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

Necrotizing enterocolitis--a highly letal disease in the newborn period--is diagnosed in about 1--2% of the admissions to a nursery. The marcroscopic lesions are basically necroses predominantly found in the ileum, colon and jejunum. Untreated they lead to perforation, peritonitis and sepsis. The predisposing factors include such as perinatal complications, immaturity and umbilical vein catheterization; the main symptoms are bile stained vomiting and blood-streaked diarrhea, followed by signs of fulminant sepsis and peritonitis. The most typical roentgenographic findings are intramural air (pneumatosis intestinalis) and in more advanced cases pneumoperitoneum (free peritoneal air) and portal vein gas. The current plan of management--consisting of immediate withdrawal of oral feeds, gastric suction, intravenous fluid therapy, treatment of shock and administration of antibiotics--and the indication for operation are discussed. Perinatal stress and secondary bacterial invasion of the intestinal lesions seem to play an important role in the etiology of the disease. An early nutrition of the healthy immature with human breast milk seems to reduce the incidence of necrotizing enterocolitis or at least has a mitigating influence on the later course of the disease. The mortality in our own series--as reported--was high (6 patients: 1 survivor, mortality: 83%) as 4 of the patients were admitted with gross symptoms of intestinal perforation and severely shocked.
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PMID:[Necrotizing enterocolitis (pediatric review)]. 33 53

The newborn infant, particularly when premature, has a haemostatic mechanism which may not be entirely capable of withstanding the onslaughts of trauma, infection, asphyxia or other complications of the neonatal period. He is at risk of local or diffuse haemorrhage, which may at times be serious or even life-threatening. The cause of haemorrhage during the newborn period can generally be ascertained by a careful history and brief physical examination directed toward recognition of any predisposing factors or underlying diseases. Screening laboratory tests can usually be correctly interpreted as long as certain laboratory artifacts and physiological peculiarities of the neonatal coagulation mechanism are kept in mind. Diagnosis of and therapy for vitamin K deficiency and haemophilia in the healthy-appearing neonate is generally carried out with little difficulty. The seriously ill neonate with bacterial sepsis, respiratory distress syndrome, or extreme immaturity presents greater problems, for laboratory tests may be more difficult to obtain and interpret and underlying conditions may be untreatable. DIC occurs commonly in such neonates, and transfusion therapy, with or without heparin, is often unsuccessful. A persistent dilemma are those neonates with fatal intravascular haemorrhage, in whom definable haemostatic abnormalities are few and transfusion therapy is futile.
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PMID:Neonatal coagulation: normal physiology and pathophysiology. 35 Apr 67

Sequential chemotherapeutic regimens, primarily used in the treatment of hematopoietic malignancies, and employing ara-C as a basic antineoplastic agent induce mucosal alterations in the entire gastrointestinal tract. These are characterized by surface and glandular epithelial atypia, immaturity, and necrosis. Glandular regeneration is characteristically delayed leading to a state of intestinal aproliferative cytopenia. Other toxic intestinal changes include telangiectasia of blood vessels and the formation of intramural hematomas. Intestinal infections develop frequently and are complicated by peritonitis, liver abscesses, pneumatosis cystoides in testinalis and sepsis. These intestinal lesions are accompanied by a predictable clinical syndrome which begins concomitantly with ara-C infusions and is characterized by diarrhea, ileus, abdominal pain, hematemesis and melena, severe hypokalemia, hypocalcemia and a protein-losing enteropathy. Additional toxic manifestations induced by ara-C include transient weight gains, fever elevations and severe bone marrow depression. The genesis of the intestinal lesions is linked to the three day dose schedule of ara-C infusions which insures both arrest of the cycling intestinal cells in the S-phase and a high cytotoxic index. The severity of these lesions is markedly augmented by prior treatment with ara-C and cyclophosphamide which causes synchronization and probable recruitment of intestinal stem cells, respectively.
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PMID:Cytosine arabinoside induced gastrointestinal toxic alterations in sequential chemotherapeutic protocols: a clinical-pathologic study of 33 patients. 70 32

