Ординатура / Офтальмология / Английские материалы / Pediatric Opthalmology_Mukherjee_2005

Simple anisometropia. In this condition one eye is emmetropic, the other eye is either myopic or hypermetropic.

Compound anisometropia. Both eyes have same type of error of refraction i.e. myopia or hypermetropia but power in one eye is more than the other.

Mixed anisometropia or Anti metropia. In this, one eye is myopic, the other eye is hypermetropic.

In simple astigmatic anisometropia one eye is emmetropic, the other has simple astigmatism.

In compound astigmatic anisometropia both the eyes are astigmatic but at different degree.

In mixed astigmatic anisometropia one eye has myopic astigmatism, the other eye has hypermetropic astigmatism.

Symptoms of anisometropia. Symptoms of anisometropia depends upon difference between the refractive status in two eyes.

Visual :

1.Binocular single vision. This is present when the difference between the two eyes is not more than 2.5D to 3.0D.

2.Uniocular vision. This happens when the difference in power in two eyes exceeds 4D. Generally one of the eye is emmetropic or has less power than the fellow eye. The eye with higher power is generally suppressed, develops and becomes amblyopic and starts squinting.

3.Alternate vision. This happens when one eye is either emmetropic or has low error of refraction and the other eye has myopia more than 2D. The patient uses the myopic eye for near vision and the other eye for distant vision. These patients may not know about their visual short coming and are comfortable. They do not seek optical aid. Such children are diagnosed on routine school survey or if they wish to join some project that requires binocular vision.

Muscle imbalance. The child may be brought with squint and discovered to have anisometropia and many a times amblyopia. Anisometropia may cause both eso or exodeviation but concomitant convergent squint is more common.

Diagnosis. Diagnosis of anisometropia is simple by doing retinoscopy which should be done under complete cycloplegia. Otherwise, it can be done by Friend test or Worth four dot test.

The Friend test. This is a simple test. It consists of a panel generally incorporated at the bottom of usual Snellen’s drum. In the chart the letter FIN are written in green and RED are written in red. The size of all the letters are same. The background is illuminated. The size of the letters correspond to size of 6/18 or 6/12. The child sits at a distance of six metres with red green glasses in the trial set or may wear a diplopi goggles. The red glass is kept in front of right eye as convention and not for any clinical significance. The child is asked to read the line

Causes of aniseikenia are

1.Optical. This is the comonest and most easily diagnosed type of aniseikonia where due to high anisometropia, images of two different sizes are formed on the retina and presented as such to the cortex. This can be congenital or acquired. The acquired cause consist of difference in power, thickness of the lens and cylinders in the lens of the spectacle prescribed.

2.Retinal

1.Shift of the retinal element towards the nodal point.

2.Separation of retinal element due to edema of the retina.

Clinical types of aniseikonia

1.Aniseikonia is said to be symmetrical when there is difference in size of the two images. The difference can be overall i.e. in all meridians or meridinal when the difference is greater in one meridian and compound when both types i.e. overall and meridinal are present.

2.Asymmetrical when there is difference in shape of the two images. It could be regular, pin cushion, barrel type or irregular. In regular type, there is progressive increase or decrease in size across the field.

Symptoms of aniseikonia vary from patient to patient. Some of the patients may not be able to express the correct symptom except diplopia. Other symptoms are asthenopia. In some patients there may be faulty stereopsis. There may be disturbances of spatial orientation in the form of objects on right side of the field looking farther away than objects of same size and distance on the left side. A flat surface slants down on the right side and up on the left. The square appears rectangular and circles seem to be elliptical.

Diagnosis. Diagnosis of aniseikonia is difficult, however, a rough estimate can be made on the basis of anisometropia present, 1% change in size per dioptre is most accepted estimate.

Treatment. Optical causes of aniseikonia are best treated by contact lens. Best treatment for unilateral aphakia is IOL implant either as primary procedure or secondary procedure.

Treatment of retinal aniseikonia is directed towards treatment of retinal condition mostly medically.

Asthenopia

Asthenopia is one of common symptoms, which the patient may not be able to express precisely. It is defined as uncomfortable vision that may cause unexplained pain and irritation in the eyes, fatigue, after near-work, heaviness of lids, sleepy feeling.

Causes of asthenopia include

1.Refractive error.

2.Muscle imbalance

3.Accommodation and convergence insufficiency.

