Cause of stillbirth and pathophysiological pathways in mothers with overweight and obesity

PurposeObesity is independently associated with stillbirth, especially in early gestation and late-term gestation. Underlying pathophysiological mechanism causing fetal death is yet not clear. The purpose of this study was to determine the association between maternal body mass index and stillbirth and its importance in potential pathophysiological mechanisms of fetal death.MethodsIn a multicenter prospective cohort study from 2002 to 2008, 1.025 women with a fetal death > 20 weeks of gestation were studied. An extensive diagnostic workup was performed including maternal blood tests, coagulation tests, autopsy and placental examination. Cause of death was classified by a multidisciplinary panel. Odds ratios for each outcome stratified by gestational age were estimated for different maternal BMI classes (underweight BMI < 18.5; overweight BMI 25.0-29.9; obesity BMI > 30.0) compared with normal weight women (BMI 18.5–24.9) by using logistic regression and cause of death was studied.ResultsWe analysed 793 women. Obese women significantly more often had pre-existing hypertension, pregnancy induced hypertension or gestational diabetes. Early fetal death (< 37 weeks) in obese women is more often caused by placental bed pathology (OR 4.10, 95% CI 1.79–9.40, P 0.001), and term fetal death by developmental placental pathology (OR 1.93, 95% CI 1.01–3.71, P 0.05).ConclusionIn obese women there are at least 2 distinct underlying pathophysiological pathways causing fetal death. The underlying mechanisms of these pathways are uncertain and should be investigated in future

Stillbirth and neonatal mortality in a subsequent pregnancy following stillbirth:a population-based cohort study

BACKGROUND: A history of stillbirth is a risk factor for recurrent fetal death in a subsequent pregnancy. Reported risks of recurrent fetal death are often not stratified by gestational age. In subsequent pregnancies increased rates of medical interventions are reported without evidence of perinatal benefit. The aim of this study was to estimate gestational-age specific risks of recurrent stillbirth and to evaluate the effect of obstetrical management on perinatal outcome after previous stillbirth. METHODS: A retrospective cohort study in the Netherlands was designed that included 252.827 women with two consecutive singleton pregnancies (1(st) and 2(nd) delivery) between 1999 and 2007. Data was obtained from the national Perinatal Registry and analyzed for pregnancy outcomes. Fetal deaths associated with a congenital anomaly were excluded. The primary outcome was the occurrence of stillbirth in the second pregnancy stratified by gestational age. Secondary outcome was the influence of obstetrical management on perinatal outcome in a subsequent pregnancy. RESULTS: Of 252.827 first pregnancies, 2.058 pregnancies ended in a stillbirth (8.1 per 1000). After adjusting for confounding factors, women with a prior stillbirth have a two-fold higher risk of recurrence (aOR 1.96, 95% CI 1.07–3.60) compared to women with a live birth in their first pregnancy. The highest risk of recurrence occurred in the group of women with a stillbirth in early gestation between 22 and 28 weeks of gestation (a OR 2.25, 95% CI 0.62–8.15), while after 32 weeks the risk decreased. The risk of neonatal death after 34 weeks of gestation is higher in women with a history of stillbirth (aOR 6.48, 95% CI 2.61–16.1) and the risk of neonatal death increases with expectant obstetric management (aOR 10.0, 95% CI 2.43–41.1). CONCLUSIONS: A history of stillbirth remains an important risk for recurrent stillbirth especially in early gestation (22–28 weeks). Women with a previous stillbirth should be counselled for elective induction in the subsequent pregnancy at 37–38 weeks of gestation to decrease the risk of perinatal death

What Can We Learn from In-Depth Analysis of Human Errors Resulting in Diagnostic Errors in the Emergency Department:An Analysis of Serious Adverse Event Reports

Introduction Human error plays a vital role in diagnostic errors in the emergency department. A thorough analysis of these human errors, using information-rich reports of serious adverse events (SAEs), could help to better study and understand the causes of these errors and formulate more specific recommendations. Methods We studied 23 SAE reports of diagnostic events in emergency departments of Dutch general hospitals and identified human errors. Two researchers independently applied the Safer Dx Instrument, Diagnostic Error Evaluation and Research Taxonomy, and the Model of Unsafe acts to analyze reports. Results Twenty-one reports contained a diagnostic error, in which we identified 73 human errors, which were mainly based on intended actions (n=69) and could be classified as mistakes (n=56) or violations (n=13). Most human errors occurred during the assessment and testing phase of the diagnostic process. Discussion The combination of different instruments and information-rich SAE reports allowed for a deeper understanding of the mechanisms underlying diagnostic error. Results indicated that errors occurred most often during the assessment and the testing phase of the diagnostic process. Most often, the errors could be classified as mistakes and violations, both intended actions. These types of errors are in need of different recommendations for improvement, as mistakes are often knowledge based, whereas violations often happen because of work and time pressure. These analyses provided valuable insights for more overarching recommendations to improve diagnostic safety and would be recommended to use in future research and analysis of (serious) adverse events

Distribution of decidual mast cells in fetal growth restriction and stillbirth at (near) term

