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At least 19 recordsLinked to original sources

Retinal detachment in retrolental fibroplasia.

Retrolental fibroplasia is a continuing problem in ophthalmology and may lead to retinal detachment. In this study, two groups of patients with retrolental fibroplasia and retinal detachment are described. The first group consists of youngsters who develop retinal detachment during their teenage years and frequently have not been diagnosed as having the disease until the retina detaches. Usually definite retinal breaks can be found near the equator and these are round or oval in appearance and without opercula. A second group of patients was noted to develop retinal detachment at an earlier age. The configuration of these detachments suggested a rhegmatogenous etiology, but retinal breaks were hard to detect because the peripheral retina was frequently obscured by a membrane or cataract. Additional evidence to support this opinion was provided when a small retinal hole was identified in one youngster whose ora could be easily seen. Because of the progressive nature of vitreoretinal adhesion in retrolental fibroplasia, it is advocated that youngsters with any evidence of retrolental fibroplasia at the time of discharge from the premature nursery be followed at one month, three months, and six months of age and at four-month intervals thereafter until the age of four years. If no difficulty develops by the time, yearly examinations suffice. Follow-up examinations are important because when prompt diagnosis of retinal detachment is made, the involved eye can often be salvaged with surgery.

Adolescent↗

Recent advances in retrolental fibroplasia.

Retrolental fibroplasia is the most common cause of preschool blindness. Changes identical to retrolental fibroplasia in humans have been produced in animals by exposing them to high oxygen concentration. Oxygen should be ordered for premature infants in a careful and precise manner. Concentrations of over 40 per cent should be avoided whenever possible. Withdrawal to air should be a gradual process.

Blindness↗

Treatment of retrolental fibroplasia.

Retrolental fibroplasia (RLF), a proliferative vascular retinopathy found almost exclusively in premature infants, continues to occur despite careful attention to oxygen administration. Much has been learned about the etiology and mechanisms of RLF over the past 30 years, and it is hoped that technological and biological research will ultimately lead to its prevention. No treatment is of proven value for the proliferative stages of RLF, although photocoagulation and cryotherapy directed at destruction of neovascularization are under study. Surgical treatment may be of value in controlling associated problems, particularly retinal detachments.

Child↗

Nonhyperoxic retrolental fibroplasia.

Retrolental fibroplasia (RLF) has most often been observed in preterm infants exposed to high ambient oxygen concentrations. This case report describes an infant near term who was never exposed to supplemental oxygen but in whom stage 4 RLF developed. The etiologic role of exchange transfusion is discussed.

Exchange Transfusion, Whole Blood↗

Retrolental fibroplasia.

Retrolental fibroplasia is more accurately referred to as retinopathy of prematurity. Host factors most clearly incriminated are the maturity of the infant and the time in oxygen therapy. A continuum of retinopathy ranges from abnormal arborization of terminal retinal vessels to a detached retina incorporated in a cicatrix behind the lens. Every high-risk infant should be examined by indirect ophthalmoscopy prior to discharge from the nursery. A thorough knowledge of the natural course of the disease is essential because many cases will resolve spontaneously.

Humans↗

Current therapy of retrolental fibroplasia. Retinopathy of prematurity.

Retrolental fibroplasia, frequently referred to now as the "retinopathy of prematurity," has shown an increased incidence in recent years. This is apparently due to advances in neonatal care, which have resulted in a four- to five-fold improvement in the survival of the extremely low birthweight infants and it is these infants who are at the highest risk of developing retrolental fibroplasia. The use of large supplements of vitamin E, a known antioxidant, is discussed along with other forms of therapy.

Child↗

[Retrolental fibroplasia--a preventable disease? (author's transl)].