Results of brain studies in 38 premature infants with severe peri- and postnatal pathology (intracranial labor trauma, asphyxia, sepsis) are presented. Clinico-morphological data detected that profound prematurity and consequently a profound immaturity of the brain, complicated by hypoxic damages during labor and early developing septic infections, lead to an expressed retardation and irreversible degenerative changes, especially in the brain structures which develop later. From the neurological point of view the most serious in relation to the prognosis are those children who are in a state of a stable inhibition of the CNS.
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PMID:[Brain histology of premature infants who have suffered hypoxia and sepsis]. 72 72

During the years 1978-89, all surviving extremely low birthweight infants (BW less than 1000 g, ELBWI) in the region of Southern Finland were admitted to the Children's Hospital, University of Helsinki and followed up to six years. The number of liveborn ELBWI increased from 30 to 50/year during the first and last third of the follow-up. During the same twelve year period, the number of the surviving infants increased from 8 to 25/year, with the number and proportion of infants with birthweights of less than 800 g and with gestational ages of less than 27 weeks increasing from 3 to 15/year. Despite of the greater proportion of smaller infants the proportion of infants without intraventricular hemorrhage increased from 50 to 85%. The proportion of children with normal neurodevelopment at two years increased from 40-70% during the first five years of the study, to 63-84% during the last three years of the study. The proportion of children with major disabilities decreased from 28 to 8%. The factors associated with poor neurodevelopment were sepsis, year of birth, intraventricular hemorrhage, and birthweight. The neurological status at one year was a valid predictor of the outcome: at four years 94% of the infants were assessed and normal remained normal as neurologically abnormal remained abnormal or slightly abnormal. The neurologically normal ELBWI were tested at six years: visuomotor coordination was immature in 50%, emotional immaturity was found in 25% and delay of language development in 13%. In our unit increased survival of ELBWI infants has not been associated with an increase in the number of ELBWI infants with handicaps.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The outcome of extremely low birthweight infants. 172 83

Continuous positive airway pressure (CPAP) administered as a mixture of oxygen and compressed air via nasal prongs has dramatically improved survival rates and lessened the frequency of barotrauma and bronchopulmonary dysplasia in the premature infant with respiratory distress syndrome. Associated with the increased use of nasal CPAP has been the development of marked bowel distension (CPAP belly syndrome), which occurs as the infant's respiratory status improves and the baby becomes more vigorous. To identify contributing factors, we prospectively compared 25 premature infants treated with nasal CPAP with 29 premature infants not treated with nasal CPAP. Infants were followed up for development of distension, defined clinically as bulging flanks, increased abdominal girth, and visibly dilated intestinal loops. We evaluated birth weight, weight at time of distension, method of feeding (oral, orogastric tube), and treatment with nasal CPAP and correlated these factors with radiologic findings. Of the infants who received nasal CPAP therapy, gaseous bowel distension developed in 83% (10/12) of infants weighing less than 1000 g, but in only 14% (2/14) of those weighing at least 1000 g. Only 10% (3/29) of infants not treated with nasal CPAP had distension, and all three weighed less than 1000 g. Presence of sepsis and method of feeding did not correlate with occurrence of distension. Neither necrotizing enterocolitis nor bowel obstruction developed in any of the patients with a diagnosis of CPAP belly syndrome. Our study shows that nasal CPAP, aerophagia, and immaturity of bowel motility in very small infants were the major contributors to the development of benign gaseous bowel distension.
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PMID:Benign gaseous distension of the bowel in premature infants treated with nasal continuous airway pressure: a study of contributing factors. 172 37

