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ARTICLE
Year : 1970  |  Volume : 18  |  Issue : 3  |  Page : 89-95

Myopia in relation to prematurity


Department of Ophthalmology, Postgraduate Institute of Medical Education and Research, Chandigarh, India

Correspondence Address:
I S Jain
Department of Ophthalmology, Postgraduate Institute of Medical Education and Research, Chandigarh
India
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Source of Support: None, Conflict of Interest: None


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How to cite this article:
Jain I S, Garg P K. Myopia in relation to prematurity. Indian J Ophthalmol 1970;18:89-95

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Jain I S, Garg P K. Myopia in relation to prematurity. Indian J Ophthalmol [serial online] 1970 [cited 2020 Aug 10];18:89-95. Available from: http://www.ijo.in/text.asp?1970/18/3/89/35071

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Table 1

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Incidence of Myopia in the Eye clinic patients as reported by Jain and Singh[21] is of the order of 15%. Myo­pia is a serious cause of blindness and one out of every 200 patients attend­ing the Eye O.P.D. is blind of high myopia, hence the importance of its early detection.

In 1955, Fletcher and Brandon drew attention to the occurrence of high myopia in premature infants. Later on many others McNei1 [22] , Gregory [18] , Alfano [1] , reported myopia among premature infants.

However, the exact pathogenesis of this association is not yet clear. Flet­cher and Brandon [10] considered it a complication of retrolental fibroplasia specially of abortive forms. Birge [2] , McNeil [22] and Alfano [1] also support the above view, while, Wagner [29] , Graham and Grey [17] do not accept this theory.

In India though the incidence of prematurity is as high as 15-20% [9] , yet it is surprising no report is avail­ - able on this problem of myopia of prematurity from our country. Hence the present study was undertaken to find out whether prematurity plays any role in the causation of myopia in Indian infants and children, as the knowledge available from western investigations may not be applicable to Indian conditions because of social, nutritional and racial factors.

The aim of the present study is to assess the refractive errors of prema­ture infants and children and to com­pare the results with the normal group.


  Material and Methods Top


The present clinical study consists of a total of 190 infants and children, of whom 90 infants and children were born prematurely while 100 infants and children served as normal controls. The following criteria of prematurity was taken:­

1. Birth weight 52 ½ lbs. or less (In­ternational Standard).

2. Gestational period less than 36 weeks.

or both

Most of the infants were examined in early infancy to a maximum age of 5 years. The cases were collected from the maternity wards and child­ren O.P.D. of the hopital attached to the Institute of Postgraduate Medical Education and Research and General Hospital, Sector 16, Chandigarh.

The birth history of the child was obtained which included birth weight, gestational age, oxygen therapy and birth trauma.

The antenatal history of maternal ill health, in particular toxaemia of pregnancy, any fever, diabetes, drugs etc. was elicited. The family history of ocular disease specially albinism and high refractive errors was record­ed.

Refraction was done under cyclo­plegia by instituting two drops of 0.05% hyoscine hydrobromide in each conjunctival cul de sac. one hour be­fore examination, as recommended by Sorsby, Sheridan, Moores and May­thorne[26].

Very young infants were examined in the wards. Baby was removed from the cradle or the incubator, shortly after feeding, and the baby's head was held steady by a nurse on a waist high table. The baby at once opened the eyes when coaxed to suck a teat dipped in glycerine. Occasion­ally lids were held apart with thumb and index finger of one hand, care­fully avoiding any pressure on the globe. No retractors were used to open the lids. Retinoscopy was done, both in the horizontal and vertical meridians by a luminous streak re­tinoscope.

Corrective lenses were held 12 mm from the cornea and correction for the working distance was made in the retinoscopic findings.


  Observations Top


Group I Normal controls (100 cases).

Group II Premature cases (90 cases).

Age and Sex Distribution

[Table - 1] shows the age and sex dis­tribution of cases studied in groups I and II. There were 58 males and 42 females in Group I, while there were 51 males and 39 females In Group II. This table further shows that the total number of cases under different ages were approximately the same in the two groups. The maxi. mum number of cases were of ages below one month and between 12-36 months.

