Hypertension in the Postpartum Woman: Clinical Update for the Hypertension Specialist

Abstract

Hypertension can persist from pregnancy or present de novo in the postpartum period and continue to pose a risk to maternal well‐being. These risks are magnified as many patients present after hospital discharge and go unrecognized because of decreased medical surveillance after delivery. Guidelines for the management of postpartum hypertension are lacking, often resulting in imprecise diagnoses and incorrect treatment strategies. As hypertension specialists are called upon to provide advice to obstetricians regarding the management of hypertension in the postpartum period, it becomes important for the hypertension specialist to develop expertise in the evaluation and treatment of hypertensive women during the postpartum period. The purpose of this clinical review article is to provide an approach to the management of postpartum hypertension.

Hypertensive disorders are the most common medical complications of pregnancy, with a prevalence of 5% to 10%, and are the second leading cause, after venous thromboembolism, of maternal death in the United States. ¹ Availability of prenatal care and specific guidelines for the management of hypertension during pregnancy has significantly decreased the morbidity associated with antenatal hypertension.

Hypertension can persist from pregnancy or present de novo in the postpartum period and continue to pose a risk to maternal well‐being. These risks are magnified as many patients present after hospital discharge and go unrecognized because of decreased medical surveillance after delivery. In very high–risk women with postpartum hypertension, complications such as cardiac failure, cerebrovascular accidents, and acute oliguric renal failure have been reported. ² Guidelines for the management of postpartum hypertension are lacking, often resulting in imprecise diagnoses and incorrect treatment strategies.

As hypertension specialists are often called upon to provide advice to obstetricians regarding the management of hypertension in the postpartum period, it becomes important for the hypertension specialist to become familiar with the evaluation and treatment of women during the postpartum period. Thus, this article reviews typical clinical scenarios of postpartum hypertension and its appropriate management.

Illustrative Cases

Case 1: Development of Postpartum Hypertension in a Primigravida Woman With No Prior History of Hypertension

A 27‐year‐old woman with an uncomplicated pregnancy presented 10 days postpartum with headache, blurred vision, nausea, mild nuchal rigidity, and hypertension. In the emergency department, her supine blood pressure (BP) was 180/110 mm Hg according to repeated determinations and her physical examination demonstrated bilateral ++ lower extremity edema and hyperreflexia of the knees and ankles.

Initial laboratory data revealed ++ proteinuria by dipstick and slightly elevated liver transaminase levels (alanine aminotransferase, 50 μ/L [normal, <34 μ/L] and aspartate aminotransferase, 48 μ/L [normal, <36 μ/L]. Complete blood cell count, serum creatinine, blood urea nitrogen, serum electrolyte, serum aldosterone, and plasma renin activity values were normal. A lumbar puncture showed an opening pressure of 110 mm H₂0, with normal chemistries and no cells. Computerized tomographic findings of the brain were unremarkable as well.

While in the emergency department, labetalol was administered intravenously to achieve a systolic BP <160 mm Hg, and a magnesium sulfate infusion was initiated. Subsequently, 24‐hour urinary collection showed 630 mg of protein and no elevations in metanephrines or normetaphrines. On the 3rd day of hospitalization, the patient was treated with hydrochlorothiazide, 25 mg once daily, and diltiazem controlled‐delivery tablets, 240 mg once daily. Assessment during the next 3 months demonstrated persistence of the hypertension necessitating chronic drug therapy. Repeat 24‐hour collection of urine showed 12 mg of protein per gram of creatinine, and the average clinic BP was 112/80 mm Hg.

Case 2: Development of Hypertension in the Immediate Postpartum Period

A previously healthy 28‐year‐old woman (gravida 2, para 2) was seen in consultation for persistently elevated BP levels on the second postoperative day following a nonemergent delivery by Cesarean section at 38 weeks’ gestation. The patient had no history of hypertension, proteinuria, or renal impairment during two pregnancies. During the first 12 hours following delivery of a healthy infant, the patient developed nausea, diffuse frontal headache, and photophobia. Supine BP was 176/108 mm Hg. The remainder of the physical examination was unremarkable. Laboratory data showed normal urinalysis, complete blood cell count, serum electrolyte, creatinine, transaminases, and uric acid values. Computerized tomographic results of the brain were normal.

