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Query: UMLS:C0243026 (sepsis)
 52,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sophisticated neonatal transport has improved the safety of transporting preterm infants, but may not substitute for the benefits of in utero transport. To describe gestational age trends and assess differences in complications between maternal (in utero) and neonatal transports, we analyzed maternal and neonatal transports, over 3 years, to the only tertiary center in the region. Those who delivered between 24 and 34 weeks' gestation were included in the analysis. Gestational age trends for each complication are described, showing, in general, decreasing morbidity with gestational age in both groups. These trends were usually parallel, but not equal. A significantly greater mean neonatal intensive care unit (p = 0.003) and total length of stay (p = 0.006) as well as longer ventilator time (p = 0.01) and oxygen therapy exposure (p = 0.018) were noted in those transported neonatally. The incidence of respiratory distress syndrome (p < 0.001), bronchopulmonary dysplasia (p = 0.027), intraventricular hemorrhage (p = 0.041), intraventricular hemorrhage grades III and IV (p = 0.008), patent ductus arteriosus (p = 0.032), and mortality (p = 0.001) were all significantly greater among the neonatal transports. The differences were not significant for retinopathy of prematurity, hyperbilirubinemia, necrotizing enterocolitis, periventricular leukomalacia, and culture proven sepsis. Specialized neonatal transport and advanced neonatology techniques have not removed the significant advantage of decreased morbidity, mortality, and length of hospital intervention resulting from maternal (in utero) transport.
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PMID:An analysis of neonatal morbidity and mortality in maternal (in utero) and neonatal transports at 24-34 weeks' gestation. 937 4

There is controversy regarding the role of mycoplasmas (MP) colonizing the neonatal respiratory tract in the development of bronchopulmonary dysplasia (BPD). To determine the association of respiratory MP colonization and BPD. Retrospective analysis of neonates (26-32 weeks of gestation) intubated for respiratory insufficiency. Tracheal aspirate cultures were obtained for MP if the lung disease was not improving by 7-10 days or there were radiographic changes suggestive of inflammation. Of 63 infants who had tracheal aspirates sent, 17 had positive MP cultures. We found no significant difference in the gestational ages (27.6 +/- 0.4 vs 27.8 +/- 0.2 weeks) or birth weights (1097 +/- 86 vs 997 +/- 42 grams) in MP positive vs negative infants. No differences were noted in antenatal or postnatal steroid use, gender, race, sepsis, RDS, PDA, air leaks, NEC, GER, days on positive pressure ventilation or days on oxygen. There were significantly (p = 0.04) more infants with severe BPD (defined as oxygen requirement at 36 weeks corrected post menstrual age) among MP positive (n = 14; 82%) versus MP negative (n = 25; 54%) infants. Presence of MP in the tracheal aspirates is associated with an increased likelihood of developing severe BPD.
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PMID:Respiratory tract colonization with mycoplasma species increases the severity of bronchopulmonary dysplasia. 959 65

In Japan, chronic lung disease (CLD) is defined as an oxygen requirement greater than that obtainable in room air at 28 days of age, with symptoms of persistent respirator distress and a hazy or emphysematous and fibrous appearance upon chest x-ray. A total of 4964 infants weighing less than 1500 g at birth and born in 1990 were admitted to and cared for at level II and III neonatal care centers in Japan. A total of 4293 infants (86.3%) survived at 28 days after birth. Analyses of infants who developed CLD through their preceding illnesses and chest x-ray findings resulted in the classification of CLD into six types. Types I and II are defined as CLD following the acute stage respiratory distress syndrome (RDS). Type I is the typical case of bronchopulmonary dysplasia (BPD) as described previously, whereas Type II shows atypical radiological findings, namely only diffuse haziness without typical emphysema and fibrosis. Type III has a history of intrauterine inflammation. Chest x-ray shows the typical bubbling and cystic appearance described in the original report of Wilson-Mikity syndrome or neonatal pulmonary emphysema in the very low birth weight infant. Type III also has atypical radiological findings in cases with intrauterine infection. Type IV does not have a history of either intrauterine inflammation or RDS but shows typical emphysematous and fibrous appearance upon chest x-ray. Type V includes those with atypical chest x-ray appearance similar to Type II but without history of RDS and intrauterine inflammation. CLD is a heterogeneous condition which shows different spectra. However, the cardinal event is common to all types--the excessive inflammatory response caused by various insults to the immature airways and alveoli, such as oxygen, barotrauma, infection and so on. The excessive inflammatory response leads to lung tissue damage and the abnormal healing process due to immaturity, (such as vitamin A deficiency and insufficient oxygen radical scavenging system) and results in dysplasia and metaplasia of the respiratory system. The treatment of respiratory distress due to CLD also acts as an insult to the lungs and thus forms a vicious cycle. The different spectra of the disease are most possibly attributed to the difference in the timing and the kind of insults to the lungs. In Type I and II CLD, the insults are given in the first hours of life when the infants with surfactant deficiency receive high concentrations of oxygen for stabilization before the surfactant replacement. In Type III and III' CLD the insults are most likely given before birth. Excessive and sustained inflammatory response in the lungs with different onset times may result in the development of Type IV and V CLD. The strategy for the prevention of CLD should be different according to the origins and causes. The prevention of Type I and II CLD, or CLD following RDS, should be accomplished by successful prophylactic surfactant replacement therapy. Another procedure may be the application of high frequency oscillatory ventilation (HFOV) in the acute stage of RDS or at the time of stabilization right after birth. Types III and III' CLD present the most difficult challenge for prevention strategy because the disease process already started before birth. At the moment there are no effective measures for prevention. The strategy for the prevention of Type IV and V CLD may reside in the early detection and treatment of patent ductus arteriosus, sepsis and airway infection including pneumonia.
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PMID:Chronic lung disease of the very low birth weight infant--is it preventable? 967 27

