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

Group B beta-hemolytic streptococcus (GBS) infection is an important cause of neonatal pneumonia and sepsis. GBS infection is frequently associated with persistent pulmonary hypertension of the newborn. To better understand the early pulmonary hypertension phase of GBS-induced acute lung injury in a conscious animal, we characterized the pulmonary and systemic hemodynamic response of spontaneously breathing, chronically instrumented newborn lambs to injections of heat-killed type Ib GBS, 0.1-9.0 x 10(9) colony forming units. Heat-killed GBS caused marked dose-dependent increases in mean pulmonary arterial pressure and calculated pulmonary vascular resistance, 190 and 370% at the maximum dose, respectively. Similarly, GBS caused dose-dependent increases in mean systemic arterial pressure and systemic vascular resistance (28.5 and 108% at the maximum dose, respectively) and a decrease in cardiac output (33.5%). Arterial oxygen tension worsened at the higher doses. GBS-induced pulmonary hypertension was decreased by two structurally unrelated, putative leukotriene D4 receptor antagonists. Pretreatment with LY171883 blocked GBS-induced pulmonary hypertension by 95%, and WY48,252 attenuated this effect by 27%. Both drugs completely blocked the hemodynamic effects of exogenous leukotriene D4. For comparison, several lambs received bolus injections of live GBS, either alone or after pretreatment with LY171883. The hemodynamic response to live GBS and attenuation of that response by LY171883 were similar to those caused by similar doses of heat-killed GBS. Thus, bolus injections of heat-killed GBS provide a reproducible model of pulmonary hypertension in conscious newborn lambs. In addition, the sulfidopeptide leukotrienes appear to be important mediators of GBS-induced pulmonary hypertension in newborn lambs.
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PMID:Hemodynamic effects of heat-killed group B beta-hemolytic streptococcus in newborn lambs: role of leukotriene D4. 131 29

We report on 50 term and near-term neonates (birth weight greater than 1800 g, gestational age greater than 33 weeks) with severe persistent pulmonary hypertension of the newborn (PPHN), referred to us from January 1987 to July 1991 after failure of maximum conventional treatment. All infants had paO2 less than 45 mm Hg when ventilated with peak inspiratory pressure greater than 38 cm H2O and FiO2 = 1.0, hence meeting entry criteria for extracorporeal membrane oxygenation (ECMO). High frequency oscillatory ventilation (HFOV) was tried in all patients. If sufficient oxygenation could not be achieved (paO2 less than 40 mm Hg for at least 2 h), ECMO therapy was begun, which was the case in 25 children. Neonates responding to HFOV (n = 25) were of a slightly younger gestational age (37.0 weeks vs 38.8 weeks, P less than 0.05), had higher Apgar scores and were less hypoxaemic before HFOV (paO2 36.6 mm Hg vs 28.8 mm Hg, P less than 0.01); during HFOV there was a significant rise in paO2 (greater than 150 mm Hg; P less than 0.001) and a fall in pCO2 to 21.6 mm Hg (P less than 0.001). Due to air leaks, which was the main complication of HFOV (52%), ECMO therapy had to be begun in two additional infants after an initial positive effect. HFOV tended to be successful in cases of primary PPHN, meconium aspiration and sepsis, but not in infants with lung hypoplasia as a result of diaphragmatic hernia or other reasons. Success or failure of HFOV could not be reliably predicted by any parameter.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:High frequency oscillatory ventilation and extracorporeal membrane oxygenation in severe persistent pulmonary hypertension of the newborn. 142 1

Ureaplasma urealyticum was isolated in pure culture from blood tracheal aspirate and lung tissue in a newborn infant, who died of a severe pneumonia within 48 h after birth. The clinical course was characterized by persistent pulmonary hypertension of the newborn (PPHN). Post-mortem examination revealed extensive hyaline membrane formation combined with signs of inflammation in both lungs. The clinical and histopathological picture resembled that of early onset group B haemolytic streptococcal pneumonia/sepsis.
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PMID:Fatal ureaplasmal pneumonia and sepsis in a newborn infant. 195 41