Prevalence of Myopia and range of Refraction:

Out of the 100 control cases only 4% had one or more myopic meri­dians in either eye, while out of the 90 premautre cases 45 cases (50%) had one or more myopic meridians of either eye, showing thereby a signifi­cantly high incidence of myopia in premature cases. Most of these cases were myopic in both the eyes.

Graphs I and IA.

The range of refraction in normal cases (200 eyes) was between -1.0D to ±5.50D. Only 8 and 7 eyes were myopic in vertical and horizontal me­ridians, while in premature cases (180 eyes) the range of refractions was between -12.5D to +5.0D, and 71 and 77 eyes were myopic in verti­cal and horizontal meridians respec­tively; while the rest of the eyes had refraction, between 0 to 5D.

Influence of sex and Age on the Incidence and Severity of Myopia of Prematurity:

[Table - 2] shows that there is no predilection for the sex of the baby. The same table demonstrates a wide range of myopia (37.0 to 60%) in premature cases of different age groups, and there is a concomitant fall in percentage, with increase in age. Higher degrees of myopia were usually seen in premature cases. [Table - 3].

Since there is a wide discrepancy in the incidence of myopia as report­ed by different authors and as this discrepancy is suspected to be partly due to the age of the subjects at the time of examination, in order to deter­mine whether any changes take place in the myopia as age of the baby advances, we preferred to subdivide our observations under 2 sub-groups.

Sub-Group A: Premature cases upto one month of age.

Sub-Group B: Premature cases older than one month.

[Table - 5] shows that myopia is more prevalent (63%) in Sub-Group A as compared to Sub-Group B 44.4%, indicating that the myopia of prema­turity behaves differently in its course than myopia of adults. It gets re­duced with advance of age.

Influence of Gestational Period, on Myopia of Prematurity:

[Table - 4]

This table clearly demonstrates that neither the myopia nor its severity bears any relationship with the period of gestation.

Influence of Tpye of Delivery on Myopia of Prematurity:

[Table - 5]

No significant influence is noted by the type of labour on myopia of pre­maturity.

Influence of Birth Weigh on Myopia of Prematurity:

[Table VI and TIT)

[Table - 6] shows a continuous fall in the incidence of myopia with rise in birth weight in all the age groups. 22 cases were examined within four weeks of life, out of which 10 cases weighed between 2-4 lbs, and an equal number between 4-5 lbs. The occur­rence of myopia was 100% and 40% in these groups respectively.

There were 2 cases weighing 5 and 5.5 lbs, but none of them was myopic.

These tables show that myopia was always present in cases of birth-weight below 4 lbs.

Influence of Multiple Birth (Triplets and Twins)

Out of 90 premature cases, there was one triplet; all these three bro­thers (100%) were myopic. There were 5 twins (9 premature cases). Only two twins (44.44%) were myo­pic. There were 38 (48.72%) myo­pes out of 78 cases born singly.

Influence of order of Birth:

Occurrence of myopia was highest in the first born children, and de­creased with the order of birth of the child.

Influence of Toxaemia of Pregn­ancy:

There were 21 cases of toxaemia of pregnancy, of which 11 issues (52%) had myopia. Comparatively, 34 issues of 63 normal deliveries (54%) had myopia. This shows that babies born to mothers having toxaemia of preg­nancy had no higher incidence of myopia.

Influence of Oxygen Therapy:

In the present series the concentra­tion of Oxygen therapy could not be established, as it was given by open method. The duration of oxygen therapy varied from one day to 20 days. None of these children who had received oxygen showed any evidence of retrolental fibroplasia.

[Table - 8], however, shows a slightly higher incidence of myopia in cases who had oxygen therapy.

Influence of Heredity of Myopic Parents

Five myopic premature cases had myopic parents, while equal number of myopic parents had normal off­ springs. Only in one case both mother and father were myopic. Detailed family history of myopia was however not available.

