Stroke in Pregnancy

Christina Mijalski Sells, MD, MPH; Steven K. Feske, MD


Semin Neurol. 2017;37(6):669-678. 

In This Article

Pregnancy-related Physiologic Changes Predisposing to Stroke

Hemodynamic Changes

Profound hemodynamic changes take place during pregnancy and the puerperium. The retention of water and sodium is associated with an increase in renin activity. The consequent increase in plasma volume is associated with an increase in cardiac output, stroke volume, and heart rate by as much as 30 to 50%. These hemodynamic adaptations may contribute to hypertension in susceptible patients. The physiologic hemodynamic changes persist for 6 to 12 weeks postpartum and may contribute to the observed increase in strokes, especially hemorrhagic, observed during this time period. Among women with hemodynamic complications during pregnancy, there is a known increased risk of stroke recurrence in subsequent pregnancies.

Changes in Connective Tissue and the Vessel Wall

Blood vessel walls undergo connective tissue changes which, especially in the setting of increased hemodynamic stress, may place vulnerable patients at increased risk for stroke. Increases in prostacyclin, progesterone, and nitric oxide are associated with a decrease in vascular resistance and a subsequent decrease in blood pressure in mid pregnancy.[4,17] However, decreases in vessel compliance in late pregnancy may confer proportional late increases in blood pressure, which might increase the risk of both ischemic and hemorrhagic stroke. While the direct effects of these vessel wall changes on stroke are poorly understood, they probably contribute to the increased risk of both ischemic and hemorrhagic stroke. In addition to the effects of blood pressure, there are theoretical concerns that remodeling of blood vessel walls may decrease their capacity to withstand hemodynamic stressors and thus contribute to the increased risk of ICH.[17] Endothelial cell dysfunction has also been described well as a factor contributing to preeclampsia–eclampsia, which significantly increases the risk of both ischemic and hemorrhagic stroke.[16]

Changes in the Coagulation System

The period of late pregnancy and the early puerperium is a physiologic hypercoagulable state, surely an adaptation to the inevitable bleeding associated with childbirth. The vascular system typically experiences an increase in compliance beginning in mid-pregnancy. This may lead to venous stasis and further encourage pathologic clotting. Pregnancy is accompanied by increases in procoagulant factors of the clotting cascade, including factors I, VII, VIII, IX, X, XII, XIII, von Willebrand factor (vWF), fibrinogen, and fibrin. Levels of the anticoagulant factor protein C remain largely unchanged, but up to one third of women will have activated protein C resistance in the late third trimester. Other anticoagulant factors, protein S and antithrombin III, undergo physiologic decreases, greatest in the late third trimester and early postpartum period.[18] The decrease in these inhibitory coagulation factors may be an important contributor to the relative hypercoagulability observed during late pregnancy and the puerperium. Local injury to blood vessels in the abdomen and pelvis may result from mass effect from the gravid uterus, and in turn, promote an increase in the levels of plasminogen activator inhibitor (PAI) and the tissue factor (TF) pathway inhibitor.[19,20]