Wednesday, April 12, 2006
Diclofenac and dystocia
It was quite a busy night last night, and it included two caesarean sections for obstructed labour. Both women had been labouring all day since elective inductions, both had received several hours of oxytocin infusion, and both delivered babies over 4 kg. The caesars went fairly will with epidural anaesthesia, but both uteri needed more massage than usual, and I administered generous doses of oxytocin and ergometrine. After the skin closures I declined the use of rectal diclofenac. This was met with some surprise because it seems in this part of the world rectal diclofenac is given almost routinely after caesarean section. But diclofenac is a COX-2 inhibitor, and thus antagonises the production of endogenous prostaglandin F2alpha which is essential in mediating myometrial contraction. PGF2a is even more crucial after oxytocin-augmented labour because oxytocin receptors become massively down-regulated during continuous intravenous infusion and the uterus is then resistant to further doses of intravenous oxytocin. And when the uterus is acidotic and truamatised from the long and obstructed labour and subsequent surgery it does not a tocolytic drug as well, which is what diclofenac and other COX-2 inhibitors are. So I leave out the diclofenac after obstructed labour and oxytocin infusion and ensure there is ready access to opioid analgesia. Postpartum haemorrhage from uterine atony remains a major cause of maternal morbidity and mortality and it shouldn't be iatrogenic.
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