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:
XN Night blindness
X1A Conjunctival xerosis
X1B Bitot’s 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 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.
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.
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.
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:
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 6
breastfed. 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.