take several forms. Small ulcers (1-3 mm) occur peripherally; they are characteristically circular, with steep margins and are sharply demarcated (Fig. 19.4). Large ulcers and areas of necrosis may extend centrally or involve the entire cornea. If appropriate therapy is instituted immediately, stromal defects involving less than one-third of corneal surface (X3A) usually heal, leaving some useful vision. However, larger stromal defects (X3B) (Fig. 19.5) commonly result in blindness.

Fig. 19.1. Xerophthalmia, stage XIA: Conjunctival xerosis.

3. X1B (Bitot’s spots). It is an extension of the xerotic process seen in stage X1A. The Bitot’s spot is a raised, silvery white, foamy, triangular patch of keratinised epithelium, situated on the bulbar conjunctiva in the inter-palpebral area (Fig. 19.2). It is usually bilateral and temporal, and less frequently nasal.

Fig. 19.3. Xerophthalmia, stage X2: Corneal xerosis.

Fig. 19.4. Xerophthalmia, stage X3A: Keratomalacia involving less than one-third of corneal surface.

Fig. 19.5. Xerophthalmia, stage X3B: Keratomalacia involving more than one-third of corneal surface.

Fig. 19.6. Xerophthalmia, stage XS: Corneal scars.

Fig. 19.7. Xerophthalmia, stage XF: Xerophthalmic fundus.

6.XS (corneal scars). Healing of stromal defects results in corneal scars of different densities and sizes which may or may not cover the pupillary area (Fig. 19.6). A detailed history is required to ascertain the cause of corneal opacity.

7.XFC (Xerophthalmic fundus). It is characterized by typical seed-like, raised, whitish lesions scattered uniformly over the part of the fundus at the level of optic disc (Fig. 19.7).

Treatment

It includes local ocular therapy, vitamin A therapy and treatment of underlying general disease.

1. Local ocular therapy. For conjunctival xerosis artificial tears (0.7 percent hydroxypropyl methyl cellulose or 0.3 percent hypromellose) should be instilled every 3-4 hours. In the stage of keratomalacia, full-fledged treatment of bacterial corneal ulcer should be instituted (see pages 120-123).

2. Vitamin A therapy. Treatment schedules apply to all stages of active xerophthalmia viz. XN, X1A, X1B, X2, X3A and X3B. Oral administration is the recommended method of treatment. However, in the presence of repeated vomiting and severe diarrhoea, intramuscular injections of water-miscible preparation should be preferred. The WHO recommended schedule is as given below:

i.All patients above the age of 1 year (except women of reproductive age): 200,000 IU of vitamin A orally or 100,000 IU by intramuscular injection should be given immediately on diagnosis and repeated the following day and 4 weeks later.

ii.Children under the age of 1 year and children of any age who weigh less than 8 kg should be treated with half the doses for patients of more than 1 year of age.

iii.Women of reproductive age, pregnant or not: (a) Those having night blindness (XN), conjunctival xerosis (X1A) and Bitot’s spots (X1B) should be treated with a daily dose of 10,000 IU of vitamin A orally (1 sugar coated tablet) for 2 weeks.

(b) For corneal xerophthalmia, administration of full dosage schedule (described for patients above

1 year of age) is recommended.

3. Treatment of underlying conditions such as PEM and other nutritional disorders, diarrhoea, dehydration and electrolyte imbalance, infections and parasitic conditions should be considered simultaneously.

Prophylaxis against xerophthalmia

The three major known intervention strategies for the prevention and control of vitamin A deficiency are:

1. Short-term approach. It comprises periodic administration of vitamin A supplements. WHO recommended, universal distribution schedule of vitamin A for prevention is as follows:

A revised schedule of vitamin A supplements being followed in India since August 1992, under the programme named as ‘Child Survival and Safe Motherhood (CSSM)’ is as follows:

First dose (1 lakh I.U.)—at 9 months of age along with measles vaccine.

Second dose (2 lakh I.U.)—at 18 months of age along with booster dose of DPT/OPV.

Third dose (2 lakh I.U.)—at 2 years of age.

2.Medium-term approach. It includes food fortification with vitaminA.

3.Long-term approach. It should be the ultimate aim. It implies promotion of adequate intake of vitamin A rich foods such as green leafy vegetables, papaya and drumsticks (Fig. 19.8). Nutritional health education should be included in the curriculum of school children.

Fig. 19.8. Rich sources of vitamin A.

Note. The short-term approach has been mostly in vogue especially in Asia. The best option perhaps is a combination of all the three methods with a gradual weaning away of the short-term approach.

OCULAR MANIFESTATIONS OF SYSTEMIC INFECTIONS

A. VIRAL INFECTIONS

Measles. Ocular lesions are: catarrhal conjunctivitis, Koplik’s spots on conjunctiva, corneal ulceration, optic neuritis and retinitis.

Mumps. Ocular involvement may occur as conjunctivitis, keratitis, acute dacryoadenitis and uveitis.

Rubella. Ocular lesions seen in rubella (German measles) are congenital microphthalmos, cataract, glaucoma, chorioretinitis and optic atrophy.

