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OCULAR MANIFESTATIONS OFSYSTEMIC DISEASES

INTRODUCTION

Ocular involvement in systemic disorders is quitefrequent. 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 NUTRITIONALDEFICIENCES

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:

SystemicOphthalmology

OCULAR MANIFESTATIONS OFSYSTEMIC DISEASES

Introduction

Nutritional deficiences

Xerophthalmia

Systemic infections Metabolic disorders

Disorders of skin and mucousmembranes

Haematological diseases

OCULAR ABNORMALITIES IN TRISOMIES

ADVERSE OCULAR EFFECTS OFCOMMON SYSTEMIC DRUGS

1919191919CHAPTER


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434 ComprehensiveOPHTHALMOLOGY

XN Night blindness

X1A Conjunctival xerosis

X1B Bitots spots

X2 Corneal xerosis

X3A Corneal ulceration/keratomalacia affecting

less than one-third corneal surface

X3B Corneal ulceration/keratomalacia affecting

more than one-third corneal surface.

XS Corneal scar due to xerophthalmia

XF Xerophthalmic fundus.

Clinical features

1.X N (night blindness). It is the earliest symptom ofxerophthalmia 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.

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/keratomala-

cia),Stromal defects occur in the late stage due to

colliquative necrosis and take several forms. Small

ulcers (1-3 mm) occur peripherally; they arecharacteristically 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 (Bitots spots). It is an extension of the xerotic

process seen in stage X1A. The Bitots 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. 19.2. Xerophthalmia, stage XIB: Bitot spots.

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


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SYSTEMIC OPHTHALMOLOGY 435

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).

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

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

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

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

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.


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436 ComprehensiveOPHTHALMOLOGY

iii. Women of reproductive age, pregnant or not: (a)

Those having night blindness (XN), conjunctival

xerosis (X1A) and Bitots 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 conditionssuch as PEM

and other nutritional disorders, diarrhoea,

dehydration and electrolyte imbalance, infections and

parasitic conditions should be consideredsimultaneously.

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:

i. Infants 6-12 100,000 IU orally every

months old and 3-6 months.

any older children

who weigh less

than 8 kg.ii. Children over 200,000 IU orally every

1 year and under 6 months.

6 years of age

iii. Lactating 20,000 IU orally once at

mothers delivery or during the next

2 months. This will raise

the concentration of vitamin

A in the breast milk and

therefore, help to protect

the breastfed infant.

iv. Infants less 50,000 IU orally should

than 6 months be given before they

old, not being attain the age of 6breastfed. months.

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 vitamin A.

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 drum- sticks (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 isa combination of all the three methods with a gradual

weaning away of the short-term approach.

OCULAR MANIFESTATIONS OF SYSTEMICINFECTIONS

A. VIRAL INFECTIONS

Measles.Ocular lesions are: catarrhal conjunctivitis,

Kopliks spots on conjunctiva, corneal ulceration,

optic neuritis and retinitis.

Mumps. Ocular involvement may occur asconjunctivitis, keratitis, acute dacryoadenitis and

uveitis.

Rubella. Ocular lesions seen in rubella (Germanmeasles) 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.

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