Errors of refraction. Uncorrected errors of refraction are commonest cause of asthenopia. High errors of refraction rarely cause asthenopia because the child is resigned to blurred vision and does not try to get a clear vision. Smaller errors of refraction cause more asthenopia. Astigmatic eyes are more likely to develop asthenopia than spherical errors. Horizontal axis and oblique axises cause more trouble than other meridians. Under corrected or over corrected errors are more likely to cause asthenopia. In myopia asthenopia develops more for near work because myope requires more convergence for clear view without or with least accommodation. The child has to depend on increased fusional convergence. Some myopic patients who had no asthenopia before correction may develop asthenopia following correction.

A hypermetropic has to use accommodation more than emmetrope for near as well as distance, putting constant strain on ciliary muscle. Hypermetropic astigmatism causes more problem because hypermetropic tries to get clear vision by accommodating, as accommodation is equal in all meridians the astigmatism is worsened in opposite meridian.

In anisometropia, the blurring of vision is unequal in two eyes and accommodation which acts equally in both eyes may worsen in one of the eyes.

Muscle imbalance. Asthenopia is more common in phorias than in tropias. The child constantly tries to keep the eye in orthophoric state and a discrepancy between amplitude of motor fusion and deviation results in asthenopia. Vertical deviations cause more asthenopia.

Accommodation convergence insufficiency. It can either be deficiency of accommodation or convergence.

Some patients with good vision with low degree of errors of refraction may be unable to accommodate without convergence.

Convergence insufficiency is seen in uncorrected myopes or hypermetropes corrected for first time. Otherwise they are orthophoric for distance.

Symptoms. The symptoms of asthenopia may be ocular or non ocular. Ocular symptoms can be visual or non visual.

The visual symptoms are intermittent. They are seen following prolonged non accustomed visual effort or general dibility. There is slight fall in vision.

Non visual symptoms are tired eyes, aching eyes and bleary eyes. The ocular pain is described variously as deep seated, boring or dull. Chronic conjunctivitis, blepharitis, styes, chalazia are common. Commonest non ocular symptom is headache. It is very common for general physicians to refer all cases of headache to ophthalmologist as asthenopia. On examination most of them may turn out to be non asthenopic. Headache in asthenopia does not follow any fixed pattern. It may be referred as browache, frontal, temporal or occipital in location. Most probable explanation for headache in asthenopia is pain referred from the ciliary body.

Management of asthenopia. Management of asthenopia is frustrating. It is directed to cause of asthenopia.

The examination that should precede management are : 1. Recording of distant and near vision.

2.Checking near point of accommodation.

3.Checking near point of convergence.

4.Assessment of muscle imbalance.

5.Refraction under cycloplegia.

Refraction should be followed by prescription of glasses that are most comfortable even with slightly reduced vision. Axis of astigmatism should be checked meticulously.

Orthoptic treatment or orthoptic exercise in the form of - adduction exercise are given for convergence insufficiency.

Prisms—Base in prisms also give good result in convergence insufficiency.

REFERENCES

1.Duke Elder S. ; Ophthalmic optics and refraction in System of ophthalmology. Vol. V, C.V. Mosby, St. Louis, 1970.

2.Duke Elder S ; The foundation in ophthalmology. System of ophthalmology. VII, Henry Kimpton, London, 1962.

3.Primrose J. ; Anomalies of refraction and accommodation in Modern Ophthalmology. Vol. III, Edited by Sorsby A. Butterworth, London, 1964.

4.Agrawal L.P. ; Principles of optics and refraction. Second edition. CBS Publishers and distributors, New Delhi, 1979.

5.Singhal N.C. ; Principles and practice of refraction and optics. JayPee Brothers, New Delhi, 1996.

6.Khurana A.K. ; Theories and practice of optics and refraction. B.I. Churchill, Livingstone, New Delhi, 2001.

7.Sharma P. ; Myopia in Essentials of ophthalmology. First edition p-21–24, Modern Publishers, New Delhi, 2000.

8.Debhorah Pavan Langston ; Refractive errors and clinical optics in Manual of ocular diagnosis and therapy. Third edition, p-361-388, Lippincot William and Wilkins, Philadelphia, 2002.

9.Khurana A.K. ; Congenital myopia in Opthalmology. Second edition, p-56, New Age International, New Delhi, 2000.

