Description, Causes and Risk Factors:
Retrolental fibroplasia also called retinopathy of prematurity (ROP) is a disorder of the retina of the eye. The retina is the back of the eye that passes visual information to the brain. In retrolental fibroplasia, the blood vessels in the retina have not developed completely, often due to premature birth. Retrolental fibroplasia is classified in five stages, ranging from mild (stage I) to severe (stage V).
There are three distinct ways in which various authors approach the problem of the etiology of retrolental fibroplasia. The first is that of the obstetrician. The factors influencing the premature birth itself, which were carefully considered by many authors are the following: Intrauterine bleeding, age of mother, multiparity, multiple fetus, sex, race, Rh factor, chronic illness of the mother, virus infection during pregnancy (e.g., rubella), toxoplasmosis, and vitamin A deficiency of the mother.
The second approach to the problem is that of the pediatrician. The factors influencing are the following: Precocious exposure to light, precocious closure of the ductus arteriosus, exposure to lower than intra-uterine temperature, lack of maternal endocrine environment, precocious rise of blood pressure, inability to assimilate vitamins, birth trauma, physiological anemia of prematurity, precocious establishment of blood groups, intra-ocular inflammation.
The third approach to the problem is that of the ophthalmologist. In babies with retrolental fibroplasia, the blood vessels in the retina grow abnormally. This can result in the formation of scar tissue and detachment of the retina, where the retina pulls loose from the back of the eye. In most cases, the blood vessels return to growing normally, but retrolental fibroplasia can cause vision problems or blindness.
Period of normality and disappearance of the hyaloid system before thecondition is observed: the fibroplasia does not develop as long as the hyaloidsystem of vessels can carry on its function.
Dilatation and tortuosity of vessels as the first clinical sign of the disease:An attempt to establish the circulation of the anterior part of the retina is causedby peripheral ischemia and metabolic breakdown.
Peripheral patches of retinal oedema and vitreous haze: the accumulatingmetabolites cause the local oedema to involve increasing areas of the retina whichthus become visible ophthalmoscopically; the vitreous in front of these areasis affected secondarily.
Retinal detachment: the natural consequence of progressing retinal edema.
Cyclitic membrane formation: a secondary inflammatory reaction provokedby the existence of a detached retina, accumulation of subretinal fluid, and metabolic failure. The anterior synechiae and mild inflammatory reaction in the uvealtract are of the same kind.
Return of retinal vessels to normal when the detachment is established:when the retina degenerates, its metabolism and nutritional requirements drop;thus the stimulus for vascularization ceases to exist.
Microphthalmos: the eye stops growing when the cyclitic membrane isformed.
Regression: this may occur with restoration to normal or as an arrest ofthe process. In the early stages of oedema or shallow detachment, it occurs as aresult of the successful establishment of circulation by retinal terminals. In thelater stages, the detached retina can become spontaneously re-attached aphenomenon known to occur in other kinds of detachment. The establishedcyclitic membrane, however, cannot regress.
The chance of having a baby with retrolental fibroplasia increases depending on how early the baby is born. About 50-70% of babies weighing less than 2.75 pounds will have retrolental fibroplasia. About 1,100-1,500 infants each year in the U.S. develop retrolental fibroplasia that is severe enough to require medical treatment. About 400-600 infants each year in the U.S. become legally blind from retrolental fibroplasia. In Virginia, about 160 babies are reported each year with some degree of retrolental fibroplasia.
Premature birth of the subject: precocious closure of the hyaloid artery,anemia, and precocious exposure to light are super-imposed on the vasculararrangements prevailing in the 7th to 8th months of pregnancy.
Retrolental fibroplasias may be mild and resolve spontaneously. However, in serious cases, it can lead to blindness. Common symptoms of retrolental fibroplasias in preterm infants are visual disturbance, retinal detachment, absent papillary light reflexes, potential blindness, dilated or twisted eye vessels, opaque retrolental eye membrane, retinal edema, and retinal hemorrhages. Other signs may include white pupils (leukocoria), abnormal eye movement (nystagmus), severe nearsightedness (myopia) and crossed eyes (strabismus).
An ophthalmologist can usually diagnose retrolental fibroplasia during an examination. All babies who are born at least 8 weeks early or weigh less than 1500 grams (less than about three pounds) need to be examined every 2 weeks. Examinations should start 6 weeks after the child is born. Examinations can stop when the blood supply to the retina has near fully grown. This is usually a couple of weeks before the date the baby was supposed to be due.
About half an hour before the examination a nurse will usually place drops in the baby's eyes. The drops will make the pupils go bigger. This lets the eye doctor see all of the back of the eye. By looking into the eye using a special lens and torch the retina can be seen. The ophthalmologist say how much of the retina does not yet have a blood supply. They can also see if any scarring or retinal detachment has started. Based on the examination the ophthalmologist can decide if any treatment is needed.
Most babies with retrolental fibroplasia do not need any treatment. If the baby's eyes do need treatment this is usually organized by the eye doctor. The treatment reduces the chance of a child developing visual impairment by between one half and one quarter.
The aim of treatment is to 'switch-off' the bits of retina at the edges that do not have a blood supply. Scarring happens in retrolental fibroplasia because these bits of retina at the edges try to make their own new blood vessels to overcome the lack of blood. The new blood vessels do not end up helping at all. They cause scarring and inflammation. This leads to retinal detachment and visual impairment. If the retina is 'switched-off' then there is no need to make the new blood vessels and retinopathy of prematurity does not develop.
These bits of retina at the edges, away from the important central part of vision, can be 'switched-off' in two ways.
By shining a hot laser into the eye, directly on to the retina.
By putting a very cold piece of metal on to the outside of the eye (cryotherapy).
Both treatments cause the retina that lacks a good blood supply to 'switch-off'. This reduces the chance of retinopathy of prematurity developing. The bits of retina that are treated usually no longer work. Despite this most children are unaware that they are missing bits of vision away at the edges. As long as their central vision remains clear it does not affect the child.
Laser is becoming the more common way to treat retrolental fibroplasia. Sometimes the laser can cause burns to the cornea or lens. These do not normally cause visual impairment and usually settle without any problems. Both types of treatment can be sore. It is often done with the child asleep under a general anaesthetic.
Many children sadly, despite treatment still develop visual impairment from retrolental fibroplasia
NOTE: The above information is educational purpose. The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition.
DISCLAIMER: This information should not substitute for seeking responsible, professional medical care.
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