Sudanese Journal of Ophthalmology

: 2014  |  Volume : 6  |  Issue : 1  |  Page : 36--39

Keratomalacia in a neonate secondary to maternal Vitamin A deficiency

Renu Magdum, Sampada Tambolkar 
 Department of Ophthalmology, Padmashree Dr D.Y. Patil Medical College, Pimpri, Pune, Maharashtra, India

Correspondence Address:
Renu Magdum
7 Panchsheel Park, Aundh, Pune - 411 007, Maharashtra


Vitamin A deficiency (VAD) is a leading cause of childhood blindness, morbidity and mortality, especially in developing countries like India. The universal Vitamin A supplementation program is mainly aimed at the age group from 6 months to 5 years. However, malnourished pregnant women with VAD and their infants, who are entirely dependent on breast milk, constitute another highly susceptible group to the blinding effects of vitamin A deficiency. We need to develop strategies aimed at safe vitamin supplementation in this vulnerable group. The aim of reporting blinding keratomalacia in a 20-day-old neonate was to emphasize on the need to revise health care strategies.

How to cite this article:
Magdum R, Tambolkar S. Keratomalacia in a neonate secondary to maternal Vitamin A deficiency.Sudanese J Ophthalmol 2014;6:36-39

How to cite this URL:
Magdum R, Tambolkar S. Keratomalacia in a neonate secondary to maternal Vitamin A deficiency. Sudanese J Ophthalmol [serial online] 2014 [cited 2020 Feb 28 ];6:36-39
Available from:

Full Text


The control of blindness in children is considered to be a high priority with the WHO Vision 2020-The Right to Sight Program. [1] There are several reasons for this. Firstly, children who are born blind or become blind and survive have a lifetime of blindness ahead, with all the associated emotional, social and economic costs to the child, the family and society. Secondly, many causes of childhood blindness are either preventable or treatable. Thirdly, many conditions associated with blindness in children such as Vitamin A deficiency (VAD), are also causes of childhood mortality. Control of blindness in children is, therefore, closely linked to child survival. [2]

"Xeropthalmia" literally means "dry eye." It encompasses a spectrum of clinical findings, beginning with night blindness and progressing to conjunctival and corneal xerosis and finally, corneal ulceration and necrosis and resultant blindness. It is generally reported in preschool children or toddlers, largely due to delayed and faulty weaning practices. It can also occur during periods when infectious disease rates are high and also during seasons when food sources rich in vitamin A are scarce. [3] Also, VAD can increase the severity of infection which, in turn, can reduce intake and accelerate body losses of vitamin A to exacerbate deficiency. [4]

Vitamin A deficiency also remains a public health problem among women, affecting an estimated 19 million pregnant women [4] Roughly 45% of vitamin A deficient and xerophthalmic children and pregnant women with low to deficient Vitamin A status live in southeast Asia and three-fourths of these live in India. [5] The prevalence across India as a whole has been estimated to be 30.8% [5] Night blindness in pregnant women is considered to be an important indicator of Vitamin A deficiency. [6] Maternal milk is deemed as having sufficient stores for a neonate and infant up to age of 6 months and colostrum is particularly rich in vitamin A, containing approximately 7 μmol/L [7],[8] Even though vitamin A content of human milk depends on maternal vitamin A status, even with low content, it is the best source of the vitamin for 0-6 months old age group. [5]

The National Prophylaxis Program against Nutritional blindness was initiated in India in 1970 as an urgent remedial measure to eliminate the unacceptably high magnitude of xerophthalmic blindness. All 1-5 year old children were to be administered an oral dose of Vitamin A once in 6 months. This was expanded in 2006 to the universal Vitamin A Supplementation Program (UVAS) and was broadened to include children between 6 months and 5 years. [9]

Hence, infants born to Vitamin A deficient women are at high risk of irreparable visual loss as both lactating mother and neonate are not covered under this program. Cases of neonatal keratomalacia in India have been reported from different states [10],[11] In a recent study of clinical spectrum and etiopathogenesis of keratomalacia in infants younger than 6 months conducted at AIIMS, New Delhi, 33 infants less than 6 months of age attending OPD over a period between June'07 to April'10 had been detected as having keratomalacia. Inadequate breastfeeding was found to be the most important contributory factor in this study [12] We are reporting a case of a 20 day old neonate who presented to our hospital with total corneal melting secondary to maternal VAD with consequent irreparable visual loss.


A 20-day-old male neonate was referred to our eye clinic with complaints of inability to open eyes, ocular discharge and white opacity in eyes since 15 days. He also had fever with cough since 4 days, difficulty in breathing and refused to accept feeds. The baby was a full term normal vaginal delivery conducted at home. He was the first child of migrant parents originally from Chhattisgarh and now working as laborers at a construction site. The baby was exclusively breast fed.