The obstetrics service initiated labetalol 5 to 10 mg intravenously every 4 to 6 hours. BP levels varied between 144/96 mm Hg and 160/112 mm Hg over the next 3 days. The visual disturbance resolved; however, the headache and mild nausea persisted. On the second postoperative day, the patient was treated with intravenous metoclopramide (1 mg/kg) and oral ibuprofen (800 mg every 8 hours).

Consultation by the hypertension service was requested due to the persistence of BP elevations into the 3rd postpartum day. At that time, physical examination was normal except for a healing surgical abdominal scar and + bilateral ankle edema. Because the patient had no plans to breastfeed her infant, hydrochlorothiazide, 25 mg once daily, was initiated and the scheduled ibuprofen was discontinued and replaced with acetaminophen 1000 mg every 8 hours as needed for pain. Off of the nonsteroidal anti‐inflammatory agent, the edema resolved by day 5 and the patient was discharged from the hospital on the thiazide diuretic and a low‐salt diet. Ten days later in an outpatient visit, the patient had a BP of 108/64 mm Hg; hydrochlorothiazide was discontinued. She remained normotensive at the 6‐week postpartum evaluation.

Case 3: Development of Hypertension 3 Weeks Into the Postpartum Period

A 33‐year‐old woman was referred to the hypertension service by her obstetrician for evaluation of new‐onset stage 1 hypertension, first detected on an episodic postpartum office visit 3 weeks after a healthy‐term delivery. Clinically relevant medical history included fatigue and palpitations in the middle of the chest. There was no history of headache, shortness of breath, or diaphoresis.

On physical examination, seated BP was 144/98 mm Hg and heart rate was 94 beats per minute. The remainder of the examination was normal. Laboratory data revealed normal urinalysis, complete blood cell count, serum electrolyte, creatinine, and blood urea nitrogen values. Serum thyroxine (T4) was 16.4 μg/dL (normal, <12 μg/dL), serum triiodothyronine (T3) was 195 ng/dL (normal, <180 ng/dL), thyroid‐stimulating hormone was 0.1 mU/L (normal, 0.5–6.0 mU/L), and free T4 was 2.2 ng/dL (normal, <1.8 ng/dL). Subsequently, it was determined that antimicrosomal and antithyroglobulin antibodies were both markedly positive with titers of 1:256. The patient declined a radionuclide assessment of thyroid function because of concerns associated with lactation. Reexamination of the thyroid gland by one of the authors, who is an endocrinologist (BT), did not reveal any abnormalities.

The clinical syndrome in this patient was consistent with postpartum thyroiditis with associated hyperthyroidism. Metoprolol tartrate 25 mg twice daily was initiated, with improvements in her clinical symptoms and BP levels (BP <130/80 mm Hg based on home and office values) within a few days. Three months later, the patient developed some mild fatigue with BPs falling into the 100 to 108/66 to 72‐mm Hg range. The β‐blocker was discontinued at that time. The patient remained normotensive and biochemically euthyroid at 10 months’ postpartum.

Commentary

Physiologic and Pathophysiologic Patterns in the Postpartum State

Pregnancy is a state of chronic volume and sodium overload that contributes to increased cardiac output, edema, and BP elevation. While much of the accumulated sodium is rapidly lost during delivery, it may take up to 2 months for the salt and water homeostasis to return to antepartum levels. ³ The pattern of physiologic return to the prepregnant state may be impaired when patients have underlying conditions such as preeclampsia, chronic hypertension, and kidney or heart disease.

In the initial postpartum period there is mobilization of extracellular fluid leading to increased intravascular volume. The volume status may be further exacerbated by the administration of intravenous fluids during labor and delivery and the first days of the postpartum period as well as by the use of high doses of nonsteroidal anti‐inflammatory drugs (NSAIDs). NSAIDs are often used for pain control, and large doses are often required in women who delivered by Cesarean section. In the general population, both NSAIDs and some selective COX‐2 inhibitors can increase mean BP by 5 to 6 mm Hg through salt and fluid retention and vasoconstriction mediated via inhibition of prostaglandin synthesis. ⁴ , ⁵ The NSAIDs also attenuate the efficacy of several classes of antihypertensive drugs including angiotensin‐converting enzyme (ACE) inhibitors, angiotensin receptor blockers, β‐blockers, and thiazide diuretics. ⁵ In contrast, the calcium antagonists and α₁–blocking agents do not demonstrate attenuation of effect by NSAIDs in studies of nonpregnant patients. ⁵ Decreased plasma proteins during pregnancy may increase the availability of NSAIDs and hence concentrations of these drugs in maternal circulation. ⁶ Women with NSAID‐induced hypertension in the postpartum period may be asymptomatic or may present with headaches, worsened or persistent edema, and renal dysfunction. Discontinuation of NSAIDs and using low to intermediate doses of acetaminophen (<3000 mg/d) and/or opioids for pain control is usually sufficient. In some cases, short‐term use of diuretics or other antihypertensive medications may be required.