Whooping cough. There may occur subconjunctival haemorrhages and rarely orbital haemorrhage leading to proptosis.

Ocular involvement in AIDS

AIDS (Acquired Immune Deficiency Syndrome) is caused by Human immunodeficiency virus (HIV) which is an RNA retrovirus.

Modes of spread include:

Sexual intercourse with an infected person,

Use of infected hypodermic needles,

Transfusion of infected blood and

Transplacental spread to foetus from the infected mothers.

Pathogenesis of AIDS. The HIV infects T-cells, T- helper cells, macrophages and B-cells and thus interferes with the mechanism of production of immune bodies thereby causing immunodeficiency.

Immune deficiency renders the individuals prone to various infections and tumours, which involve multiple systems and finally cause death.

Ocular manifestations. These occur in about 75 percent of patients and sometimes may be the presenting features of AIDS in an otherwise healthy person or the patient may be a known case of AIDS when his eye problems occur. Ocular lesions ofAIDS may be classified as follows:

1. Retinal microvasculopathy. It develops from vaso-occlusive process which may be either due to direct toxic effects of virus on the vascular endothelium or immune complex deposits in the precapillary arterioles.

It is characterised by non-specific lesions (Fig. 19.9):

Multiple ‘cotton-wool spots’ occur in 50 percent cases,

Superficial and deep retinal hemorrhages occur in 15-40 percent cases.

Microaneurysms and telangiectasia may also be seen rarely.

Fig. 19.9. Retinopathy in AIDS.

2. Usual ocular infections. These are also seen in healthy people, but occur with greater frequency and produce more severe infections in patients withAIDS. These include:

Herpes zoster ophthalmicus,

Herpes simplex infections,

Toxoplasmosis (chorioretinitis),

Ocular tuberculosis, syphilis and fungal corneal ulcers.

3.Opportunistic infections of the eye. These are caused by microorganisms which do not affect normal patients. They can infect someone whose cellular immunity is suppressed by HIV infection or by other causes such as leukaemia. These include: cytomegalovirus (CMV) retinitis (see page 253 Fig 11.5), candida endophthalmitis, cryptococcal infections and pneumocystis carini, choroiditis.

4.Unusual neoplasms. Kaposi’s sarcoma is a malignant vascular tumour which may appear on the eyelid or conjunctiva as multiple nodules. It is seen in about 3 percent cases of AIDS. Burkitt’s lymphoma of the orbit is also seen in a few patients.

5.Neuro-ophthalmic lesions. These are thought to be due to CMV or other infections of the brain. These include isolated or multiple cranial nerve palsies resulting in paralysis of eyelids, extraocular muscles, loss of sensory supply to the eye and optic nerve involvement causing loss of vision.

Management. It consists of the measures directed against the associated infection/lesions. For example:

CMV infections can be treated by zidovudine, gancyclovir and foscarnet (see page 422).

Kaposi’s sarcoma responds to radiotherapy.

Horpes zoster ophthalmicus, is treated by acyclovir.

B. BACTERIAL INFECTIONS

1.Septicaemia. Ocular involvement may occur in the form of metastatic retinitis, uveitis or endophthalmitis.

2.Diphtheria. There may occur: membranous conjunctivitis, corneal ulceration, paralysis of accommodation and paralysis of extraocular muscles.

3.Brucellosis. It may involve the eye in the form of iritis, choroiditis and optic neuritis.

4.Gonococcal ocular lesions are: ophthalmia neonatorum, acute purulent conjunctivitis in adults and corneal ulceration.

5.Meningococcal infection may be associated with: metastatic conjunctivitis, corneal ulceration, paresis of extraocular muscles, optic neuritis and metastatic endophthalmitis or panophthalmitis.

6.Typhoid fever. It may be complicated by optic neuritis and corneal ulceration due to lagophthalmos.

7.Tuberculosis. Ocular lesions seen are granulomatous conjunctivitis, phlyctenular keratoconjunctivitis, interstitial keratitis, nongranulomatous and granulomatous uveitis, Eales’ disease, optic atrophy (following chiasmal arachnoiditis secondary to meningitis), and papilloedema (due to raised intracranial pressure following intracranial tuberculoma).

8.Syphilitic lesions (acquired) seen in primary stage are conjunctivitis and chancre of conjunctiva. In secondary stage there may occur iridocyclitis. Tertiary stage lesions include chorioretinitis and gummata in the orbit. Neurosyphilis is associated with optic atrophy and pupillary abnormalities. Ocular lesions of congenital syphilis are: interstitial keratitis, iridocyclitis and chorioretinitis.

9.Leprosy. Ocular lesions of leprosy include cutaneous nodules on the eyelids, madarosis, interstitial keratitis, exposure keratitis, granulomatous uveitis and dacryocystitis.

C. PARASITIC INFECTIONS

1.Toxoplasmosis is known to produce necrotising chorioretinitis (see page 157).

2.Taenia echinococcus infestation may manifest as hydatid cyst of the orbit, vitreous and retina.