The mother was examined and a detailed dietary history was taken. History revealed that due to certain religious fads prevalent in the area, she had consumed only potatoes and cereals during her entire pregnancy. She also had symptoms of night blindness during entire pregnancy and also at present.

The neonate had weight of 2.6 kg, length was 52 cm, Heart rate was 150/min, respiratory rate was 52/min, temperature was 100° F. Systemic examination showed subcostal and intercostal retractions with crepitations, suggestive of pneumonitic patch in right lung. The chest X-Ray showed bilateral patchy infiltrates.

Baby kept both eyes tightly closed and seemed to be photophobic. Ocular examination revealed characteristically dry looking, wrinkled conjunctivas. There was total absence of any congestion that is a hallmark of xerophthalmia uncomplicated by superimposed infections. Both corneas showed central melting with exposure of iris tissue. (Stage × 3B) [Figure 1].{Figure 1}

Ocular examination of mother revealed presence of Bitot's spots and a dry looking muddy conjunctiva. Both corneas were normal. The child's father was also examined and was found to have normal eyes.

Both mother and baby were investigated for S. Vitamin A levels which were found to be very low at 6.45 micrograms/dl and 19 micrograms/dl (ref. values-30-120 micrograms/dl) respectively measured by High performance liquid chromatography method.

Typically, a newborn has far lower cord plasma retinol concentration values, even under normal circumstances, than the mother. The comparatively higher values in the baby is consistent with a known preferential maternal transport for vitamin A into mammary glands to support lactation at maternal cost [8] It seems possible that the infant was born with a far lower vitamin A level, consistent with the clinical signs, but that may have been rising through intensive breast feeding, making the mother even more replete.

A diagnosis of keratomalacia with bilateral pneumonitis was made and treatment was started immediately in the form of I/V fluids, antibiotics, a parenteral dose of 25 000 IU of Vitamin A along with ocular antibiotics, cycloplegics and artificial tears with eye patching. The serum retinol levels of the neonate after 2 days of Vitamin A supplementation was 29.6 micrograms/dl. The baby and the mother were treated with total 3 doses of Vitamin A and after adequate counseling about diet, the baby was discharged. One month follow up of the baby showed dense corneal opacities in both eyes.


During pregnancy, Vitamin A is essential for the health of the mother as well as for development of the fetus. This is because vitamin A is important for cell division, fetal organ and skeletal growth and maturation, maintenance of the immune system to strengthen defenses against infection, and development of vision in the fetus as well as maintenance of maternal eye health and night vision. [13],[14]

Comprehensive recommendations for the assessment and control of VAD were rigorously reviewed and revised by a working group and presented for discussion at the XX International Vitamin A Consultative Group meeting in Hanoi, Vietnam. These recommendations include standardized definitions of VAD and VAD disorders. VAD is defined as liver stores below 20 μg (0.07umol) of retinol per gram. VAD disorders are defined as any health and physiologic consequences attributable to VAD, whether clinically evident (xerophthalmia, anemia, growth retardation, increased infectious morbidity and mortality) or not (impaired iron mobilization, disturbed cellular differentiation and depressed immune response). A maternal history of night blindness during a recent pregnancy was added to the clinical criteria for assessing vitamin A status of a population, and the serum retinol criterion for a "public health problem" was revised to 15% or more of children sampled having levels of less than 20 ug/dl(0.7 umol/L). [15]

Infants are born with negligible liver stores which are sufficient only for a few days of vitamin A. When a mother is deficient in vitamin A the newborn child's reserves are even smaller. Colostrum and early breast milk are concentrated sources of vitamin A [16] To enable some storage of the vitamin, the infant needs to be predominantly breast fed with milk containing at least 30 ug/dl. Studies by Belvady and Gopalan in India have shown that infants fed by vitamin A deficient mothers whose breast milk provides as little as 120+/−15 microgm DE/day grow normally as their basal requirement(minimum daily intake that prevents the appearance of clinical signs of VAD) are met with. [17] Accordingly, the FAO/WHO recommends basal requirement for infants at 120 microgm/day, increased to 180 ug RE/day to account for variability in growth rates. [18]

The concentration of Vitamin A in breast milk is maintained by maternal retinol stores and maternal dietary vitamin A intake. These can get depleted during lactation. Vitamin A in breast milk is in form of retinyl esters and provitamin A carotenoids. The relative proportion is dependent on the usual diet of the mother, so carotenoids account for a larger proportion of the vitamin A in breast milk of women from developing countries. [19]