Despite indomethacin therapy, many premature infants require surgical closure of their patent ductus arteriosus (PDA). Between January 1985 and December 1997, 176 premature infants underwent surgical closure of PDA by vascular clip after failure of medical treatment. The median gestational age and birth weight were 26 weeks (range 23-36 weeks) and 847.5 g (range 400-2300 g), respectively. The median age at diagnosis and at surgery was 4 days (range, 1-37) and 21 days (range, 4-60) respectively. The median weight at surgery was 982.5 g (range 475-2740 g). Of these infants, 168 (95%) were intubated prior to surgery and the median time to extubation was 21 days (range 1-273 days). There were no operative deaths but 11 infants (6.4%) died from complications of prematurity (sepsis, bronchopulmonary dysplasia and pulmonary hemorrhage). The frequency of chest tube insertion at surgery decreased from 41.7% to 10% between the 1985-88 and 1996-97 periods (P<0.01). Three infants (1.7%) developed vocal cord paralysis directly related to the position of the vascular clip. Echocardiography confirmed PDA closure in 43 infants (24.4%) while the remaining 133 had no clinical signs of PDA. Surgical closure of PDA by vascular clip carries a very low morbidity in premature infants.
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PMID:Is surgical closure of patent ductus arteriosus a safe procedure in premature infants? 1009 62

Prematurity, intrauterine infection and perinatal brain injury have been reported to be significant risk factors of cerebral palsy (CP). We examined the perinatal predictors of cerebral palsy and delayed development (DD) in 184 high risk infants. Thirty-five infants were diagnosed as cerebral palsy and delayed development at 12 months corrected age. Antenatal, intrapartum, and neonatal factors were prospectively evaluated in 2 groups of high risk infants compared with controls; Group A (n = 79), infants weighing less than 2,000 g; Group B (n = 43), infants weighing 2,000 g or more. In univariate analysis, there were no significant antenatal and intrapartum factors associated with cerebral palsy and delayed development in either group. We found that significant postnatal risk factors of CP in group A included sepsis (p = 0.008), BPD (bronchopulmonary dysplasia) (p = 0.028), IVH (intraventricular hemorrhage) (p = 0.042), ventriculomegaly (VM) (p = 0.001) and a longer duration of mechanical ventilation (p = 0.001); while in group B, sepsis (p = 0.047) and neonatal seizure (p = 0.027) were significant risk factors. In multivariate analysis, sepsis in group B was a moderate risk factor of CP (OR (odds ratio) 1.47; 95% CI (confidence interval) 1.02-2.13). In conclusion, neonatal sepsis may contribute to the development of cerebral palsy and delayed development. We suggest that high risk infants who have sepsis should be carefully followed for cerebral palsy and delayed development. The prevention of cerebral palsy may be feasible by decreasing neonatal risk factors such as sepsis during the neonatal period.
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PMID:Prospective evaluation of perinatal risk factors for cerebral palsy and delayed development in high risk infants. 1048 40

Short-term inhaled dexamethasone therapy was evaluated in a double blind placebo controlled trial in 36 ventilator dependent preterm neonates (BW < 1500 gm, postnatal age > 7 days) who were at risk for bronchopulmonary dysplasia. Pulmonary and systemic effects were compared at early (day 3), late (7-10 days) and post (14 days after initiation) phases of therapy. Airflow mechanics improved as demonstrated by a net 101% improvement in pulmonary resistance (a decrease from 139 to 101 cm H2O/L/s in the dexamethasone treated infants as compared to an increase from 153 to 267 cmH2O/L/s in the placebo treated infants during the early phase of therapy); this was associated with a 45% increase in inspiratory airflow (1.29 +/- 0.43 to 1.87 +/- 0.978 L/min; p < 0.01), and 37% increase in expiratory airflow. These changes resulted in a significant reduction in the work of breathing such that the mean tidal driving pressure significantly decreased from 13.6 cmH2O to 9.4 cm H2O with inhaled steroid administration. Though the brief duration of therapy did not result in cessation of ventilatory support, the level of support was significantly reduced (decreased values of oxygen supplementation, mean airway pressure and oxygenation index and increased ventilatory efficiency index). The inhaled dexamethasone therapy was also associated with systemic absorption of the drug as evidenced by transient but apparently reversible reduction in serum cortisol levels. No systemic side effects of hypertension, hyperglycemia or nosocomial sepsis were observed. These data demonstrate beneficial effects of short-term inhaled dexamethasone on the resistive airflow properties of preterm infants at risk for BPD and may provide adjunctive means to facilitate weaning in the ventilator dependent neonates.
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PMID:Respiratory and systemic effects of inhaled dexamethasone on ventilator dependant preterm infants at risk for bronchopulmonary dysplasia. 1077 73