Extracorporeal membrane oxygenation (ECMO) has rescued moribund infants with respiratory failure from a variety of causes. We report the experience from 58 United States and 7 overseas ECMO centers between 1980 and 1989. Voluntarily submitted data forms provided details of diagnosis, clinical condition, ECMO indications, morbidity, and mortality. Of 3,528 infants with a predicted mortality greater than 80% treated with ECMO, 83% survived. Entry diagnoses and aggregate survival were: meconium aspiration syndrome (MAS) 1,356 (93%), persistent pulmonary hypertension of the newborn (PPHN) 480 (83%); congenital diaphragmatic hernia (CDH) 585 (62%); hyaline membrane disease (HMD) 532 (84%); sepsis 416 (77%); and other 185 (77%). ECMO indications were a-AdO2 greater than 600 for 6 to 8 hours (22%), oxygenation index greater than 40 for 4 hours (18%), acute deterioration (14%), maximal therapy failure (34%), and barotrauma (1%). Annual survival improved over 9 years except for CDH, which decreased from 70% (1987) to 56% (1989) P less than .01). Survivors differed from non-survivors (P less than .05) by birth weight (greater than 2 kg), gestational age (greater than 37 weeks), entry diagnosis (MAS, PPHN, HMD, sepsis v CDH), inborn versus outborn, pre-ECMO pH, and ECMO duration. Technical complications in 25% of patients and medical complications in 75% adversely affected survival. Annual sepsis survival improved to 75% (1989) but had significantly greater complication rates (P less than .05) than other diagnoses. Multicenter data yield information not available from single institution experience. Although entry criteria and conventional therapy continue to evolve, ECMO currently improves survival from an estimated 20% to 83% overall. Individual prognosis depends on entry diagnosis, clinical condition, and complications.
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PMID:Extracorporeal membrane oxygenation and neonatal respiratory failure: experience from the extracorporeal life support organization. 206 12

Persistent pulmonary hypertension of the newborn (PPHN), initially described by Gersony et al as persistent foetal circulation (PFC syndrome), results from a flawed transition from foetal to extrauterine pulmonary circulation. It is characterised by the maintenance of a high pulmonary vascular resistance and right-to-left shunting through the ductus arteriosus and foramen ovale. Infants with a wide variety of underlying clinical conditions develop PPHN. According to Rudolph three main anatomic types of PPHN can be identified: normal pulmonary vascular development increased pulmonary vascular smooth muscle development decreased cross-sectional area of pulmonary vascular bed. It is important to realize that several pathophysiologic mechanisms may coexist and interact. Besides metabolic and respiratory acidosis, hypercapnia and hypoxaemia some other factors induce pulmonary vasoconstriction. Thromboxane, leukotrienes and prostaglandins play a decisive role. Since PPHN can be associated with a broad spectrum of clinical conditions, a specific clinical picture is lacking. The baby is usually term or post-term, cyanotic immediately after birth or some hours later. Birth asphyxia, hyperviscosity, sepsis and aspiration of meconium have been recognized as predisposing factors. The diagnosis can be confirmed by echocardiography. Contrast echo will indicate right-to-left shunting with normal anatomy. Currently hyperventilation, tolazolin, chlorpromazin and dopamine/dobutamine have been advocated as central foci for clinical therapy. Recently prostacyclin was introduced as a specific pulmonary vasodilatator.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Persistent pulmonary hypertension of newborn. The PFC syndrome]. 229 36

Necrotising enterocolitis is the most common gastrointestinal complication of pre-term infants. In order to determine the strength of the association of hypoxia/ischaemia and infection as causative factors in necrotising enterocolitis, we evaluated all liveborn pre-term infants with a birthweight less than 1500 g and/or gestational age less than 32 weeks in The Netherlands in 1983. The factors related to hypoxia/ischaemia included: asphyxia, respiratory distress syndrome, ventilatory assistance, persistent fetal circulation, persistent ductus arteriosus, apnoea, bradycardia, exchange transfusion and peri/intraventricular haemorrhage; those related to infection were: congenital infections, pneumonia, sepsis and meningitis. Of the 1338 infants enrolled, 1187 survived for more than 24 hours and had complete data. Mean (+/- s.d.) birthweight was 1278 (+/- 297) g and mean (+/- s.d.) gestational age 30.7 (+/- 2.6) weeks. Seventy-three (6.1%) infants developed necrotising enterocolitis: 46 (63.0%) stage I disease (clinically very suspect), 11 (15.1%) stage II (pneumatosis intestinalis) and 16 (21.9%) stage III (intestinal perforation). Mean +/- s.d. birthweight of the infants with necrotising enterocolitis (1197 +/- 284 g) was lower (P less than 0.02) than in those without necrotising enterocolitis (1283 +/- 297 g). Gestational ages were comparable. Mortality in the group with necrotising enterocolitis was 21.9% versus 15.8% in the non-necrotising enterocolitis group (NS). Stepwise logistic regression analysis indicated that among those factors studied, only sepsis and birthweight were truly associated with the occurrence of necrotising enterocolitis.
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PMID:A prospective survey of necrotising enterocolitis in very low birthweight infants. 265

