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 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The impact of implementation of the National Health Insurance on the outcome, cost, and length of hospitalization of very-low-birth-weight (VLBW) infants is not clear in Taiwan. These data are important for the planning of medical care and regionalization in this area. This study was an attempt to examine these questions. We retrospectively collected mortality, morbidity, and length and cost of hospitalization data of VLBW (BW < 1500 g) infants between March 1995 and February 1998. There were totally 162 patients enrolled. The overall mortality rate was 21.6%; the birth weight (BW)-specific mortality rate was 72%, 31%, 19%, and 3% for infants with BWs of < 750 g, 750-999 g, 1000-1249 g, and 1250-1499 g, respectively. The incidence of morbidities were: respiratory distress syndrome (74%), patent ductus arteriosus (36%), necrotizing enterocolitis (9%), sepsis (42%), intraventricular hemorrhage (15%), retinopathy of prematurity (31%), failure to pass auditory brainstem response (ABR) (34%), and chronic lung disease (17%). The average length of hospitalization was 67.2 days, and the cost per infant was 62 x 10(4) NT dollars; 108 +/- 38 days, 73 +/- 32 x 10(4) NT dollars if BW < 750 g; 94 +/- 15 days, 99 +/- 35 x 10(4) NT dollars if BW 750-999 g; 66 +/- 23 days, 64 +/- 36 x 10(4) NT dollars if BW 1000-1249 g; and 43 +/- 14 days, 39 +/- 37 x 10(4) NT dollars if BW 1250-1499 g. In conclusion, VLBW infants are associated with high mortality and morbidity rates. They have long lengths and high costs of hospitalization, and therefore deserve attention in the implementation of the National Health Insurance and regionalization.
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PMID:Mortality, morbidity, length and cost of hospitalization in very-low-birth-weight infants in the era of National Health Insurance in Taiwan: a medical center's experience. 1119 36

Persistent pulmonary hypertension of the newborn (PPHN) remains one of the most challenging situations in the neonatal intensive care unit, and it is associated with high mortality and morbidity. The optimal treatment for PPHN is controversial. We report our 9-year experience in the management of PPHN through a retrospective review of 29 neonates with persistent pulmonary hypertension. The diagnosis of PPHN is made by echocardiography and/or preductal and postductal oxygen tension difference. The treatment modalities include supportive medical care, vasodilator therapy, mechanical ventilation and correction of underlying conditions. The wide diversity of etiologies of PPHN, the complications of vasodilator therapy, the management of assisted ventilation, the mortality and the morbidity are evaluated. There are 29 patients enrolled in this study, including 18 male and 11 female babies. Twenty-two patients (72%) are referred from other hospitals. The mean birth body weight is 2707 +/- 693 grams (range: 1450-4100 grams) and the mean gestational age is 37.1 +/- 3.1 weeks (range: 31-41 weeks). The underlying clinical conditions include meconium aspiration syndrome (n = 8), perinatal asphyxia (n = 7), respiratory distress syndrome (n = 5), sepsis and/or pneumonia (n = 4), congenital diaphragmatic hernia (n = 3) and idiopathic persistent fetal circulation (n = 2). In addition to supportive medical care and correction of underlying clinical conditions, most of the patients receive vasodilator therapy (Tolazoline) and nonhyperventilation respirator management. The overall mortality rate is 27.6% (8/29). The duration on ventilator therapy in the survival group (9.3 +/- 8.6 days) is not significantly different from in the mortality group (6.0 +/- 7.1 days) (p = 0.13). There is also no statistically significant difference between these two groups both in the maximal alveolar-arterial oxygen tension difference (594 +/- 53 mmHg and 613 +/- 37 mmHg, p = 0.145) and in the maximal oxygenation index (49.7 +/- 29.6 and 61.1 +/- 36.9, p = 0.172) before vasodilator therapy. However, twenty-four hours after treatment, these two parameters change significantly with the former changes to 426 +/- 198 mmHg and 643 +/- 7 mmHg, respectively (p < 0.001), and the latter changes to 21.6 +/- 15.8 and 82.3 +/- 54.8, respectively (p < 0.001). Skin rash, gastrointestinal hemorrhage, hypotension and hyponatremia are the most common complications of Tolazoline therapy. Eight patients have pulmonary complications including pneumothorax (n = 5) and pulmonary interstitial emphysema (n = 3). Two patients develop chronic lung disease. Three patients have neurodevelopmental handicap. In conclusion, we achieve a survival rate of nearly 75% in PPHN mainly with the administration of Tolazoline therapy and the nonhyperventilation respirator approach. Further well-controlled and multicenter studies with newer treatment modalities are crucial for the improvement of survival of PPHN in Taiwan.
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PMID:Persistent pulmonary hypertension of the newborn: experience in a single institution. 1135 72

