Low dose aspirin in pregancy to prevent PIH

 Other health care organizations also have published guidelines for preeclampsia prevention using low-dose aspirin based on risk factors. Published in 2011, the World Health Organization guideline recommended that low-dose aspirin (75 mg/day) be initiated before 20 weeks of gestation for women at high risk of preeclampsia; eg, women with a history of preeclampsia, diabetes, chronic hypertension, renal disease, autoimmune disease, and multiple gestations. The National Institute of Health and Care Excellence published a quality statement, Antenatal Assessment of Pre-eclampsia Risk, in July 2013 that asked health care providers to prescribe low-dose aspirin (75 mg/day) to pregnant women at increased risk of preeclampsia at the first prenatal visit, to be taken daily from 12 weeks of gestation until birth .The degree of risk of preeclampsia was based on the presence of one or more high-risk factors (hypertensive disease in previous pregnancy, chronic kidney disease autoimmune disease, type 1 or type 2 diabetes, and chronic hypertension) or more than one moderate-risk factor (first pregnancy, maternal age of 40 years or older, a body mass index greater than 35, family history of preeclampsia, and multiple pregnancy) 

Pathophysiology

Aspirin (acetylsalicylic acid) is a nonsteroidal antiinflammatory drug (NSAID) that works primarily through its inhibition of two cyclooxygenase isoenzymes (COX-1 and COX-2), which are necessary for prostaglandin biosynthesis. The COX-1 isoform is present in the vascular endothelium and regulates the production of prostacyclin and thromboxane A₂, prostaglandins with opposing regulatory effects on vascular homeostasis and platelet function. Prostacyclin is a potent vasodilator and inhibitor of platelet aggregation, whereas thromboxane A₂ (TXA2) is a potent vasoconstrictor and promotes platelet aggregation. The COX-2 isoform is inducible and expressed almost exclusively following exposure to cytokines or other inflammatory mediators. The effect of aspirin on COX-dependent prostaglandin synthesis is dose dependent. At lower dosages (60–150 mg/day) aspirin irreversibly acetylates COX-1, resulting in decreased platelet synthesis of TXA2 without affecting vascular wall production of prostacyclin . At higher doses, aspirin inhibits both COX-1 and COX-2, effectively blocking all prostaglandin production.

Evidence suggesting that an imbalance in prostacyclin and TXA2 metabolism was involved in the development of preeclampsia prompted the initial studies of aspirin for preeclampsia prevention because of its preferential inhibition of TXA2 at lower doses . However, it is likely that preeclampsia is a result of poor placentation from a variety of causes, including ischemia, reperfusion, or dysfunctional maternal inflammatory response towards the trophoblast . Whether low-dose aspirin improves early placental perfusion is unknown, and likewise, the precise mechanism by which low-dose aspirin prevents preeclampsia in some women is also uncertain 

Risks of Aspirin Use in Pregnancy

Maternal Risks

The majority of systematic reviews of randomized controlled trials (RCTs) have found no increase in hemorrhagic complications associated with low-dose aspirin during pregnancy