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Query: UMLS:C0029713 (immaturity)
 4,335 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors presented their own material of years 1974-1977. During this period 8788 children were born, in it 737 (8,3%) with low birth weight (below 2500 g). Retrolental fibroplasia was diagnosed in 4 children, it was 0,5% of newborns with low birth weight, and 0,04% of the all live-borns. The retrolental fibroplasia was diagnosed in: 1) the child born in 27 week of pregnancy with 1000 g of body weight, 2) in two children born in 32-33 week of pregnancy with 1450 g and 1350 g of body weight, 3) in a child born in 31 week of pregnancy with 1600 g of body weight. The infants were nursed in incubators with about 30% of oxygen during 36 to 46 days. Contemporary hypoglycemia, hypoproteinemia, atelectasia of lungs with respiratory insufficiency were diagnosed. In the discussion the authors underlined the role of immaturity and hypoxia of the premature baby, which play the role in the secondary injury of vessel's walls of retina. The disturbancy of carbohydrate and protein metabolism were certainly secondary pathogenic agent sin retrolental fibroplasia. There exists the necessity of oxygen therapy of premature baby, but to take cre of the infant in the incubator does not mean the necessity of oxygen therapy . Even with controlled oxygen dosage in incubator the retrolental fibroplasia may occur as a result of relative hyperoxydation induced by the constriction of retina vessels. The authors underlined the necessity of repeated ophthalmologic examination of premature babies in about every 2 weeks, what makes very early diagnosis possible.
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PMID:[Risk of damage to the organ of vision in low birth weight infants]. 26 40

Visual acuity was assessed in 72 patients who weighed 750 g or less at birth, had intact visual pathways as confirmed with computed tomography or magnetic resonance imaging, and had at least one eye evaluated for cicatricial sequelae after active, untreated retinopathy of prematurity without macular detachment (stage 4a or better). Visual acuities were obtained for 137 untreated, sighted eyes. Severity parameters for retinopathy of prematurity (stage of retinopathy of prematurity, refraction [in spherical equivalents], macular ectopia [in disc diameters], and vessel traction [in 30 degrees sectors]) was were significant predictors of visual acuity (P less than .0001) based on results of linear regression and stepwise regression analyses; however, parameters of retinal immaturity (birth weight, gestational age, and zone of retinopathy of prematurity) were not significant predictors of visual acuity. Visual acuity of the study eyes was good (median, 20/30; geometric mean, 20/33.58), with no statistical differences between eyes evaluated on last examination with linear Allen figures and those evaluated with linear Snellen test types.
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PMID:Visual acuity correlates with severity of retinopathy of prematurity in untreated infants weighing 750 g or less at birth. 149 21

We reviewed the records of 32 consecutive children (43 eyes) who underwent lensectomy/vitrectomy between January 1988 and August 1990 at the Medical Center of the University of California at San Francisco, to study the incidence and characteristics of clinically significant postoperative inflammation (CSPI). No eyes of patients 18 months old or younger (22 eyes) developed CSPI; nine of 21 eyes of older patients did develop CSPI. Other ocular abnormalities (microphthalmos, persistent hyperplastic primary vitreous, retinopathy of prematurity, and Axenfeld's syndrome) and systemic syndromes did not influence the incidence of CSPI. Prolonged inflammation delayed refractive and amblyopia therapy but did not affect final visual acuity. The absence of CSPI in younger patients may be related to the general immaturity of their immune system and a resultant weak inflammatory response, or to their specific immunologic tolerance to lens crystallins.
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PMID:Inflammation after cataract surgery in children. 151 45

The pathogenesis of NC in VLBW infants appears to be multifactorial. The vulnerability of extreme immaturity and the underdevelopment of renal function may be the most important variables. In some ways, we view this problem as similar to that of retinopathy of prematurity. (Clearly the exposure of the retina to high partial pressures of oxygen contributes to the development of retinopathy of prematurity but other variables--some known, such as an immature retina, and others not yet defined--must be present.) Hypercalciuria is common in the VLBW infant, yet not all develop NC. Decreased glomerular filtration rate, low citrate excretion, and frequently an alkaline urine are in part due to the immaturity of renal function of these infants. The need for prolonged hyperalimentation resulting in increased oxalate excretion and the development of BPD frequently requiring diuretics that may cause phosphaturia and magnesium depletion and that may increase calcium excretion are more common in the smallest and sickest of premature infants. Even transient insults to the kidneys, such as hypoxia or hypotension or the use of nephrotoxic drugs that provoke tubular injury and cell death with the probability of crystal formation and growth by way of heterogeneous nucleation, are likely to occur more frequently in this vulnerable population.
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PMID:Nephrocalcinosis. 157 67

The object of this investigation was to review the neonatal mortality among infants with very low birthweights (less than or equal to 1,500 gram) in the County of North Jutland and to determine the distribution of the main causes of death. It is important to note that, in a review of this type, the material was unselected. The period involved was 1988-1989. During this period, 86 infants with very low birthweights were born and 63 of these survived for longer than 28 days, corresponding to a neonatal survival of 73%. The survival increased from 11% in infants weighing 500-700 gram at birth to 93% for infants with birthweights between 1,250-1,500 gram from 0% with gestational ages of 24-25 weeks to 98% with gestational ages greater than or equal to 30 weeks. No significant differences in survival were observed as regards sex, place of delivery, method of delivery and singleton/twin delivery but survival was markedly dependent on whether the infants had asphyxia on delivery. The commonest causes of death were the respiratory distress syndrome, periventricular haemorrhage and asphyxia, followed by sepsis, enterocolitis necrotans and immaturity. The incidence of immediate sequelae in the form of chronic pulmonary disease and the retinopathy of prematurity were low.
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PMID:[Neonatal mortality in infants with very low birth weights in the county of North Jutland. Retrospective study]. 195 90

