Hypertensive Disorders In Pregnancy Flashcards
Intro to Hypertensive disorders in pregnancy
Hypertensive disorders in pregnancy are a group of conditions in pregnancy characterised by the elevation of blood pressure as the cardinal sign and the occurrence of other manifestations in several organ systems such as the brain and CNS, cardio-pulmonary system, liver, kidneys and the coagulation systems. They complicate about 5-10% of pregnancies and are important cause of obstetric emergencies. They lead to significant adverse maternal and fetal outcomes.
Pregnancy 🤰 induced hypertension
GESTATIONAL HYPERTENSION
Gestational hypertension, formerly known as pregnancy-induced or transient hypertension, is defined as blood pressure 140/90 mm Hg on two separate oc- casions, at least 4 hours apart, after 20 weeks’ gestational age. This can also be diagnosed within the first 2 weeks postpartum without a history of chronic hyper- tension and without the signs and symptoms of preeclampsia. However, if blood pressures remain persistently elevated postpartum, that should warrant a diagnosis of chronic hypertension.
Gestational hypertension is the most common etiology of hypertension in preg- nancy, affecting 6% to 7% of nulliparous and 2% to 4% of parous women. The incidence increases with a history of preeclampsia and in multiple gestations. Earlier diagnosis of gestational hypertension increases the risk of preeclampsia; up to 50% of those with hypertension before 30 weeks will progress to preeclampsia.
• Prognosis and management depend on timing and severity.
• If 37 weeks, monitor closely for progression to severe hypertension, pre-
eclampsia, and fetal growth restriction.
• Delivery is indicated between 37 0/7 weeks and 38 6/7 weeks’ gestation for those
without severe-range blood pressures and as early as 34 weeks for those with
severe-range pressures.
• If delivery becomes indicated prior to 37 weeks and the patient has yet to re-
ceive a course of antenatal steroids, then a course of antenatal steroids can be administered. However, delivery should NOT be delayed for an antenatal ste- roid course to be completed, especially in the setting of worsening maternal or fetal status.
• Gestational hypertension may be predictive of chronic hypertension later in life and is important in regard to patient counseling and preventative medical decisions.
PRE ECLAMPSIA
Preeclampsiaisdiagnosedbyelevatedbloodpressureandproteinuriaafter20weeks’ gestation in a patient known to be previously normotensive. Trophoblastic disease or multiple gestation can present with preeclampsia before 20 weeks’ gestation.
• Mild preeclampsia is defined by the following criteria:
¢ Blood pressure 140/90 mm Hg confirmed on two measures at least 4 hours apart
¢ Proteinuria 300 mg on a 24-hour urine collection or spot urine protein/ creatinine ratio of 0.3 or greater. If neither test is available, a less reliable op- tion is two random urine dipstick results of at least 30 mg/dL (“1”).
¢ The 24-hour urine collection remains the gold standard for diagnosing preeclampsia.
• Preeclampsia with severe features is classified by the following criteria:
¢ Blood pressure of 160 mm Hg systolic or 110 mm Hg diastolic which
is persistent
¢ Signs, symptoms, or lab values of severe preeclampsia with any elevated
¢ Of note, proteinuria is no longer a diagnostic marker of severe pre-
eclampsia because level of proteinuria is not associated with maternal or
fetal outcomes.
¢ Signs and symptoms of severe preeclampsia include cerebral or visual distur-
bances (eg, persistent headache, blurred vision, scotomata), persistent epigas-
tric or right upper quadrant pain, and pulmonary edema.
¢ Symptoms that can be seen with severe preeclampsia but are not diagnostic include nausea and vomiting, decreased urine output, hematuria, or rapid weight gain 5 lb in 1 week. An additional sign that does not establish a
diagnosis of preeclampsia but does warrant increased surveillance for pre- eclampsia is the elevation of 15 mm Hg diastolic and 30 mm Hg systolic of the patient’s blood pressure from baseline.
