Differences between conjunctival and ciliary congestion

S. no. Feature Conjunctival congestion Ciliary congestion 1. Site More marked in the fornices More marked around the limbus 2. Colour Bright red Purple or dull red 3. Arrangement of vessels Superficial and branching Deep and radiating from limbus 4. On moving conjunctiva Congested vessels also move Congested vessels do not move 5. On mechanically squeezing out Vessels fill slowly from Vessels fill rapidly from the blood vessels fornix towards limbus limbus towards fornices 6. Blanching, i.e., on putting one Vessels immediately blanch Do not blanch drop of 1 in 10000 adrenaline 7. Common causes Acute conjunctivitis Acute iridocyclitis, keratitis (corneal ulcer)

Ocular Manifestations Of 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, Descemets 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 fibre- vascular 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

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 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 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 (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. 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 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 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.

PUPILLARY REFLEXES AND THEIR ABNORMALITIES

PUPILLARY REFLEXES Light reflex When light is shone in one eye, both the pupils constrict. Constriction of the pupil to which light is shone is called direct light reflex and that of the other pupil is called consensual (indirect) light reflex. Light reflex is initiated by rods and cones. Pathway of light reflex (Fig. 12.6). The afferent fibres extend from retina to the pretectal nucleus in the midbrain. These travel along the optic nerve to the optic chiasma where fibres from the nasal retina decussate and travel along the opposite optic tract to terminate in the contralateral pretectal nucleus. While the fibres from the temporal retina remain uncrossed and travel along the optic tract of the same side to terminate in the ipsilateral pretectal nucleus. Internuncial fibres connect each pretectal nucleus with Edinger-Westphal nuclei of both sides. This connection forms the basis of consensual light reflex. Efferent pathway consists of the parasympathetic fibres which arise from the Edinger-Westphal nucleus in the mid-brain and travel along the third (oculomotor) cranial nerve. The preganglionic fibres

enter the inferior division of the third nerve and via the nerve to the inferior oblique reach the ciliary ganglion to relay. Post-ganglionic fibres travel along the short ciliary nerves to innervate the sphincter pupillae. Near reflex Near reflex occurs on looking at a near object. It consists of two components: (a) convergence reflex, i.e., contraction of pupil on convergence; and (b) accommodation reflex, i.e., contraction of pupil associated with accommodation. Pathway of convergence reflex (Fig. 12.7). Its afferent pathway is still not elucidated. It is assumed that the afferents from the medial recti travel centrally via the third nerve to the mesencephalic nucleus of the fifth nerve, to a presumptive convergence centre in the tectal or pretectal region. From this the impulse is relayed to the Edinger-Westphal nucleus and the subsequent efferent pathway of near reflex is along the 3rd nerve. The efferent fibres relay in the accessory ganglion before reaching the sphincter pupillae. Pathway of accommodation reflex (Fig. 12.7). The afferent impulses extend from the retina to the parastriate cortex via the optic nerve, chiasma, optic tract, lateral geniculate body, optic radiations, and striate cortex. From the parastriate cortex the impulses are relayed to the Edinger- Westphal nucleus of both sides via the occipito-mesencephalic tract and the pontine centre. From the Edinger-Westphal nucleus the efferent impulses travel along the 3rd nerve and reach the sphincter pupillae and ciliary muscle after relaying in the accessory and ciliary ganglions. Psychosensory reflex It refers to dilatation of the pupil in response to sensory and psychic stimuli. It is very complex and its mechanism is still not elucidated. ABNORMALITIES OF PUPILLARY REACTIONS 1. Amaurotic light reflex. It refers to the absence of direct light reflex on the affected side (say right eye) and absence of consensual light reflex on the normal side (i.e., left eye). This indicates lesions of the optic nerve or retina on the affected side (i.e., right eye), leading to complete blindness. In diffuse illumination both pupils are of equal size. 2. Efferent pathway defect. Absence of both direct and consensual light reflex on the affected side (say right eye) and presence of both direct and consensual light reflex on the normal side (i.e., left eye) indicates efferent pathway defect (sphincter paralysis). Near reflex is also absent on the affected side. Its causes include: effect of parasympatholytic drugs (e.g., atropine, homatropine), internal ophthalmoplegia, and third nerve paralysis. 3. Wernickes hemianopic pupil. It indicates lesion of the optic tract. In this condition light reflex (ipsilateral direct and contralateral consensual) is absent when light is thrown on the temporal half of

the retina of the affected side and nasal half of the opposite side; while it is present when the light is thrown on the nasal half of the affected side and temporal half of the opposite side. 4. Marcus Gunn pupil. It is the paradoxical response of a pupil of light in the presence of a relative afferent pathway defect (RAPD). It is tested by swinging flash light test. For details see page 474. 5. Argyll Robertson pupil (ARP) . Here the pupil is slightly small in size and reaction to near reflex is present but light reflex is absent, i.e., there is light near dissociation (to remember, the acronym ARP may stand for accommodation reflex present). Both pupils are involved and dilate poorly with mydriatics. It is caused by a lesion (usually neurosyphilis) in the region of tectum. 6. The Adies tonic pupil. In this condition reaction to light is absent and to near reflex is very slow and tonic. The affected pupil is larger (anisocoria). Its exact cause is not known. It is usually unilateral, associated with absent knee jerk and occurs more often in young women. Adies pupil constricts with weak pilocarpine (0.125%) drops, while normal pupil does not.