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1.
  • Jonsson, Maria, 1966- (författare)
  • Use and Misuse of Oxytocin During Delivery
  • 2009
  • Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
    • Obstetric malpractice claims, concerning delivery during a period of eight years, were analysed for motives behind disciplinary actions, and for the frequency of inappropriate oxytocin use.Failure to respond to signs of foetal distress, injudicious use of oxytocin and a failure to effect a timely delivery were the recurrent problems that accounted for the majority of disciplinary actions. Inappropriate use of oxytocin was more frequent than reported in earlier studies. (Paper I) In a case-control study, differences in the obstetric management in neonates born with and without acidaemia (umbilical artery pH < 7.05), was evaluated. Out of 28,486 deliveries during 1994–2004, 305 neonates were born with acidaemia. Uterine hyperactivity and oxytocin use were independently associated to acidaemia at birth. The increased uterine activity was related to oxytocin treatment in 75 % of cases. Pathological cardiotocographic patterns occurred significantly more often in the case group. The results indicate that guidelines on oxytocin use and foetal surveillance are not followed. The duration of bearing down is less important when uterine contraction frequency has been considered. (Paper II) In a subset of study II, cases with metabolic acidosis (umbilical artery pH < 7.05 and base deficit ≥12 mmol/L) and controls were audited for the occurrence of suboptimal intrapartum care, and the nature of such care. It was found that suboptimal care occurred in half (49%) of the cases, while it was less frequent but not uncommon among controls (13%). Suboptimal care consisted of injudicious use of oxytocin and a failure of appropriate action upon signs of foetal distress. A high rate of NICU admissions and diagnosis of encephalopathy in the case group confirms that metabolic acidosis should be avoided. We estimate that metabolic acidosis could probably have been prevented in 40-50% of the cases.(PaperIII) Women (n=103) scheduled for elective caesarean section in regional anaesthesia were randomised to 5 or 10 units oxytocin, given as an intravenous bolus (double blinded), and electrocardiograms were analysed for ST depressions as a sign of myocardial ischaemia. ST depressions were associated with oxytocin administration significantly more often in subjects receiving 10 compared with 5 units. A dose of 10 units resulted in a more marked decrease of the mean arterial blood pressure, but no difference in increase of the heartrate. There was no difference in estimated blood loss. (paper IV)
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2.
  • Wikström, Anna-Karin, 1965- (författare)
  • Biochemical and Epidemiological Studies of Early-Onset and Late-Onset Pre-Eclampsia
  • 2007
  • Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
    • Biochemical and epidemiological aspects of pre-eclampsia were investigated, with the main focus on possible pathophysiological differences between early-onset and late-onset disease.In pre-eclamptic women poor correlation was found between albumin-creatinine ratio (ACR) in a random urine sample and total amount of albumin in a 24-hour urine collection. (Paper I) In a cohort of women giving birth in Sweden in 1973-82 we estimated the adjusted incidence rate ratio (IRR) for ischaemic heart disease (IHD) during the years 1987–2001. The adjusted IRR for development of IHD was 1.6-2.8 in woman exposed to gestational hypertensive disease during her pregnancy compared with unexposed women. The higher risk represents more severe or recurrent hypertensive disease. (Paper II)Before delivery, in early-onset pre-eclampsia (24-32 weeks) there were pronounced alterations in plasma concentrations of soluble fms-like tyrosine kinase 1 (sFlt1) and placental growth factor (PlGF), and also a higher placental 8-iso-PGF2α concentration and an elevated serum ratio of plasminogen-activator inhibitor (PAI)-1 to PAI-2 compared with early controls. In late-onset pre-eclampsia (35-42 weeks) there were only moderate alterations in sFlt1 and PlGF concentrations, and the placental 8-iso-PGF2α concentration and PAI-1/ PAI-2 ratio were similar to those in late controls. (Papers III, V) There was a rapid postpartum decrease in sFlt1 concentration in all groups. One week postpartum the sFlt1 concentration was persistently higher, however, in women with early-onset pre-eclampsia compared with early controls. (Paper IV)In conclusion: random ACR cannot replace 24-hour urine collections for quantification of albuminuria in pre-eclamptic women; gestational hypertensive disease, especially severe or recurrent, increases the risk for later IHD; early-onset, but not late-onset pre-eclampsia is associated with pronounced alterations of angiogenesis-related markers and only early-onset pre-eclampsia is associated with placental oxidative stress and an increased PAI-1/ PAI-2 ratio, all suggesting a stronger link between early-onset than late-onset pre-eclampsia and a dysfunctional placenta.
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