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Background: Clinical guidelines improve outcomes, but poor compliance with recommendations is common. Insight into perceived barriers and enablers to the implementation of guidelines can engage maternity care providers and inform strategies for effective implementation. Aim: To identify the perceived barriers and enablers to implementing the 2020 'Induction of Labour [IOL] in Aotearoa New Zealand; a Clinical Practice Guideline.' Materials and Methods: Electronic anonymous survey of clinical leaders in midwifery, obstetrics, and neonatology in New Zealand, from August to November 2021. Recruitment of participants was initially through provided lists of national clinical leads, followed by chain sampling. Results: There were 32 of 89 surveys returned (36%). The most frequently identified enablers were implementation tools such as 'standardised IOL request form' and 'peer review process,' and administrative support and dedicated time. Six maternity hospitals already had peer review in place, whereby IOL requests that did not adhere to guidelines were reviewed by a multidisciplinary group of senior colleagues or peers, with individual feedback to the referring clinician. Attitudes in the form of 'existing systems, routines and culture' was the most frequently identified barrier, followed by external barriers such as 'lack of human resources.' Conclusions: Overall, few barriers were identified to implementing this guideline, and some of the key enablers were already in place. The identified enablers warrant future research to develop and evaluate effectiveness in improving outcomes. [ABSTRACT FROM AUTHOR]

Background: Birth‐related third‐ and fourth‐degree perineal trauma is common and associated with short‐ and long‐term complications. Aim: To conduct a review of clinical audits investigating management of women with perineal trauma. Materials and Methods: We identified all audits undertaken in eight New Zealand public hospitals between 2005 and 2014 that investigated whether women with birth‐related third‐ and fourth‐degree perineal trauma were receiving care according to clinical guidelines. We aggregated audit results and calculated the proportion of women receiving the recommended standard of care. Results: During the review period, 25 audits investigated intra‐operative (n = 11), post‐operative (n = 14) and outpatient care (n = 18). Baseline audits showed variation in care by site; intra‐operative care (range 39–96% for repair conducted under anaesthesia, 60–96% for repair by or under supervision of a senior clinician, and 33–54% for completion of Accident Compensation Corporation forms); post‐operative care (range 40–93% for prescribed antibiotics and 33–96% for stool softeners) and outpatient care (45–84% for referral to outpatient clinic and 54–78% for physiotherapy follow‐up). Sustained high quality of care and improvements in adherence with recommendations were seen for most of the follow‐up audits (eg 90% adherence for prescribed stool softeners over three audits; over 50% increase in prescribed antibiotics over seven years). Conclusions: These clinical audits exemplify the need to measure patient care against standards, learn from the findings, implement changes to improve patient experience and reduce life‐long sequelae from perineal trauma. This review showed some progress in some care services and highlighted where further changes are needed to close evidence‐practice gaps. [ABSTRACT FROM AUTHOR]

Preeclampsia is triggered by an as yet unknown toxin from the placenta. Antiphospholipid antibodies (aPL), a strong risk factor for preeclampsia, have been shown to induce the production of toxic trophoblastic debris from the placenta. High mobility group box 1 (HMGB1) is a proinflammatory danger signal, and the expression of it has been reported to be increased in preeclampsia. This study examined whether aPL or preeclamptic sera increase the expression of HMGB1 in the syncytiotrophoblast or trophoblastic debris. Trophoblastic debris from normal placental explants that had been cultured with aPL or preeclamptic sera was exposed to endothelial cells. Endothelial cell activation was quantified by cell-surface ICAM-1 expression and U937 monocyte adhesion. The expression of HMGB1 in placental explants and trophoblastic debris that had been treated with aPL or preeclamptic sera was measured by immunohistochemistry and western blotting. The expression of the receptor for advanced glycation end products (RAGE) in endothelial cells was quantified by western blotting. Compared with controls, the expression of HMGB1 in the cytoplasm of the syncytiotrophoblast and trophoblastic debris was increased by treating placental explants with aPL or preeclamptic sera. The increased levels of HMGB1 contributed to endothelial cell activation, mediated in part by the RAGE. Preeclamptic sera and aPL both induced an increase in the cytoplasmic levels of the danger signal HMGB1 in trophoblastic debris. This increased HMGB1 in trophoblastic debris may be one of the toxic factors released from the placenta in preeclampsia. [ABSTRACT FROM AUTHOR]