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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report our experience of medical treatment, chiefly based on prolonged artificial ventilation, of 33 preterm infants with PDA and heart failure whose survival rate was 88%. All of them had clinical criteria used by others to indicate surgical ligation of the ductus arteriosus. This conservative approach seems to give better results than surgical ligation, despite a high frequency of bronchopulmonary dysplasia among survivors.
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PMID:Conservative management of patent ductus arteriosus in preterm infants. 43 23

During the period from February, 1971 to February, 1973, 30 premature infants underwent surgical ligation of patent ductus arteriosus. The gestational ages ranged from 25 to 36 wk (mean 30), and the birth weights ranged from 760 to 2010 g (mean 1274). The patients were divided into two groups on the basis of the indications for assisted ventilation. Group I consisted of 21 patients with severe hylanine membrane disease who required assisted ventilation during the first 2 days of life and could not be weaned off the respiratory by 10 days of age. Group II was composed of nine infants who required intermittent positive-pressure breathing after a mean age of 8 days because of repeated apneic spells secondary to uncontrollable heart failure. All infants in Group II survived the operation and left the hospital well. Fourteen of the 21 patients in Group I survived; the seven deaths were all due to underlying severe pulmonary disease (bronchopulmonary dysplasia). The value of PDA ligation in premature infants with uncontrollable heart failure is demonstrated in this study; this procedure also appears to be beneficial in neonates with severe respiratory distress syndrome.
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PMID:Surgical closure of patent ductus arteriosus in the premature infant with respiratory distress. 109 12

Thirty-two consecutive preterm infants with birth weights under 1,500 grams and with respiratory distress syndrome (RDS) complicated by a patent ductus arteriosus (PDA) underwent ligation of PDA. The indications for operation were massive left-to-right shunting associated with heart failure (cardiomegaly and pulmonary edema) unresponsive to medical treatment. The clinical manifestations of heart failure were related to the severity of RDS. Infants with mild-to-moderate RDS (21) often recovered and later developed typical findings of PDA (bounding pulses, hyperactive precordium, and murmur). They are now operated upon as soon as respiratory support is required. Infants with severe RDS (11) develop cardiomegaly earlier, and retrograde aortography may show massive left-to-right shunting before the presence of a murmur. Ligation is indicated when blood-gas values deteriorate despite medical treatment. Nineteen (59 per cent) of these extremely preterm infants survived to be discharged and 16 (50 per cent) are developing normally. Three have neurologic impariment. None of the survivors has clinical respiratory disease, and their radiologic findings of bronchopulmonary dysplasia are improving.
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PMID:Improving the results of ligation of patent ductus arteriosus in small preterm infants. 124 41

Natural surfactant (Surfactant TA, Survanta, CLSE, SF-RI 1, Curosurf and human surfactant obtained from amniotic fluid) therapy for RDS in very premature infants has been evaluated in 17 controlled clinical trials. Uniformly intratracheal surfactant administration caused a decreased intensity of mechanical ventilation during the first hours (reduced inspiratory pressure, reduced oxygen requirements) as an immediate effect of surfactant administration. Metanalysis reveals barotraumatic pulmonary complications mainly, pneumothorax and pulmonary interstitial emphysema to occur less frequently in surfactant-treated infants in virtually all trials; an increased incidence of survival without bronchopulmonary dysplasia following surfactant treatment was observed in 10 controlled clinical trials. The incidence of other complications of prematurity (intracranial hemorrhage, patent ductus arteriosus and necrotizing enterocolitis) was unchanged following natural surfactant treatment. Dosing of natural surfactant is still under investigation, however recent data indicate that the initial dose should not be less than 100 mg/kg b.w. and retreatment should be given to infants with unsatisfactory response (i.e. fraction of inspired oxygen (FiO2) > 40%). Timing of surfactant treatment still remains controversial. Prophylactic treatment shortly following birth has been compared with rescue-treatment, i.e. surfactant administration to infants suffering from manifest RDS in most studies 4-8 h after birth. Conflicting data from 5 controlled trials may be interpreted as follows: prophylactic treatment seems to be favourable for extremely premature infants (GA < or = 26 weeks) and rescue treatment seems to be adequate for infants of 27-30 weeks of gestation. Intratracheal surfactant instillation in very premature infants did not result in an improved lung function for 24 h to 48 h in all patients. Ten--25% of study infants were reported to be "non-responders", i.e. infants without sustained decrease in oxygen requirements (i.e. FiO2 > 40%). Various factors may be operative including congenital bacterial infections (sepsis or pneumonia), lung hypoplasia and cardiac failure. Inactivation of surface properties of natural surfactant caused by a leakage of proteins across the alveolar-capillary membrane was observed in experimental and clinical studies. Current investigations focus on a combination of postnatal steroids and surfactant treatment to improve lung function and outcome in "non-responders". As long as any controlled clinical studies are being published, this approach remains experimental. Up to now, any controlled clinical trials have been performed to assess different modes of artificial ventilation (e.g. high frequency oscillating ventilation versus conventional ventilation) combined with surfactant therapy. Data obtained from premature animals given natural surfactant indicate any advantage with respect to gas exchange and lung histology to result from high frequency ventilation.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Natural surfactant for neonatal respiratory distress syndrome in very premature infants: a 1992 update. 129 66