Retinopathy of prematurity has reappeared in the neonatal nursery after largely disappearing 35 years ago. The major factor in its reemergence is the progressive improvement in neonatal care, resulting in salvage of infants who formerly would have been lost. Oxygen is now recognized to be but one of many interacting factors in the development of retinopathy of prematurity, with extreme immaturity being the primary factor. Methods of examination, classification and treatment of retinopathy of prematurity are discussed.
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PMID:Retinopathy of prematurity. 219 77

Identification of a suitable animal model is essential for the continued study of retinopathy of prematurity (ROP). Since 1984 we have used the newborn rat for the study of oxygen-induced retinopathy (OIR). The rat retina is highly immature at birth. Like those of humans, the retinal vessels arise from mesenchymal precursors, but contrary to that which occurs in humans, canalization of the rats inner retinal vessels is not related to the presence of cystoid spaces. In addition, only immature Stage I photoreceptors are present around the optic disk at birth. This extreme immaturity makes the rat retina highly susceptible to direct damage from oxygen. Oxygen-induced retinopathy can be produced by exposing the newborn rat to 80% oxygen for the first 7-10 days of life. We have demonstrated that OIR does not develop when oxygen is administered under conditions of moderate hyperbarism (+1.8 atm). It is possible that hyperbarism exerts a protective effect on the immature retinal vessels by inducing a vasoconstrictive response which reduces the amount of oxygen transported from the choroid to the inner retina during hypoxia. I recently hypothesized that this vasoconstriction might also affect the ciliary body, thus reducing the quality of aqueous produced, and we are currently studying the relationship between development of the immature retinal vessels in the rat and production and drainage of the aqueous. The question we are attempting to answer is whether a condition of relatively increased intraocular pressure is capable of promoting the development of OIR.
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PMID:Oxygen-induced retinopathy in the rat model. 220 74

Retinopathy of prematurity (ROP) has increased in the United States in the past decade. Its resurgence has been attributed to advances in medical care which have increased the survival of infants less than 1000 g. Retinal immaturity and exposure to supplementary oxygen are generally accepted as the principal factors associated with ROP, however precocious exposure of the immature retina to light may also contribute. The preterm infant is routinely exposed for the duration of hospital stay to bright continuous light at levels which produce retinal damage in animals. A recent study has provided evidence implicating light in ROP. Preterm infants for whom the light levels were reduced had a lower incidence of ROP, compared to a similar group of preterms exposed to standard levels of nursery light. Given the problems of a non-randomized design, the results must be considered preliminary; however the findings are substantiated by parallel results in both hospitals studied and by an effect of exposure to light within the treatment group. Speculations regarding the mechanisms of light as a contributor to ROP include: alterations of retinal metabolism, cellular damage by phototoxicity, and the generation of free radicals. Mechanisms of phototoxicity are compatible with theories of oxygen toxicity. Light may not be necessary for ROP to occur, but it may increase the risk.
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PMID:Light and the developing retina. 220 77

The authors present the protocol currently used in their institution for initial and follow-up evaluation of infants at high risk for developing retinopathy of prematurity (ROP). After topical anesthesia and lid speculum insertion, the examination is carried out using an indirect binocular ophthalmoscope with a +20 or +28-diopter lens. Mydriasis is achieved by instilling one drop of 1% tropicamide, followed by one drop of 0.5% tropicamide + 2.5% phenylephrine 15 minutes later and after an additional 15 minute interval, another drop of 1% tropicamide. If mydriasis is insufficient after one hour, one drop of a 0.5% tropicamide-5.0% phenylephrine solution may be instilled. The initial examination is performed between the third and fourth weeks of life. If any areas of retinal immaturity are found, the examination is repeated every other week and, later, every three to four weeks, until vascularization has reached the ora serrata. Should any sign of ROP be present during the first examination, the patient is examined weekly or every other week depending on the severity of clinical findings.
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PMID:Retinopathy of prematurity (ROP): optimal timing of clinical evaluation and standard procedures. 220 81

The study includes all infants in a Danish county born 1982-87 considered at risk of acquiring retinopathy of prematurity (n = 411; 178 girls, 233 boys). 325 had birthweight (BW) less than or equal to 1750 g and/or gestational age (GA) less than or equal to 34 weeks. The remaining referrals were on account of functional immaturity/significant oxygen treatment (n = 86). With a median onset age of 6.5 weeks (range 5-9 weeks) ROP was recorded in 63 infants. A negative correlation (r = -0.34) between GA and ROP onset age suggested a later onset in the very immature infant. ROP appeared in 60% of those born at GA less than or equal to 28 weeks (n = 30) and in 50% of survivals with BW less than or equal to 1000 g (n = 20). With BW and GA beyond the limits of 32 weeks and 1750 g only 5 cases of ROP were observed. Out of the 14 infants with at least stage 3 ROP 6 became blind in both eyes after few months (GA at delivery 25-31 weeks/BW 920-1595 g). All considered, 57 of the 63 with ROP showed spontaneous regression, however, leaving myopia of prematurity in 8 subjects.
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PMID:Retinopathy of prematurity. Clinical findings in a Danish County 1982-87. 235 10


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