¢ Laboratory findings diagnostic of severe preeclampsia include platelet count below 100 000 platelets per L, serum creatinine greater than 1.1 mg/dL OR a doubling of the patient’s baseline creatinine, liver enzyme (aspartate aminotransferase/alanine aminotransferase) elevation of more than double the upper limit of normal.
• Nondiagnostic, but other lab abnormalities that may be seen are decreased he- moglobin secondary to severe hemolysis in hemolysis, elevated liver enzymes, and low platelets (HELLP) syndrome, microangiopathic hemolytic anemia with abnormal findings on peripheral smear, increased serum bilirubin, elevated serum lactate dehydrogenase, elevated uric acid level, decreased serum haptoglo- bin, signs of coagulopathy such as prolonged partial thromboplastin time and prothrombin time, and decreased fibrinogen.
• Fetal findings associated with preeclampsia may include intrauterine growth restriction (IUGR), oligohydramnios, and other signs of uteroplacental insuf- ficiency. However, none of these findings is diagnostic of preeclampsia or pre- eclampsia with severe features.
• Superimposed preeclampsia is defined as preeclampsia in the setting of ma- ternal chronic hypertension, occurring in 13% to 40% of pregnancies compli- cated by chronic hypertension. Exacerbation of chronic hypertension versus superimposed preeclampsia can be difficult, especially if there is baseline pro- teinuria. Superimposed preeclampsia with severe features accounts for any of the aforementioned lab abnormalities with elevated blood pressure and new/ worsening proteinuria in a patient with chronic hypertension. Persistently ele- vated blood pressure (160 mm Hg systolic or 110 mm Hg diastolic) without proteinuria in a patient with chronic hypertension is not diagnostic of superim- posed preeclampsia with severe features.
• Hemolysis, elevated liver enzymes, and low platelets syndrome is a variant of preeclampsia defined by the following criteria:
¢ Hemolysis identified by burr cells and schistocytes on an abnormal peripheral
smear, an elevated serum bilirubin (1.2 mg/dL), or lactate dehydrogenase
level (600 IU/L), or a low serum haptoglobin
¢ Thrombocytopenia with platelets 100 000/L is the most consistent find-
ing in HELLP syndrome.
¢ Elevated liver function tests (ie, transaminases) more than double the upper
limit of normal
¢ Note that hypertension may be absent (12%-18% of cases), mild (15%-50%),
or severe (50%). Proteinuria may be absent as well (13%).
Risk factors for Preeclampsia
PREECLAMPSIA
Preeclampsia occurs in 2% to 7% of healthy nulliparous women and 1% to 5% of parous women. The incidence is higher in twin pregnancies (14%) and for women with a history of preeclampsia (18%). It is the third leading cause of maternal mortality, responsible for over 17% of maternal deaths, and a major cause of neonatal morbidity and mortality.
Risk factors for preeclampsia include the following:
• Nulliparity
• Multiplegestation
• Obesity
• Chronichypertension
• Systemic lupus erythematosus or other autoimmune disorder
• Thrombophilia
• Pregestationaldiabetes
• Kidneydisease
• History of preeclampsia or eclampsia
• Lowsocioeconomicstatus
• Family history of preeclampsia, eclampsia, or cardiovascular disease
• Molarpregnancy
• Conception via assisted reproductive technologies
• Advanced maternal age (40 years)
• The pathophysiology of preeclampsia has been studied extensively over the past de- cade. It is clear that preeclampsia is a systemic disease, and the placenta is the root cause of preeclampsia. The proposed insult to the placenta is an immunologic alter- ation in trophoblastic function and reduction in trophoblast invasion. This in turn reduces vascular remodeling, reducing perfusion, and increasing velocity of blood in the intervillous space. This leads to both inflammation and endothelial damage and dysfunction. Due to this, angiogenesis and angiogenic factors have been studied ex- tensively. Two particular proteins of interest are soluble fms-like tyrosine kinase 1 (sFlt-1), which is an antiangiogenic agent, and placental growth factor. The sFlt-1 par- ticularly has been shown to be increased 4 to 5 weeks prior to any clinical manifesta- tions of preeclampsia (see “Prediction of Preeclampsia” under “Preeclampsia” section).