Etiologies of Postpartum Hypertension

Common clinical causes and syndromes of postpartum hypertension are shown in Table I . While most of these diagnoses are fairly familiar to the hypertension specialist, some are specific to the recent pregnancy and immunologic changes often seen during the transition from pregnancy to the postpartum state.

Table I.

 Potential Causes of Postpartum Hypertension

Chronic hypertension (both primary or secondary)

Gestational hypertension

Preeclampsia, unresolved with delivery

Volume excess associated with fluid or drug administration (eg, nonsteroidal anti‐inflammatory drugs for postoperative pain)

Postpartum hyperthyroidism (thyroiditis)

Preeclampsia and Related Disorders

Pregnancy‐induced hypertensive disorders including gestational hypertension, preeclampsia, or eclampsia may cause hypertension in the postpartum period. Both preeclampsia and eclampsia are states of systemic vasospasm related to the production of placental factors that mediate arterial dysfunction and endothelial injury. ⁷ While delivery of the fetus and placenta is considered the definitive treatment, not uncommonly, BP remains elevated after delivery. The incidence of delayed postpartum preeclampsia (up to 6 weeks after delivery) is approximately 6%. ⁷ In fact, a substantial number of these patients may present without any evidence of preeclampsia in the antepartum or peripartum period. ⁷ , ⁸ , ⁹ Typically, patients with preeclampsia have generalized edema, proteinuria >300 mg per 24 hours, and, if untreated, can progress to eclampsia with the development of seizures. Other diagnostic symptoms and signs include headache, blurred vision, photophobia, and altered mental status, along with hyperuricemia and evidence of microangiopathy on the peripheral blood smear.

Pharmacologic treatment with antihypertensives, and in many cases parenteral magnesium sulfate, is indicated in most patients with preeclampsia. The preeclampsia syndrome, including associated hypertension, may take several days to weeks to resolve. In a study of preeclamptic women by Podymow and colleagues, ¹⁰ 43% of patients had BPs that normalized by the end of the first postpartum month, but 57% remained hypertensive for up to 6 months. In patients whose BP remains elevated for more than 6 months’ postpartum, etiologies other than delayed preeclampsia should be considered.

Secondary Forms of Hypertension

Similar to the nonpregnant patient population, causes of secondary hypertension should be considered in women with postpartum hypertension, including fibromuscular disorders of the renal arteries, Cushing’s syndrome, hyperaldosteronism, pheochromocytoma, and hyperthyroidism. Of note, since the dynamic volume status resulting from the transition of pregnancy to the postpartum state can markedly influence diagnostic testing (eg, plasma renin activity, serum aldosterone, and urinary sodium excretion), it is prudent to wait 2 to 4 weeks after delivery prior to performing the assays that would be deranged by pregnancy.

Postpartum thyroiditis may cause transient hyperthyroidism and/or hypothyroidism for the first postpartum year. It is often a form of subacute autoimmune thyroiditis similar to Hashimoto’s disease precipitated at the end of pregnancy due to the immunologic flare after the partial immunosuppression of pregnancy. ¹¹ The prevalence of postpartum thyroiditis is estimated to range from 1.1% to 16.7% and is more common in women with type 1 diabetes mellitus. ¹¹ , ¹² Although noted to be more common in women who are positive for antithyroid peroxidase antibodies, there is no widely accepted screening method to identify women who would be at risk for developing postpartum thyroiditis. ¹² In this syndrome, the classical presentation of hyperthyroidism, followed by hypothyroidism and subsequent return to euthyroid state, is rare. More typically, the clinical presentation of postpartum thyroiditis is the development of permanent hypothyroidism without any overt symptoms of hyperthyroidism. ¹³ In cases in which symptomatic hyperthyroidism develops (palpitations, tremors, heat intolerance, fatigue, irritability, and nervousness) with systolic hypertension, a short course of β‐blockade may be useful, as seen in our case 3 above. If symptoms of hyperthyroidism persist beyond several weeks, other causes of thyrotoxicosis such as Grave’s disease should be considered. ¹¹ , ¹² As both Grave’s disease and thyroiditis have suppressed thyroid‐stimulating hormone (TSH) and elevated T4 and T3 early in the course, these two diagnoses can be differentiated by decreased uptake on nuclear imaging of the thyroid in postpartum thyroiditis.

