myopia & hypermetropia.pptx

Myopia

1. MYOPIA AND HYPERMETROPIA

2. MYOPIA Myopia or shortsightedness is a type of refractive error in which parallel rays of light coming from infinity are focused in front of the retina when accommodation is at rest.

3. Etiological dassification Axial myopia results from increase in anteroposterior length of the eyeball. It is the commonest form. Curvatural myopia occurs due to increasedcurvature of the cornea, lens or both. Positional myopia is produced by anterior placement of crystalline lens in the eye. Index myopia results from increase in the refractive index of crystalline lens associated with nuclear sclerosis. Myopia due to excessive accommodation occurs in patients with spasm of accommodation.

4. Grading of myopia American OptometricAssociation (AOA) has defined three grades of myopia: Low myopia , when the error is s-3D. Moderate myopia , when the error is berween-3D to -6D. High myopia , when the error is > - 6D.

5. Clinical varieties of myopia Congenital myopia. Simple or developmental myopia. Pathological or degenerative myopia. Acquired or second.ray myopia which occurs secondary to some other disease/ factors are as follows: post-traumatic , post- keraritic , drug-induced , pseudomyopia , space myopia, night myopia, and consecutive myopia.

6. CONGENITAL MYOPIA Present since birth, the congenital myopia, is usually diagnosed by the age of 2- 3 years. Most of the time the error is unilateral but rarely , it may be bilateral. High degree of error, about 8 to 10D, is usually present , which mostly remains constant. Convergent squint may develop in order to preferentially see clear at its far point (which is about 10- 12cm ).

7. Associations may include other congenital anomalies such as- Cataract , microphthalmos , aniridia , Megalocornea congenital separation of retina. Early correction of congenital myopia is desirable.

8. Simple myopia Most common type of myopia which progresses during the childhood and adolescence and rarely exceed 5 to 6 D. It generally begins b/w ages 7 to 8 years and stop to progress by the age of 21 years and the BCVA is always normal (6/6). It is considered as a physiological error not associated with any disease of eye .

9. Clinical features- It rarely present at birth. Most of such patients are rather born hypermetropioc but during development the normal mark is overshooted and child becomes myopic. There is no effective method for halting the progress of this so called “SCHOOL myopia” once it has started.

10. Symptoms- 1- Poor vision for distance ( shortsightness ) 2-Asthenopic symptoms- occurs with small degree of myopia . Strain develops due to dissociation between convergence and accommodation. 3-Change in psychological outlook- These children take the poor far-vision indoor for granted and concentrated their energy in to indoor activities.

11. Signs- 1- Eyes are typically large and some what prominent. 2- A/C deep 3- Pupil are large size (and a bit sluggish reaction) 4- Fundus –is normal; rarely may show myopic crescent at the temporal margin of the disc. 5- The error does not exceed 6 to 8 diopters.

12. Pathological myopia Pathological myopia is essentially a degenerative and progressive condition which manifest in early childhood. Etiology- It is unequivocal that the pathological myopia results from a rapid axial growth of the eyeball which is out side the normal biological variations ( i.e. 20 to 30 D)of development. To explain the spurt in axial growth , various theories have been put forward. So far no satisfactory hypothesis has emerged to explain the etiology of pathological myopia . However , it is definitely linked with Heredity and General growth process.

13. ( i ) Role of hereditary- the condition has a strong hereditary tendency and is more common in women than in man. - Autosomal dominant pathological myopia has been linked to genes 18p11.31 and 12q2123. (ii) Role of general growth process- Lengthening of the posterior segment of the globe commences only during the period of active growth and probably ends with the termination of the active growth. Therefore , the factors ( such as nutritional deficiency, debilitating diseases, endocrinal disturbances, general health etc) which effect the general growth process may also have some influence on the progress of myopia.

14. Etiological hypothesis- summarized More growth of retina. Stretching of sclera Genetic Factors General growth process * Increase axial length * Degeneration of choroid * Degeneration of retina * Degeneration of vitreous

15. Clinical features Symptoms- 1- Defective vision- The inability to see distant object clearly and holding the book too close to the eye while reading are the usual complaints of parents. Further due to progressive degeneration changes an uncorrectable loss of vision may occurs. 2- Muscae volitantes – Floting black opacities in front of the eyes are also complained of by many patients. Theses occur due to degenerated liquified vitreous.

