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

Bacterial sepsis continues to be an important cause of morbidity and mortality in neonates. Neutropenia in the newborn, as a result of decreased bone marrow neutrophil storage pool reserves and myeloid committed progenitor cells, increases the risk of sepsis and is associated with a poor prognosis. The hematopoietic colony-stimulating factors G-CSF (granulocyte colony stimulating factor) and GM-CSF (granulocyte-macrophage colony stimulating factor) increase the number of circulating neutrophil number by stimulating neutrophil precursors proliferation. In a number of clinical trials in very low birthweight neonates and in neonates with preeclampsia-associated neonatal neutropenia, both hematopoietic growth factors significantly increased the circulating absolute neutrophil count. However, no larger study showed that prophylactic G-CSF or GM-CSF treatment resulted in a reduction of infectious complications or in an improved overall survival. Similar results were seen in studies evaluating G-CSF and GM-CSF as intervention therapy in septic neonates. Therefore, experts do not recommend the routine use of the expensive growth factors in preterm and term neonates. However, prospective clinical trials are still needed to evaluate whether specific treatment groups will benefit from the use of G-CSF or GM-CSF. In this regard, efforts must be directed at better defining the endpoints and in particular assigning value to reduction in treatment of possible infectious complications, such as days in hospital, antibiotic usage and costs. In addition, randomized studies are required to evaluate the proper dosage and duration of therapy, which most likely will vary between groups of patients.
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PMID:[Hematopoietic growth factors in prevention and therapy of infectious complications in premature and newborn infants]. 1172 63

In most instances, tissue factor (TF) exposed to the circulation is the sole culprit underlying the initiation of disseminated intravascular coagulation (DIC), although notable exceptions because of a more direct activation of the coagulation system, by snake venoms, for example, do occur. Peripheral monocytes and subendothelial structures are the potential sources of such TF; in the former, TF emerges on the cell surface on synthesis induction and in the latter it becomes available subsequent to permeability changes or damage to the endothelium. Subendothelial TF is constitutively present in fibroblasts, pericytes, and macrophages and at a higher than normal level in tumor-associated macrophages. This scenario of coagulation activation probably describes the principal events underlying emerging acute DIC states under pathophysiological conditions such as abruptio placentae, septic abortion, amniotic fluid embolization, and pregnancy toxemia. Under disease conditions associated with DIC, the continuous exposure to excess TF typically exhausts the available tissue factor pathway inhibitor (TFPI), leading to rampant thrombin generation, persistent feedback activation of factor XI (FXI) by the generated thrombin, and hence virtually uncheckable ongoing fibrin generation (DIC). Recently, it was shown that patients subject to meningococcal sepsis had comparatively large amounts of mainly monocyte-derived circulating TF-containing microparticles. Because phosphatidylserine (PS) is exposed on such particles, in addition to TF, they probably contribute crucially to DIC during meningococcal sepsis. Although endothelial cells (EC) have been shown to express large amounts of TF in vitro, this observation hardly relates to the situation in vivo, where, in contrast, synthesis and exposure of EC TF is very limited and not likely to be of any significance in emerging and ongoing DIC.
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PMID:The tissue factor pathway in disseminated intravascular coagulation. 1174 Jun 84

OBJECTIVE: Life-threatening conditions cause severe changes in the organization and conformation of macromolecules, creating urgent requirements for protein repair to ensure survival. As molecular chaperones, heat shock proteins (HSP) that have specialized functions in protein folding are now well established to restore homeostasis in cells and organisms. Augmentation of HSP synthesis is tightly regulated by stress-inducible heat shock factors (HSF), which are part of a transcriptional signaling cascade with both positive (e.g., HSP) and negative (e.g., proinflammatory cytokines) properties. In this review, we discuss the biological roles and mechanisms of HSP-mediated protection in pathophysiologic conditions (ischemia, sepsis, and preeclampsia) and the regulation for stress-dependent HSP synthesis and speculate about future applications for harnessing HSF and HSP partners as cytoprotective agents. DATA SOURCES: Reactive oxygen species are major pathogenic factors in cell death pathways (e.g., necrosis, apoptosis), in part, because of proteotoxic effects. In intact organisms, forced overexpression of HSP per se affords effective counterbalance against ischemia challenges (e.g., heart and brain) and systemic conditions (e.g., sepsis). Besides stressful conditions, gene-targeting studies have uncovered new functions for heat shock transcription factors (e.g., maintenance of intrauterine pregnancy) in mammals. In parallel, pharmacologic studies using small molecules are paving the way for future prospects to exploit the beneficial properties of HSP, albeit an important but presently elusive goal. CONCLUSIONS: Together, HSF and HSP partners are attractive targets in therapeutic strategies designed to stimulate endogenous protective mechanisms against deleterious consequences of oxidative stress. With further technological advances, it is anticipated that the spotlight on HSP, alone or in combination with other stress response pathways, could, ultimately, reduce injury and accelerate functional recovery of susceptible organs in living organisms including humans.
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PMID:Heat shock factor 1 and heat shock proteins: Critical partners in protection against acute cell injury. 1183 44