Severe bronchopulmonary dysplasia (BPD) is frequently associated with asthma. The combination is often severe enough to necessitate corticosteroid therapy. There are no commercially available nebulizer solutions of corticosteroids for use in infants and young children. Seven infants and small children with very severe BPD and asthma aged 6-24 months, were treated with flunisolide, 187-250 micrograms q.i.d. in the form of nasal spray delivered by nebulizer. After treatment for 2.5-20 months, four patients showed clinical improvement, one initially improved but later deteriorated and died of cardiac failure, and two patients showed no improvement and died within 3 months. The number of days of hospitalization was significantly reduced from 8.4/month to 2.5/month (P less than 0.05). No side-effects were detected and it was felt that the three patients who died, did so as a consequence of very severe BPD and its cardiac consequences. The suspension remained stable for 80 min when mixed with normal saline, cromolyn sodium, albuterol, or acetylcysteine. It is concluded that nebulized flunisolide is a potentially useful treatment for infants and young children with asthma and BPD.
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PMID:Clinical observations of nebulized flunisolide in infants and young children with asthma and bronchopulmonary dysplasia. 152 30

Assessing the short-term prognosis of bronchopulmonary dysplasia (BPD) (duration of mechanical ventilation, of O2 therapy, and risk of death) is often uncertain at the early stages of the disease. From a retrospective study of 124 cases of BPD, we made a search for factors of poor prognosis which could be recognized early. Among the 124 BPD, 56 (45%) had a severe disease (mechanical ventilation for greater than 3 months and/or O2 for greater than 4 months), and 24 of them (20%) died. Two types of factors have been identified as linked to a poor prognosis (risk of evolution towards a severe disease in a proportion of 70 to 90%): some respiratory events (refractory hypoxemia, recurrent pneumothorax, interstitial emphysema, no improvement of hyaline membrane disease at 3-4 days of life in babies less than 32 weeks gestational age) and hemodynamic failures (cardiac failure due to persistent ductus arteriosus, collapse following infection or anoxia). We have also defined different values of a ventilatory index (I = mean airway pressure x FiO2) which allows the neonatologists to estimate the final prognosis of BPD during the first two months of life.
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PMID:[Evaluation of short term prognosis of bronchopulmonary dysplasia]. 207 7

Pulmonary hypertension is a relatively common complication of chronic lung disease in children that can cause diminished right ventricular performance (RVP) and, eventually, cor pulmonale and heart failure. Since oxygen may decrease pulmonary artery pressure in these patients, we questioned whether RVP would also improve concomitantly. We evaluated the effect of oxygen on RVP in two young hypoxemic patients by radionuclide angiography. A child with bronchopulmonary dysplasia and cor pulmonale who was not clinically in heart failure had acutely better RVP while breathing oxygen and a further improvement after continuous oxygen therapy for 1 year. In a young adult with cystic fibrosis who was suspected of being in heart failure RVP acutely improved when the FIO2 was increased. We conclude that oxygen may improve RVP in hypoxemic patients and speculate that the observation of such improvement may be valuable for the early detection of patients who can benefit from long-term oxygen therapy.
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PMID:Effect of oxygen on right ventricular performance evaluated by radionuclide angiography in two young patients with chronic lung disease. 303 45

