Keratomalacia in a neonate secondary to maternal vitamin a deficiency
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《美国医学杂志》
Department of Pediatrics, Regional Institute of Maternal and Child Health, Umaid Hospital for Women and Children and Dr. S.N. Medical College, Jodhpur, India
Abstract
A 40-day-old male child was admitted with complaints of not opening eyes from 2-3 days after birth. A diagnosis of X3-B keratomalacia was made. The treatment was done with vitamin-A to which the patient had responded. The mother of the baby had a history of night blindness throughout the pregnancy for which she was also treated. Keratomalacia secondary to vitamin-A deficiency is rare in neontes, although in children it is reported form developing countries.
Keywords: Keratomalacia; Vitamin-A deficiency; Neonates.
Keratomalacia (Limbus to Limbus Corneal Xerosis) in secondary to vitamin A deficiency is rare in neonates, although in children it is reported from developing countries. Malnutrition is one of the major causes of blinding malnutrition due to vitamin A deficiency.
We are reporting a neonate 40 days old who has presented to us with keratomalacia. His mother also had a history of night blindness all through the period of pregnancies.
Case report
A 40-day-old male child was admitted with complaints of not opening his eyes since 2-3 days after birth. The patient was preterm (34 weeks), normal delivery at home with immediate cry at birth, and he was on exclusive breastfeeding, although the yield of milk was poor. According to the mother he was opening his eyes for the first three days of life, when there developed a yellow color discharge from both the eyes, and since then was unable to open his eyes. Upto one month, the patient had not taken any treatment. Thereafter, he was shown to an ophthalmologist who diagnosed the problem as corneal ulcer. The patient was later referred to the authors for any systemic disease associated with it. One of the significant findings in the family history was that the mother had history of night blindness during the present and previous pregnancy and was also having night blindness at the time of admission in the ward.
The weight of the child was 3.5kg, length 52cms and head circumference 36cms. On examination, both the eyes were tightly closed due to marked photophobia; and on opening the eyes forcibly, there was a presence of corneal ulcer with opacities and discharge from both the eyes. In the investigations conducted Hb, Total nd Differential leucocyte count (TDLC) and X-ray chest were normal. Neonatel reflexes (NNR) and systemic examination were also normal.
The ophthalmologist's opinion was same that it is bilateral corneal ulcer with scar and diagnosis is made as X3-B keratomalacia.
As a treatment the patient was given 50,000 I.U. of vitamin A I.M. daily for two days. With this treatment, the patient showed some improvement; he started opening his eyes and the discharge from eyes had also lessened. Simultaneously, the mother was also treated for night blindness with parental doses of vitamin A.
Discussion
Xerophthalmia, literally, means dry eye. It encompasses a spectrum of clinical findings, beginning with night blindness arising from loss of function of the rod photoreceptors and progressing to conjunctival or corneal xerosis with photophobia, and finally corneal ulceration and necrosis. It is generally agreed that when keratomalacia develops, there is no hope of visual rehabilitation. In a diet entirely devoid of vitamin A, night blindness heralds the onset of conjunctival and corneal degeneration by 2 to 3 months. [1],[2],[3],[4],[5],[6],[7],[8],[9],[10]
In developing countries, vitamin A deficiency is associated with general malnutrition and protein deficiency, with high mortality and morbidity rates.[2],[3] There are generally two peaks of prevalence: first in early infancy (less than 6 months) and second, after 3-4 years. The first peak probably reflects maternal nutrition and the second peak is diet related.[4] The present case belonged to the first peak and is related to maternal vitamin A deficiency.
Western Rajasthan has the largest arid zone in India (62%), and nearly half of this area is a desert with poor or no rainfall.[5] It has been seen that at times of drought and famine, the prevalence of vitamin A deficiency in desert area region is high, but similar in urban (13.7%) as in rural (16.2%) areas.[6] A study conducted by G.S.Toteja et al[7] in Western Rajasthan (Bikaner) had shown prevelance of Bitot's spots (0.64%) and night blindness (0.5%) in children, and prevalence of night blindness in pregnant mother was nil.
In rural area, the reason for vitamin A deficiency is that the rural population still does not consume vitamin A enriched foods. However, the availability of vitamin A enriched food is seasonal and they are not popular food items.[8] The mother of the child had night blindness and this night blindness, according to her, was still persisting in the post partum period and thereafter. The other members of the family including other children and the father who came with the index case, on examination, were found to have X1A and X1B lesions indicating vitamin A deficiency in the family.