Introduction: Placental pathology and pregnancy complications are associated with unfavorable regulation of the maternal immune system. Although much research has been performed towards the role of immune cells like macrophages and T cells in this context, little is known about the presence and function of mast cells (MC). MC can be sub classified in tryptase-positive (MCT) and tryptase- and chymase-positive (MCTC). This study investigates the presence of MC in the decidua of pregnancies complicated by fetal growth restriction (FGR) and stillbirth (SB). Methods: Placental tissue from FGR (n = 250), SB (n = 64) and healthy pregnancies (n = 42) was included. Histopathological lesions were classified according to the Amsterdam Placental Workshop Group criteria. Tissue sections were stained for tryptase and chymase. Decidual MC were counted manually, and the results were expressed as number of cells/mm2 decidual tissue. Results: A significant lower median number of MCTC was found in the decidua of FGR (0.40 per mm2; p < 0.001) and SB (0.51 per mm2; p < 0.05) compared to healthy controls (1.04 per mm2). No difference in MCT number (1.19 per mm2, 1.88 per mm2 and 1.37 per mm2 respectively) was seen between the groups. There was no difference in number of MCT and MCTC between placental pathological lesions. Discussion: Our findings suggest a shift in decidual MC balance towards MCT in pregnancy complications. No difference in numbers of MC subtypes was found to be related to histopathologic lesions

What Can We Learn From In-Depth Analysis of Human Errors Resulting in Diagnostic Errors in the Emergency Department: An Analysis of Serious Adverse Event Reports

INTRODUCTION: Human error plays a vital role in diagnostic errors in the emergency department. A thorough analysis of these human errors, using information-rich reports of serious adverse events (SAEs), could help to better study and understand the causes of these errors and formulate more specific recommendations. METHODS: We studied 23 SAE reports of diagnostic events in emergency departments of Dutch general hospitals and identified human errors. Two researchers independently applied the Safer Dx Instrument, Diagnostic Error Evaluation and Research Taxonomy, and the Model of Unsafe acts to analyze reports. RESULTS: Twenty-one reports contained a diagnostic error, in which we identified 73 human errors, which were mainly based on intended actions (n = 69) and could be classified as mistakes (n = 56) or violations (n = 13). Most human errors occurred during the assessment and testing phase of the diagnostic process. DISCUSSION: The combination of different instruments and information-rich SAE reports allowed for a deeper understanding of the mechanisms underlying diagnostic error. Results indicated that errors occurred most often during the assessment and the testing phase of the diagnostic process. Most often, the errors could be classified as mistakes and violations, both intended actions. These types of errors are in need of different recommendations for improvement, as mistakes are often knowledge based, whereas violations often happen because of work and time pressure. These analyses provided valuable insights for more overarching recommendations to improve diagnostic safety and would be recommended to use in future research and analysis of (serious) adverse events

What Can We Learn from In-Depth Analysis of Human Errors Resulting in Diagnostic Errors in the Emergency Department: An Analysis of Serious Adverse Event Reports

Introduction: Human error plays a vital role in diagnostic errors in the emergency department. A thorough analysis of these human errors, using information-rich reports of serious adverse events (SAEs), could help to better study and understand the causes of these errors and formulate more specific recommendations. Methods: We studied 23 SAE reports of diagnostic events in emergency departments of Dutch general hospitals and identified human errors. Two researchers independently applied the Safer Dx Instrument, Diagnostic Error Evaluation and Research Taxonomy, and the Model of Unsafe acts to analyze reports. Results: Twenty-one reports contained a diagnostic error, in which we identified 73 human errors, which were mainly based on intended actions (n=69) and could be classified as mistakes (n=56) or violations (n=13). Most human errors occurred during the assessment and testing phase of the diagnostic process. Discussion: The combination of different instruments and information-rich SAE reports allowed for a deeper understanding of the mechanisms underlying diagnostic error. Results indicated that errors occurred most often during the assessment and the testing phase of the diagnostic process. Most often, the errors could be classified as mistakes and violations, both intended actions. These types of errors are in need of different recommendations for improvement, as mistakes are often knowledge based, whereas violations often happen because of work and time pressure. These analyses provided valuable insights for more overarching recommendations to improve diagnostic safety and would be recommended to use in future research and analysis of (serious) adverse events

Distribution of decidual mast cells in fetal growth restriction and stillbirth at (near) term

Introduction: Placental pathology and pregnancy complications are associated with unfavorable regulation of the maternal immune system. Although much research has been performed towards the role of immune cells like macrophages and T cells in this context, little is known about the presence and function of mast cells (MC). MC can be sub classified in tryptase-positive (MCT) and tryptase- and chymase-positive (MCTC). This study investigates the presence of MC in the decidua of pregnancies complicated by fetal growth restriction (FGR) and stillbirth (SB). Methods: Placental tissue from FGR (n = 250), SB (n = 64) and healthy pregnancies (n = 42) was included. Histopathological lesions were classified according to the Amsterdam Placental Workshop Group criteria. Tissue sections were stained for tryptase and chymase. Decidual MC were counted manually, and the results were expressed as number of cells/mm2 decidual tissue. Results: A significant lower median number of MCTC was found in the decidua of FGR (0.40 per mm2; p < 0.001) and SB (0.51 per mm2; p < 0.05) compared to healthy controls (1.04 per mm2). No difference in MCT number (1.19 per mm2, 1.88 per mm2 and 1.37 per mm2 respectively) was seen between the groups. There was no difference in number of MCT and MCTC between placental pathological lesions. Discussion: Our findings suggest a shift in decidual MC balance towards MCT in pregnancy complications. No difference in numbers of MC subtypes was found to be related to histopathologic lesions