Since 1996, maternal mortality is registered as part of a permanent confidential inquiry in France. The National Committee has studied all cases recorded to assess the cause of death and the avoidable obstetrical complications involved. Recommendations are proposed. In 1996 and 1997, there were 196 maternal deaths in France; 165 could be analyzed. The cause was obstetrical in 123 cases (74%), non-obstetrical in 26 (16%), and unidentified in 16 (10%). Ninety-seven direct deaths occurred (78% of the obstetrical mortality cases); 31 cases of hemorrhage including 19 post partum, 20 cases of pregnancy-induced hypertension, 10 cases of eclampsia and 7 of pre-eclampsia, 16 cases of amniotic fluid embolism, 11 cases of thromboembolism and 10 cases of sepsis. The National Committee considered that 54% of these deaths were avoidable: 87% for hemorrhage, 80% for sepsis, and 65% for hypertensive diseases. The deaths due to amniotic fluid embolism were not considered avoidable. This mortality stemmed from substandard care, delayed treatment, missed diagnosis, and professional errors. Clinical recommendations are proposed for post partum hemorrhage, pre-eclampsia and eclampsia, prevention of maternal infection, and thromboembolism prophylaxy.
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PMID:[Maternal mortality: avoidable obstetrical complications]. 1188 12

A review of maternal mortality at the University of Nigeria Teaching Hospital (UNTH) Enugu between January 1976 and December 1985 has been made. Deaths up to 6 weeks of puerperium from direct, indirect, and incidental causes were included but abortions were excluded. There were 47,361 deliveries and 127 maternal deaths giving a maternal mortality rate of 2.7/1000. There has been a downward trend in the mortality rate from 5.46 in 1976 to 1.99 in 1985. Comparing mortality rates according to booking status, it was observed that mortality rates were 48 times higher in unbooked patients. It was observed that overall that deaths increased with increasing maternal age except in the 26-30 age group. Whereas only 0.16% of women aged 26-30 died, 2% of women 40 died. The highest mortality rates are in primigravida and grand multipara. The main causes of death were obstructed labor plus ruptured uterus (35%), obstetric hemorrhage (25.98%), eclampsial severe/preeclampsia (11%), and sepsis (10.24%). Other causes of death include anesthetic, amniotic fluid embolism, jaundice in pregnancy, congestive cardiac failure, pulmonary embolism, and severe anemia. Factors influencing this high mortality include antenatal care, maternal age, and parity. The majority of these deaths are avoidable through adequate blood transfusions, attention to details and better case management, improved medical services, recognition of severe problems by patients and family, and immediate medical care. Futhermore, faults may lie either with the patient, the hospital, the medical team, the government or the system or a combination of these factors. The ways to reduce the high maternal mortality are improved standard of living, raising the literacy level, improved structural facilities and social amenities, better communication and transportation, increased number of hospitals, blood transfusion services, better case management, and a high level of utilization of available facilities.
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PMID:Maternal mortality at the University of Nigeria Teaching Hospital, Enugu: a 10-year survey. 1217 83

This reviews 431 maternal deaths over 3 periods of 3-4 years each from January 1958 to December 1968. Trends in mortality are noted. A steady decline was noted. Associated diseases increased maternal mortality but age and parity had no significant influence. 47% of the deaths were intrapartum, 35% postpartum, and 18% antenatal. Major causes were hemorrhage, preeclampsia, eclampsia, sepsis, and anemia, in that order. Deaths due to infection diminished markedly during the period. 58.2% of the deaths were considered avoidable. Delay by patient or doctor and lack of facilities in rural areas were principle avoidable factors. Extension of obstetrical service to villages, emergency mobile squads, and periodic review of mortality statistics are recommended.
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PMID:Maternal mortality at government maternity hospital. Hyderabad, Andhra Pradesh (a review of 431 cases). 1230 76

Until the 20th century, women and families worldwide knew that it was always a possibility that women would die from childbearing (e.g., over 2000 maternal deaths/100,000 births in Europe). Increased knowledge about pregnancy and its complications and the application of that knowledge in maternal health care systems in developed countries reduced maternal mortality considerably (e.g., 20 in northern Europe). Improvements in delivery management helped greatly to reduce maternal deaths, which include aseptic techniques, appropriate use of forceps, safe blood transfusion, sulphonamides, and proper management of preeclampsia and eclampsia. Maternal mortality is still high in developing countries (e.g., 5% of women in some parts of Africa die from a pregnancy-related condition) where 99% of all maternal deaths occur. These pillars of family life die in the prime of their life and often leave other children. Their loss adversely affects social and economic development. Just 78 countries (35% of the world's population) have a vital registration system recording causes of death, thereby making it difficult to understand the extent of maternal mortality. The 1st cause of maternal death to fall in developed countries and now in developing countries is sepsis. Other causes of maternal death are obstetric hemorrhage, eclampsia, ectopic pregnancy, unsafe abortions, and obstructed labor. Lack of access to maternal health services keeps many women with pregnancy complications from receiving the care they need to survive. Trained persons help only about 50% of women worldwide with labor and delivery. Upgrading of local health centers and training midwives in recognizing complications and in aseptic delivery techniques are needed to improve the quality of maternal health care. Each health center must have the means to transport women to district hospitals. Health centers must offer contraception to prevent unwanted pregnancies. Countries need to reduce the social inequalities that women face.
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PMID:Maternity care for all. 1231 74