Ureaplasma urealyticum was isolated from the lower respiratory tract of three infants with persistent pulmonary hypertension of the newborn. In one, cultures positive for U urealyticum were obtained on multiple occasions from trachea, blood, and pleural fluid prior to the infant's death on postnatal day 6. Autopsy findings confirmed the presence of severe pneumonia and the organism was again recovered from multiple sites. A second infant had no apparent predisposing factors for development of persistent pulmonary hypertension of the newborn but U urealyticum and Staphylococcus epidermidis were recovered from the trachea antemortem and from lung tissue obtained during autopsy on the 12th postnatal day. The third infant had persistent pulmonary hypertension of the newborn and a pulmonary infiltrate within hours after birth with tracheal cultures positive for both U urealyticum and Mycoplasma hominis. Erythromycin was given for ten days, and the infant gradually improved. Prolonged ventilation with supplemental oxygen was necessary, and chronic lung disease developed. This is the first report of neonatal ureaplasmal pneumonia with sepsis and persistent pulmonary hypertension of the newborn as well as the first time a microorganism other than streptococci has been specifically implicated in the pathogenesis of persistent pulmonary hypertension of the newborn. Respiratory infections with U urealyticum or other bacteria should be considered as possible causative or contributory factors in infants with persistent pulmonary hypertension of the newborn.
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PMID:Ureaplasmal pneumonia and sepsis associated with persistent pulmonary hypertension of the newborn. 290 79

No therapeutic agent consistently decreases pulmonary arterial pressure (PAP) more than aortic pressure in neonates with persistent pulmonary hypertension of the newborn. We have investigated whether nitroglycerin (NG) or nitroprusside (NP) selectively decreases PAP in an animal model of sepsis-induced pulmonary hypertension. Piglets were anesthetized, intubated, and ventilated. Pulmonary hypertension was induced by an iv infusion of group B Streptococci. Piglets were then divided into three groups with group B Streptococci infusion ongoing. Neither PAP nor the pulmonary vascular resistance index was decreased significantly by either NP or NG. NP decreased significantly both mean aortic pressure and the systemic vascular resistance index. Cardiac index decreased significantly during both NG and placebo infusion. These data suggest that neither NP nor NG is likely to be beneficial in sepsis-induced pulmonary hypertension in newborns.
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PMID:Neither nitroglycerin nor nitroprusside selectively reduces sepsis-induced pulmonary hypertension in piglets. 311 93

Twenty-seven infants with severe persistent pulmonary hypertension of the newborn were seen in 33 months. Asphyxia with or without meconium aspiration was the cause in the majority of cases. Other causes were group B streptococcal sepsis and acute fetal blood loss. The mortality rate was 11%. Twenty-three of the 24 survivors were followed. Their age at follow-up ranged 12-37 months. The mean score for mental development was within the normal range while that for psychomotor development was 1 standard deviation below normal. Seven infants were judged to be at risk of attention deficit disorder. Predictor variables related to these outcomes were cardiotocography, meconium aspiration, first pH, highest PaCO2 after resuscitation and mother's education. All infants except one were perceived as normal by their parents.
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PMID:Persistent pulmonary hypertension of the newborn treated with hyperventilation: clinical features and outcome. 314 64

Extracorporeal membrane oxygenation (ECMO) has been successful (greater than 80% survival) in 35 centers in greater than 900 newborns with severe respiratory failure having an estimated mortality of greater than 80% on conventional management. During the last 3 years we have treated 79 newborns with 74 survivors (94%). Their diagnoses included meconium aspiration, persistent fetal circulation, respiratory distress syndrome, congenital diaphragmatic hernia, and sepsis. Seven patients (9%) had life-threatening intrathoracic complications requiring emergent intervention while on ECMO: tension hemothorax (3), tension pneumothorax (2), and pericardial tamponade (2). Pericardial tamponade and tension hemothorax and pneumothorax show a similar pathophysiology of increasing intrapericardial pressure and decreasing venous return. Perfusion is initially maintained by the nonpulsatile flow of the ECMO circuit before further decrease in venous return results in decreasing ECMO flow and progressive hemodynamic deterioration. Each of the seven patients demonstrated a clinical triad that includes increasing PaO2 and decreasing peripheral perfusion (as evidenced by decreasing pulse pressure and decreasing SvO2) followed by decreasing ECMO flow with progressive deterioration. The diagnoses were confirmed by transillumination, chest x-ray, or cardiac echocardiogram. Initial emergent placement of a percutaneous drainage catheter was temporizing in all seven cases. However, four patients required emergent thoracotomy for definitive treatment while still on ECMO. All seven patients were weaned from ECMO and are short-term survivors (6 months to 3.5 years). As use of ECMO for newborn severe respiratory failure increases, responsible physicians must be familiar with life-threatening intrathoracic complications and appropriate treatment strategies.
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PMID:Life-threatening intrathoracic complications during treatment with extracorporeal membrane oxygenation. 320 57


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