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 28,634 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The rationale for surfactant therapy in premature infants is presented, along with a discussion of the characteristics of surfactant and a review of clinical trials of surfactant for the prevention and treatment of neonatal respiratory distress syndrome (RDS). RDS is a major complication of prematurity, affecting up to 40,000 infants in the United States and Canada annually. Poor lung compliance due to a functional or quantitative deficiency of surfactant causes progressive collapse of the lungs. Surfactant, a mixture of phospholipids, neutral lipids, and proteins synthesized by pneumocytes during gestation, reduces surface tension and stabilizes alveoli, which increases lung compliance and decreases the work of breathing. Mammalian, human, and artificial surfactants are being investigated for use in premature infants. Several controlled trials of exogenous surfactant therapy have demonstrated reductions in mortality and pulmonary air-leak phenomena and improved gas exchange, but these results are not seen consistently, and no significant reductions in bronchopulmonary dysplasia have been observed. Surfactant has no appreciable toxicity, although the potential for immunogenicity exists. Typical doses range from 60 mg to 200 mg/kg administered endotracheally either before the first breath or after development of RDS. Surfactant is a safe investigational agent that appears promising for the prevention and treatment of neonatal RDS, although additional clinical trials with long-term follow-up are needed to determine its true efficacy.
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PMID:Use of surfactant in the prevention and treatment of neonatal respiratory distress syndrome. 267 Mar 98

In a large Swedish 2 1/2-year population of fullterm infants the incidence of early neonatal sudden death (ENSD) was 0.12 per 1000 newborn infants considered healthy at birth but presenting with sudden cardiovascular collapse between 6 and 100 hours after birth. In the total neonatal mortality the rate of ENSD was 11%. Well-known risk infants, e.g. prematurity, perinatal asphyxia, difficult delivery or congenital malformations were not included. In an inborn population of 20 123 fullterm newborns the rate of ENSD was 0.15 per 1000. In the same population near-missed ENSD occurred in 0.35 per 1000 liveborn infants. Possible causative factors were infections in 4 and anaemia in 2 cases. But in 7 of 13 infants thorough epidemiological examinations and postmortem sterile autopsies did not reveal the cause of death or near death. These are probably cases of sudden infant death syndrome hitherto unrecognized in the first days of life.
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PMID:Early neonatal sudden infant death and near death of fullterm infants in maternity wards. 409 Sep 60

Early onset group B streptococcal disease was reviewed for the seven year period between 1975 to 1981 at Vanderbilt University Medical Center. One hundred and twenty cases were identified. The disease varied from asymptomatic bacteremia to fatal cardiopulmonary collapse. Factors associated with a poor outcome were prematurity, low Apgar score at 5 min, the presence of shock, leukopenia, rupture of membranes for more than 12 hours, and a delay in treatment after the onset of symptoms. A scoring system for probability of death based on these 6 factors was then developed. Over the seven year period mortality decreased from 50% to 10%. The only factor identified with the decrease in mortality was a significant decrease in the number of hours between the onset of symptoms and the beginning of treatment. Early recognition and prompt treatment seem to be the major causes of the decreasing mortality over the seven years of this report.
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PMID:Early onset group B streptococcal disease. Seven year experience and clinical scoring system. 635 49

Twenty-four fatal cases of echo 11 infection in the eleven years 1968-78 are presented. All were children, and could be divided into two groups according to age at death and clinical presentation. The first group comprised 12 babies who died aged between 5 and 11 days after a short illness characterised by collapse, acidosis, and bleeding. At necropsy there was evidence of disseminated intravascular coagulation with haemorrhage into many organs including the renal medulla, suprarenal glands, gastrointestinal tract, and central nervous system. Six cases showed hepatic necrosis which was massive in three. Virus was present in many tissues. Infection was probably acquired from the mothers at delivery in 3 cases. Low maternal neutralising antibody titres and prematurity were thought to be adverse factors in the outcome. The second group consisted of 12 children aged between 9 weeks and 4 years 10 months who died suddenly. Pathological findings included upper respiratory tract infection, pneumonia, encephalitis, and gastroenteritis. Six of this group had been classified as 'cot deaths'. The role of echo 11 in the death of some of these older children is unknown. This report shows the danger of echo 11 to neonates, especially if unprotected by maternal antibody.
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PMID:Fatal infection with echovirus 11. 719 96

