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

In newborn and premature infants whose lung immaturity entails a limited capacity for O2 detoxification, the use of supplemental oxygen should be continuously and non-invasively monitored. Pulse oximetry and transcutaneous O2 monitoring are the systems most used in the NICU. Major limitations of pulse oximetry are motion artifact, sensitivity to excessive light, cutaneous hypoperfusion, hypothermia, venous congestion, arterio-venous shunting, strong skin pigmentation, anemia and high percentage of abnormal hemoglobin. Alarm habituation is a further major risk. New oxymeters show less motion, artifact and higher accuracy during low oxygen saturation. The accuracy during high oxygen saturation is very dependent on the specific oxymeter model used. Transcutaneous O2 monitoring is usually combined with transcutaneous PCO2 monitoring, hence enabling evaluation of oxygenation as well as ventilation. A major risk of this method is related to the heated electrode sensor, which can induce skin burns. A combined ear sensor for pulse oximetry and PCO2 monitoring seems promising.
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PMID:[Oxygen therapy in newborn: equipments for non-invasive monitoring]. 1576 30

Marsupials at birth are small and relatively undeveloped. At birth, the lung in some species is at the canalicular stage of development and though lung diffusion and metabolic rate are strongly correlated, the allometric exponent suggests that smaller newborns have relatively smaller diffusing capacity with respect to their demand for oxygen. Without improvement in functional or structural parameters newborn marsupials are reliant to varying degrees on skin gas exchange to compensate for the immaturity of the lung. Indeed, in some species there is complete reliance on the skin for gas exchange at birth. Nevertheless, with an early dependence on ventilation, the CNS would appear already to contain neurons with properties and connections that permit rhythmic motor output at birth and pulmonary reflexes mature soon after. Despite appropriate neural control and the presence of surfactant, the highly compliant nature of the newborn chest wall results in substantial chest wall distortion during inspiratory effort which reduce the efficacy of the lung for ventilation. This review explores the morpho-functional development of the respiratory system, including oxygen transport and cardiac shunts, and the establishment of convective requirement in marsupials, a group that places emphasis on extended postnatal development.
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PMID:Development of the respiratory system in marsupials. 1678 Dec 4

Perinatal brain injury in survivors of premature birth has a unique and unexplained predilection for periventricular cerebral white matter. Periventricular white-matter injury (PWMI) is now the most common cause of brain injury in preterm infants and the leading cause of chronic neurological morbidity. The spectrum of chronic PWMI includes focal cystic necrotic lesions (periventricular leukomalacia; PVL) and diffuses myelination disturbances. Recent neuroimaging studies support that the incidence of PVL is declining, whereas focal or diffuse noncystic injury is emerging as the predominant lesion. Factors that predispose to PVL during prematurity include hypoxia, ischemia, and maternal-fetal infection. In a significant number of infants, PWMI appears to be initiated by perturbations in cerebral blood flow that reflect anatomic and physiological immaturity of the vasculature. Ischemic cerebral white matter is susceptible to pronounced free radical-mediated injury that particularly targets immature stages of the oligodendrocyte lineage. Emerging experimental data supports that pronounced ischemia in the periventricular white matter is necessary, but not sufficient to generate PWMI. The developmental predilection for PWMI to occur during prematurity appears to be related to both the timing of appearance and regional distribution of susceptible oligodendrocyte progenitors. Injury to oligodendrocyte progenitors may contribute to the pathogenesis of PWMI by disrupting the maturation of myelin-forming oligodendrocytes. Chemical mediators that may contribute to white-matter injury include reactive oxygen species glutamate, cytokines, and adenosine. As our understanding of the pathogenesis of PWMI improves, it is anticipated that new strategies for directly preventing brain injury in premature infants will develop.
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PMID:Perinatal white matter injury: the changing spectrum of pathology and emerging insights into pathogenetic mechanisms. 1680 10