The objective of this paper is a retrospective study of all infants treated for congenital chylothorax at the Royal Children's Hospital (RCH), Melbourne, Australia and King Fahad National Guard Hospital (KFNGH), Riyadh, Kingdom of Saudi Arabia. The charts of all infants with congenital chylothorax admitted to RCH over a period of 13 years, June 1982-August 1994, and admissions to KFNGH over a 7-year period, June 1992-August 1998 inclusive, were reviewed including management outcome and complications. There were 19 infants, 13 from RCH and 6 from KFNGH; 11 females and 8 males. Three infants were managed antenatally. Fifteen infants presented immediately after birth. Seven were born with hydrops fetalis, 6 infants had syndromes and 10 infants were born prematurely. Regular infant feeding formula and/or breast milk were used successfully in 12 infants, while in 7 infants medium chain triglycerides (MCT) rich formula was used. Sixteen infants were mechanically ventilated with 75% of them ventilated for < or = 28 days. Fifteen infants received total parenteral nutrition (TPN), and in 80% for < or = 32 days. Hydropic infants had longer duration of mechanical ventilation and hospital stay with mean (range) of 33.9 (3-120) and 115 (23-225) days, respectively, compared with 18 (1-62) and 34.3 (14-88) days for nonhydropic infants. Five infants underwent surgery with failure in four. Sepsis and bronchopulmonary dysplasia were the main complications. The survival rate was 100% regardless of the mode of therapy. The prognosis of Isolated congenital chylothorax in term, and preterm infants is good even in the presence of hydrops. Breast milk and/or regular infant feeding formula should be used initially before proceeding to MCT-rich formula, which may be necessary in some cases. Surgery should be considered if conservative management of congenital chylothorax fails after 4-5 weeks.
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PMID:Congenital chylothorax. 1101 35

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

Birthweight-specific neonatal mortality for Alaska Natives is higher than for non-natives for the years 1987-1996. We investigated the reasons for this based on Level III Neonatal Intensive Care Unit information available from 1991-1996. We also investigated whether differences in mortality extended to measures of morbidity. There were less Native patients born at the tertiary care center for babies with birthweight < 1500 grams and 1500-2499 grams (64% for Natives and 87% for non-natives, p = .000). Differences in antenatal referral were only apparent for the population residing within the Anchorage/Mat-Su area. There were also less cesarean deliveries for Native infants that were born outside of the tertiary care center for both birthweight categories (25% for Native vs. 53% for non-native infants < 1500 grams, p = .01; 27% for Native vs. 48% for non-native infants 1500-2499 grams, p = .01). For Alaska Native babies < 1500 grams there was more necrotizing enterocolitis (13% in Native vs. 4.9% in non-native, p = .01), more severe retinopathy of prematurity (12% in Native vs. 4.6% in non-native, p = .01), and more bronchopulmonary dysplasia (49% in Native vs. 34% in non-native, p = .04). For Alaska Native babies 1500-2499 grams that needed ventilatory assistance there was more intraventricular hemorrhage (19% in Native vs. 7.4% in non-native, p = .003), more severe (grade 3-4) intraventricular hemorrhage (9.5% in Native vs. 0.9% in nonnative, p = .001), and more acquired sepsis (7.1% in Native vs. 1.7% in non-native, p = .02). Differences in access to Level III perinatal care and intrapartum care (cesarean delivery rates) are likely factors that contribute to the worse outcomes in the Alaska Native population.
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PMID:Racial differences in newborn intensive care morbidity in Alaska. 1143 33

Cytomegalovirus causes pneumonia, hepatitis, thrombocytopenia, and hemolytic anemia. Cytomegalovirus adrenalitis in premature infants, however, is rare. This report described a premature newborn who had progressively worsening hyperbilirubinemia, pancytopenia, and hepatosplenomegaly at the age of 4 days. The baby's mother had prolonged rupture of amniotic membrane for about 8 weeks. The infant received exchange blood transfusion, empiric antibiotics treatment, and mechanical ventilation. Pneumonia and sepsis developed at the age of 18 days. Serum anticytomegalovirus immunoglobulin M and urine virus culture were positive for cytomegalovirus. The baby died at the age of 22 days. Autopsy showed cytomegalovirus infection complicated with interstitial pneumonitis and pulmonary edema, subacute bronchopulmonary dysplasia with interstitial fibrosis, and adrenalitis. We concluded that the functional status of the adrenal glands in cytomegalovirus-infected premature newborns who have unexplained electrolytes imbalance, fever, diarrhea, weight loss, or hypotension should be closely followed because of the possible involvement of adrenal glands.
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PMID:Perinatal cytomegalovirus infection complicated with pneumonitis and adrenalitis in a premature infant. 1182 12


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