During the final prenatal period of fetal lung development in humans, important maturational processes occur, including the production of surfactant necessary to decrease surface tension at the air-liquid interface of the alveoli. During early gestation, the glucocorticoid receptor is expressed in the fetal lung, and glucocorticoids stimulate the production of surfactant-associated proteins and increase phospholipid synthesis by enhancing the activity of phosphatidylcholine. Other glucocorticoid-induced effects may include stimulation of cell maturation and differentiation, inhibition of DNA synthesis, changes in interstitial tissue components, stimulation of antioxidant enzymes, and regulation of pulmonary fluid metabolism. Recently, it was suggested that glucocorticoids are also important in postnatal pulmonary development, and may be related to the development of neonatal lung disease in preterm infants. Surfactant deficiency that can be prevented by antenatal corticosteroid treatment causes infant respiratory distress syndrome and requires mechanical ventilation. Ventilation by itself or in combination with high levels of oxygen, fluid overload, pulmonary infections, sepsis, and air leak syndrome causes an acute pulmonary inflammatory reaction that may result in chronic lung disease or bronchopulmonary dysplasia. Glucocorticoids are effective in the treatment of chronic lung disease of prematurity and regulate the inflammatory response by the interaction with transcription factors such as nuclear factor kappaB and activated protein 1. Indeed, inflammatory cells and the levels of chemokines and cytokines in bronchoalveolar fluid decrease after dexamethasone treatment. However, treatment of fetuses and preterm infants with repeated and/or high doses of corticosteroids may have considerable long-term side effects on somatic, brain, and lung growth. The difficult balance between short-term gain and the possible long-term side effects of glucocorticoids in preterms remains a difficult issue.
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PMID:Glucocorticoids and lung development in the fetus and preterm infant. 1141 80

Respiratory muscle dysfunction associated with ventilatory loading may be partially attributed to respiratory muscle injury. Exertion-induced muscle injury can be defined as structural alterations of the muscle, however, a better understanding of the biochemical, morphologic, and functional correlates of injured respiratory muscles will facilitate discrimination of how injury, fatigue, and weakness contribute to respiratory muscle dysfunction. In addition to the increased loads associated with lung disease, many factors such as poor arterial blood gases, immobilization, sepsis, decreased nutrition, and corticosteroids may increase susceptibility to exertion-induced respiratory muscle injury. Respiratory muscle injury in humans is not well-described, however, more extensive evidence has been shown in animal models of increased ventilatory loading. Potential mechanisms of respiratory muscle injury are mechanical stress, metabolic stress, and inflammation. In order to optimize therapeutic interventions, a better understanding of these mechanisms and the patients that are most susceptible to respiratory muscle injury needs to be determined.
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PMID:Respiratory muscle injury: evidence to date and potential mechanisms. 1148 9

The authors carried out an experiment on mice infected with dark-pigmented micromicetes Aspergillus clavitus and Exophiala dermatitidis, preplanted from lung operational material of patients with chronic non-specific lung disease and destructive tuberculosis. The infection was produced by the peroral method in the first group of animals and by the intranasal method in the second group. By day 30 the test animals developed mycotic sepsis, fifty percent of the animals had malignant lung growths (adenocarcinoma, squamous cell carcinoma and angiopericytoma). Established in the experiment was toxicity and cancerogenity of dark-pigmented micromicetes Aspergillus clavitus and Exophiala dermatitidis. A model of mycotic sepsis and micromicete-induced lung cancer has been created.
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PMID:[Deep mycosis and lung tumor induced by dark-pigmented micromycetes]. 1169 96

Over the past year, human studies have confirmed and expanded the involvement of macrophage migration inhibitory factor (MIF) in a number of diseases that had originally been studied in animals. In addition to sepsis, rheumatoid arthritis, glomerulonephritis and inflammatory lung disease, elevated MIF levels have been described in patients suffering from ulcerative colitis, inflammatory neurological diseases and cancer. Cellular studies indicate that in addition to macrophages, MIF affects the activities of CD4+ and CD8+ T cells, natural killer cells, fibroblasts and endothelial cells, actions that may explain the contribution of MIF to inflammatory diseases and cancer. Molecular studies have identified direct interactions between MIF and several intracellular regulatory proteins (Jab1, PAG and p53) that control cellular growth and proliferation; however, how interactions with these proteins fit into a general scheme to explain MIF's biological activity has not been elucidated. The three-dimensional structure of MIF has offered some surprising clues and if the potential enzymatic sites identified are involved with MIF-associated diseases, they may provide good targets for therapeutic intervention.
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PMID:Glucocorticoid counter regulation: macrophage migration inhibitory factor as a target for drug discovery. 1175 24