Classification of Postpartum vs Gestational Hypertension

Currently there is little consensus on the exact timing that BP should normalize after delivery in women with gestational hypertension or preeclampsia. Guidelines from both the United States and Europe define transient hypertension in pregnancy as BP that normalizes by 6 to 12 weeks’ postpartum, ¹³ , ¹⁴ and preexisting and gestational hypertension may persist up to 6 weeks’ postpartum. Hypertension that has resolved by 6 weeks’ postpartum is typically classified as gestational hypertension. ¹⁴ In the Prevention and Treatment of Postpartum Hypertension review by Cochrane Collaboration, “de novo” postpartum hypertension is defined as BP ≥140/90 mm Hg measured twice at least 4 hours apart between delivery and at 6 weeks’ postpartum. ¹⁵ The duration of hypertension in the postpartum period has been related to both the severity of gestational hypertension as well as renal dysfunction. ¹⁶

Diagnostic Evaluation of Postpartum Hypertension

Laboratory testing in all cases of postpartum hypertension should include a complete hematologic assessment to assess for anemia, thrombocytopenia, and signs of hemolysis. This is particularly relevant when the HELLP syndrome (hemolysis, elevated liver enzymes, low platelets) may be complicating postpartum hypertension and preeclampsia (see case 1). Similar to any secondary hypertension evaluation process, complete renal function testing with serum potassium, uric acid, and urinary protein levels should be assessed for possible underlying diagnoses of hyperaldosteronism and chronic kidney diseases. In patients with symptoms and signs suggestive of postpartum thyroiditis and hypertension, thyroid function testing including TSH, free T4, T3, TSH receptor antibodies, and thyroid peroxidase antibodies should be obtained. ¹¹ , ¹²

Management of Postpartum Hypertension

Treatment of hypertension in the postpartum period is guided both by the underlying etiology of the BP elevation and whether the patient is lactating and planning to breastfeed her infant. Drug therapy may not be required for some women during the postpartum period, especially if the BP values are <150/90 mm Hg and the patient has no history or evidence of chronic hypertension. Furthermore, coexisting conditions such as pain and/or anxiety should be addressed at the time of consultation. As noted in case 2 above, large doses of NSAIDs are often used in the postpartum period for pain control and may elevate BP substantially in some patients, particularly those with impaired kidney function or preexisting fluid overload and those on a high‐salt diet. In these cases, acetaminophen and short‐term use of opioids should be considered in lieu of NSAIDs.

In mothers who choose not to breastfeed, drug choice is based on the same factors as in any nonpregnant patient. Age, individual risk factors and comorbidities, history of allergies, and prior intolerances as well as cost of treatment should be used in the medical decision‐making process. If the patient has initiated breastfeeding, then the excretion of antihypertensive drugs into breast milk would be a consideration. Unfortunately, assays for drug excretion in breast milk are not readily available to the clinician; hence, what is known about the clinical pharmacology of a drug as it relates to drug disposition in breast milk will have to be derived from small published reports in the medical literature (Table II ). Nearly all antihypertensive drugs are excreted into human breast milk in varying degrees, allowing for the treating physician to cautiously advise the lactating mother on which antihypertensive agent may be appropriate in her case. It is not likely that placebo‐controlled, prospective, randomized trials will be performed in pregnant or lactating women, thus, the availability of data will likely always remain limited. While there is a tendency to use older antihypertensive agents (eg, α₂ agonists and β₁ selective adrenergic blockers) during pregnancy and into the postpartum period, many newer agents may be equally safe and more effective in treating hypertension in mothers during lactation.

Table II.