The identification of the biologic properties of nitric oxide (NO) is one of the key scientific discoveries of the century, but its potential for treating human disease is yet to be fully realized. NO has a basic role in regulating vascular tone of the pulmonary circulation, and recent animal models have suggested a more wide reaching influence on perinatal lung development. In animal models, NO has effects on lung growth, angiogenesis, airway smooth muscle proliferation, vascular remodeling, surfactant function, inflammation, and pulmonary mechanics. However, despite extensive basic science investigation and completion of several large clinical trials, the role of NO in the treatment of the premature infant with respiratory distress syndrome remains unclear. One must conclude that the interaction of lung immaturity, ventilator and oxygen-induced lung injury, and NO biology in the premature newborn is incompletely understood. Clinical trial results of inhaled NO therapy in the premature infant are accumulating, but the results do not suggest a clear-cut advantage for the population at greatest risk for death and disability. Whether trial design, dose, duration of therapy, or other factors are responsible has not been determined. Further research is needed to answer these questions and more clearly define the population of premature infants who may derive benefit from this new therapy.
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PMID:The use of inhaled nitric oxide in the premature infant with respiratory distress syndrome. 1700 53

The potential negative impact of early blood oxygenation on development of specific cognitive and motor outcomes in children born at very low birth weight (VLBW; 1000-1500g) has not been examined even though these infants are exposed to varying durations and amounts of oxygen as part of their neonatal care. While this is the largest group of preterm infants, they receive much less research attention than extremely low birth weight infants (ELBW<1000g). Although neonatologists are questioning the routine use of oxygen therapy for all neonates, research has focused primarily on the more medically fragile ELBW infants. To date there are no systematic studies available to guide decision making for oxygen supplementation for a large segment of the preterm infant population. The aim of the present study was to determine if there is an association between blood oxygenation in the first 4h of life and specific cognitive and motor skills in preterm infants with acute respiratory disorders but no severe intracranial insult using a selected cohort from a longitudinal study children recruited in 1991 and 1992 designed to examine the role of biological immaturity as defined by gestational age and parenting in development. From this cohort, 55 children had acute respiratory disorders without severe intracranial insult. Of these, 35 children had at least one partial pressure of oxygen obtained from arterial blood (PaO2) during the first 4h of life as part of their clinical care. Higher early PaO2 values were associated with lower impulse control and attention skills in the elementary school age period. Models that were examined for relations between PaO2 values that also included birth weight and parenting quality across the first year of life revealed that higher PaO2 remained associated with impulse control but not attention skills. Birth weight was not associated with any outcomes. These results suggest that hyperoxia may be a risk factor for developmental problems that are not expressed until school age.
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PMID:The association of early blood oxygenation with child development in preterm infants with acute respiratory disorders. 1798 19

Patent ductus arteriosus (PDA) complicates the hospital course of premature infants. Impaired oxygen (O2)-induced vasoconstriction in preterm ductus arteriosus (DA) contributes to PDA and results, in part, from decreased function/expression of O2-sensitive, voltage-gated potassium channels (Kv) in DA smooth muscle cells (DASMCs). This paradigm suggests that activation of the voltage-sensitive L-type calcium channels (CaL), which increases cytosolic calcium ([Ca2+]i), is a passive consequence of membrane depolarization. However, effective Kv gene transfer only partially matures O2 responsiveness in preterm DA. Thus, we hypothesized that CaL are directly O2 sensitive and that immaturity of CaL function in preterm DA contributes to impaired O2 constriction. We show that preterm rabbit DA rings have reduced O2- and 4-aminopyridine (Kv blocker)-induced constriction. Preterm rabbit DASMCs have reduced O2-induced whole-cell calcium current (ICa) and [Ca2+]i. BAY K8644, a CaL activator, increased O2 constriction, ICa, and [Ca]i in preterm DASMCs to levels seen at term but had no effect on human and rabbit term DA. Preterm rabbit DAs have decreased gamma and increased alpha subunit protein expression. We conclude that the CaL in term rabbit and human DASMCs is directly O2 sensitive. Functional immaturity of CaL O2 sensitivity contributes to impaired O2 constriction in premature DA and can be reversed by BAY K8644.
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PMID:Developmental absence of the O2 sensitivity of L-type calcium channels in preterm ductus arteriosus smooth muscle cells impairs O2 constriction contributing to patent ductus arteriosus. 1809 58