The average breast milk concentration of women in industrialized countries is 60 ug/dl as compared with 50 ug/dl in poorer countries, where individual values are often less than 30 ug/dl. [20]

Lactating mothers become vitamin A depleted in many developing countries. Night blindness among pregnant and lactating women in rural Nepal ranges from 8 to 16% in the Terai and 52% at higher elevations. [21] WHO recommends that all breastfeeding women in vitamin A deficient areas should be supplemented with a single dose of 60 mg RE during the first 2 months post partum. Thereafter, they should not be given more than 3 mgRE per day or 25 mgRE per week because of possibility of new pregnancy, when the high dose supplement could cause fetal malformations. [22] When low income Bangladeshi women were given a single dose of 60 mg of vitamin A 24 h after delivery, there was a significant increase in maternal serum retinol through 3 months of lactation when compared with controls. [23]

Poor absorption of vitamin A is a problem during diarrhoeal disease and febrile infections, during which there is a higher rate of utilization of the vitamin. Human milk contains a latent lipase that is activated by bile salts in the duodenum and may hydrolyze the retinyl esters in the milk. Zinc and iron deficiency also interfere with the transport and utilization of stored retinol, Hence, such factors should be kept in mind when evaluating need of supplements in this group.

There is relatively little information on the effects on breast milk retinol when mothers are given smaller doses of vitamin A in pregnancy or lactation. Low income Indian women supplemented with 31.5 umol (9mgRE) daily during the last trimester of pregnancy had a higher vitamin A concentration in colostrum and in breast milk until 10 days postpartum. [24]

Breast milk retinol concentration can improve as a result of vitamin A fortification programs such as Vitamin A fortified monosodium glutamate in Indonesia [25] or sugar as in Guatemala. [26] These studies suggest that smaller, sustained doses of vitamin A can sustain increase in breast milk retinol concentration.

The health benefits of vitamin A supplementation in infants have also been studied. Different studies conducted in Bangladesh in which 7.5-15 mg RE of vitamin A given to infants along with the three doses of DPT/OPV to infants did not improve serum retinol concentration significantly. [27] It has been suggested that this may be due to inappropriate cutoffs for vitamin A indicators in this age group and also because relatively little of the supplement is retained at 3 and 6 months.

Existing WHO recommendations for vitamin A supplementation during pregnancy are that independent of vitamin A status, 10 000IU or 3000 microgm RE per day is the maximum daily supplement to be recommended at any time during pregnancy. In vitamin A deficiency endemic areas, the recommendations are same or a weekly supplement not exceeding 25 000IU (8500 microgm) at any time during pregnancy. Both dietary and supplemental forms of Vit A are safe at these levels. [28]

Pregnant women are also denied good food due to false beliefs. Papaya, a rich source of Vitamin A, is considered to be an abortificient and is hence often banned. Illiterate women are also unlikely to consume sufficient green vegetables, seasonal fruits and meat. [29],[30] Moreover, the availability of vitamin A enriched food is seasonal and they are not popular food items [31] Poor vitamin A status has also been reported as one of the factors associated with a higher prevalence of prematurity and intrauterine growth retardation [32] Hence, pregnant women should be encouraged to receive adequate nutrition, which is best achieved by consumption of a healthy balanced diet. However, in a poor country like ours, the role of vitamin A supplementation for pregnant women and neonates especially in areas with high incidence of maternal night blindness needs to be revised and reviewed.