 Antihypertensive Drug Excretion in Breast Milk

Drug	Daily Dose, mg	Average Concentration in Milk	Milk to Plasma Ratio	Transfer to Infant
Atenolol	100	0.6 μg/mL	3.0	10 μg/mL; may induce neonatal depression
Captopril	300	5.0 μg/mL	0.1	Not studied
Chlorthalidone	50	0.3 ng/mL	0.05	Not studied
Clonidine	0.15	1.5 ng/mL	1.5	Not studied
Diltiazem	240	200.0 ng/mL	1.0	Not studied
Enalapril	20	1.74 ng/mL	0.01	Not studied
Hydralazine	150	0.8 μg/mL	0.5	Not studied
Hydrochlorothiazide	50	100.0 ng/mL	0.4	Not detected (<1 ng/mL)
Methyldopa	1000	1.0 μg/mL	0.3	Plasma level of 0.09 μg/mL; no adverse effects noted
Metoprolol	200	1.7 μg/mL	3.0	Not studied
Nadolol	80	0.35 μg/mL	5.0	Not reported
Nicardipine (intravenous)	4.5–5.5 mg/h	5.1–18.5 ng/mL	Not reported	<300 ng/d was estimated
Nifedipine	90	10 ng/mL	–	Not studied
Nitrendipine	10	5.0 ng/mL	2.5	Not studied
Oxprenolol	160	130.0 ng/mL	0.3	Not elevated
Quinapril (quinaprilat)	20	27.9 μg/L/d	0.12	Estimated at 1.6% of maternal dose
Propranolol	160	50.0 ng/mL	0.6	No adverse effects noted
Sotalol	160	4 μg/mL	5.6	Not studied
Timolol	15	16.0 ng/mL	0.8	Not studied
Verapamil	240	20.0 μg/mL	0.4	Not detected in infants’ plasma

Factors Affecting Drug Excretion Into Breast Milk

The effects of the medication on the neonate depends on a number of factors including the maternal dose, the rate of passage of the drug into milk, the peak concentrations in milk, and the mechanism of action of the drug as well its effect on milk production. Furthermore, neonatal kidneys and excretory systems are immature and this can alter the estimated neonatal blood levels. ¹⁷

Antihypertensive drugs can be in the unbound form in the maternal blood or they may be bound to plasma proteins such as albumin. In general, the extent and affinity with which drug binds to plasma vs milk protein will determine the concentration of drug in whole milk. ¹⁷ Highly plasma protein–bound drugs do not readily pass into milk, whereas drugs more tightly bound to milk proteins are concentrated in breast milk, leading to a high milk to plasma (M/P) concentration.

Drugs exist in either ionized or nonionized forms in plasma depending on its pKa value, and this will also affect its transfer and concentration in breast milk. Large drug particles pass from the plasma into milk across semipermeable lipid membranes until equilibrium is reached. The diffusion is faster for the nonionized portion of the drug compared with the ionized portion. Therefore, agents that primarily exist in the ionized form at a physiologic pH level diffuse much more slowly into milk. The pH value of human plasma is 7.4 and that of human milk is more acidic at 7.0. Drugs that are weak bases will remain nonionized in the maternal plasma and pass readily into breast milk where they will become ionized and may not diffuse back into the plasma space. Finally, hydrophilicity and lipophilicity are important as lipid‐soluble drugs pass more rapidly into milk than do more water‐soluble drugs. ¹⁷

The timing of breastfeeding relative to the timing of maternal dosing of antihypertensive therapy can affect the concentration of drug exposure in milk to the neonate. Some antihypertensive drugs may diffuse rapidly into breast milk, and levels in milk may persist due to slow back‐diffusion. Frequent dosing of such agents will lead to high peak levels in the infant. As noted in Table II , these pharmacokinetic effects may reduce the safety profile of these agents compared with others for use during lactation.

Antihypertensive Drugs in the Postpartum Period and Impact During Lactation

Diuretics

Diuretics are typically avoided during pregnancy due to concerns of possible interference with normal plasma volume expansion that could lead to intrauterine growth retardation. While these concerns are mitigated after delivery, diuretics would not be considered a preferred option in women who choose to breastfeed. Thiazide diuretics are known to decrease milk production and have even been used to suppress lactation when used in large doses. ¹⁷ , ¹⁸ Other hypothetical concerns with thiazide use include neonatal thrombocytopenia, hypokalemia, and jaundice, but these have not been shown to occur with increased frequency with maternal thiazide use. ¹⁹ Loop diuretics can also decrease milk production and are excreted in breast milk. Potassium‐sparing diuretics such as spironolactone, amiloride, and triamterene may be compatible with breastfeeding. ¹⁹