• It has also been hypothesized that alteration in the prostacyclin-thromboxane bal- ance plays a role in preeclampsia. Given this, low-dose aspirin (81 mg), which blocks thromboxane production, has been studied as a preventative agent for pre- eclampsia. Small initial studies showed promising results but larger randomized trials showed nonsignificant reduction in preeclampsia. The largest meta-analysis showed a 17% risk reduction in women at high risk for the disease. Patients at high risk for preeclampsia include those with the following:
• Previouspreeclampticpregnancy
• Chronichypertension
• Renaldisease
• Multifetalpregnancy
• Pregestationaldiabetes
• Systemic lupus erythematosus or other autoimmune disorder (antiphospholid
syndrome)
• For pregnancies at high risk for preeclampsia (those that meet the above criteria), we recommend initiating low-dose aspirin between 12 and 28 weeks (ideally before 16 wk) and continue until delivery. No increased risk of signifi- cant bleeding or abruptio placentae has been noted with low-dose aspirin.
• Other factors that increase preeclampsia risk include nulliparity, family history of preeclampsia, low sociodemographic factors (low socioeconomic status, African American ethnicity), maternal age 35 years, obesity, in vitro fertilization, and previously poor pregnancy outcomes. It is unclear if prophylactic aspirin provides any benefit in these conditions. If a patient has two or more of these aforemen- tioned factors, an informed discussion with the patient about the possible benefits of low-dose aspirin should take place.
• Other important measures for preeclampsia prevention are early evaluation and risk reduction through optimizing prepregnancy and maternal health. Women with preeclampsia in the second trimester have a recurrence rate as high as 65%. In patients at high risk for development of preeclampsia, supplementation with fish oil and vitamins C and E has been studied and has been shown to be ineffective. Strict hypertension goals have not been shown to decrease preeclampsia risks either. Calcium supplementation in patients who have a deficiency has been shown to decrease the risk of preeclampsia development, although it is very unlikely that a patient would be calcium deficient in the United States and calcium supplementa- tion is, at this time, not recommended. Dietary salt restriction has also been studied in preeclampsia prevention; however, it has not been shown to provide benefit.
• Prediction of preeclampsia has been an area of growing research and debate. Uter- ine artery velocity Doppler and various biomarkers (sFlt-1, soluble endoglin, pla- cental growth factor) have been shown in small studies to be predictive of future preeclampsia development, especially when studied in the second trimester; how- ever, use of these biomarkers has yet to show improvement in either maternal or fetal outcomes during pregnancy and none is approved by the US Food and Drug Administration for clinical use. There are ongoing studies evaluating the combi- nation of biomarkers plus uterine artery Doppler studies to create a prediction algorithm, and ongoing research is warranted.
• Uricacid:Atestthatisreadilyavailableisuricacid,andarecentprospectivestudy showed a uric acid level of 5.2 mg/dL correlated with a positive predictive value of 91.4%. Using uric acid in rare circumstances to evaluate a patient with worsening gestational hypertension for possible progression to preeclampsia is a reasonable option, although regularly checking uric acid levels should not be part of routine care and should not be the principle guiding force in patient management.
• Diagnosis of preeclampsia is by symptoms and signs, including elevated blood pressure, proteinuria, and abnormal laboratory findings (described above).
Management of Preeclampsia
• Definitive management for gestational hypertension, preeclampsia, and eclampsia is delivery because the placenta is the insulting agent and removal of the placenta will lead to resolution of the disease process.
Management of Preeclampsia Without Severe Features
• In general, preeclampsia without severe features (also known as mild preeclamp- sia, see definitions above) at term is treated by delivery, typically at 37 weeks or at time of diagnosis if after 37 weeks.