Apnea, defined as cessation of breathing resulting in pathological changes in heart rate and oxygen saturation, is a common occurrence especially in preterm neonates. It is due to immaturity of the central nervous system (apnea of prematurity) or secondary to other causes such as metabolic disturbances etc. Secondary causes of apnea should be excluded before a diagnosis of apnea of prematurity is made. Methylxanthines and continuous positive airway pressure form the mainstay of treatment. Mechanical ventilation is reserved for apnea resistant to the above therapy. An approach to the management of apnea in neonates is described.
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PMID:Apnea in the newborn. 1824 37

Cerebral white matter injury, characterised by loss of premyelinating oligodendrocytes (pre-OLs), is the most common form of injury to the preterm brain and is associated with a high risk of neurodevelopmental impairment. The unique cerebrovascular anatomy and physiology of the premature baby underlies the exquisite sensitivity of white matter to the abnormal milieu of preterm extrauterine life, in particular ischaemia and inflammation. These two upstream mechanisms can coexist and amplify their effects, leading to activation of two principal downstream mechanisms: excitotoxicity and free radical attack. Upstream mechanisms trigger generation of reactive oxygen and nitrogen species. The pre-OL is intrinsically vulnerable to free radical attack due to immaturity of antioxidant enzyme systems and iron accumulation. Ischaemia and inflammation trigger glutamate receptor-mediated injury leading to maturation-dependent cell death and loss of cellular processes. This review looks at recent evidence for pathogenetic mechanisms in white matter injury with emphasis on targets for prevention and treatment of injury.
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PMID:Pathogenesis of cerebral white matter injury of prematurity. 1829 74

A considerable proportion of premature infants requires mechanical ventilatory support and supplemental oxygen. Due to their immaturity, exposure to these forms of respiratory support contributes to the development of lung injury, oxidative stress and abnormal retinal development. These conditions are associated with poor long-term respiratory and neurological outcome. Mechanically ventilated preterm infants present with frequent fluctuations in ventilation and gas exchange. Currently available ventilatory modes and manual adjustment to the ventilator or supplemental oxygen cannot effectively adapt to these recurrent fluctuations. Moreover, the respiratory support often exceeds the infant's real needs. Techniques that adapt the mechanical ventilatory support and supplemental oxygen to the changing needs of preterm infants are being developed in order to improve stability of gas exchange, to minimise respiratory support and to reduce personnel workload. This article describes the preliminary evidence on the application of these new techniques in preterm infants and animal models.
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PMID:Automated respiratory support in newborn infants. 1882 5

The history of retinopathy of prematurity (ROP) gives a prime example of how dangerous the uncontrolled introduction of a new medical treatment--particularly in the field of neonatology--may be. The most important risk factors for the development of ROP are the immaturity of premature infants as well as uncontrolled and/or inadequate treatment with oxygen. In comparison to the fetus, the premature infant is exposed to a nonphysiologically high oxygen concentration. This hyperoxia leads to formation of aggressive oxygen radicals on the one hand and, on the other hand, to temporarily reduced production of growth factors such as vascular endothelial growth factor and erythropoietin, which both play an important role in the pathogenesis of ROP. The most important measure to prevent ROP is restrictive and carefully monitored oxygen treatment. Medical treatment to prevent ROP includes injection of D-penicillamine and retinol, but the available data are still limited, particularly with regard to the long-term effects of this treatment. A higher oxygenation in prethreshold ROP does not lead to recovery of ocular findings, but it increases the incidence of pulmonary complications. A reduction of light intensity in neonatal intensive care units proved not to be efficient for preventing ROP. To avoid blindness, standardized screening of the risk group is needed.
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PMID:[Risk factors and prevention of retinopathy of prematurity]. 1906 7


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