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

Prematurity apnea remains a major clinical problem that requires treatment choices which are sometimes difficult. Prematurity apnea occurs in most infants of gestational age at birth less than 33 weeks. It is a developmental disorder which usually reflects a "physiological" immaturity of respiratory control. However, neonatal diseases may be associated and play an additive role, resulting in an increased incidence of apnea. Careful screening should therefore be performed in order to make sure that no other factor than immaturity is involved in the occurrence of apnea. Short apnea (less than 10s, without hypoxemia and bradycardia), due to immaturity, are not clinically relevant. More prolonged apnea, that last for more than 15 or 20s, and / or apnea associated with bradycardia or oxygen desaturation, results in short-term disturbances of cerebral haemodynamics and oxygenation, which may negatively impact on neurodevelopmental outcome. Evaluating the immediate severity of apnea and the risks that apnea may affect long-term outcome remains a challenge. The choice of treatments is based on a few evidences. Caffeine citrate, which reduces the incidence of apnea, has been used for decades. However, a thorough evaluation of risks and benefits of this medication has been performed only recently. Caffeine citrate was found to be safe and resulted in unexpected benefits. In treated infants, compared with controls, indeed, a decreased incidence of the following complications was recorded: bronchopulmonary dysplasia at 36 weeks of conceptional age, patent ductus arteriosus, cerebral palsy at 18 months of age. Nasal CPAP can be used in association with caffeine citrate, when the latter is not effective enough.
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PMID:[Apnea of prematurity: what's new?]. 1994 73

Enhancing functional maturity of the high-risk preterm fetus is aimed at decreasing the life-threatening neonatal disorders that increase the burden of chronic disease. A course of antenatal glucocorticoids before 35 weeks of pregnancy substitutes endogenous activation of the hypothalamic-adrenal axis that spontaneously enhances functional maturity and augments cytokine-induced preterm lung maturity. It is the main fetal therapy that decreases the functional prematurity-related neonatal morbidity in the era of surfactant therapy. Tocolytic agents potentiate the effect of glucocorticoids on the fetus. Repeating an antenatal glucocorticoid course may be recommended if the preterm fetus remains undelivered for more than 7 days and very preterm birth is imminent. However, the follow-up results are still incomplete, and available preliminary studies warn against adverse neurological and metabolic consequences following several antenatal repeat courses of glucocorticoids. Administration of glucocorticoids after 34 weeks of pregnancy may be considered in selected high-risk cases, preferably with documented lung immaturity. We recommend delaying elective delivery in low-risk pregnancies without established lung maturity until 40 weeks, unless labor starts earlier. In a selected high-risk population 17alpha-hydroxyprogesterone acetate decreases the prematurity rate. However, this drug has a limited impact on functional maturity of the preterm fetus and its effects on the development of the child remain to be studied further.
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PMID:Enhancing functional maturity before preterm birth. 2055 6

Apnea of prematurity (AOP) is a developmental sleep disorder which is yet to be completely understood. Although there is some evidence of brainstem immaturity, there is nothing to suggest that infants with AOP have gross deficits in respiratory control. It appears, however, that the early (and frequent) occurrence of hypoxemia during apnea in preterm infants is related to their low expiratory lung volume, which falls even further during apnea, while the accompanying bradycardia results from this combination of apnea and hypoxemia. Feeding is an important trigger for AOP. While hypoxemia during feeding is most likely related to an immature coordination between sucking, swallowing and breathing and potentially also to an immature laryngeal chemoreflex, hypoxemia after feeding may be caused by diaphragmatic fatigue; gastro-esophageal reflux only rarely plays a role. The time course of AOP, i.e., its increased occurrence during the second and third rather than the first week of life, together with data from physiological studies, also suggests a role for diaphragmatic fatigue. Additional factors include upper airway obstruction, persistence of the fetal response to hypoxia, i.e., ventilatory depression, and the close proximity between the eupneic and apneic CO(2) thresholds in neonates. Observational data cannot provide definite answers on cause-and-effect issues but may provide a starting point for further studies into mechanisms involved in AOP and for the development of new therapeutic interventions. First, however, we need to better define how much AOP can be tolerated in an infant without endangering neurodevelopment.
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PMID:Apnea of prematurity: What can observational studies tell us about pathophysiology? 2062 58

