FP1193 : Correlation of Apgar Scoring and Retinopathy of Prematurity

Dr. Jeevan Singh, M19036, Dr. Perwez Khan, Dr. Gupta  Ramesh Chandra, Dr. Mohan Shalini, Dr. Rajnath Singh Kushawaha

INTRODUCTION

Retinopathy of prematurity (ROP) is a vasoproliferative retinopathy that affects the developing retinal vessels of premature infants. Despite being a treatable disorder, in its more severe forms, it can lead to traction retinal detachment and blindness. ^[1-3]

ROP is the main cause of visual impairment in premature infants. ^[4] Advances in Neonatology and improvements in the quality care have resulted in an increasing number of premature and extremely low birth weight (ELBW) babies surviving the neonatal period leading to an increase in the population at risk for developing ROP. ^{[5, 6]}

ROP is a leading cause of blindness in children ^{[7, 8]} and accounts for up to 10% of childhood blindness worldwide. ^[9–11]

It is considered a multi-factorial disease; the immaturity of vascularisation is the key factor that causes the increased susceptibility of the retina to oxidative damage and to a number of perinatal factors. ^[12]

Classification of the stages of ROP is necessary for the standardization of treatment practices, and so that interventions can be assessed at a definite stage when progression to blindness is likely.

The stages of ROP are classified according to the recommendations summarized in the Interna­tional Classification of Retinopathy of Prematurity first published in 1985 and later on revised in 2005. ^{[13, 14]} 

LOCATION OF DISEASE

Zone I (the innermost zone) consists of a circle, the radius of which extends from the center of the optic disc to twice the distance from the center of the optic disc to the center of the macula.

Zone II extends centrifugally from the edge of zone I to the nasal ora serrata.

Zone III is the residual crescent of retina anterior to zone II.

By convention, zones II and III are considered to be mutually exclusive.

EXTENT OF DISEASE

Recorded as the hours of the clock or as 30° sectors.

As the observer looks at each eye, the 3-o’clock position is to the right and nasal in the right eye and temporal in the left eye, and the 9-o’clock position is to the left and temporal in the right eye and nasal in the left eye.

The boundaries between sectors lie on the clock hour positions; that is, the 12-o’clock sector extends from 12 o’clock to 1 o’clock

STAGES OF DISEASE

There are 5 stages that are used to describe the abnormal vascular response at the junction of the vascularised and avascular retina.

Stage 1: Demarcation Line

This line is a thin but definite structure that separates the avascular retina anteriorly from the vascularised retina posteriorly

Stage 2: Ridge

The ridge is the hallmark of stage 2 ROP. It arises in the region of the demarcation line, has height and width, and extends above the plane of the retina.

Stage 3: Extra retinal Fibrovascular Proliferation

Neovascularisation extends from the ridge into the vitreous. This extra retinal proliferating tissue is continuous with the posterior aspect of the ridge, causing a ragged appearance as the proliferation becomes more extensive.

Stage 4: Partial Retinal Detachment

Divided into extrafoveal (stage 4A) and foveal (stage 4B) partial retinal detachments.

Generally concave and most are circumferentially oriented

Stage 5: Total Retinal Detachment

Retinal detachments are generally tractional and may occasionally be exudative.

PLUS DISEASE

Along with the changes described earlier at the leading edge of the abnormally developing retinal vasculature, additional signs indicating the severity of active ROP may occur. These include increased venous dilatation and arteriolar tortuosity of the posterior retinal vessels and may later increase in severity to include iris vascular engorgement, poor pupillary dilatation (rigid pupil), and vitreous haze. This important constellation of signs in the original classification was referred to as plus disease. A + symbol is added to the ROP stage number to designate the presence of plus disease.

In the majority of the infants, ROP is a mild disease and undergoes spontaneous regression with no significant visual sequelae. However, in a significant number of case progression to advanced ROP occurs resulting in severe visual impairment. Long-term morbidity of ROP has a spectrum ranging from mild myopia to blindness.

APGAR SCORE

APGAR score (Activity, Pulse, Grimace, Appearance, and Respiration) provides an accepted and convenient method for reporting the status of the newborn infant immediately after birth and the response to resuscitation if needed (figure 1)

The test is generally done at one and five minutes after birth, and may be repeated later if the score is and remains low. Scores 7 and above are generally normal, 4 to 6 fairly low, and 3 and below are generally regarded as critically low.

An APGAR score that remains below 3 at later times—such as 10, 15, or 30 minutes—may indicate long-term neurological damage, including a small but significant increase in the risk of cerebral palsy. However, the APGAR test’s purpose is to determine quickly whether a newborn needs immediate medical care. It is not designed to predict long term health issues. ^[16]

A score of 10 is uncommon, due to the prevalence of transient cyanosis, and does not substantially differ from a score of 9. Transient cyanosis is common, particularly in babies born at high altitude.