This small series however demon­strates that myopia in parents had no influence on myopia of prematurity.


  Discussion Top


Various investigators, from time to time, have tried to explain the aetio­logical factors of myopia but the pro­blem is still far from being solved.

The role of heredity in the patho­genesis of myopia is well known al­though the mode of transmission is doubtful (Franeois[12]). Out of the environmental factors, less consump­tion of first class proteins (Gardiner [13],[14] ), toxaemias of Pregnancy (Gardiner and James [15] ), malnutrition (Sood and Gupta [25] ) and premature births (Brige [2] ), Fletcher and Bran­don [30] ), have been pointed out as the causes, which affect the refractive state of the eyes.

In the literature, conflicting reports have appeared about the presence of myopia in premature cases. Wa1d [28] and Hiat, Cortenbader and Albert [19] do not find myopia in premature cases, while Fletcher and Brandon have reported myopia in almost all prema­ture cases. Observations from the present study, however, show frequent occurrence of myopia in premature cases and thus lend support to the observations of Graham and Grey [17] and Hosaka [20] .

The degree of myopia upto a ma­ximum of -12.0D in the present se­ries also confirm the similar findings reported by Birge [2] , Wagner [29] , Cur­tin [8] . Bilaterality (99.5%) in our present series also confirms the earlier observations of Brige [2].

Incidence of Myopia, of Prema­turity.

A wide variation ranging from denial (Wald [28] and Hiat [19] et al) to oc­currence in almost all cases (Fletcher and Brandon [10],[11] ) has been reported, while in the present series the over­all occurrence of myopia is 50%. This discrepancy in the incidence can partly be explained by the method of exa­mination, age at the time of examina­tion and the birth weight of prema­ture cases.

Fletcher and Brandon [10] used the ophthalmoscope only, as the method of examination to assess the degree of myopia and no cycloplegic refrac­tion was done, which may have been responsible for 100% incidence, re­ported by them.

The second factor is the age of the child at the time of examination. Contrary to the general trend in myopia the incidence of myopia of prematurity decreases with increase in age as has been observed in the pre­sent study.

The incidence of 60% at the age of one month fell to 37% when examin­ed from 1-5 years.

This assumption gains support from the studies of Fletcher and Brandon[10] who reported 100% incidence when examined immediately after birth.

Hosaka[20] examined within 4-5 weeks after birth and reported 25% incidence, while Castrens reported an incidence of 3.7% as he examined cases between 9-11 years of age.

The third factor, for the disparity in incidence may be the level of birth weight of the cases studied.

Our observation of the occurrence of myopia to the extent of 100% in babies weighing 4 lbs. or less at birth and decreasing to 40% between 4-5 lbs and nil in babies weighing 5-5Z lbs. point to the fact that there is a continuous fall in the incidence of myopia, with increase in the birth weight.

This finding indirectly supports the suggestion of Ghosh and Berim[16] and Nair[23] that 4 lbs be taken as the upper limit of prematurity in India. Further, the equal occurrence of myo­pia in premature cases of gestational ages above and below 38 weeks fur­ther supports the view that "prema­ture infant" be better defined in terms of birth weight rather than gestational age.

Sex of the baby, method of delivery or type o f labour, was found to have no bearing on the myopia of prema­turity, however, no report from the literature is available regarding the study of such parameters. While multiple births could only give rise to lesser weight of the babies and thus cause an apparent higher incidence of myopia.

Influence of Heredity

Myopia in parents had no influence on myopia of prematurity, and this observation of ours is supported by McNeil[22] and Alfano [1] who consider­ed myopia of prematurity as non­familial and non-hereditary.

Influence of Toxaemia of Pregn­ancy:

From the present study, it is appa­rent that toxaemia of pregnancy had no influence in the causation of myo­pia of prematurity. Gardiner and James[15], however found that 50% of the mothers of congenital myopes had toxaemia of pregnancy, but they made this statement irrespective of the birth weight. Our observations go a step further, that inspite of premature birth, in cases of toxaemia of preg­nancy, the occurrence of myopia was not more in children of these mothers than those who had no toxaemia.