16. 3- Eye strain and headache- may occurs due to an imbalance between accommodation and convergence in myopia. 4- Flashes of light 5-Night blindness- may be complained by very high myopes having marked chorio -retinal degenerative changes.

17. Signs- 1- Prominent eyes- appearing elongated and even simulating an exophthalmos . (The elongation is probably not due to stretching but to a primary degeneration of the coats of the eye including the posterior half of the sclera; the part of eye Anterior to the equator may be normal). 2- Cornea – large size 3- A/C- Deep 4- Pupil- Large size 5- Refractive error- May progress until mid 30s and frequently results in myopia of 10-20D.

18. 5- Fundus examination- A- Optic disc- ( i ) Large and pale (ii) Temporal crescent (iii) Nasal Supertraction crescent

19. B- Degenerative changes in retina and choraid - ( i ) Tigroid appearance of fundus - due to visible prominent large choroidal vessels following atrophy of RPE and choriocapillaris . -In late stages White atrophic patches seen due to total disappearance of choroidal tissue (Post. pole).

20. (ii) Foster- fuchs ’ spot- Dark red circular patch due to subretinal neovascularization and choroidal haemorrhage , may be present at macula.

21. (iii) Cystoid degeneration- may be seen at the periphery ( iv) Total retinal atrophy – at central area (v) There may be associated lattice degeneration / Snail track lesion. (vi) Retinal hole/ tear, hemorrhage and even Retinal detachment.

22. C- Posterior staphyloma - In high degree of myopia, the sclera may bulge out at the posterior pole to form a posterior staphyloma . D- Degenerative changes in vitreous- it includes: - Liquefaction -Vitreous opacities -Posterior vitreous detachment(PVD)(Weiss’ ring)

23. E- Visual field- show concentric and in some cases ring scotoma may be seen. F- Electroretinogram (ERG)- subnormal

24. Complications- Retinal tear / R. D Hemorrhage Complicated cataract Nuclear sclerosis POAG (common association)

25. Treatment of myopia 1- Optical Correction 2-Contact lenses 3-Surgical correction 4- General health 5- Low vision aids 6- Genetic Counseling

26. 1- Optical correction- Concave lenses ( Problem of high minus glass- Minification of object, bright image, distortion of image, reduced fiel of vision, eye appears smaller behind the glass) Basic rule of correction of myopia - The minimum acceptance providing maximum vision. - Children- below 8 years of age- full correction -Adults- * < 30 yrs of age- accept their full myopic * > 30yrs – Undercorrected distance vision - Irrespective of age , full correction can rarely be tolerated in case of high myopia (more then -10 D).

27. 2- Contact lenses- Have most important role in myopic correction. Advantage: * Less minification of image * Image distortion can be eliminated * Field of vision is increased * Glass free

28. 3- Surgical correction- For pt. who do not wish to use glasses , refractive surgery to correct the myopia is an option. -Radial keratotomy (RK) - Photorefrective keratectomy(PRK) -Intra corneal ring (ICR) -Laser-assisted in situ keratomileusis (LASIK) - Phakic lens implantation(ICL) -Refractive lens exchange( Fukala’s operation)

29. 4- General health- The general health of a myopic child should be attended to. Nutritious diet, out door activities and regular exercises should be encouraged. - Advised to do near work in good illumination . - Avoid blunt ocular trauma .

30. 5- Low vision Aid- in pathological myopia low vision aids may be of some help to the patient, particularly in reading. 6- Genetic counseling- Genetic counseling may stop hereditary propagation of the disease in the family. -Two highly myopic adults with degenerative myopia should never, from the medical point if view, have child.

31. HYPERMETROPIA Hypermetropia is also known as ‘far sight’. In this dioptric condition of the eye, with the accommodation at rest, incident parallel rays come to a focus posterior to the light sensitive layer of the retina.

32. Etiology types of hypermetropia Axial Curvarural Index Positional Due to absence of crystalline lens. Consecutive hypermetropia

33. Axial hypermetropia It is the commonest form, and i n this condition, the total refractive power of eye is normal but there is an axial shortening of eyeball. About 1 mm shortening of the antero-posrerior diameter of the eye results in 3 dioptres of hypermetropia .

34. Curvatural hypermetropia It is the condition in which the curvature of cornea, lens or both is flatter than the normal resulting in a decrease in the refractive power of eye. About l mm increase in radius of curvature results in 6 dioptres of hypermetropia .