The child and mother were treated with parental doses of vitamin A to ensure the complete doses and speedy recovery from the disease. The mother has shown remarkable improvement with her night blindness. But the child has both eyes blinded because of ulceration and keratomalacia. We took the opinion of ophthalmologist regarding the corneal grafting, but according to them, there was no hope of revival of vision. However, we advised follow-up to evaluate the possibility of corneal graft in later life, otherwise the child has no problem. The family was told about the diet and other members were also given vitamin A.
References
1. Sommer A, Tjakarasudjatma S et al. Vitamin A responsive panocular xerophthalmia in a healthy adult. Arch Ophthalmol 1978; 96 : 1630-1634.
2. Kie-Tong Y. Protein deficiency in Keratomalacia. Br J Ophthalmol 1956; 40 : 502-503.
3. Venktaswamy G. Ocular manifestations of vitamin A deficiency. Br J Ophthalmol 1967; 51 : 854-859.
4. Rahmathullah L, Raj MS, Chandrawath TS. Aetiology of severe vitamin A deficiency in children. Natl Med J India 1997; 10 : 62-65.
5. Ramakrishna YS. Climatic changes in relation to desertification in the Indian arid zone. In Tiwari AK, ed. Desertification - Monitoring and Control. 1st edn. Jodhpur; Scientific Publishers, 1988; 99-133.
6. Desai NC. The xerophthalmic profile in desert regions. Afro - Asian J Ophthalmol 1986; 5 (1) : 20-22.
7. Toteja GS, Padam Singh, Dhillon BS and Sexena BN. Vitamin A deficiency disorders in 16 Districts of India. Ind J Pediatr 2002; 69 (7): 603-605.
8. Desai S, Desai R, Desai NC. Compendium of dietry sources of vitamin A in the Thar desert. Ind J Ophthalmol 1992 ; 40 (4) : 106-108.
9. Jensen O.A et al. Necrotizing keratitis (Keratomalacia) with corneal perforation and expulsive hemorrhage in newborn. Acta Opthalmol (Copenhen) 1968; 46(2) : 215-217.
10. Changing trends in Vitamin A deficiency in children below five years of age. Xerophalmic Club Bulletin 1994 ; 56 : 1-4.(Gupta Mukesh, Jora Rakesh)
Abstract
A 40-day-old male child was admitted with complaints of not opening eyes from 2-3 days after birth. A diagnosis of X3-B keratomalacia was made. The treatment was done with vitamin-A to which the patient had responded. The mother of the baby had a history of night blindness throughout the pregnancy for which she was also treated. Keratomalacia secondary to vitamin-A deficiency is rare in neontes, although in children it is reported form developing countries.
Keywords: Keratomalacia; Vitamin-A deficiency; Neonates.
Keratomalacia (Limbus to Limbus Corneal Xerosis) in secondary to vitamin A deficiency is rare in neonates, although in children it is reported from developing countries. Malnutrition is one of the major causes of blinding malnutrition due to vitamin A deficiency.
We are reporting a neonate 40 days old who has presented to us with keratomalacia. His mother also had a history of night blindness all through the period of pregnancies.
Case report
A 40-day-old male child was admitted with complaints of not opening his eyes since 2-3 days after birth. The patient was preterm (34 weeks), normal delivery at home with immediate cry at birth, and he was on exclusive breastfeeding, although the yield of milk was poor. According to the mother he was opening his eyes for the first three days of life, when there developed a yellow color discharge from both the eyes, and since then was unable to open his eyes. Upto one month, the patient had not taken any treatment. Thereafter, he was shown to an ophthalmologist who diagnosed the problem as corneal ulcer. The patient was later referred to the authors for any systemic disease associated with it. One of the significant findings in the family history was that the mother had history of night blindness during the present and previous pregnancy and was also having night blindness at the time of admission in the ward.
The weight of the child was 3.5kg, length 52cms and head circumference 36cms. On examination, both the eyes were tightly closed due to marked photophobia; and on opening the eyes forcibly, there was a presence of corneal ulcer with opacities and discharge from both the eyes. In the investigations conducted Hb, Total nd Differential leucocyte count (TDLC) and X-ray chest were normal. Neonatel reflexes (NNR) and systemic examination were also normal.
The ophthalmologist's opinion was same that it is bilateral corneal ulcer with scar and diagnosis is made as X3-B keratomalacia.