Role of Oxygen

The role of oxygen in the causa­tion of myopia of prematurity could not be evaluated with certainty from the present study, but Gregory [18], McNeil[22], Wagner [29] , Graham and Grey [17] could not find any association of myopia with administration of oxygen.

Thus, inspite of the study of vari­ous parameters vis-a-vis myopia of prematurity, in the present report, no definite explanation can be put for­ward regarding its pathogenesis. However, it is abundantly clear that there is a definite tendency towards myopic refraction in premature cases and the myopia shows a progressive fall with increase in birth weight and the age of the patient.

The explanation, therefore, has to be sought in the organogenesis of the embryonic eye. Sondermann [24] felt that there was 'sclerectasia posterior' during embryonic life, which flatten­ed after the 6th foetal month and dis­appeared at birth. Persistence of this may be responsible for the myopic refraction. Tait [27] and Curting men­tion the spherical shape of the lens in the immature eye, as the causative factor for myopia of prematurity.

Recent studies [6],[7] in the "chick eye" have indicated that the vitreous vo­lume increase is the essential elonga­tion force of the developing eye. The variation in vitreous volume may not only be due to changes in its initial growth, but may also be influenced by factors such as systemic hydration and intraocular pressure.

Thus the myopia of prematurity in all likelihood, may be occasioned by the development of a macrohya­loid body: Fluctuating increased ocular tension together with shallow­ing of the anterior chamber point to an intravitreal transudation, as the probable pathogenic mechanism.

This theory could also explain why there is progressive fall in myopic refraction with increasing birth weight and the age of the patient.


  Summary & Conclusions Top


50% of premature cases had one or more myopic meridia in either eye, and this myopia was almost always bilateral. A continuous fall in the incidence of myopia was seen with increase in birth weight and with in­crease in age of the patient.

In this series, myopia in parents, toxaemia in mother during pregnancy, gestational age, single or multiple births, type of delivery, sex of the baby and oxygen therapy, show no influence on the incidence of myopia of prematurity.

In no case any evidence of retro­lental fibroplasia was seen.

Vitreous Volume increase may be acting as an elongating force for the globe of the developing eye, thus the myopia of prematurity may be occa­sioned by the development of a mac­rohyaloid body.

Exact pathogenesis of myopia of prematurity still remains unsolved, perhaps the answer would be found from more critical studies of organo­genesis of the embryonic eye.



 
  References Top

1.
Alfano, J. E.: Myopia of prematurity, Amer. J. Ophth. 46, 45 Part 1 (1958).  Back to cited text no. 1
    
2.
Birge, H. L.: Myopia caused by pre­maturity, Tr. Oph. Soc. U.K. 53; 219, (1955).  Back to cited text no. 2
    
3.
Idem: Amer. J. Ophth. 41; 292, (1956).  Back to cited text no. 3
    
4.
Idem: Prematurity in causation of ocular anomalies. Modern Ophthalmology (1963) Ed. Sorsby, A. Butter­worth, London. Vol. 2, P. 3.  Back to cited text no. 4
    
5.
Castren, J.: The significance of pre­maturity on the eye. Acta Ophth. 44 (Supp) (1955) Quoted by Graham et al in 17.  Back to cited text no. 5
    
6.
Coulombre, A. J.: Role of Intra­ocular pressure in the development of the chick eye. (1) Control of eye size: Journal of Experimental Zoo­logy, 133: 211 (1956).  Back to cited text no. 6
    
7.
Idem, & Coulombre, J. L.: Lens development. Role of lens in Eye growth. Journal of experimental Zoology: 156: 39 (1964).  Back to cited text no. 7
    
8.
Curtin, B. J.: Pathogenesis of con­genital myopia. Arch. Ophth. (Chi­cago) 69: 166-173 (1963).  Back to cited text no. 8
    