One hundred one infants with chronic respiratory failure (CRF) who required prolonged mechanical ventilation were cared for in the pediatric intensive care unit at The Children's Hospital of Philadelphia between January 1967 and December 1984. Chronic respiratory failure of infancy is a condition that requires mechanical ventilation for more than 28 days in the first year of life. Thirty-six children had severe bronchopulmonary dysplasia, 50 had congenital anomalies, and 15 had neuromuscular disorders. The mean duration of mechanical ventilation for the 101 patients was 12.3 months. Seventy-one children were alive, and 53 (75%) of the 71 had been weaned from mechanical ventilation as of Dec 31, 1984. Pulmonary insufficiency and cardiac failure were the predominant causes of death in 17 of 22 infants in the first two years after the onset of CRF; four of eight deaths that occurred beyond two years were caused by airway- and ventilator-related accidents. Mechanical ventilatory support was emphasized for as long as necessary to provide normal blood gas tensions, nutrition, growth, and development rather than weaning as rapidly as possible. This clinical experience demonstrates that it is feasible to save over 70% of infants with the severest forms of CRF and prolonged ventilator dependency.
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PMID:Chronic respiratory failure in infants with prolonged ventilator dependency. 368 38

Bronchopulmonary dysplasia is caused by several factors. Avoidance of bronchopulmonary dysplasia is directed at its causes and should always attempt the rapid weaning of the patient from the respirator. Some of the preventive measures include a) avoiding an oxygen injury; b) prevention of barotrauma; 3) sufficient moisturization and warming of the respiratory gases; d) regular cleaning of the respiratory tract and bacterial controls of the tracheal secretion; e) administration of vitamin E; f) reconsideration (restricting the use) of parenteral nutrition. Assistance in the weaning from the respiratory means a) avoidance of an open ductus arteriosus; b) paced reduction of FiO2, respiratory pressure and frequency up to intermittent mandatory ventilation and final transition to spontaneous respiration with increased mean respiratory pressure; c) avoidance of cardiac insufficiency; d) administration of corticosteroids; e) theophyllin, and f) physical therapy. The number of patients with bronchopulmonary dysplasia has remained the same in the last six years. However, the mortality until 1979 round about 50% has been reduced to 1/3, in the years 1980/81.
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PMID:[Clinical management of bronchopulmonary dysplasia]. 649 44

Pulmonary edema is an important feature of many newborn lung diseases, including respiratory distress from severe perinatal asphyxia, heart failure, hyaline membrane disease, pneumonitis from group B beta-hemolytic streptococcus, and chronic lung disease (bronchopulmonary dysplasia). Neonatal pulmonary edema often results from increased filtration pressure in the microcirculation of the lungs. This occurs during sustained hypoxia, in left ventricular failure associated with congenital heart disease or myocardial dysfunction, following excessive intravascular infusions of blood, colloid, fat, or electrolyte solution, and in conditions that increase pulmonary blood flow. Low intravascular protein osmotic pressure from hypoproteinemia may predispose infants to pulmonary edema. Hypoproteinemia is common in infants who are born prematurely. Large intravascular infusions of protein-free fluid further decrease the concentration of protein in plasma and thereby facilitate edema formation. Lymphatic obstruction by air (pulmonary interstitial emphysema) or fibrosis (long-standing lung disease) also may contribute to the development of edema. Bacteremia, endotoxemia, and prolonged oxygen breathing injure the pulmonary microvascular endothelium and cause protein-rich fluid to accumulate in the lungs. The risk of neonatal pulmonary edema can be reduced by several therapeutic measures designed to lessen filtration pressure, increase plasma protein osmotic pressure, and prevent or reduce the severity of lung injury.
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PMID:Edema formation in the lungs and its relationship to neonatal respiratory distress. 657 79


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