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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Six full-term newborn infants are described who suffered from severe adult respiratory distress syndrome (ARDS). The triggering event was intrauterine/perinatal asphyxia in five, and group B streptococcal (GBS) septicemia in three. All had severe respiratory distress/failure and were ventilated mechanically with high concentrations of inspired oxygen and positive end-expiratory pressure. Radiography of the chest showed dense bilateral consolidation with air bronchograms and reduced lung volume. Persistent pulmonary hypertension (PPH) was documented in all cases. The coincidence of ARDS and PPH rendered respiratory management extremely difficult. For this reason high-frequency ventilation was instituted in all patients in order to improve CO2 elimination and induce respiratory alkalosis. Acute complications of respiratory therapy were encountered in five patients (pneumothorax, pulmonary interstitial emphysema, pneumopericardium). Three infants died (irreversible septic shock, progressive severe hypoxemia, and sudden cardiac arrest) after 17, 80, and 175 h of life. Histologic examination of the lungs was possible in all fatal cases and revealed typical changes of acute to subacute stages of ARDS. Three infants survived, the mean time of mechanical respiratory support being 703 h. Two patients were still dependent on oxygen after 1 month of life, and all survivors had increased interstitial markings and increased lung volumes on their chest roentgenograms at this time.
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PMID:The paradox of adult respiratory distress syndrome in neonates. 200 41

From July 1987 to October 1991, we experienced 10 full-term newborn infants with severe adult respiratory distress syndrome (ARDS). The triggering events were intrauterine/perinatal asphyxia in 6 and sepsis in 4. All had severe respiratory distress/failure and were mechanically ventilated with high concentration of inspired oxygen and positive end-expiratory pressure. Radiography of the chest all showed bilateral dense consolidation (white out lungs) and reduced lung volume. Persistent pulmonary hypertension (PPHN) was documented in 9 cases (90%). The concomittent occurrence of ARDS and PPHN rendered respiratory management extremely difficult. High-rate ventilation and tolazoline infusion were used in all these 9 PPHN cases. Acute complication of respiratory therapy (pneumothorax) was encountered in 5 patients. Only 3 cases survived, all belonging to the asphyxia group. Of these 3 survivors, 1 developed bronchopulmonary dysplasia, 1 had cerebral palsy on follow up and the other one was lost on follow up. The outcome of neonatal ARDS was generally poor.
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PMID:Adult respiratory distress syndrome in full term neonates. 817 41

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

Persistent pulmonary hypertension in the newborn (PPHN) is characterised by increased medial and adventitial thickness in the lung vasculature. This study describes morphometry of lung vasculature after extracorporeal membrane oxygenation (ECMO) in newborns with PPHN, due to meconium aspiration syndrome, sepsis or idiopathic persistent pulmonary hypertension of the newborn (i-PPHN). Three groups were studied: newborns with PPHN treated with ECMO (n=9), newborns with PPHN not treated with ECMO (n=12) and age-matched controls without PPHN (n=11). In pulmonary arteries with an external diameter of less than 150 microm, arterial media, adventitia and total wall thickness, expressed as a percentage of the external diameter, and their cross-sectional areas were calculated. Newborns with PPHN, compared with controls, demonstrated increased percentage of media thickness, adventitia thickness and total wall thickness, and increased medial, adventitial and total wall cross-sectional area. Newborns treated with ECMO, compared with those not treated so, showed a decreased percentage of media thickness and medial cross-sectional area in arteries with an external diameter less than 75 microm, and decreased percentage of media thickness and decreased medial, adventitial and total wall cross-sectional area in arteries with an external diameter of 75-150 microm. ECMO for persistent PPHN, due to meconium aspiration syndrome, sepsis or i-PPHN, reduces the abnormal morphometry of small pulmonary arteries. The underlying mechanisms contributing to this improved morphometry are yet unknown.
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PMID:Morphometric analysis of the lung vasculature after extracorporeal membrane oxygenation treatment for pulmonary hypertension in newborns. 1517 81

Persistent pulmonary hypertension (PPHN) is a disease characterised by the disruption of the transition from fetal to neonatal circulation with the persistence of high pulmonary vascular resistances and right-to left shunting. This condition, occurring in about 1-2 newborns per 1000 live births, causes severe hypoxemia. Despite significant improvements in treatment, the mortality of PPHN varies from 10 to 20 % of affected newborns. Pulmonary hypertension is frequently observed in some cardiac malformation and in congenital diaphragmatic hernia, in meconium aspiration syndrome, neonatal sepsis, podalic presentation and male sex. Maternal risk factors are tobacco smoking, cesarean section, low socio-economic conditions, diabetes and urinary infections. Another predisposing condition is antenatal or postnatal exposure to some drugs. The medications involved in drug-induced pulmonary hypertension and the mechanisms involved are reviewed.
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PMID:Drug-induced pulmonary hypertension in newborns: a review. 1743 Feb 17

Persistent pulmonary hypertension (PPHN) is a consequence of failed pulmonary vascular transition at birth and leads to pulmonary hypertension with shunting of deoxygenated blood across the ductus arteriosus (DA) and foramen ovale (FO) resulting in severe hypoxemia, and it may eventually lead to life-threatening circulatory failure. PPHN is a serious event affecting both term and preterm infants in the neonatal intensive care unit. It is often associated with diseases such as congenital diaphragmatic hernia, meconium aspiration, sepsis, congenital pneumonia, birth asphyxia and respiratory distress syndrome. The diagnosis of PPHN should include echocardiographic evidence of increased pulmonary pressure, with demonstrable right-to-left shunt across the DA or FO, and the absence of cyanotic heart diseases. The mainstay therapy of PPHN includes treatment of underlying causes, maintenance of adequate systemic blood pressure, optimized ventilator support for lung recruitment and alveolar ventilation, and pharmacologic measures to increase pulmonary vasodilation and decrease pulmonary vascular resistance. Inhaled nitric oxide has been proved to treat PPHN successfully with improved oxygenation in 60-70% of patients and to significantly reduce the need for extracorporeal membrane oxygenation (ECMO). About 14%-46% of the survivors develop long-term impairments such as hearing deficits, chronic lung disease, cerebral palsy and other neurodevelopmental disabilities.
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PMID:Beyond the inhaled nitric oxide in persistent pulmonary hypertension of the newborn. 2892 74