1Global Initiative for the elimination of avoidable blindness. Geneva: World Health Organisation; 1998 (unpublished document WHO/BL/97.61).
2Gilbert C, Foster A. Childhood blindness in the context of VISION 2020-the Right to Sight. Bull World Health Organ 2001;79:227-32.
3Underwood BA. Prevention of vitamin A deficiency. In: Howson C, Kennedy E, Horwitz A, editors. Prevention of micronutrient deficiencies: Tools for policy makers and public health workers. Washington, DC: National Academy Press; 1998. p.103-66.
4Global prevalence of vitamin A deficiency in populations at risk 1995-2005. WHO Global Database on Vitamin A deficiency. Geneva: World Health Organisation; 2009.
5Stoltzfus RJ, Underwood BA. Bulletin of WHO, 1995. Available from: [Last accessed on 2013 Dec 13].
6Sommer A, Davidson FR. Annecy Accords. J Nutr 2002;132(9 suppl):28455-505.
7Chappell JE, Francis T, Clandinin MT. Vitamin A and E content of human milk at early stages of lactation. Early Hum Dev 1985;11:157-67.
8Allen LH, Haskell M. Vitamin A requirements of infants under six months of age. Food Nutr Bull 2001;22:214-34.
9Oliva MS, Schottman T, Gulati M. Turning the tide of corneal blindness. Curr Ophthalmol 2012;60:423-7.
10Gupta M, Jora R, Bhatia R, Pareek A. Keratomalacia in a Neonate Secondary to Maternal Vitamin A Deficiency. Indian J Pediatr 2005;72:881-2.
11Haldavar PV, Vasanthkumar HS, Siddibhavi BM. Neonatal Keratomalacia. Indian J Matern Child Health 1990;1:84-5.
12Gupta N, Tandon R. Sociodemographic features and risk factor profile of keratomalacia in early infancy. Cornea 2012;31:864-6
13Downie D, Antipatis C, Delday MI, Maltin CA, Sneddon AA. Moderate maternal vitamin A deficiency alters myogenic regulatory protein expression and perinatal organ growth in the rat. Am J Physiol Regul Integr Comp Physiol 2005;288:73-9.
14Food and Nutrition Board, Institute of Medicine. Vitamin A. In: Dietary reference intakes for vitamin A, vitamin K, arsenic, boron, chromium, copper, iodine, iron, manganese, molybdenum, nickel, silicon, vanadium, and zinc. Washington, DC: National Academy Press; 2001. p.82-146.
15Sommer A, Davidson FR. Assessment and control of vitamin A deficiency: The Annecy Accords. J Nutr 2002;132:2845S-50S.
16Sommer A. Vitamin A deficiency and its consequences: A field guide to detection and control. 3 rd ed, Geneva: World Health Organisation; 1995. p. 15.
17Belvady B, Gopalan C. Chemical composition of milk in poor Indian women. Indian J Med Res 1959;47:234-45.
18FAO/WHO. Requirements of vitamin A, iron, folate and vitamin B-12. Rome: Food and Agricultural Organisation; 1988.
19Wallingford JC, Underwood BA. Prediction of minimum maternal vitamin A status necessary to provide fully replete maternal and fetal tissue levels of vitamin A. Fed Proc 1984;43:470.
20Newman V. Vitamin A and breastfeeding: A comparison of data from developed and developing countries. San Diego, Calif, USA: Wellstart International;1993.
21Katz J, Khatry SK, West KP Jr, Humphrey JH, LeClerc SC, Kimbrough E, et al. Night Blindness is prevalent during pregnancy and lactation in rural Nepal. J Nutr 1995;125:2122-7.
22WHO. Safe vitamin A dosage during pregnancy and lactation. Geneva: World Health Organisation; 1997.
23Roy S, Islam A, Molla A, Akramuzzaman S, Jahan F, Fuchs G. Impact of a single megadose of vitamin A at delivery on breastmilk of mothers and morbidity of their infants. Eur J Clin Nutr 1997;51:302-7.
24Venkatachalam P, Belavady B, Gopalan C. Studies on vitamin A nutritional status of mothers and infants in poor communities in India. Trop Pediatr 1962;61:262-8.
25Muhilal, Murdiana A, Azis I, Saidin S, Basuni Jahari A, Karvadi D. Vitamin A-fortified monosodium glutamate and vitamin A status: A controlled field trial. Am J Clin Nutr 1988;48:1265-70.
26Arroyave G, Aguilar JR, Flores M, Guzman MA. Evaluation of sugar fortification with vitamin A at the national level. Washington DC: Pan American Health Organisation; 1979.
27Mahalanabis D, Rahman M, Wahed M, Islam M, Habte D. Vitamin A megadoses during early infancy on serum retinol concentration and acute side effects and residual effects on 6 month follow up. Nutr Res 1997;17:649-59.
28World Health Organisation. Safe vitamin A dosage during pregnancy and lactation. Vol. 98, Ottawa: Micronutrient Initiative; 1998. p.1-34.
29Chatterjee M. Socio-economic and socio-cultural influences on women's nutritional status. In: Gopalan C, Kaur S, (Editors). Women and Nutrition in India. New Delhi: Nutrition in India. New Delhi: Nutrition Foundation of India, Spl. Pub; Seri. No. 5 1989:297-323.
30Christian P, West KP Jr, Khatry SK, Katz J, Shreshtha SR, Pradhan EK, et al. Night Blindness of pregnancy in rural Nepal-nutritional and health risks. Int J Epidemiol 1998;27:231-7.
31Desai S, Desai R, Desai NC. Compendium of dietary sources of vitamin A in the Thar desert. Indian J Ophthalmol 1992;40:106-8.
32Shah RS, Rajalakshmi R. Vitamin A status of the newborn in relation to gestational age, body weight, and maternal nutritional status. Am J Clin Nutr 1984;40:794-800.