A 34-year-old primigravida presented with a fetal death in utero at 36+ weeks having had no fetal movements for 24 hours previously. Her blood pressure was then 140/100 and the protein/creatinine ratio was 144 mg/mmol. She had given the GP and obstetricians a strong family history of pre-eclampsia in her mother, sister and maternal aunt. Her blood pressure during pregnancy had been 100/65 at booking at 23-6 and had remained within normal limits until 36 weeks. Her urine had only been infrequently tested for proteinuria and her schedule of antenatal visits had not been as frequent as would even be normally expected: no visit between 31 weeks and 36 weeks. When the baby was delivered it weighed 1400g (<3rd percentile) and the placenta weighed only 258 g (<5th percentile).
Can Low Dose Aspirin Prevent This?
Preeclampsia is a complication of pregnancy secondary to placental dysfunction. Initially, vascular uterine re-modelling is altered, leading to decreased maternal blood supply to the placenta. Progressively, placental hypoxia and oxidative stress result in generalized dysfunction of the villous trophoblast. This placental dysfunction induces release into the maternal circulation of factors (free radicals, oxidized lipids, cytokines, sFlt-1) that cause generalized endothelial dysfunction, leading to clinical signs of the disease.
The first evidence of the obstetrical efficacy of aspirin was noted in 1985 by Beaufils et al., in a randomized study of preventive treatment with aspirin in 102 patients at high risk of preeclampsia and/or intrauterine growth restriction. The prevalence of preeclampsia was significantly reduced in the aspirin group compared with the untreated group (0/48 vs 6/45 p < 0.05).