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

Lesional pulmonary edema caused by substances which are directly caustic for the gastrointestinal pathways (strong acids and bases, inhaled vomit) are opposed by their immediate and long-term gravity with those due to cardiotropic medicamentatous toxins or volemic overloading which lead to curable pulmonary edema. Material and human factors, in favour of accidental intoxication are compensated for by the fact that many toxins produce vapours which are strongly irritant for the upper respiratory pathways: this prevents prolonged exposure and therefore wards off edema. Drug intoxication by ingestion can lead to pulmonary edema by relative or absolute volemic overload, by allergic accidents or by immaturity of the enzyme degradation systems. It seems to us that the notions of "neurological" and "metabolic" toxic edema should be abandoned. In lesional edema the treatment is that of the acute respiratory failure. The combination of pethidine, promethazine, and chlorpromazine gives good immediate results. Owing to careful follow-up, hemodynamic pulmonary edema should most frequently be avoided.
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PMID:[Nonhemodynamic pulmonary edema due to toxins]. 0 74

Surfactant is now available for general clinical use in infants with RDS. While surfactant is effective, it does not prevent lung disease in many preterm infants because of other aspects of lung immaturity. In experimental models, corticosteroids alter the fetal lung by improving compliances, increasing lung volumes, decreasing pulmonary edema, and altering surfactant-compliance dose response curves. These effects are independent of changes in surfactant pools but augment the responses of the lungs to surfactant treatment. Optimal outcomes for the preterm require the combined use of fetal maturation strategies and postnatal surfactant.
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PMID:Surfactant in the perinatal period. 139 80

Pulmonary surfactant is an important chemical component of the lung. It decreases surface tension in the alveolar cells to help stabilize the alveoli, and it may help prevent pulmonary edema. Currently, naturally and synthetically derived surfactants are being used to treat neonatal respiratory distress syndrome, a leading cause of death in premature infants. Surfactant is recommended for prophylactic therapy in infants weighing less than 1,350 g (3 lb) and in infants weighing more than 1,350 g who show signs of pulmonary immaturity and for rescue therapy in infants with respiratory distress syndrome. Surfactant is administered by endotracheal tube, and the recommended dose is 5 mg per kg. Three doses, given 12 hours apart, is the recommended regimen for prophylactic therapy. Rescue therapy consists of one dose of surfactant given at the onset of respiratory distress and another dose given 12 hours later.
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PMID:Surfactant: clinical applications. 162 34

Respiratory failure in the preterm results from not only surfactant deficiency but also the immaturity of a number of other elements that have a structural basis. Airway, alveolar, fluid clearance, and epithelial and endothelial barrier functions also are important to lung function. Immaturities in these lung elements have identifiable adverse consequences for lung function such as pulmonary interstitial emphysema and pulmonary edema. The maturation of each of these elements appears to be achievable by agents such as corticosteroids, and maturation will result in an improved response to surfactant treatments. While surfactant treatments can improve respiratory failure by minimizing lung injury, other aspects of lung immaturity continue to contribute to respiratory compromise in the preterm. A thorough understanding of respiratory failure in the newborn depends on a better appreciation of the contribution of immaturity of the different structural elements of the lung on lung function.
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PMID:Pathogenesis of respiratory failure in the preterm infant. 177 25

There is a wide variability in the therapeutic responsiveness to exogenous surfactant, a drug that has become generally available for the treatment of lung immaturity and respiratory distress syndrome. Recent studies have demonstrated evidence that therapies decreasing lung edema improve the effectiveness of surfactant substitution. In addition, exogenous surfactant may acutely decrease pulmonary perfusion since the airway pressures are effectively transmitted to airspaces, compressing alveolar capillaries, especially in hypovolemia. Therapies aimed at decreasing lung edema, improving cardiac output, and stepwise weaning from oxygen and ventilatory pressures are cornerstones in the successful management of patients undergoing surfactant therapy.
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PMID:Factors affecting surfactant responsiveness. 177 26

Many questions are raised in this review about the role of adult donor granulocyte transfusions in the setting of overwhelming bacterial neonatal sepsis. There clearly exists a number of variables, which influence the survival and morbidity associated with bacterial sepsis. The important differences in these studies highlight the need for prospective large multicenter studies to definitely clarify these issues. Important criteria, which are yet to be established and which impact significantly, include the time of administration of adjuvant granulocytes, the number of granulocytes that need to be harvested, which group of neonates require early granulocyte transfusions, the best method for optimal and easy granulocyte collection, the frequency and intervals of granulocyte transfusions, and improved methods for the early identification of neonatal candidates who would benefit from the granulocyte transfusions. The benefits of granulocyte transfusions (ie, the improvement in morbidity and mortality) in septic neutropenic neonates must be weighed against the possible and reported side effects associated with such transfusions. Adverse reactions including graft-versus-host disease, CMV, HIV and hepatitis infection, fluid retention and pulmonary edema, blood group sensitization, and pulmonary insufficiency may all result from the use of granulocyte transfusions in a host who has evidence of developmental immaturity. All future studies must continue to evaluate these potential complications to balance and analyze the true benefits of survival with reported treatment results. Recently, a number of investigators including ourselves, have begun to examine the role of alternate adjuvant immunotherapy in enhancing neonatal host defense in the clinical setting of overwhelming bacterial sepsis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The use of granulocyte transfusion in neonatal sepsis. 213 12