SUBJECTS  AND METHODS

It was a hospital based observational cross sectional study done over a period of one year i.e. January 2016 to December 2016. INCLUSION CRITERIA–

1) Premature neonates with gestational age <32weeks born in obstetrics and gynaecology department of our institute with the documented APGAR score.

EXCLUSION CRITERIA–

1) Major congenital abnormalities preventing good assessment of fundus.

2) Premature infants born at home or in other hospitals and transferred after birth because of lack of information regarding APGAR.

Patients fitting into inclusion criteria were selected from the neonatal intensive care unit (NICU) of the department of Paediatrics and screened for ROP.

METHODOLOGY– A total of 107 newborns were screened.

1) Fundus examination was performed using indirect ophthalmoscope and a 20 D lens with speculum and scleral depression after pupillary dilatation using 2.5% phenylephrine and 0.5%tropicamide eye drops.

Screening was done according to the criteria laid down by The American Academy of Paediatrics and Ophthalmology ^[17] after taking informed consent from the parents

The first examination was performed between 3-4 weeks of postnatal age. Retinopathy was graded into stages and zones as per the ICROP classification. ^[14]

2) Gestational age,gestational weight,duration of oxygenation, APGAR at 1 minute and 5 minutes were also recorded for each study participant.

STATISTICAL ANALYSIS

Continuous data were presented as mean with a standard deviation. To compare continuous data, unpaired t test was used. Groupcomparisons were done by the Chi-squared (χ²) test or Fisher’s exact test for categorical variables was used.

Statistical significance was set at p< 0.05.

RESULTS

Total 107 infants were screened, including 58 males and 49 females. The mean gestational age  and birth weight of the  infants screened were 30.14 + 1.51 weeks and 1248 + 140.07 grams respectively.

ROP was seen in 25 cases (23.36%) with male to female ratio being 1.27:1. Mean gestational age of the infants with ROP was 28.88 + 1.481 weeks  and mean birth weight was 1194 +155.67 grams.

Table 1 shows stage wise distribution of ROP. Stage 1 retinopathy had the highest incidence (64%) followed by decreased incidence pattern in stage 2, 3. No infants with stage 4, stage 5 ROP were found in our study.

Table 2 shows the relation between ROP and risk factors.

ROP was significantly associated with gestational age (p<0.0001), low birth weight (p=0.02), oxygen therapy (p=0.04), low APGAR score at 1 and 5 minutes (p<0.0001).However, there was no significant association of ROP with gender, mode of delivery, duration of oxygen therapy (p>0.05)

DISCUSSION

ROP is a multifactorial disease. The immaturity of vascularisation is the key factor that causes the increased susceptibility of the retina to oxidative damage. ¹²Low gestational age and low birth weight are the most consistent factors associated with ROP.

Low APGAR is a predictor of poor long term postnatal outcome. It highlights the newborns in immediate need of resuscitation. ROP is a disease of premature infants who also have a poor postnatal course. That is why, this study was done to find out how ROP is related with APGAR.

A total of 107 premature infants were screened out of which ROP was found in 25 cases. Thus, the incidence of ROP in our study was 23.36 %.

In our study ROP cases had significantly low APGAR score at 1 minute (p<0.0001) as well as 5 minutes (p<0.0001) as compared to the neonates not having ROP.

Similar to ours Alajbegovic J.et.al^[21] in their study found out that low APGAR score at 1 minute (3.20 ± 1.304) and 5 minutes (5.20 ± 1.095) were significantly associated (p=0.002; p=0.001respectively) with the occurrence of ROP.

Also in a study conducted by Chirico G et.al ^[19] the association of ROP was significantly associated with low APGAR score at 1 minute and 5 minutes (p<0.001;p<0.0001 respectively).

However, in a study conducted by Arrne M. et.al^[18] low APGAR score at 1 minutes (p<0.0001) was significantly associated with the occurrence of ROP. Though APGAR at 5 minute (p=0.05) was not quite significantly associated but was positively correlated with the occurrence of ROP.

So, our study highlights the importance of recording APGAR score for every new-born and providing resuscitation measures accordingly. However, screening for ROP should be done for every premature infant irrespective of gestational weight, duration of oxygen therapy or low APGAR.

Conclusion

Low APGAR score at 1 minute and 5 minutes is significantly associated with the occurrence of ROP.

