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

Of 124 patients with Takayasu arteritis studied over a period of 20 years (1979-1999), 12 female patients experienced 24 pregnancies. The mean age was 23.6+/-3.6 years. The presenting features during pregnancy were severe hypertension (11 patients), congestive heart failure (two patients) and unequal pulses (one patient). Aortography revealed that abdominal aorta was involved in 11 patients and renal arteries in nine patients. Of 17 live babies born, intrauterine growth retardation was present in five babies and premature deliveries were encountered in four patients. Pregnancies resulted in abortion in two patients and intrauterine death in five patients. Maternal complications included superimposed pre-eclampsia in four patients, congestive heart failure and progression of renal insufficiency in two patients each and post partum sepsis in one patient. All patients with poor perinatal outcome had abdominal aortic involvement and a significant delay in seeking medical attention.
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PMID:Outcome of pregnancy in Takayasu arteritis. 1098 Mar 56

The objective of this paper is to examine whether growth-restricted preterm infants have a different neonatal outcome than appropriately grown preterm infants. All consecutive, singleton preterm deliveries between 27-35 weeks' gestation were included over a 4-year period. Infants with congenital anomalies and infants of diabetic mothers were excluded. Infants were categorized as small-for-gestational-age (SGA) when birth weight was at or below the 10th percentile, and appropriate-for-gestational-age (AGA) when between the 11th and 90th percentiles. Outcome variables included: neonatal death, respiratory distress syndrome (RDS), sepsis, intraventricular hemorrhage (IVH), and necrotizing enterocolitis (NEC). Neonatal morbidity and mortality were examined by univariate and stepwise multivariate logistic regression analyses. Factors controlled for during the analysis included: maternal age; gestational age; mode of delivery; presence of preeclampsia, HELLP syndrome, prolonged premature rupture of membranes (PROM), placental abruption, placenta previa, prenatal steroid exposure, infant gender, and low Apgar score. Seventy-six infants were included in the SGA group and 209 in the AGA group. SGA infants had a higher mortality rate (p = 0.003). They also had more culture-proven sepsis episodes (p = 0.001). No differences were found with respect to the other outcomes. The results were similar when analyzed separately for the group of infants born at or below 32 weeks' gestation. Growth-restricted preterm infants were found to have both higher mortality and infection rates compared with AGA preterm infants. Growth restriction in the preterm neonate was not found to protect against other neonatal outcomes associated with prematurity. When considering elective preterm delivery for this high-risk group of pregnancies, the increased risks in the neonatal period should be taken into account.
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PMID:Neonatal outcome in growth-restricted versus appropriately grown preterm infants. 1104 40

Perinatal mortality rates are considered in the western world to be a quantitative barometer of maternity care. This 6-year prospective perinatal audit was conducted at a tertiary hospital in order to determine foetal outcome, and the common causes of foetal and early neonatal deaths. Of a total of 30,987 births, there were 469 stillbirths and 391 early neonatal deaths, giving a perinatal mortality rate of 27.7 per 1000 total births. The leading causes of stillbirths were the hypertensive disorders of pregnancy, abruptio placentae, diabetes mellitus, intrapartum foetal distress and lethal congenital anomalies. Neonatal deaths were mainly due to the respiratory distress syndrome (57.8%), birth asphyxia (22.2%) and sepsis (13.5%). A dedicated medical team, including a neonatologist, to manage pre-eclampsia, and more senior obstetric involvement in the labour ward are recommended.
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PMID:An audit of perinatal mortality. 1139 86

Anaesthetic and analgesic techniques in the critically ill are determined largely by the nature of the presenting illness. The commonest conditions likely to present as life-threatening emergencies are pre-eclampsia, obstetric haemorrhage, cardiac disease and severe sepsis. Issues dictating choice of anaesthetic technique are the patient's ability to maintain her airway, coagulation status, intravascular volume and haemodynamic dependence upon sympathetic drive, and requirements for ventilatory support and intensive care. Fetal well-being is an issue in the antepartum period, uteroplacental blood flow should be maintained and hypotension avoided. Maternal survival takes priority, however, and occasionally general anaesthetic techniques must be used which lead to neonatal respiratory depression and requirement for ventilatory support. Anaesthesia itself is associated with known hazards. The risks of each technique must be balanced against possible benefits in the context of the presenting illness.
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PMID:Anaesthesia and analgesia for the critically ill parturient. 1147 12

Healthy pregnancy is accompanied by changes in the haemostatic system which convert it into a hypercoagulable state vulnerable to a spectrum of disorders ranging from venous thromboembolism to disseminated intravascular coagulation (DIC). This latter is always a secondary phenomenon triggered by specific disorders such as abruptio placentae and amniotic fluid embolism due to release of thromboplastin intravascularly or endothelial damage resulting from pre-eclampsia and sepsis. In modern obstetric practice the most common cause is haemorrhagic shock with delay in resuscitation leading to endothelial damage. The initial management of massive obstetric haemorrhage is the same whether associated with coagulopathy initially or not. Low-grade DIC, associated with pre-eclampsia, is monitored haematologically by serial platelet counts and serum fibrin degradation products (FDPs). Supportive measures and removal of the triggering mechanism are the key to successful management. Outcome depends primarily on our ability to deal with the trigger and not on direct attempts to correct the coagulation deficit.
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PMID:Disseminated intravascular coagulation. 1147 19

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


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