During 1981-1986, 86 maternal deaths transpired at the obstetrics department of the Jawaharlal Institute of Postgraduate Medical Education and Research in Pondicherry, India. The maternal mortality rate stood at 5.8/1000 births. 31.4% were primigravidae. The percentage of maternal deaths characterized as gravidae 2-4, 5, and multigravidae was 42.9%, 9.3%, and 16.4%, respectively. The leading causes of death were sepsis (41.9%), especially septic abortion (30.2%); eclampsia-severe preeclampsia (10.5%); ruptured uterus (9.3%); and hemorrhage and prolonged labor (8.1% each). Direct obstetric causes of death accounted for 81.4% of all maternal deaths. Indirect obstetric causes of death were hepatitis (5.8%), heart disease (4.7%), and severe anemia (2.3%). Most of the women who died were illiterate (97.6%), poor (98.8%), and had received no prenatal care (94.2%). 47.7% traveled more than 60 km to the hospital. Quacks or untrained traditional birth attendants had excessively interfered with about 33% before they reached the hospital, especially the septic induced abortion, obstructed labor, and ruptured uterus cases. Among the 48 women who delivered before dying, there were 24 live births (5 of whom died during the early neonatal period) and 24 still births. These findings indicate a need for a cooperative effort to improve and expand maternal and child health care in the community.
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PMID:Determinants of maternal mortality: a hospital based study from south India. 1231 6

The objective of this study is to identify the risk factors for neonatal thrombocytopenia among preterm infants. During a 4-year study period all consecutive, singleton preterm deliveries (between 27 and 35 weeks of gestation) were evaluated, and separate cohorts were compared-growth restricted (small-for-gestational-age; SGA) and appropriately grown (appropriate-for-gestational-age; AGA) infants. An initial comparison was done for the presence of thrombocytopenia (platelet count below 150,000/mL) and marked thrombocytopenia (below 100,000/mL). Following that, a comparison was made between the groups as determined by platelet count for various possible risk factors. Three hundred and five preterm infants were included in the study. Mean platelet count was significantly lower in the SGA group (p = 0.0009). Ninety-three neonates (31%) were thrombocytopenic and 212 infants with a normal platelet count served as controls. In the thrombocytopenic group, the rate of preeclampsia was significantly higher (p = 0.002). Thrombocytopenic infants had a significantly lower average gestational age at delivery (p = 0.002), lower birth weight (p = 0.0001), and low 5-minute Apgar score (p = 0.0002). They were more likely to suffer from intraventricular hemorrhage (IVH) ( p = 0.04) and sepsis (p = 0.002). Growth restriction, lower gestational age and low 5-minute Apgar score (<7) were found to be significantly independent risk factors for marked thrombocytopenia, when analyzed separately. Growth restriction, lower gestational age at delivery, and low 5-minutes Apgar score are significantly associated with neonatal thrombocytopenia in preterm infants, which may lead to significant morbidity. Screening these high-risk groups for thrombocytopenia might be beneficial in terms of early diagnosis and management.
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PMID:Risk factors for neonatal thrombocytopenia in preterm infants. 1263 81

L-Selectin is an adhesion molecule shed from the surface of lymphocytes and granulocytes upon activation. Soluble L-selectin in the plasma can thus reflect immune activation and is elevated in several pathological states. Our objective was to evaluate plasma levels of L-selectin as an immune activation marker in neonates and to determine whether it can serve as a marker of infection, either neonatal or congenital, or if it is affected by the mode of delivery and obstetrical or perinatal complications. A solid-phase ELISA was used on 89 sera from neonates less than 2 days of age, according to the manufacturer's instructions. Levels of soluble L-selectin in the neonate were lower than those of older infants and children and comparable to the levels seen in adults. There was no difference between levels of soluble L-selectin of premature (median, 1172 ng/ml) and full-term babies (median, 1151 ng/ml) or between babies born via vaginal (median, 1233 ng/ml) or cesarean delivery (median, 1146 ng/ml). Conditions such as preeclampsia or administration of steroids to the mother did not affect the levels of L-selectin in the neonate. In contrast, the presence of maternal clinical chorioamnionitis resulted in an increase in levels of L-selectin in the neonate (median, 1377 vs 1072 ng/ml, p = 0.02), as did neonatal sepsis (median, 1331 vs 1149 ng/ml, p = 0.026). Soluble L-selectin, and thus immune activation level, is highest in neonates with neonatal infection and needs to be further evaluated as a surrogate marker for diagnosing sepsis in the neonate.
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PMID:Soluble L-selectin, a marker of immune activation, in neonatal infection. 1459 21


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