β‐Adrenergic–Blocking Agents

While β‐adrenergic blockers have not been shown to have teratogenic effects, concerns with low birth weight have limited widespread use of these drugs in pregnancy. In the postpartum period, they often are very useful for management of hypertension since patients are typically younger than 40 years and respond well to this class of therapy. Numerous studies have shown that β‐blockers are excreted and accumulated in breast milk. The M/P ratio is quite variable for different agents in this class ( Table II ). Rarely, β‐blockers including propranolol, atenolol, and acebutolol attain high enough levels in breast milk to transfer to the neonate and may induce signs of neonatal β‐blockade. ¹⁷ , ²⁰ , ²¹ Metoprolol also accumulates in milk but the levels aren’t significantly high in infants with normal liver function. ¹⁷ , ¹⁹ As noted in case 3 above, β‐blocker use may be particularly helpful for the treatment of symptoms of thyrotoxicosis and hypertension in postpartum thyroiditis. ¹¹

The combined α–β‐blocker labetalol is efficacious and relatively safe during lactation. In our experience, most maternal‐fetal medicine physicians are familiar with its use in severe hypertension in the hospitalized patient. It can be used parenterally during a hypertensive urgency and easily converted to oral administration. However, due to its short duration of action, multiple daily dosing is often required for adequate BP control, making its utility after hospital discharge less attractive. Data are lacking for the vasodilating β‐blockers carvedilol and nebivolol during lactation.

Calcium Channel Blockers

The calcium channel blockers (CCBs) are used in pregnancy hypertension and have been shown to be effective for the treatment of hypertension during the postpartum period. Among the dihydropyridines, nifedipine, perhaps due to its longevity, has data supporting its safety for use in pregnancy and lactation. ¹³ Nifedipine is highly bound to plasma proteins and has a M/P <1, with insignificant amounts transferred into breast milk. ¹⁷ In contrast, the dihydropyridine nicardipine attains larger concentrations in breast milk relative to maternal plasma concentrations and would generally be avoided in hypertensive breastfeeding mothers. Due to insufficient data on amlodipine, no recommendation can be currently made by for its use during lactation. ¹⁷ , ²¹ The nondihydropyridines CCBs verapamil and diltiazem are highly protein bound with M/P ratios <1 and have been reported as effective alternatives to β‐blockers and dihydropyridine CCBs during lactation. ²¹

Renin‐Angiotensin–Blocking Agents

As the renin‐angiotensin–blocking drugs are considered teratogenic, they should never be used in hypertension during pregnancy. ²² , ²³ During the postpartum period, these agents may be very beneficial, especially in women with type 2 diabetes or chronic kidney disease. Data on the use of captopril, enalapril, and quinapril during lactation ( Table II ) show that the concentrations achieved in milk lead to minute amounts of medication delivered to the infant, hence these agents can typically be used as antihypertensives during lactation. Similar data do not exist for other ACE inhibitors, angiotensin receptor blockers, or renin inhibitors, so these should be used with caution during lactation, and the potential benefits associated with their use should be weighed against the possible harm to the neonate. ²²

α‐Blockers, CNS Active Drugs, and Hydralazine

Methyldopa has a long safety record for its use in pregnancy hypertension and is often continued into the postpartum period by maternal‐fetal medicine physicians. However alpha‐methyldopa is a relatively weak antihypertensive agent susceptible to tolerance due to volume retention, and, in large doses, can cause lethargy and cognitive impairment in the mother that may interfere with the demands of a neonate. α₁‐Antagonists are infrequently used in the setting of postpartum hypertension and would be reserved for use as a fourth or fifth antihypertensive agent. There are few data and little experience regarding their use in lactating women and there are no pharmacokinetic data on excretion into breast milk.

Hydralazine, a direct‐acting arteriolar vasodilator, is often used parenterally during severe elevations of BP in the hospitalized postpartum woman, but it has an unpredictable antihypertensive effect and a short duration of action and reflex tachycardia. Oral and parenteral use of hydralazine should not be considered for the routine treatment of hypertension even though it has relatively low concentrations in breast milk ²⁴ (Table II ).

Follow‐Up in the Ambulatory Setting

Following hospitalization, it is strongly recommended that women with postpartum hypertension be reevaluated by the consulting hypertension specialist. In today’s setting of short hospital stays, even following Cesarean section and persistent postpartum, it is typical for patients to be discharged on the fourth postpartum day. This may leave unanswered questions regarding diagnostic test results and poor insight by patients regarding their management since a diagnosis of hypertension is often a new one. Since many cases of postpartum hypertension are due to “residual” preeclampsia or the effect of volume and/or NSAID therapy, reevaluation of patients in 2 to 4 weeks of hospital discharge is quite reasonable. During this immediate postdischarge period, we also advocate regularly measured home or self–BP measurement as an important step to follow any transitions in BP that might occur in women with postpartum hypertension.