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

A three-day-old female infant was transferred to the Pediatric Intensive Care Unit with chief presenting problems of progressive change of cyanosis and respiratory distress. Physical examination revealed tachypnea, acrocyanosis, hepatomegaly, undetectable pulse of extremities and oozing over the place of venous puncture. Chest roentgenograms revealed slight cardiomegaly; other X-rays were within normal limits. Complete electrocardiograms showed right axis deviation and right ventricular hypertrophy. Because of an impression of neonatal sepsis, the patient was put in an incubator with oxygen and antibiotics were given. Persistent anuria appeared associated with sighs of cardiac and renal failure; the ventilator was applied; dopamine and lasix were also given. Unfortunately, the cyanosis worsened progressive. Despite several attempts at resuscitations, the infant expired eight hours later. Pathology disclosed the heart size as normal; hypoplasia of ascending aorta as 0.4 cm in diameter; a PDA with 1 cm in diameter; a diminutive bean-sized left ventricle; hypertrophy of right ventricle and atresias of aortic and mitral valves. There was no evidence of septicemia.
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PMID:[Hypoplastic left heart syndrome due to aortic and mitral atresias: report of one case]. 263 9

Pulmonary complications secondary to postburn sepsis are a major cause of death in burned patients. Using an in vitro organotypic culture system, we examined the effect of E. coli endotoxin (LPS) on lung cell surfactant synthesis. Our results showed that E. coli endotoxin (1.0, 2.5, 10 micrograms LPS/ml) was capable of suppressing the incorporation of 3H-choline into de novo synthesized surfactant, lamellar bodies (LB), and common myelin figures (CMF) at 50%, 68%, and 64%, respectively. In a similar study, we were able to show that LPS also inhibited 3H-palmitate incorporation by cultured lung cells. LPS-induced suppression of surfactant synthesis was reversed by hydrocortisone. Our results suggest that LPS may play a significant role in reducing surfactant synthesis by rat lung cells, and thus contribute to the pathogenesis of sepsis-related respiratory distress syndrome (RDS) in burn injury.
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PMID:Endotoxin suppresses surfactant synthesis in cultured rat lung cells. 264 10

Phosphatidylglycerol (PG) in amniotic fluid is recognized as a good indicator of fetal lung maturity and is unaffected by moderate amounts of blood or meconium contamination. A rapid immunologic agglutination assay, Ultrasensitive AmnioStat-FLM (FLM), was compared with two-dimensional thin-layer chromatography (TLC) and an enzymic, colorimetric procedure (E-PG). Eighty amniotic fluid specimens were analyzed. FLM results were reported as high (H), intermediate (I), or low positive (L). TLC was compared with FLM:H (n = 27), mean 0.14 (fraction of total phospholipids); I (n = 7), mean 0.11; L (n = 9), mean 0.03; negative results had no detectable PG by TLC. In 33 cases E-PG was compared with FLM:H (n = 9), mean 7.0 mumol/L; I (n = 5), mean 8.1 mumol/L; L (n = 3), mean 3.0 mumol/L; negative (n = 16), mean 3.2 mumol/L. Records were reviewed in 70 cases. Thirty cases were excluded: sample to delivery time was greater than 72 hours; steroids were given or sepsis was documented. Fetal lung immaturity was clinically present in six cases: respiratory distress syndrome in three cases and transient tachypnea of the newborn (TTN) in three cases. One false positive result was identified (TTN, FLM:H). FLM sensitivity for fetal lung maturity was 85.3%, specificity was 83.3%, and the positive predictive value for fetal lung maturity was 96.7%. FLM is a fast, reliable indicator of fetal lung maturity.
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PMID:Phosphatidylglycerol in amniotic fluid. Comparison of an "ultrasensitive" immunologic assay with TLC and enzymatic assay. 264 6

Multiple organ failure continues to be the primary cause of death after trauma and sepsis. This clinical syndrome represents the transition from a hypermetabolic response to injury to a syndrome of progressive organ failures and death. Risk factors include: perfusion deficits, persistent foci of dead or injured tissue, an uncontrolled focus of infection, the presence of the respiratory distress syndrome, persistent hypermetabolism, and preexisting fibrotic liver disease. Once initiated, most treatment modalities for the organ failure syndrome become progressively ineffective including: ventilation, antibiotics, nutrition, and surgery. The best treatment remains prevention and rapid control of risk factors including restoration of oxygen transport and aggressive nutrition support. There seems to be no treatment "magic bullet" either experimentally or clinically once the syndrome has occurred. The metabolic response to injury involves alterations in physiology and in the metabolism of carbohydrate, fat and amino acids. These changes seem to reflect the modulation of the end-organs by the mediator systems activated in response to the stress stimuli. The transition from hypermetabolism to organ failure appears to reflect the clinical appearance of liver failure. It is hypothesized that this liver failure may represent a state of regulatory dysfunction induced in large part by the activated hepatic macrophage, the Kupffer cell. The activation of these macrophages is hypothesized to represent the final stage of a series of stimulating events, eg. hypoxia, endotoxin, bacteria, and gut translocated toxins. The precise monokine(s) responsible are not yet completely characterized, although Interleukin-1 (IL-1) and tumor necrosis factor (TNF) appear to be involved as do prostaglandins (Pg) such as PgE2.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of monokines in altering hepatic metabolism in sepsis. 264 13