3.Taenia solium infestation. Cysticercus cysts are known to involve conjunctiva, vitreous, retina, orbit and extra-ocular muscles.

4.Toxocara infestation may be associated with endophthalmitis (see page 158).

5.Onchocerciasis is a common cause of blindness in African countries. Its ocular features include sclerosing keratitis, uveitis, chorioretinitis and optic neuritis invariably ending in optic atrophy.

D. FUNGAL INFECTIONS

OCULAR MANIFESTATIONS OF COMMON ENDOCRINAL AND METABOLIC DISORDERS

Gout

Ocular lesions of gout include:

Episcleritis,

Scleritis, and

Uveitis.

Diabetes mellitus

Ocular involvement in diabetes is very common. Structure-wise ocular lesions are as follows:

1.Lids. Xanthelasma and recurrent stye or internal hordeolum

2.Conjunctiva. Telangiectasia, sludging of the blood in conjunctival vessels and subcon-junctival haemorrhage

3.Cornea. Pigment dispersal at back of cornea, decreased corneal sensations (due to trigeminal neuropathy), punctate kerotapathy, Descemet’s folds, higher incidence of infective corneal ulcers and delayed epithelial healing due to abnormality in epithelial basement membrane

4.Iris. Rubeosis iridis (neovascularization)

5.Lens. Snow-flake cataract in patients with IDDM, posterior subcapsular cataract, early onset and early maturation of senile cataract

6.Vitreous. Vitreous haemorrhage and fibrevascular proliferation secondary to diabetic retinopathy

7.Retina. Diabetic retinopathy and lipaemia retinalis (see page 259).

8.Intraocular pressure. Increased incidence of POAG, neovascular glaucoma and hypotony in diabetic ketoacidosis (due to increased plasma bicarbonate levels)

9.Optic nerve. Optic neuritis

10.Extraocular muscles. Ophthalmoplegia due to diabetic neuropathy

11.Changes in refraction. Hypermetropic shift in hypoglycemia, myopic shift in hyperglycemia and decreased accommodation

Galactosemia

It is usually associated with congenital cataract (page 181).

Homocystinuria

Systemic fungal infections may be associated with corneal ulceration and endophthalmitis.

It is associated with bilateral subluxation of lens (page 202).

Mucopoly saccharidosis

Ocular lesions include:

Corneal opacification,

Pigmentary retinopathy,

Glaucoma, and

Optic atrophy

Hyperthyroidism

Ocular lesions include:

Thyroid ophthalmopathy (see page 390)

Superior limbic keratoconjunctivitis (page 111), and

Optic disc oedema

Hypoparathyroidism

Ocular lesions include:

Fasciculation

Cataract and

Optic disc oedema

Wilson disease

Ocular lesions include:

Kayser - Fleisher ring

Sunflower cataract

OCULAR MANIFESTATIONS OF COMMON DISORDERS OF SKIN AND MUCOUS MEMBRANES

1.Atopic dermatitis. It may be associated with conjunctivitis, keratoconus and cataract.

2.Rosacea. Its ocular lesions include blepharitis, conjunctivitis, keratitis and rosacea pannus.

3.Dermatitis herpetiformis. Its ocular complications include recurrent bullae, ulceration and cicatrization.

4.Epidermolysis bullosa. Ocular complications, when they occur, take the form of cicatrizing conjunctivitis and keratitis.

5.Stevens-Johnson syndrome. Stevens-Johson syndrome is an acute illness often caused by hypersensitivity to drugs, particularly sulphonamides. It is characterized by acute ulceration of the conjunctiva and other mucous membranes like that of mouth and vagina. Conjunctival ulceration is followed by cicatrizing conjunctivitis. The clinical picture at this stage is the same as in ocular pemphigoid.

OCULAR MANIFESTATIONS OF

HAEMATOLOGICAL DISEASES

1.Anaemias. Anaemic retinopathy may occur in severe anaemia of any etiology (see page 264).

2.Leukaemias. Ocular involvement in leukaemias may occur in the form of:

Proptosis due to leukaemic deposits in the orbital

tissue.

Leukaemic retinopathy is of common occurrence in lymphocytic as well as myeloid leukaemias

(see page 264).

3.Sickle cell disease. Ocular involvement may occur

as:

Dilated conjunctival vessels and

Sickle cell retinopathy (see page 264)

4.Lymphomas may cause following ocular lesions:Lid and/or orbital deposits, and

Uveitis

OCULAR ABNORMALITIES IN

TRISOMIES

Trisomy 13 (D Trisomy or Patau Syndrome)

Microphthalmos

Colobomas (almost 100%)

Retinal dysplasia

Cataract

Corneal opacities

Optic nerve hypoplasia

Cyclopia

Intra-ocular cartilage

Trisomy 18 (E trisomy or Edwards syndrome)

Blepharophimosis

Ptosis

Epicanthal fold

Hypertelorism

Microphthalmos

Uveal coloboma

Congenital glaucoma

Corneal opacities

Trisomy 21 (G Trisomy or Down’s syndrome)

Upward slanting palpebral fissure (Mongoloid slant)

Almond-shaped palpebral fissure

Epicanthus