Clinical and laboratory-based studies of pulmonary edema have usually focused on the mechanisms responsible for the production of the edema and how therapeutic maneuvers can oppose or treat such processes. Recently, there has been increasing interest in the mechanisms involved in the clearance of airspace fluids. These studies have demonstrated that active transport of Na+ by the distal lung epithelium plays an important physiologic role in the clearance of pulmonary edema fluid. Specifically, the ability of the lung to clear its fluid by active transport processes correlates with survival from high-pressure or high-permeability pulmonary edema. Also, studies have shown that immaturity of Na+ transport processes and, specifically, inadequate expression of Na+ channels contribute to the pathogenesis of respiratory distress syndrome in the newborn.
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PMID:The role of active Na+ transport by lung epithelium in the clearance of airspace fluid. 758 65

Approximately 20% to 30% of infants with respiratory distress syndrome (RDS) do not respond to surfactant replacement therapy. Unfortunately there is no uniform definition of 'response' or 'non-response' to surfactant therapy. Response was based on improvement in a/A PO2 and/or mean airway pressure (MAP) by some and on improvement in FIO2 and/or MAP by others. Even the point of time at which evaluation of response was done is different in various reports. There is an urgent need to adopt an uniform definition. Most premature babies are surfactant deficient which is the aetiological factor of RDS. Generally good antenatal care and perinatal management are essential in avoidance of premature birth. Babies with lung hypoplasia and who are extremely premature (less than 24 weeks of gestation) do not respond well to exogenous surfactant replacement because of structural immaturity. Prompt management of asphyxiated birth and shock are necessary as there may be negative response to surfactant replacement. Foetal exposure to glucocorticoids improves responsiveness to postnatal administration of surfactant. Antenatal steroid therapy has become an important part of management of RDS with surfactant replacement. The premature lungs with high alveolar permeability tend to develop pulmonary oedema. With the presence of plasma-derived surfactant inhibitors, the response to exogenous surfactant may be affected. These inhibitors may also be released following ventilator barotrauma. The standard of neonatal intensive care such as ventilatory techniques has an important bearing on the outcome of the RDS babies.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Factors affecting responses of infants with respiratory distress syndrome to exogenous surfactant therapy. 826 36

Human status epilepticus (SE) is consistently associated with cognitive problems, and with widespread neuronal necrosis in hippocampus and other brain regions. In animal models, convulsive SE causes extensive neuronal necrosis. Nonconvulsive SE in adult animals also leads to widespread neuronal necrosis in vulnerable regions, although lesions develop more slowly than they would in the presence of convulsions or anoxia. In very young rats, nonconvulsive normoxic SE spares hippocampal pyramidal cells, but other types of neurons may not show the same resistance, and inhibition of brain growth, DNA and protein synthesis, and of myelin formation and of synaptogenesis may lead to altered brain development. Lesions induced by SE may be epileptogenic by leading to misdirected regeneration. In SE, glutamate, aspartate, and acetylcholine play major roles as excitatory neurotransmitters, and GABA is the dominant inhibitory neurotransmitter. GABA metabolism in substantia nigra (SN) plays a key role in seizure arrest. When seizures stop, a major increase in GABA synthesis is seen in SN postictally. GABA synthesis in SN may fail in SE. Extrasynaptic factors may also play an important role in seizure spread and in maintaining SE. Glial immaturity, increased electronic coupling, and SN immaturity facilitate SE development in the immature brain. Major increases in cerebral blood flow (CBF) protect the brain in early SE, but CBF falls in late SE as blood pressure falters. At the same time, large increases in cerebral metabolic rate for glucose and oxygen continue throughout SE. Adenosine triphosphate (ATP) depletion and lactate accumulation are associated with hypermetabolic neuronal necrosis. Excitotoxic mechanisms mediated by both N-methyl-D-aspartate (NMDA) and non-NMDA glutamate receptors open ionic channels permeable to calcium and play a major role in neuronal injury from SE. Hypoxia, systemic lactic acidosis, CO2 narcosis, hyperkalemia, hypoglycemia, shock, cardiac arrhythmias, pulmonary edema, acute renal tubular necrosis, high output failure, aspiration pneumonia, hyperpyrexia, blood leukocytosis and CSF pleocytosis are common and potentially serious complications of SE. Our improved understanding of the pathophysiology of brain damage in SE should lead to further improvement in treatment and outcome.
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PMID:Pathophysiological mechanisms of brain damage from status epilepticus. 838 2

The pathophysiology of functional deficiency of pulmonary surfactant in the neonatal respiratory disorders represented by MAS, hemorrhagic lung edema and ARDS was discussed. The removal of inhibitor(s) is the cardinal procedure for MAS and the lavage with surfactant solution seems to be promising. In case of replacement therapy, we should consider using a different dose compared to the one used in RDS due to lung immaturity, in order to optimize results.
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PMID:Functional pulmonary surfactant deficiency and neonatal respiratory disorders. 1009 35


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