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

A 32-year-old woman with acute salpingitis had signs and symptoms of sepsis, with hypotension, renal failure, acute respiratory distress syndrome, and disseminated intravascular coagulation. Streptococcus pyogenes group A was grown from blood cultures taken at the onset of illness, and salpingitis was confirmed at laparotomy. The patient recovered after appropriate antimicrobial and intensive supportive therapy.
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PMID:Septic shock and acute respiratory distress syndrome after salpingitis caused by Streptococcus pyogenes group A. 265 6

To assess the previously reported association of intraventricular hemorrhage (IVH) with neutropenia, we prospectively followed during a 38-month study period infants with birth weight less than or equal to 1500 gm who survived greater than 72 hours and underwent serial cranial sonography and neutrophil counts for the first 14 days of life. Neutrophil counts were interpreted according to a widely employed reference range. Infants with conditions other than IVH reported to be associated with neutropenia (sepsis, maternal hypertension, 5-minute Apgar score less than or equal to 5) were excluded. Final study groups included 38 infants with IVH and 114 without IVH. No significant differences were found for birth weight, gestational age, respiratory distress syndrome, mechanical ventilation, prolonged rupture of membranes, patent ductus arteriosus, route of delivery, pneumothorax, or sex. The occurrence of neutropenia before 14 days of age was not significantly different between the groups (50% with IVH, 56% without IVH), nor were differences found at individual postnatal ages. Comparison of immature neutrophil count and immature/total neutrophil ratio also revealed no differences. The high incidence of neutropenia in our non-IVH group raises questions about application of these widely accepted reference ranges to very low birth weight infants.
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PMID:Neutropenia and intraventricular hemorrhage among very low birth weight (less than 1500 grams) premature infants. 265 58

In a prospective, randomized, double-blind, multicentre trial the effect of antenatal treatment with betamethasone phosphate was compared with placebo in the prevention of the respiratory distress syndrome (RDS) in preterm infants. The dose of betamethasone was 4 mg every 8 h for six doses, unless delivery occurred. The 251 women who were enrolled gave birth to 262 liveborn infants, 130 in the beta-methasone and 132 in the placebo group; the two groups were evenly matched in most respects. The diagnosis of RDS in the newborn was confirmed by two independent assessors. Seven of the 130 infants in the betamethasone group and 16 of the 132 in the placebo group developed RDS. In infants whose mothers had received at least three injections, RDS was also less frequent in the steroid group than in the placebo group (3/104 and 10/104 respectively; P less than 0.05). There was a significant reduction of RDS in those born between 24 h and 6 days after entry into the trial (0/30 and 8/45 respectively; P less than 0.05). The largest difference in frequency of RDS occurred in the subgroup of infants born before 34 weeks gestation, within 8 days of trial entry, and whose mothers had received at least three injections (0/27 steroid group and 7/32 placebo group; P = 0.03), and there were also significantly fewer neonatal deaths (2/27 and 13/32, respectively; P less than 0.01) in this subgroup. Betamethasone did not provoke earlier delivery. Premature rupture of the membranes and maternal hypertension did not seem to contraindicate the use of steroids: there was no increase in maternal or neonatal sepsis nor in stillbirth in hypertensive pregnancies in the steroid group. Neonatal jaundice was significantly less frequent in the steroid (55/129) than in the placebo group (81/127; P less than 0.01) but not in the subgroups born before 34 completed weeks gestation.
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PMID:Antenatal administration of betamethasone to prevent respiratory distress syndrome in preterm infants: report of a UK multicentre trial. 266

Group B streptococcal sepsis was associated with delayed presentation of an unsuspected right-sided diaphragmatic hernia in two neonates. These unusual clinical observations and a review of 24 similar cases from the literature form the basis of this report. Infants present with respiratory distress during the first few hours of life and have group B streptococcal sepsis confirmed by results of blood cultures. The right side of the diaphragm appears normal on the initial chest roentgenogram in the majority of cases. After initial improvement with antibiotic therapy and ventilatory support, sudden deterioration of respiratory status may occur. Subsequent chest roentgenograms often demonstrate herniated viscera in half of the cases, while ultrasound examination, isotopic liver scan, and peritoneography are useful in achieving a diagnosis in the other cases. If recognized, survival is 100% following hernia repair. Persistent respiratory symptoms in a neonate who is recovering from group B streptococcal sepsis should prompt a careful evaluation of the right side of the diaphragm for the presence of an unsuspected posterolateral hernia.
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PMID:Delayed presentation of a right-sided diaphragmatic hernia and group B streptococcal sepsis. Two case reports and a review of the literature. 267 42

Multiple organ failure continues to be the primary cause of death after trauma and sepsis. This clinical syndrome follows shock and resusitation and the transition from a hypermetabolic response to a syndrome of progressive organ failures and death. Risk factors include: perfusion deficits, persistent foci of dead or injured tissue, an uncontrolled focus of infection, the presence of the respiratory distress syndrome, and preexisting fibrotic liver disease. The imitation of the syndrome represents the clinical manifestation of hepatic failure. It is hypothesized that this hepatic failure results from paracrine amplification with Kupffer cell induced hepatocyte cytotoxicity. The best treatment remains prevention and rapid control of risk factors including restoration of oxygen transport and aggressive nutrition support. There seems to be no treatment "magic bullet" either experimentally or clinically once the syndrome has occurred.
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PMID:Hepatic dysfunction in multiple systems organ failure as a manifestation of altered cell-cell interaction. 267 63


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