10.Agrawal L.P. ; Myopia in Essentials of Ophthalmology. First edition, p-469–473, CBS Publication, New Delhi, 2000.

11.Basak S.K. ; Myopia in Essentials of ophthalmology. Second edition, p-56–60, Current Book International, Calcutta, 1999.

12.D.S.T. Clair Roberts ; Fundus changes in myopia in Modern ophthalmology. Vol. 4, p-761–762, Edited by Sorsby A. Butterworth, London, 1964.

13.Miller S.J.H. ; Myopic choroido retinal degeneration in Parsons diseases of the eye. Seventeenth edition, p-165–166, Churchill Livingstone, London, 1984.

14.Kanski J.J. ; Myopic maculopathy in Clinical ophthalmology. Second edition, p-360, Butterworth London, 1989.

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17.Duke Elder S. ; Congenital aphakia in System of ophthalmology. Vol. III, Part I, p-688, Henry Kimpton, London, 1964.

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20.Phyllis L. Rakow ; Soft lenses and astigmatic eye in Contact lenses. First edition, p-49–61, Jay Pee Brothers, New Delhi, 1989.

21.C.Y. Khoo ; 101 Questions and answers about contact lenses. P.G. Publication, New Delhi, 1985.

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Congenital stationary night blindness. They have early onset of diminished vision that may be moderate or crippling. The children have normal field when tested in normal illumination. Their colour sense is impaired. The fundi are normal except myopic changes due to associated moderate myopia. Myopia is common accompaniment in stationary congenital night blindness. The condition does not progress much. It is bilateral.

The condition is genetic, there are three types of genetic presentation i.e. Recessive either X linked or autosomal and autosomal dominant.

Children with autosomal variety have normal vision while other two have diminished distant vision due to associated myopia. Children with diminished vision may have strabismus and or nystagmus.

The children have abnormal ERG and EOG. There is no known treatment.

Oguchis disease. This is a very rare congenital anomaly of rods, mostly seen in Japanese. It is an autosomal recessive disorder with high incidence of consanguinity. The main symptom is night blindness (nyctalopia) followed by diminished distant vision which is moderate, mostly due to myopia. The condition is non progressive.

The diagnosis lies in the fundus picture. The fundus has a yellowish gray phosphorescent sheen2 that spreads from disc to periphery. Occasionally only peripheral sheen is also met with. The choroidal vessels are not visible. It is difficult to differentiate between the retinal arteries and veins as they have almost same dark colour.

The confirmatory feature is Mizuo sign or Mizuo phenomenon that consists of reversal of fundus finding from yellowish gray sheen to normal fundus picture if the eyes are kept closed for 2 to 3 hours. Then the retina returns to its yellowish gray colour after exposure to normal light in half an hour to one hour. Colour vision is not affected. ERG shows only scotopic ‘a’ wave, ‘b’ wave is extinct, EOG is normal.

There is no known treatment.

Fundus albipunctatus5. This is a condition of congenital night blindness of autosomal recessive type. The condition is stationary in nature. There is a progressive type which is a tapeto retinal dystrophy and is called retinitis punctata albescens. Both the conditions have uniform sized white or yellow white dots scattered all over the fundus. The dot may increase in number and area but do not involve the macula. The retinal vessels are of normal size. The disc does not undergo atrophic changes that is common in true retinal dystrophies. The peripheral fields are within normal limits. The ERG results are variable. EOG is normal. There is no known treatment.

Developmental causes of night blindness. This comprises a number of conditions of diverse etiology and pathology with common features of night blindness, constricted field and fundus changes in the form of pigmentation. The condition may be localised to eyes only or may be associated with number of systemic condition.

All of them are genetically determined conditions, are most probably present at birth but clinically manifest after few years hence they are put in category of developmental disorders.

They are all abiotrophies. They can be put into two broad groups according to parts of the eye involved :

1.A large number of conditions that are retinal in origin.

2.A smaller number of uveal dystrophies.

Though some of them are called degeneration, they are in fact dystrophies. The retinal conditions are also known as tapetoretinal degeneration. Some of the terms like retinitis pigmentosa may suggest an inflammatory etiology. They are non infective or inflammatory.

The retinopathies may be confined to the eye only like in primary retinitis pigmentosa or may have systemic involvement like Laurence Moon Biedl Bardet Syndrome. The number of systemic conditions with night blindness is a long one. See page. 433–439 also.