There is growing evidence that sepsis-related complications in neonates are crucially mediated by the action of proinflammatory cytokines. It has previously been demonstrated that elevated IL-6 and IL-8 levels can predict brain damage and chronic lung disease in preterm infants. However, it is the current view that neonates have a reduced capability to produce proinflammatory cytokines. To clarify this issue, we analyzed the inflammatory response in term and preterm infants directly at the single cell level by flow cytometry. Endotoxin challenge was performed under defined conditions on monocytes obtained from 50 healthy adults and 119 neonates, which consist of 45 term infants, 63 preterm infants (26.1-36.7 wk of gestational age), and 11 preterm infants with proven infection (24.6-29.9 wk). Our results challenge the existing view of an immature inflammatory response by demonstrating that term infants and preterm infants display a higher percentage of IL-6- and IL-8-positive cells than adults. After preincubation with dexamethasone the number of cytokine-positive cells decreased in all groups, but the number of IL-8-positive cells remained higher in term and preterm infants >32 wk compared with adults. These observations demonstrate not only a well-developed but also an enhanced inflammatory response in term and preterm infants. Under consideration of several detrimental effects of IL-6 and IL-8, our data may have major implications on the pathophysiology of inflammatory-triggered neonatal diseases.
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PMID:Enhanced interleukin-6 and interleukin-8 synthesis in term and preterm infants. 1271 93

Persistent pulmonary hypertension is seen in association with a number of diseases and conditions in the newborn including perinatal asphyxia, meconium aspiration syndrome, Group B strep sepsis, and certain surgical conditions such as congenital diaphragmatic hernia. The conventional therapy of persistent pulmonary hypertension is discussed as well as the adjunctive role of surfactant replacement therapy and high frequency ventilation. The mechanism of action of inhaled nitric oxide as a selective pulmonary vasodilator is explained. Human neonatal clinical experience is chronicled from the original studies of Roberts in 1992 and Kinsella in 1993. A review of three large prospective randomized trials of nitric oxide is presented as well as a summary of new areas of investigation including the use of nitric oxide in pre-term infants and the use of nitric oxide in the prevention of chronic lung disease. Current dosing recommendations are presented as well as guidelines recently published from the American Academy of Pediatrics. A review of follow up literature in relationship to patients receiving inhaled nitric oxide is also summarized.
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PMID:Status report: inhaled nitric oxide in persistent pulmonary hypertension/hypoxic respiratory failure of neonate. 1210 54

This article describes three extremely low birth weight infants with Staphylococcus aureus septicemia associated with insertion of a percutaneous central venous catheter who later developed endocarditis. Echocardiography demonstrated large vegetations although only one infant had a murmur. Following a 6-week course of intravenous flucloxacillin and netilmicin, the endocarditis completely resolved and further intervention was unnecessary, although one baby died later as a result of volvulus and chronic lung disease. Echocardiography should be performed to exclude invasive infection in infants with S. aureus septicemia even when there is no murmur or other evidence of endocarditis. If endocarditis is identified, a good outcome is possible with appropriate aggressive antibiotic therapy.
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PMID:Staphylococcus aureus endocarditis in preterm neonates. 1215 43

The survival rate for extremely preterm or extremely low-birth-weight (LBW) newborns born at the threshold of viability (25 or fewer completed weeks of gestation) improved in the early 1990s, largely as the result of a greater use of assisted ventilation in the delivery room and surfactant therapy. Increased use of antenatal and neonatal corticosteroids also may have influenced survival rates. However, this improvement in survival has not been associated with an equal improvement in morbidity. The incidence of chronic lung disease, sepsis, and poor growth remains high and may even have increased. There is concern that the treatment of extremely preterm and extremely LBW newborns may result in unforeseen effects into adulthood, and that the neurodevelopmental outcome and cognitive function of extremely preterm and extremely LBW infants may be suboptimal. The purpose of this document is to describe the potential consequences of extremely preterm birth and to provide clinical management guidelines based on the best available data.
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PMID:ACOG Practice Bulletin: Clinical Management Guidelines for Obstetrcian-Gynecologists: Number 38, September 2002. Perinatal care at the threshold of viability. 1222 Jul 92


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