One hundred and five infants treated with adrenaline or atropine, or both, as part of resuscitation on 124 occasions were studied retrospectively. Adrenaline was administered to 98 infants, in 40 of whom it was in combination with atropine, and seven infants received atropine alone. Twenty infants were treated solely on the delivery unit, 81 on the neonatal medical unit, and four in both places. Twelve infants treated on the delivery unit and 13 treated on the neonatal unit survived. Follow up studies showed that 13 infants were handicapped with nine severely handicapped. Extreme prematurity, the need for early or repeated resuscitation using these drugs, particularly for episodes of collapse without a clear precipitating cause, and asystole rather than bradycardia were associated with a worse outcome. Evidence is accumulating to support a view that the use of these drugs for resuscitation at birth and in the first week of life of extremely preterm infants may be inappropriate.
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PMID:Use of adrenaline and atropine in neonatal resuscitation. 811 24

Surfactant protein A (SP-A) is a major apo-protein of pulmonary surfactant, which lines the alveolar walls, lowering the surface tension to prevent lung collapse. Pregnant rats were divided into two groups which received a diet with either 5% or 20% protein from gestational day 9. By a sensitive immunoassay, SP-A levels in the fetal lungs and the amniotic fluid showed a dramatic increase with advancing gestation after the initial appearance on gestational day 18 in both diet groups. Significantly lower levels of SP-A in pregnant rats fed 5% protein diet than those in pregnant rats fed 20% protein diet were observed in the fetal lungs on gestational day 21 and in the amniotic fluid on gestational days 20 and 21. The profiles of increased SP-A levels in the amniotic fluid reflected those in the fetal lungs during gestation. Immunohistochemical examination with anti-rat SP-A antibody at 21 days of gestation showed that the immunoreactive staining of bronchiolar epithelial Clara cells and alveolar type II cells were weaker in the fetal lung sections from pregnant rats fed 5% protein diet than in those from pregnant rats fed 20% protein diet. It is concluded that protein malnutrition in pregnant rats affects the biosynthesis of SP-A in the fetal lungs, which may have important consequences for prematurity and decreased respiratory functions in the neonatal lungs at birth.
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PMID:Levels of pulmonary surfactant protein A in fetal lung and amniotic fluid from protein-malnourished pregnant rats. 886 57

Pulmonary surfactant is a complex and highly surface active material composed of lipids and proteins which is found in the fluid lining the alveolar surface of the lungs. Surfactant prevents alveolar collapse at low lung volume, and preserves bronchiolar patency during normal and forced respiration (biophysical functions). In addition, it is involved in the protection of the lungs from injuries and infections caused by inhaled particles and micro-organisms (immunological, non-biophysical functions). Pulmonary surfactant can only be harvested by lavage procedures, which may disrupt its pre-existing biophysical and biochemical micro-organization. These limitations must always be considered when interpreting ex vivo studies of pulmonary surfactant. A pathophysiological role for surfactant was first appreciated in premature infants with respiratory distress syndrome and hyaline membrane disease, a condition which is nowadays routinely treated with exogenous surfactant replacement. Biochemical surfactant abnormalities of varying degrees have been described in obstructive lung diseases (asthma, bronchiolitis, chronic obstructive pulmonary disease, and following lung transplantation), infectious and suppurative lung diseases (cystic fibrosis, pneumonia, and human immunodeficiency virus), adult respiratory distress syndrome, pulmonary oedema, other diseases specific to infants (chronic lung disease of prematurity, and surfactant protein-B deficiency), interstitial lung diseases (sarcoidosis, idiopathic pulmonary fibrosis, and hypersensitivity pneumonitis), pulmonary alveolar proteinosis, following cardiopulmonary bypass, and in smokers. For some pulmonary conditions surfactant replacement therapy is on the horizon, but for the majority much more needs to be learnt about the pathophysiological role the observed surfactant abnormalities may have.
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PMID:Pulmonary surfactant in health and human lung diseases: state of the art. 1044 27

