Lying Down after Premature Rupture of the Membranes in Term Singleton Pregnancies: An Evidence-Based Recommendation?

Objectives: In many countries pregnant women in term singleton pregnancies are advised by obstetricians and midwives to lie down immediately after rupture of membranes until engagement of the foetal head is confirmed. The horizontal positioning aims to prevent the prolapse of the umbilical cord. The objective of this systematic review is to assess the effects of the maternal lying down measure in term singleton pregnancies. Search methods: We searched the databases of MEDLINE/PubMed, EMBASE/Ovid and CENTRAL (Issue 10, 2015) from their inception until September 30th, 2015. Additionally, we searched selected trial registers, the reference lists of potentially relevant studies and national and international obstetrical clinical guidelines. All types of studies without language restriction were selected. Main results: One retrospective study was found. Only one woman with a term singleton pregnancy had the event of an umbilical cord prolapse following premature rupture of membranes (0.008%). The study did not report on the presence of an engaged foetal head in this woman. Conclusions and implications: Recommendations cannot be made in favour or against the lying down positioning based solely on the single identified study. For that reason, the widespread recommendation given by obstetricians and midwives should be critically reassessed. Also, induction of maternal anxiety and increased costs to the healthcare system following transportation to the delivery unit have to be considered in the light of the given minimal risk of umbilical cord prolapse in conjuncture with lacking evidence for the utility of the common recommendation.

Effects of N-, P/Q- and L-type calcium channel blockers on nociceptive neurones of the trigeminal nucleus with input from the dura.

In anaesthetized rats, extracellular recordings were made from neurones of the spinal trigeminal nucleus, involved in the processing of nociceptive input from the dura. Blockers of voltage-gated calcium channels (VGCCs) were administered topically to the exposed brainstem. Blockade of N-type (CaV2.2) channels reduced spontaneous activity and responses of the neurones to cold and chemical stimuli applied to the dura, suggesting that N-type channels regulate excitatory synaptic activation. Blockade of L-type (CaV1) channels enhanced spontaneous discharges of the neurones. Blockade of P/Q-type (CaV2.1) channels slightly decreased responses to chemical and cold stimuli but markedly increased spontaneous activity, an effect which was absent during concomitant application of GABA to the brainstem. The data suggest that P/Q-type VGCCs regulate a tonic synaptic inhibitory control of the brainstem neurones. The risk of migraine by genetic modifications of P/Q-type channels may thus be sought in disturbed inhibition in the network that processes nociceptive dura input.

Dimethylthiourea, but not dimethylsulfoxide, reduces canine myocardial infarct size.

We studied the effect of treatment with two diffusible, low molecular weight scavengers of toxic oxygen metabolites, dimethylthiourea (DMTU) and dimethylsulfoxide (DMSO), on canine infarcts caused by 90 min of ischemia and 3 h of reperfusion. Infarct size was determined by incubating ventricular slices with triphenyl tetrazolium chloride. Areas at risk were determined by autoradiography of 99Tc microspheres injected in vivo during ischemia and were similar (p greater than 0.05) in DMTU, DMSO, and saline treated dogs. However, the ratio of infarct size to area at risk was reduced (p less than 0.05) in dogs treated 30 min before reperfusion with 500 mg/kg DMTU (31.1 +/- 4.6%, n = 9) compared with saline treated dogs (53.4 +/- 4.6% n = 9). In contrast, the ratio of infarct size to area at risk was not significantly different (p greater than 0.05) in dogs treated with 2000 mg/kg DMSO 30 min before reperfusion (43.7 +/- 4.3%) compared to saline treated dogs. The serum concentration of DMTU (4.5 mM) was one-tenth that of DMSO (48 mM) in early reperfusion. Therefore, DMTU but not DMSO protected against post-ischemic cardiac reperfusion injury.