Corneal clouding, a rare observation in neonates, has been
linked to causes such as infections and metabolic disorders.
We describe a case of an extreme preterm with bilateral,
reversible corneal clouding – possibly due to hyperglycemia.
This preterm (25 weeks) male infant was
born vaginally to a primigravida mother; birth weight was
840 g. The child was managed with surfactant, ventilation,
parenteral nutrition, cefotaxime and amikacin. On 4th day,
baby developed seizures requiring phenobarbitone.
Neurosonogram revealed grade-I germinal matrix hemorrhage.
On 6th day, infant developed
hyperglycemia, which was managed by insulin infusion.
Hyperglycemia lasted for 22 hours (highest blood glucose:
890 mg/dL). Antibiotics were changed to vancomycin and
meropenem. Child also developed bilateral diffuse corneal
clouding suggestive of corneal edema. There was no
conjunctival or circumciliary congestion or eye discharge.
View to the anterior chamber and fundus was hazy; a red glow
was present. Iris details could not be visualized. Cornea
became clearer in the next few days. Mild haze persisted
till 28 days and cleared completely by 39 days. The infant
was diagnosed to have retinopathy of prematurity (ROP) at 28
days which progressed bilaterally requiring laser treatment
at 41 days. At discharge (81st day) and at 6 months, the
cornea remained clear.
Opacification of the cornea in a newborn
may occur in congenital glaucoma, corneal dystrophies,
Peter’s anomaly, sclerocornea, infection, trauma, limbal
dermoids and metabolic disorders like mucopolysaccharidoses
[1]. The case presented had no signs of ophthalmic infection
or dysmorphism. Corneal clouding was reversible unlike in
mucopoly-saccharidoses. ROP is an unlikely cause since
cornea had cleared when ROP had progressed. Drugs given to
this infant are also not known to cause corneal edema.
In this infant, severe hyperglycemia
could have caused endothelial dysfunction and corneal edema.
The Na,K-ATPase in the basolateral membrane of the
cornea, is responsible for the pump function [2]. Animal
studies show that hyperglycemia reduces Na,K-ATPase activity
of cornea [3,4]. In adult humans, acute hyperglycemia
affects corneal hydration control [5]. Another mechanism
could be hydration of lens, leading to angle closure and
rise in intra-ocular pressure resulting in corneal edema.
However, digital tonometry was normal in this infant.
We could not find any reported case of
corneal clouding in neonates due to hyperglycemia. Although
60-80 percent of extreme preterms develop hyperglycemia,
very high levels as observed in this case are rare. We
hypothesize that severe hyperglycemia may have an adverse
effect on the cornea of extreme preterms. With early
optimization of blood glucose levels, the corneal prognosis
appears to be good.
1. de Alba Campomanes AG, Binenbaum G,
Quinn GE. Disorders of the Eye. In: Gleason CA, Devaskar SU,
editors. Avery’s Diseases of the Newborn. 9th ed.
Philadelphia: Elsevier Saunders; 2012. p.1423-40.
2. Cornea NT. In: Krachmer JH, Mannis MJ, Holland EJ,
editors. Cornea. 2nd ed. London: Elsevier Mosby;
2005. p. 3-26.
3. Herse PR, Adams L. Effect of
hyperglycemia duration on rabbit corneal thickness and
endothelial ATPase activity. Acta Ophthalmol
Scand.1995;73:158-61.
4. Whikehart DR. The inhibition of
sodium, potassium-stimulated ATPase and corneal swelling:
the role played by polyols. J Am Optom Assoc.1995;66:331-3.
5. Mc Namara NA, Brand RJ, Polse KA,
Bourne WM. Corneal function during normal and high serum
glucose levels in diabetes. Invest Ophthalmol Vis Sci. 1998;
39:3-17.