Incidence

The exact incidence of postpartum hypertension is difficult to ascertain. In clinical practice, most women will not have their blood pressure (BP) checked until the 6 weeks’ postpartum visit in physician’s offices or in postpartum clinics. As a result, women with mild hypertension who are asymptomatic are usually not reported. In addition, postpartum women who have hypertension in association with symptoms such as headaches or blurred vision are often seen and managed in the emergency department and will not be coded as hypertensive unless they are hospitalized.

Research studies dealing with postpartum hypertension are usually limited by analysis of data from a single center, focused on inpatients in the immediate postpartum period (2-6 days), or describing patients who were readmitted because of preeclampsia-eclampsia, severe hypertension, or complications related to hypertension. Despite the limitations, the reported prevalence of de novo postpartum hypertension or preeclampsia ranges from 0.3–27.5%.

Etiology and differential diagnosis

The etiology and different diagnosis of postpartum hypertension is extensive ( Table ), but it can be focused based on clinical and laboratory findings as well as response to treatment of BP. GH-preeclampsia (new onset or preexisting prior to delivery) is the most common cause, however, other life-threatening conditions such as pheochromocytoma and cerebrovascular accidents should also be considered.

Etiology and differential diagnosis

The etiology and different diagnosis of postpartum hypertension is extensive ( Table ), but it can be focused based on clinical and laboratory findings as well as response to treatment of BP. GH-preeclampsia (new onset or preexisting prior to delivery) is the most common cause, however, other life-threatening conditions such as pheochromocytoma and cerebrovascular accidents should also be considered.

New-onset postpartum hypertension-preeclampsia

Normal pregnancy is characterized by increased plasma volume in association with sodium and water retention in the interstitial tissue. This is further exaggerated in women with multifetal gestation. In addition, many women receive intravenously a large volume of fluids during labor, delivery, and postpartum. Large volumes of fluids are also given because of regional analgesia-anesthesia or during cesarean section. In some women, acute or delayed mobilization of large volume of fluid into the intravascular space, particularly in association with suboptimal renal function, can lead to a state of volume overload resulting in hypertension.

Some medications that cause vasoconstriction are often used for pain relief, in women having perineal lacerations, episiotomy, or cesarean delivery. Such women usually require large doses of nonsteroidal antiinflammatory drugs such as ibuprofen or indomethacin that are associated with vasoconstriction and sodium and water retention, both of which can result in severe hypertension. In addition, some women receive frequent injections of ergot alkaloids (ergometrine or methylergonovine) for treatment of uterine atony. The action of these medications is mediated through alpha adrenergic receptors, which can lead to peripheral vasoconstriction with resultant hypertension or aggravation of hypertension, cerebral vasoconstriction, and stroke. These medications are also associated with nausea, vomiting, and headaches, symptoms that are similar to those in severe GH-preeclampsia.

Persistence/exacerbation of hypertension-proteinuria in women with preexisting GH-preeclampsia

Maternal hypertension and proteinuria will usually resolve during the first week postpartum in most women with GH or preeclampsia, however, there are conflicting data regarding the time it takes for resolution in such women. The differences among various studies are due to the population studied, severity of disease process (mild, severe, with superimposed preeclampsia, HELLP syndrome), duration of follow-up, management (aggressive vs expectant), and criteria used for hypertension or proteinuria. In women with preeclampsia, there is a decrease in BP within 48 hours, but BP increases again between 3-6 days postpartum. In some patients, cerebral manifestations and/or deterioration in maternal laboratory findings will manifest for the first time postpartum leading to the development of eclampsia and/or HELLP syndrome.

Persistence/exacerbation of hypertension in chronic hypertension

Women with chronic hypertension during pregnancy are at increased risk for exacerbation of hypertension and/or superimposed preeclampsia. The risk depends on severity of hypertension, presence of associated medical conditions (obesity, type 2 diabetes, renal disease), or whether antihypertensive medications were used during pregnancy. Hypertension or exacerbation of hypertension postpartum may be due to either undiagnosed essential chronic hypertension (women with limited medical care prior to or early in pregnancy), or due to exacerbation of hypertension after delivery in those with superimposed preeclampsia.

Two studies in patients with superimposed preeclampsia suggest that systolic and diastolic BP increases at 3-6 days postpartum in such women.

Postpartum hypertension or preeclampsia can also be secondary to ≥1 of the underlying medical disorders listed in the Table .

Maternal complications

Maternal complications depend on ≥1 of the following: severity and etiology of the hypertension, maternal status at presentation (presence of organ dysfunction), and the quality of management used. Potential life-threatening complications include cerebral infarction or hemorrhage, congestive heart failure or pulmonary edema, renal failure, or death. Maternal outcome is usually good in those with only isolated hypertension or preeclampsia, whereas it is poor with pheochromocytoma, stroke, thrombotic thrombocytopenic purpura/hemolytic uremic syndrome, and with delayed diagnosis and inadequate control of persistent severe hypertension.