The mortality of very preterm infants has significantly improved after introducing into clinical practice the antenatal use of glucocorticoid steroids prior to premature births and postnatal treatment with pulmonary surfactant which effectively decreases the tendency of the alveoli to collapse. The period of necessary mechanical ventilation was shortened. Reducing the concentration of inspired oxygen and inflation pressures became possible. In spite of this, long-term damage of lung tissue in immature infants is still a major clinical problem. However, its origin seems to be slightly different. A new form of bronchopulmonary dysplasia (BPD) has been recently evaluated. The most important factors in the pathogenesis of the "new" BPD are: lung tissue immaturity, infections initiating a cascade of events caused by formation of free oxygen radicals and cytokines and the presence of persistent patent ductus arteriosus. Primary prevention of BPD is possible by reducing the rates of prematurity and intrauterine infections. Secondary prevention includes antenatal steroids administration and postnatal surfactant treatment according to the accepted known standards. When protracted mechanical ventilation is necessary, low and subsequently reduced doses of i.v. glucocorticoid steroids in the second and third week of life are administrated, together with diuretics, bronchodilators and suitably high calorie feeding.
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PMID:[Changes in the clinical picture of bronchopulmonary dysplasia]. 1132 69

A medical officer for the Expanded Program on Immunization (EPI) of the World Health Organization (WHO) calls for staff at all health facilities to screen and, if appropriate, immunize every infant, child, and woman of reproductive age attending health facilities. Routine immunization services tend to miss many women and children who should be immunized. Three important components comprise the health team approach needed to avoid missed opportunities: awareness to screen, a well-organized referral system within each health facility, and regular availability of vaccines. In the health facility, the nonimmunized child is at risk of contracting measles, so all such children should be immunized before they leave the health facility. The WHO/EPI medical officer presents five ways to avoid missed opportunities: screen and immunize at every opportunity, administer all required vaccines, stress real and avoid false contraindications, train staff, and open new vials of vaccine when needed. Contraindications to immunization include severe adverse reactions after a dose of vaccine (collapse or shock, convulsions without fever, anaphylaxis, or encephalitis/encephalopathy), neurological disease (for vaccines containing whole cell pertussis), immune deficiency diseases or immunosuppression due to drugs (generally for live vaccines), and symptomatic HIV infections (for BCG or yellow fever vaccines). The following conditions do not preclude immunization: minor illnesses (e.g., upper respiratory infections); allergy, asthma, hay fever, or "snuffles"; prematurity, small-for-date infants; malnutrition; breast feeding; family history of convulsions; treatment with antibiotics, low-dose corticosteroids, or locally acting steroids; eczema or localized skin infection; chronic diseases of the heart, lung, kidney, or liver; stable neurological conditions (e.g., Down syndrome), and history of jaundice after birth. WHO/EPI has an exit survey for use at district-level clinics or hospitals available so program managers can learn if they are missing chances to immunize children.
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PMID:Opportunities to immunise. 1229 31

Sudden unexpected death in infancy (SUDI) is a category used to represent the largest single group of infant deaths. Although there are several theories, the cause of SUDI remains unknown and the mechanism of co-sleeping associated deaths are also undetermined. We investigate a possible biomechanical mechanism which may be common in SUDI and may provide an explanation for the association of the known risk factors for SUDI such as co-sleeping, prematurity, prone sleeping position, overwrapping, overheating and maternal smoking. The neonatal lung has few, if any, true septa but from about four weeks of age, a period of rapid alveolarisation commences. The developing alveolar walls (septae) have little fibre support against surface tension forces as they grow but are supported by a double layer of capillaries. Until the elastin/collagen supporting network is laid down these nascent septal walls are vulnerable to collapse against sac or duct walls during this transitional period. We hypothesise that such collapse will prevent one side of the septa, and the wall it overlays, from alveolar gas exchange and a functional left-right shunt is formed which may result in hypoxia. Furthermore, lung stretch receptors in bronchi running through or adjacent to collapsed regions will be activated, falsely signalling lung inflation to the brain stem with resultant respiratory inhibition, so precipitating further collapse. The process will continue until lung volume falls below residual capacity, when normal tidal breathing efforts will no longer result in significant air flow, even if stretch receptor signals have not produced complete apnoea. Large inspiratory efforts are then required to break the surface tension seal, which damages capillaries to produce petechial haemorrhages. Many epidemiological risk factors for SUDI could influence such a mechanism, leading to the proposal that Alveolar Septal Collapse in Infancy (ASCI) is a core mechanism via which these factors act.
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PMID:Alveolar septal collapse in the transitional infant lung: a possible common mechanism in sudden unexpected death in infancy. 1528 74


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