Nosocomial infections are one of the major causes of morbidity and mortality in the newborn intensive care unit (NICU). They result in prolonged hospital stays and increased hospital costs. Neonates are susceptible hosts because of prematurity of organ systems, immaturity of immune system, low birth weight and the use of invasive devices. Most infections are endemic others can occur during outbreaks. As advances in medical technology improve mortality in the tiniest of infants, it is imperative that health care providers identify effective interventions to minimize the risks of nosocomial infections in the NICU. Recommended infection control and prevention strategies are: hand washing promotion, decreased use of invasive procedures, limited antitibiotic exposure, environmental hygiene. In this context infection surveillance is the first step to recognize and analyze problems, to effectively target infection control measures and feedback. Any suspicion of an outbreak should lead to a review of general infection control procedures to prevent the spread of the pathogens as quickly as possible. A multidisciplinary approach can be an effective means of developing a plan of action to apply prolonged and strict adherence to isolation precautions', to detect potential reservoirs or source of infections, to educate every member of the patient care team and to review NICU protocols.
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PMID:[Surveillance of infection events in neonatal intensive care]. 2109 73

Most abnormalities of ventilatory control in infants are due to immaturity or abnormal development of ventilatory control. This includes a broad range, from rare disorders like congenital central hypoventilation syndrome to common problems such as apnoea of prematurity. Development of the ventilatory control system, including central respiratory rhythmogenesis and central and peripheral chemoreception, begins early in gestation and continues for weeks or months after birth. Development of the neural components of central rhythmogenesis and their highly complex interconnectivity results from complex, timing-sensitive interactions between patterning and other genes, transcription factors and neurotrophic factors. At birth, nearly all aspects of ventilatory control remain immature, especially in preterm infants; and postnatal maturation can be altered by hypoxia, toxins and other stressors. Clinical care may be greatly enhanced by increased awareness of ventilatory control maturation and related disorders.
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PMID:Development of ventilatory control in infants. 2110 77

Apnea of prematurity (AOP) is a significant clinical problem manifested by an unstable respiratory rhythm reflecting the immaturity of respiratory control systems. This review will address the pathogenesis of and treatment strategies for AOP. Although the neuronal mechanisms leading to apnea are still not well understood, recent decades have provided better insight into the generation of the respiratory rhythm and its modulation in the neonate. Ventilatory responses to hypoxia and hypercarbia are impaired and inhibitory reflexes are exaggerated in the neonate. These unique vulnerabilities predispose the neonate to the development of apnea. Treatment strategies attempt to stabilize the respiratory rhythm. Caffeine remains the primary pharmacological treatment modality and is presumed to work through blockade of adenosine receptors A(1) and A(2). Recent evidences suggest that A(2A) receptors may have a greater role than previously thought. AOP typically resolves with maturation suggesting increased myelination of the brainstem.
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PMID:Apnea of prematurity: pathogenesis and management strategies. 2112 67

Apnea of prematurity (AOP) is a common problem affecting premature infants, likely secondary to a "physiologic" immaturity of respiratory control that may be exacerbated by neonatal disease. These include altered ventilatory responses to hypoxia, hypercapnia, and altered sleep states, while the roles of gastroesophageal reflux and anemia remain controversial. Standard clinical management of the obstructive subtype of AOP includes prone positioning and continuous positive or nasal intermittent positive pressure ventilation to prevent pharyngeal collapse and alveolar atelectasis, while methylxanthine therapy is a mainstay of treatment of central apnea by stimulating the central nervous system and respiratory muscle function. Other therapies, including kangaroo care, red blood cell transfusions, and CO(2) inhalation, require further study. The physiology and pathophysiology behind AOP are discussed, including the laryngeal chemoreflex and sensitivity to inhibitory neurotransmitters, as are the mechanisms by which different therapies may work and the potential long-term neurodevelopmental consequences of AOP and its treatment.
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PMID:Apnea of prematurity: from cause to treatment. 2130 66