Acquired night blindness

Acquired night blindness in children is a serious ophthalmic problem in developing countries, which if not managed may lead to permanent loss of vision.

The commonest cause is vitamin A deficiency either due to short supply in malnutrition, high depletion in measles or poor absorption in diarrhoea. It may be seen in many children in the same family. It is fully preventable as well as curable in early stages. It is generally associated with xerophthalmia, which may precede onset of night blindness, may accompany night blindness. In lesser number of children, night blindness may be the first symptom that develops over few weeks. This is called chicken blindness because the child fumbles in diminished light.

Other causes of acquired night blindness in children are less common.

They are high myopia with extensive chorioretinal degeneration, peripheral cataract and juvenile glaucoma.

Day blindness. This is less common than night blindness and not serious enough to cause blindness. Nonetheless there is a troublesome symptom that comprises of constriction of pupil resulting in lowering of vision. The lesion is either in front of the pupil i.e. dense central corneal opacity or behind the pupil as in central nuclear or posterior polar cataract. Large macular lesion also causes diminished vision in bright light.

Day blindness should not be confused with glare and photophobia. Glare is intolerance to bright light without loss of vision as seen in - Coloboma of iris, congenital or surgical, aniridia, albinism, myopia and following mydriasis either therapeutic or neurologic.

In photophobia the child involuntarily shuts the lid in presence of light or may turn the head away from the light, may bury the face under the pillow. This is due to irrigation of trigeminal nerve. It has not been conclusively proved if photophobia can be present in absence of light perception. Common causes of photophobia in children are - Interstitial keratitis, corneal abrasion, corneal ulcer, phlyctenular kerato conjunctivitis, fascicular ulcer, buphthalmos, hydrops of cornea, acute iridocyclitis, meningitis and encephalitis. It is also seen in congenital achromatopsia.

Photopsia. This represents seeing flashes of light. This is due to irritation of visual elements of the retina. This is a serious symptom that is almost always a warning to development of retinal detachment especially in myopic children and eyes that have sustained

injury. Cases of photopsia should not be dismissed casually. All children complaining of flashes of light should undergo complete ocular examination, which should include indirect ophthalmoscopy with scleral indentation.

Rarely cerebral irritation may also cause flashes of light.

Chromatopsia. In this condition, the persons gets a coloured hue on a light coloured object i.e. white washed wall, white cloth etc.

This is mostly due to faulty absorption of a particular colour due to changes in the lens or may be drug induced.

Erythropsia (Seeing red). This is common following lens extraction in first few days. Occasionally a child with fresh thin blood film in front of the pupil or a fresh vitreous haemorrhage can complain of red coloured vision. It also occurs in snow blindness.

Cyanopsia (seeing blue). This is also a common complain after lens extraction.

Xanthopsia (seeing yellow). Commonest cause is jaundice. There is a big list of drugs that cause xanthopia.

Changes in the form of objects (Metamorphopsia) :

Micropsia. When the things took smaller than their actual size. This is due to crowding of cones. In contrast to this, minification is smaller image formation on retina by minus glasses as is seen in myopic correction.

Macropsia. When the things look larger than its actual size due to separation of cones. Magnification like minification is an optical phenomenon where the image of the object real or virtual look larger than its actual size as in hypermetropic correction, aphakic correction, use of magnifiers.

Metamorphopsia is distorted shape, this is best appreciated on Amsler grid.

Micropsia, macropsia and metamorpopsia are signs of macular lesion and retinal detachment.

Colour Blindness

Human eye have a highly developed colour sense. Most of the animals and birds have poor colour sense. A species nearer the human beings has better colour sense than those away from human beings. None of the animals have colour sense as good as human. Human eyes can perceive about 200 colours between 380-760 nm. The visible spectrum ranges between 397 nm to 723 nm roughly between 400-725 nm.5 The visible spectrum is called white light. Ultra violet has shortest wave length while infrared has longest wave length.

Colour vision is mediated through cones and is transmitted via optic pathway like white light. Hence defect in retina specially in macula and disorders of anterior optic pathway lead to colour defect.

Red, green and blue are the three primary colours. Others are made up of various combinations.

There are three types of cones responsible for red, green and blue colour sense. The cones contain three different types of pigments one for red, the other for green and last for blue.