Up to 10% of women scheduled for ERCS go into labour before
39+0 weeks. Therefore it is good practice to to discuss and document a plan for delivery if labour starts prior to the scheduled date.

Do not use pad tests in the routine assessment of women with urinary
incontinence.

• Clinicians should consider the use of intravenous tranexamic acid (0.5–1.0 g), in addition to oxytocin, at caesarean section to reduce blood loss in women at increased risk of PPH.
• Consideration should be given to the use of tranexamic acid in the management of PPH.
• According to a Cochrane review- blood loss greater than 400 or 500 ml was less
  common in women who received tranexamic acid in addition to the usual uterotonic agent after vaginal
  birth or caesarean section in a dosage of 1 or 0.5 g intravenously. Tranexamic acid was effective in
  decreasing the incidence of blood loss greater than 1000 ml in women who had undergone caesarean section but not vaginal birth. Further studies are required to investigate the risk of serious adverse effects, including thromboembolic events.

Where delivery is planned, either by elective caesarean section or induction of labour, LMWH maintenance therapy should be discontinued 24 hours prior to planned delivery.

Regional anaesthetic or analgesic techniques should not be undertaken until at least 24 hours
after the last dose of therapeutic LMWH.
LMWH should not be given for 4 hours after the use of spinal anaesthesia or after the epidural catheter has been removed, and the epidural catheter should not be removed within 12 hours of the most recent injection.

Regarding 'Prophylactic dose'-Regional techniques should be avoided if possible until at least 12 hours after the previous
prophylactic dose of LMWH.
LMWH should not be given for 4 hours after use of spinal anaesthesia or after the epidural catheter has been removed and the catheter should not be removed within 12 hours of the most recent injection.

If women do not achieve satisfactory benefit from bladder training programmes, the combination of an overactive bladder medicine with bladder training should be considered if frequency is a troublesome symptom.

Codeine is converted to active metabolites, mainly morphine. The ultrarapid metaboliser phenotype is due to duplications of the CYP2D6 gene, and prevalence varies by ethnic origin.

Ultrarapid metabolisers who take codeine can have up to 50% higher plasma concentrations
of its active metabolite morphine than extensive metabolisers, with the consequence that there is a risk of serious toxicity even at therapeutic doses of codeine in such individuals.