35. Index Hypermetropia It occurs due to decrease in the refractive index of the lens in old age due to cortical sclerois . Positional Hypermetropia It results from posteriorly placed crystalline lens.

36. Absence of crystalline lens It can be either congenital or acquired and it leads to aphakia (absence of lens)- a condition of high hypermetropia . Consecutive hypermetropia Overcorrected myopia after refractive surgery, implantable contact lens Underpowered IOL in cataract surgery

37. Clinical types of hypermtopia Simple hypermetropia Pathological hypermetropia Functional hypermetropia

38. SIMPLE HYPERMETROPIA It is the commonest form It results from normal biological variations in the development of the eyeball It includes- Axial hypermetropia Curvatural hypermetropia

39. PATHOLOGICAL HYPERMETROPIA It results due to congenital or acquired conditions to the eyeball which are outside the normal biological variations of development It is of 2 types- Congenital Acquired

40. CONGENITAL PATHOLOGICAL HYPERMETROPIA Microphthalmos Microcornea Congenital posterior subluxation of lens Congenital aphakia Microphthalmos Microcornea

41. ACQUIRED PATHOLOGICAL HYPERMETROPIA Senile hypermetropia Curvatural Index hypermetropia Positional hypermetropia Aphakia Consecutive hypermetropia Retrobulbar orbital tumours , by pushing the posterior wall of the eyeball anteriorly

42. Functional hypermetropia It results from paralysis of accommodation as seen in patients with 3rd nerve palsy and internal ophthalmoplegia

43. Hypermetropia : Variation with age At birth , the eyeball is relatively short, having +2 to +3 hypermetropia , which is gradually reduced. By the age of 5-7 years , the eye is emmetropic and remains so till the age of about 50 years. After 50 years of age, senile hypermetropia is due to changes in the crystalline lens, with a hypermetropia of +2 to +3

44. Clinical features Symptoms Asymptomatic . A small amount of refractive error in young patients is usually corrected by mild accommodative effort without producing any symptom. Asthenopic symptoms - These include: tiredness of eyes frontal or frontotemporal headache Watering mild photophobia

45. Defective vision with asthenopic symptoms. When the amount of hypermetropia is such that it is not fully corrected by the voluntary accommodative efforts, then the patients complain of defective vision which is more for near than distance and is associated with asthenopic symptoms due to sustained accommodative efforts. Defective vision only . Wh en the amount of hypermetropia is very high, the patients usually do not accommodate (especially adults) and there occurs marked defective vision for near and distance.

46. Signs Size of eyeball may appear small as a whole especially in high hypermetropia . Cornea may be slightly smaller than the normal. Anterior chamber is comparatively shallow. Retinoscopy and autorefractometry reveals hypermetropic refractive error. Shallow anterior chamber

47. Fundus examination reveals a small optic disc which may look more vascular with ill-defined margins and even may simulate papillitis . The retina as a whole may shine due to greater brilliance of light reflections (shot silk appearance). A-scan ultrasonography (biometry) may reveal. A short anteroposterior length of the eyeball in axial hypermetropia .

48. GRADING OF HYPERMETROPIA Hypermetropia can be classified as : -low (up to 2 D) - moderate (2.25–5D) - high (more than 5D) and rarely exceeds 6–7 D, which is equivalent to a 2 mm shortening of the optic axis.

49. Complications Recurrent styes , blepharilis or chalazia may occur, Accommodative convergent squint Amblyopia Predisposition to develop primary narrow angle glaucoma.

50. Treatment Optical treatment. Basic principle of treatment is to prescribe convex (plus) lenses, so that the light rays are brought to focus on the retina. Fundamental rules for prescribing glasses in hypermetropia include: Total amount of hypermetropia should always be discovered by performing refraction under complete cycloplegia . The spherical correction given should be comfortably acceptable to the patient. However, the astigmatism should be fully corrected.

51. Gradually increase the spherical correction at 6 months interval till the patient accepts manifest hypermetropia . ln the presence of accommodative convergent squint, full cycloplegic correction should be given at the first sitting. If there is associated amblyopia , full correction with occlusion therapy should be started.

52. SURGICAL TREATMENT Conductive keratoplasty /corneal refractive therapy Laser thermal keratoplasty Photorefractive Keratectomy and their variants Hyperopic LASIK Phakic IOLs Refractive lens exchange

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