Retrolental Fibroplasia has a high incidence in premature infants of low gestational age. The most susceptible period for developing retrolental fibroplasia is the immature vascularisation of the retina during the 28th to 40th gestational week. The disease is caused by the direct effect of oxygen administration. Retrolental fibroplasia is associated with the concentration of oxygen administered and the length of time in supplemental oxygen. There is also a significant association between its development and severe apnea requiring bag and mask resuscitation maintaining ambient oxygen concentration during the procedure. Furthermore there is an association between retrolental fibroplasia and the amount of adult blood transfused. Infants with these factors are at high risk to develop retrolental fibroplasia. Preductal PaO2-level should be kept between 60 and 70 mm Hg and supervised by continuous transcutaneous readings. There is some concern about intermittent arterial sampling. Problems of interpreting PaO2-analyses are discussed. 25 mg Vitamin E are recommended for prevention. There are many management protocols and techniques during neonatal intensive care of premature infants for prevention of the disease. Premature infants at risk should have a close time schedule for ophthalmoscopy.

Blood Transfusion↗

THE PRESENT STATUS OF RETROLENTAL FIBROPLASIA.

The incidence of retrolental fibroplasia in premature babies has been greatly reduced since the curtailment of oxygen concentration and exposure time. However, in infant care, cases still occur in premature infants who have respiratory distress and cyanosis. The incidence is lowest where oxygen in excess of 40 per cent is never administered, regardless of the status of the infant. The mechanism by which oxygen causes obliteration of retinal vessels has not been discovered. A sampling of teaching institutions revealed that more than 30 cases have been seen since 1959.

Cyanosis↗

Retinal and central nervous system abnormalities: syndromes which resemble retrolental fibroplasia.

Recently, the mechanism of the development of severe retrolental fibroplasia has been shown to occur by gap junction formation between adjacent mesenchymal spindle cells in the nerve fiber layer. Multiple syndromes with oculo-cerebral malformations give rise to retinal dysplasia (disturbances of neuroectodermal migration and/or differentiation) or retinal vascular abnormalities (disturbances of mesenchymal differentiation) which resemble clinically retrolental fibroplasia. Case 1 is an example of retinal dysplasia (disturbed neuroectodermal migration and/or differentiation) with normal retinal vascularization simulating superficially an active peripheral retinal detachment of retrolental fibroplasia in the preterm infant. Case 2 is an example of normal retinal differentiation with abnormal retinal vascularization (disturbed mesenchymal differentiation) simulating identically cicatricial dragging of the retinal vessels temporally of retrolental fibroplasia in the preterm infant. Thus, cases of central nervous system malformation should prompt an early ophthalmologic examination to document retinal abnormalities in term infants which occur without the administration of oxygen congenitally, from true retrolental fibroplasia in preterm infants which occurs following changes in oxygen tension approximately 8 weeks postnatally.

Abnormalities, Multiple↗

Vascular tufts in retrolental fibroplasia.

Three cases of retrolental fibroplasia with vascular tufts at different locations are described. They probably represent mesenchymal proliferation in response to severe hypoxia. The tufts are reddish-pink in color and angiographically do not leak fluorescein. When present posterior to the equator they suggest an immature retinal circulation and the visual prognosis is poor.

Adolescent↗

Retrolental fibroplasia: a medical dilemma.

Retrolental fibroplasia (RLF) remains as a leading cause of visual impairment in infants. The pathophysiology of RLF is discussed as well as the significant risk factors. The clinical course of the disease is considered including the various stages of RLF and the differential diagnosis. Finally, the management and treatment options of RLF are discussed.

Diagnosis, Differential↗

The relationship of blood transfusions to retrolental fibroplasia.

The medical records of 53 premature infants weighing less than 1,360 g at birth were examined. The retinas of 32 infants remained normal, while mild active retrolental fibroplasia developed in 17 babies, and severe active retrolental fibroplasia developed in four babies. The birth weight, duration of exposure of supplemental oxygen, and the amount of blood they received as transfusions were recorded. There was no significant difference in these values for those babies whose retinas remained normal and for those babies in whom mild retinopathy of prematurity developed. However, the infants in whom severe retrolental fibroplasia developed were significantly smaller in weight at birth and received more supplemental oxygen and transfused blood. There was a close correlation between the amount of blood transfused and days of exposure to supplemental oxygen. In addition, the ratio of transfused blood to days of supplemental oxygen exposure was greater in those infants in whom no retrolental fibroplasia developed and least in those infants in whom severe active retrolental fibroplasia developed.

Birth Weight↗