Bibliography

1. Prendiville A, Schulenburg WE. Clinical factors associated with retinopathy of prematurity. Arch Dis Child. 1988;63(5):522-7.
2. Termote J, Schalij-Delfos NE, Brouwers HA, Donders AR, Cats BP. New developments in Neonatology: Less severe retinopathy of prematurity. J Pediatr Ophthalmol Strabismus. 2000;37(3):142-8.
3. Cloherty JP, Eichenwald EC, Stark AR. Manual of Neonatal Care. 5th Ed. Philadelphia: Lippincott Williams and Wilkins; 2004. p. 667-83.
4. Purohit DM, Ellison RC, Zierler S, Miettinen OS, Nadas AS. Risk factors for retrolental fibroplasia: Experience with 3,025 premature infants. National Collaborative Study on Patent Ductus Arteriosus in Premature Infants. Pediatrics 1985; 76 (3): 339-44.
5. Gibson DL, Sheps SB, Uh SH, Schechter MT, McCormick AQ. Retinopathy of prematurity-induced blindness: Birth weight-specific survival and the new epidemic. Pediatrics 1990; 86 (3): 405-12.
6. Hussain N, Clive J et.al. Current incidence of retinopathy of prematurity, 1989-1997. Pediatrics. 999; 104 (3): e26
7. Nissenkorn I, Wijsenbeek Y, Cohen S. Etiology of blindness in Childrenin Israel in recent years.Acta Concilium      ophthalmologicum . 1987;25:742–744.
8. Steinkuller PG, Du L, Gilbert C, Foster A, Collins ML, Coats DK.Childhood blindness.J AAPOS. 1999;3:26–32.
9. Goggin M, O’Keefe M. Childhood blindness in the Republic of  Ireland: a national survey.Br J Ophthalmol. 1991;75:425–449.
10. Fleck BW, Dangata Y. Causes of visual handicap in the Royal    Blind School, Edinburgh, 1991–1992..   1994;78:421.
11. Gibson DL, Sheps SB, Schechter MT, Wiggins S, McCormickRetinopathy of prematurity: a new epidemic? Pediatrics.1989;83: 486–492.
12. Charan R, Dogra MR, Gupta A, et al. The incidence of ROP in   a neonatal care unit. Indian J Ophthalmol 1995; 43 (3): 123–6.
13. An international classification of ROP. Pediatrics 1984; 74:127–33.
14. International Committee for the Classification of RetinopathyOf Prematurity. The International Classification of Retinopathy of Prematurity revisited.2005; 123:991–99.
15. 15.Casey, McIntire, Leveno, K. J. (2001). “The continuing value of the APGAR score for the assessment of  newborn infants”.
16. Apgar Virginia(1953). “A proposal for a new method of  evaluation of the newborn infant”American Academy of Pediatrics, Section on Ophthalmology.  Screening examination of premature infants for retinopathy  of prematurity. Pediatrics. 2001;108:809–811
17. Mette Arrne and Birgit Peitersen; Retinopathy of prematurity:Review of a seven-year period in a Danish neonatal intensive care unit. Acta Pzdiatr (1994)83: 501-5.
18. G. Chirico; The Italian ROP Study Group; Italian multicentre  study on retinopathy of prematurity; Eur J Pediatr (1997) 156:  939 ± 943.
19. Woo SJ, Park KH, Lee SY, et al. The relationship between cord   blood cytokine levels and perinatal factors and retinopathy of prematurity: A gestational age-matched case control study.  Invest Ophthalmol Vis Sci. 2013;54:3434–3439.
20. Halimic Jasmina Alajbegovic, Denisa Zvizdic et.al Risk Factors for Retinopathy of Prematurity in Premature Born Children; Med Arh. 2015 Dec; 69 (6): 409-413.

Legends

Figure 1- APGAR Score

Table 1:Stages of ROP

Stages of ROP	No. of infants	Plus Disease
Stage 1	16(64%)	5
Stage 2	7(28%)	2
Stage 3	2(8%)	1
Stage 4	0	0
Stage 5	0	0

Table 2: ROP and Risk Factors

Risk factors		ROP present	ROP absent	p value
Gender	Male	14	44	1.0*
	Female	11	38
Mode of delivery	Caesarean	16	44	0.37
	Vaginal	9	38
Gestational age (weeks) (Mean+ SD)		28.88 +1.48 (n=25)	30.52 + 1.30 (n=82)	<0.0001‡
Birth weight (grams) (Mean+ SD)		1194+155.67 (n=25)	1267.07 + 128.43 (n=82)	0.02‡
Oxygen therapy (n=92)		18	74	0.04 OR=0.278
Duration of Oxygen therapy	<1 week (55)	11	44	0.91
	>1 week (37)	7	30
APGAR Score (Mean + SD)	at 1minute	4.16 + 0.473 (n=25)	6.48 + 0.71 (n=82)	<0.0001‡
	at 5 minute	5.52 + 1.0 (n=25)	7.01 + 0.76 (n=82)	<0.0001‡
APGAR Score	< 7	17	35	0.02 OR= 2.854
	> 7	8	47

^*Fisher’s exact test, Chi Square test, ^‡Unpaired t test