As a treatment the patient was given 50,000 I.U. of vitamin A I.M. daily for two days. With this treatment, the patient showed some improvement; he started opening his eyes and the discharge from eyes had also lessened. Simultaneously, the mother was also treated for night blindness with parental doses of vitamin A.
Discussion
Xerophthalmia, literally, means dry eye. It encompasses a spectrum of clinical findings, beginning with night blindness arising from loss of function of the rod photoreceptors and progressing to conjunctival or corneal xerosis with photophobia, and finally corneal ulceration and necrosis. It is generally agreed that when keratomalacia develops, there is no hope of visual rehabilitation. In a diet entirely devoid of vitamin A, night blindness heralds the onset of conjunctival and corneal degeneration by 2 to 3 months. [1],[2],[3],[4],[5],[6],[7],[8],[9],[10]
In developing countries, vitamin A deficiency is associated with general malnutrition and protein deficiency, with high mortality and morbidity rates.[2],[3] There are generally two peaks of prevalence: first in early infancy (less than 6 months) and second, after 3-4 years. The first peak probably reflects maternal nutrition and the second peak is diet related.[4] The present case belonged to the first peak and is related to maternal vitamin A deficiency.
Western Rajasthan has the largest arid zone in India (62%), and nearly half of this area is a desert with poor or no rainfall.[5] It has been seen that at times of drought and famine, the prevalence of vitamin A deficiency in desert area region is high, but similar in urban (13.7%) as in rural (16.2%) areas.[6] A study conducted by G.S.Toteja et al[7] in Western Rajasthan (Bikaner) had shown prevelance of Bitot's spots (0.64%) and night blindness (0.5%) in children, and prevalence of night blindness in pregnant mother was nil.
In rural area, the reason for vitamin A deficiency is that the rural population still does not consume vitamin A enriched foods. However, the availability of vitamin A enriched food is seasonal and they are not popular food items.[8] The mother of the child had night blindness and this night blindness, according to her, was still persisting in the post partum period and thereafter. The other members of the family including other children and the father who came with the index case, on examination, were found to have X1A and X1B lesions indicating vitamin A deficiency in the family.
The child and mother were treated with parental doses of vitamin A to ensure the complete doses and speedy recovery from the disease. The mother has shown remarkable improvement with her night blindness. But the child has both eyes blinded because of ulceration and keratomalacia. We took the opinion of ophthalmologist regarding the corneal grafting, but according to them, there was no hope of revival of vision. However, we advised follow-up to evaluate the possibility of corneal graft in later life, otherwise the child has no problem. The family was told about the diet and other members were also given vitamin A.
References
1. Sommer A, Tjakarasudjatma S et al. Vitamin A responsive panocular xerophthalmia in a healthy adult. Arch Ophthalmol 1978; 96 : 1630-1634.
2. Kie-Tong Y. Protein deficiency in Keratomalacia. Br J Ophthalmol 1956; 40 : 502-503.
3. Venktaswamy G. Ocular manifestations of vitamin A deficiency. Br J Ophthalmol 1967; 51 : 854-859.
4. Rahmathullah L, Raj MS, Chandrawath TS. Aetiology of severe vitamin A deficiency in children. Natl Med J India 1997; 10 : 62-65.
5. Ramakrishna YS. Climatic changes in relation to desertification in the Indian arid zone. In Tiwari AK, ed. Desertification - Monitoring and Control. 1st edn. Jodhpur; Scientific Publishers, 1988; 99-133.
6. Desai NC. The xerophthalmic profile in desert regions. Afro - Asian J Ophthalmol 1986; 5 (1) : 20-22.
7. Toteja GS, Padam Singh, Dhillon BS and Sexena BN. Vitamin A deficiency disorders in 16 Districts of India. Ind J Pediatr 2002; 69 (7): 603-605.
8. Desai S, Desai R, Desai NC. Compendium of dietry sources of vitamin A in the Thar desert. Ind J Ophthalmol 1992 ; 40 (4) : 106-108.
9. Jensen O.A et al. Necrotizing keratitis (Keratomalacia) with corneal perforation and expulsive hemorrhage in newborn. Acta Opthalmol (Copenhen) 1968; 46(2) : 215-217.
10. Changing trends in Vitamin A deficiency in children below five years of age. Xerophalmic Club Bulletin 1994 ; 56 : 1-4.(Gupta Mukesh, Jora Rakesh)