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Originally Posted by bharat A male infant is born markedly prematuraly at 25 weeks of gestation.
Due to the immaturity of his lung, therapy with oxygen is used. Because of the extensive medical innervaion, this premature infants survives, but unfortunately he is found to be blind resulting from the use of oxygen.
Which of the listed pathologic abnormalities correctly describe the pathology
that causes the infant's blindness?
A. Accumulation of abnormal material in the ganglion cells of retina.
B. Fibrous Oblitration of the canal of Schlemm.
C. Formation of Fibrovascular mass behind the lens.
D. Lipid accumulation at the periphery of the cornea.
E. Severe Degeneration of the medulla. |
Oak is righ the Correct answer is C. Formation of Fibrovascular mass behind the lens.
bharat I congratulate for bringing this issue in the MCQs, because most of us are unware of this fact as we are posted to Gyn/Obs and Paediatrics we encounter a lot of problem where we do have to give O2 to the premature infant.
It was a burning issue in ealry 1950 where premature infant ended up with blindness for life after high O2 therapy during their birth as part of neonatal resuscitation.This resulted in a decreased incidence of cerebral palsy and death but increased incidence of blindness later in the life.
This is now known as Retinopathy of Prematurity (ROP), originally called retrolental fibroplasia, was the leading cause of blindness in children in the 1940s and 1950s. It was first described in the medical literature in 1942 by Terry.
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The problem occurs when an infant is given supplemental oxygen at birth to aid his or her underdeveloped lungs. At that time, the blood vessels in the childıs retinas are still developing, and oxygen therapy can cause these blood vessels to grow abnormally. After the abnormal growth begins, vessels that are supposed to remain with the retina of the eye can actually grow into the center of the eye, causing retinal detachment. The only way to repair the problem is with invasive laser therapy, which can cause damage to healthy retinal tissue.
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If we go back to the cause: We know that organigenesis occur from 3rd week to 8th week of intrauterine life and from 16 weeks to birth, retinal blood vessels grow out from the optic nerve to reach the peripheral retina. The last twelve weeks of a normal 40 week gestation are crucial in the development of fetal eyes. In premature infants, the normal growth of blood vessels stops. It is theorized that the area without adequate blood supply emits a chemical trigger to stimulate growth of the abnormal vessels. These vessels lead to a formation of a ring of scare tissue attached to both the retina and the vitreous gel that fills the center of our eyes. As the scar contracts, it may pull on the retinal creating a retinal detachment. Regardless of the gestation age at birth, ROP seems to occur at about 37 to 40 weeks.
But recenet understanding of ROP is changing. Traditionally the view was that high oxygen exposure was the cause. While it is certainly one of the major factors, studies now show that it is not just exposure to oxygen or other toxic agents after birth, but may also relate to actions that occur to the fetus prior to birth. Both chronic hypoxia (lack of oxygen) and intrauterine growth retardation may relate to ROP development. As many as one third of ROP cases may be the result of prenatal conditions. Light exposure has been suggested as another factor. To date, scientific studies have not confirmed light as a cause.
If anyone of you are interested to know more detail about ROL visit the following links:
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02-07-2006, 08:01 AM
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