Congenital hypothyroidism is screened for in the UK using blood spot thyroid-stimulating hormone (TSH) screening at 5-8 d of age. Although standards are set by the UK Newborn Screening Programme Centre, there are variations in TSH cut-offs used. The introduction of repeat screening of preterm babies at 36 weeks' gestational age in 2005 was controversial in its utility and timing. Two cases of preterm babies are presented, who had normal blood spot TSH values on the first test and who became screen positive when re-tested at term. The first with Trisomy 21 was born at 29 + 6 weeks with an initial blood spot TSH of 3.3 mU/L rising to 263 mU/L at term-corrected gestational age (plasma TSH 476.5 mU/L). The second was born at 24 + 6 weeks' gestational age and on day 7, the heel prick blood spot TSH was <2 mU/L, rising to 6.4 mU/L at 36 weeks corrected gestational age. After a barium enema, the plasma TSH increased to 66.6 mU/L with a free thyroxine of 7.6 pmol/L at day 101. Both cases were treated with thyroxine until death due to complications of prematurity. These cases illustrate the difficulties in screening for congenital hypothyroidism in preterm infants, due to the immaturity of the hypothalamo-pituitary-thyroid axis, and the effect of intercurrent illness and drugs on thyroid function. Despite a reassuring published review of 2200 preterm infants, these cases suggest that it may be unwise not to re-screen ex-preterm infants for congenital hypothyroidism at term.
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PMID:Hypothyroidism in preterm infants following normal screening. 2190 4

Continuous improvements in perinatal care have allowed the survival of ever more premature infants, making the task of protecting the extremely immature lung from injury increasingly challenging. Premature infants at risk of developing chronic lung disease or bronchopulmonary dysplasia (BPD) are now born at the late canalicular stage of lung development, just when the airways become juxtaposed to the lung vasculature and when gas-exchange becomes possible. Readily available strategies, including improved antenatal management (education, regionalization, steroids, and antibiotics), together with exogenous surfactant and exclusive/early noninvasive ventilatory support, will likely decrease the incidence/severity of BPD over the next few years. Nonetheless, because of the extreme immaturity of the developing lung, the extent to which disruption of lung growth after prematurity and neonatal management lead to an earlier or more aggravated decline in respiratory function in later life is a matter of concern. Consequently, much more needs to be learned about the mechanisms of lung development, injury, and repair. Recent insight into stem cell biology has sparked interest for stem cells to repair damaged organs. This review summarizes the exciting potential of stem cell-based therapies for lung diseases in general and BPD in particular.
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PMID:Lung injury in preterm neonates: the role and therapeutic potential of stem cells. 2240 Aug 13

Due to the functional and structural immaturity of different organ systems, preterms have a higher rate of morbidity and mortality. The prevention and treatment of the complications of prematurity is a major challenge in perinatal health care. Recently, there have been several multicenter research trials analysing the impact of prematurity or low birth weight on the health problems of children and adolescents. Many of these studies deal with the issue of pediatric hypertension. An analysis of 15 studies conducted in the years 1998-2011, in which blood pressure values in ex-preterm children were measured, was performed. Comparison was based on several issues: measurement method, cohorts age, size, and birthweight. It has been proven that hypertension occurs more often in former preterm infants; however the etiologic pathways that cause this condition still remain unclear. Moreover, pediatric hypertension is a significant problem, because of its transformation into adult hypertension and increased cardiovascular risk later in life. Therefore it is crucial to introduce wide-spread screening and detection of elevated blood pressure, especially among prematurely born children.
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PMID:Prematurity-related hypertension in children and adolescents. 2251 77


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