Premature infants and neonates are vulnerable to bacterial sepsis. This susceptibility may be due to the relative immaturity of their immune systems. To determine if neonates and, in particular, premature infants have decreased polymorphonuclear leukocyte (PMN) phagocytosis, we tested PMN phagocytosis of Staphylococcus aureus as a function of gestational age in the fetal lamb model. Because phagocytosis is made more efficient by the presence of opsonins in plasma, fetal and postnatal PMN phagocytosis were also measured after exposure to fetal and adult plasma. PMNs were isolated from fetal lambs at 104, 114, 124, and 141 days' gestation (term gestation for the fetal lamb is 145 days), as well as from 10-day-old neonatal sheep and adult sheep. Labeled S aureus were opsonized by incubation in either fetal or adult plasma, or left unopsonized for baseline values. Phagocytosis was measured as a percent of adult PMN phagocytosis after adult plasma opsonization. It was found that fetal PMN function is limited by two factors during the early third trimester: a primary defect in the ability of the PMN to phagocytose S aureus despite adequate opsonization, and the diminished ability of autologous fetal plasma to opsonize bacteria. The defect in PMN phagocytosis disappears late in the third trimester, but the inability of the fetal plasma to opsonize effectively continues until after birth.
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PMID:Ontogeny of fetal sheep polymorphonuclear leukocyte phagocytosis. 189 98

Out of 6957 deliveries of the years 1987 and 1988 (7.2%) pregnant women have been analysed because premature rupture of fetal membranes. In 23.4 per cent symptoms of amniotic infection could be observed. In 31 per cent pathogenic germs could be identified from cervical swabs. In 33.6 per cent gestational period could be prolonged from 2 to 7 days, in 4.2 per cent more than 7 days. We found upon 32nd week of pregnancy a significant reduction of respiratory adaptation disturbances of 22%. Neonatal sepsis had been found at 50% till completion of 32nd week of pregnancy. Reasons for neonatal mortality are sepsis, immaturity and dysontogenesis. Conclusions have been made for practice in diagnostics and treatment.
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PMID:[Obstetric management and results of premature amniotic rupture]. 192 6

The object of this investigation was to review the neonatal mortality among infants with very low birthweights (less than or equal to 1,500 gram) in the County of North Jutland and to determine the distribution of the main causes of death. It is important to note that, in a review of this type, the material was unselected. The period involved was 1988-1989. During this period, 86 infants with very low birthweights were born and 63 of these survived for longer than 28 days, corresponding to a neonatal survival of 73%. The survival increased from 11% in infants weighing 500-700 gram at birth to 93% for infants with birthweights between 1,250-1,500 gram from 0% with gestational ages of 24-25 weeks to 98% with gestational ages greater than or equal to 30 weeks. No significant differences in survival were observed as regards sex, place of delivery, method of delivery and singleton/twin delivery but survival was markedly dependent on whether the infants had asphyxia on delivery. The commonest causes of death were the respiratory distress syndrome, periventricular haemorrhage and asphyxia, followed by sepsis, enterocolitis necrotans and immaturity. The incidence of immediate sequelae in the form of chronic pulmonary disease and the retinopathy of prematurity were low.
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PMID:[Neonatal mortality in infants with very low birth weights in the county of North Jutland. Retrospective study]. 195 90

We report a premature infant with severe hypoglycemia (serum glucose: 6 mg/dl) and cholestasis (serum total bile acids: 211.55 mumol/L) caused by hypoplasia of the interlobular bile ducts. This patient had developed intracranial hemorrhage and sepsis while undergoing treatment for hypoglycemia. As a result of endocrine evaluation, we made a diagnosis of idiopathic panhypopituitarism, congenital absence or hypoplasia of the pituitary gland. Moreover, we found abnormal bile acid profiles: The ratio of cholic acid to chenodeoxycholic acid was abnormally low in serum (0.04) and in biliary bile (0.33). However, 3 alpha,7 alpha,12 alpha-trihydroxy-5 beta-cholestan-26-oic acid and bile alcohols were not detected. We therefore suspected that the severe cholestasis and abnormal bile acid profiles in the serum and biliary bile in this patient were related to physiologic immaturity of the enterohepatic circulation of bile acids and immaturity of hepatic 12 alpha-hydroxylation.
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PMID:Abnormal low ratio of cholic acid to chenodeoxycholic acid in a cholestatic infant with severe hypoglycemia. 207 33


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