9.
Dawn, C. S.: Text book of obste­tric. Sreemoti Arati Dawn 54, Suren­dra Nath Banerjee Road, Calcutta-14 (1962).  Back to cited text no. 9
    
10.
Fletcher, M. C. and Brandon, S.: Myopia of prematurity. Am. J. Ophth. 474-481 (1955).  Back to cited text no. 10
    
11.
Il. Idem: The developing fundus oculi of the premature infant: Journal of Paediatrics: 43(2) 499, 1953,  Back to cited text no. 11
    
12.
Francois, J.: Heredity in Ophthal­mology (1961) St. Louis, C. V. Mosby Co. P. 198.  Back to cited text no. 12
    
13.
Gardiner, P. A.: (1956) Quoted by Sood and Gupta, 1966.  Back to cited text no. 13
    
14.
Idem: (1958), Quoted by Sood and Gupta, 1966.  Back to cited text no. 14
    
15.
Gardiner, P. A. & James, G.: Asso­ciation between maternal disease and myopia in the child. Brit. J. Ophth. 44: 172 (1960).  Back to cited text no. 15
    
16.
Ghosh, S. & Berim, S. T.: Standard of prematurity for North Indian Ba­bies: Indian J. of Child Health; 11, 210, (1962).  Back to cited text no. 16
    
17.
Graham, M. V. & Grey, O. P.: Re­fraction of premature babies eye, Brit. Med. Jour. 1: 1452, (1963).  Back to cited text no. 17
    
18.
Gregory, I. D. R.: Retinopathy of prematurity (Retrolental fibroplasia), Brit. J. Ophth., 41: 321 (1957).  Back to cited text no. 18
    
19.
Hiatt, R. L., Costenbader, F. D. and Albert, D. G.: Clinical Evaluation of congenital myopia; Arch. Oph. 74: 31-35, (1965).  Back to cited text no. 19
    
20.
Hosaka, Akio: The ocular findings in the premature infants especially on the premature signs. Jap. J. Oph. 7: 2: 77 (21), (1963).  Back to cited text no. 20
    
21.
Jain, I. S. and Singh, K.: A clinical study of myopia (High myopia - I) Orient. Arch. Ophth. 5: 67-75 (1967).  Back to cited text no. 21
    
22.
McNeil, N.: Some ocular manifes­tations of prematurity: Brit. J. Ophth. 40, 24, (1956).  Back to cited text no. 22
    
23.
Nair, N. S.: Study of birth weight of term infants at Calicut: J. Obst. Gynae. India: 13: 488, (1963).  Back to cited text no. 23
    
24.
Sondermann: Klin. Mbl. Aug.: 111, 573. Cited by Genetics and Ophthal­mology. Ed. Waardenburg, 1963, P. 123 (1950).  Back to cited text no. 24
    
25.
Sood, N. N., and Gupta, S.: Refrac­tive changes in malnourished child­ren : Orient. Arch. Ophth : 4 : 264­-269, (1966).  Back to cited text no. 25
    
26.
Sorsby, A, Sheridan, Moores and Maythorne: Hyoscine cycloplegia in children. Lancet, July 30, P. 214 (1955).  Back to cited text no. 26
    
27.
Tait, E. F.: Discussion of Fletcher and Brandon, Survey of Ophth. 1: 105, cited by Alfano (1956).  Back to cited text no. 27
    
28.
Wald, K. C.: Hereditary Myopia, Arch. Ophth. 42: 225 (1949).  Back to cited text no. 28
    
29.
Wagner, G.: Klin. Mbl. Aug. 131: 326, Quoted from Brit. Med. Journal (1960) Annotation: The Eye of  Back to cited text no. 29
    
30.
Premature: 2: 45 (1957).  Back to cited text no. 30
    



 
 
    Tables

  [Table - 1], [Table - 2], [Table - 3], [Table - 4], [Table - 5], [Table - 6], [Table - 7], [Table - 8]



 

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