• Optimal treatment prior to 37 weeks is usually expectant management. The
benefits of antihypertensive medications and early hospitalization are not clearly established. There is no role for bed rest in the management of preeclampsia without severe features.
Close maternal and fetal observation is essential, but there is no standard proto- col for testing or frequency.
• Fetal monitoring can include growth ultrasound and amniotic fluid assessment every 3 to 4 weeks, umbilical artery Doppler velocimetry, and once or twice weekly NST or BPP.
• Maternal monitoring can include weekly or semiweekly blood pressure check and evaluation, and periodic lab testing such as 24-hour urine protein or urine protein/creatinine ratio, serum creatinine, platelet count, and serum transami- nases to detect progression to severe preeclampsia.
• A gestational age of 34 weeks with uncontrolled hypertension and abnormal fetal testing should warrant further investigation, and if severe features identi- fied, prompt delivery.
Management of Preeclampsia With Severe Features
• The first priority in treating preeclampsia with severe features is to assess and stabilize the mother.
• At34weeks,deliveryisindicated,althoughimmediatecesareandeliveryisnot
usually warranted, rather urgent delivery after maternal stabilization is indicated.
¢ Patients with a vertex fetus and no contraindication to labor can deliver
vaginally.
¢ Careful monitoring, at least hourly assessments, and strict intake/output re-
cordings should be maintained. Furthermore, assessment of labs such as CBC and comprehensive metabolic panel should be checked serially (typically every 6-12 h) during an induction of a severely preeclamptic patient to monitor for development of HELLP syndrome.
• Between 24 and 34 weeks expectant management is acceptable if blood pres- sure is adequately controlled with antihypertensive agents, fetal status is reassur- ing, and the mother is not developing worsening HELLP syndrome.
¢ Magnesium sulfate (MgSO4) and IV antihypertensives may be given initially
while betamethasone is administered for fetal lung maturity.
¢ Fluid status should be monitored.
¢ The CBC, platelets, and liver function tests should be checked daily.
¢ Fetal surveillance with NST or BPP should be performed at least weekly, and
patients should be instructed regarding maternal assessment of fetal movement.
¢ Delivery is indicated by the following: worsening IUGR, nonreassuring fetal tracing, eclampsia, neurologic deficits, pulmonary edema, right upper quad- rant/epigastric pain, worsening renal status, disseminated intravascular coag-
ulation, HELLP, placental abruption, or uncontrolled severe blood pressure.
• Prior to 24 weeks’ gestation, expectant management is associated with high
maternal morbidity and limited perinatal benefit.
• Expectant management of severe preeclampsia with IUGR has been associated
with increased risk of fetal death (rate of perinatal death is 5.4%) and should be
performed cautiously.
• Seizure prophylaxis during labor and for 24-hour postpartum is recommended
for patients with preeclampsia. Some patients with severe persistent preeclampsia may need seizure prophylaxis for longer periods before and after delivery.
• Magnesium sulfate is the agent of choice for eclamptic seizure prophylaxis. The
MgSO4 has been shown to decrease the risk of eclampsia by more than 50%.
¢ For prophylaxis, we administer a loading dose of 6 g MgSO4 intravenously
over 15 to 20 minutes.
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Maintenance dose is 2 g/hr intravenously (dose should be titrated down if the patient has poor urine output, poor kidney function, or an elevated serum creatinine).
If there is no IV access, the loading dose is 5 g MgSO4 (50% solution) admin- istered intramuscularly in each buttock (10 g total), with a maintenance dose of 5 g in alternating buttocks every 4 hours. Thetherapeuticserummagnesiumlevelforseizureprophylaxisdependsonthe laboratory. In general, the therapeutic range is 4.8 to 8.4 mg/dL or 4 to 6 mEq/L. However, it is our practice to follow magnesium levels only for those patients in whom we are unusually concerned for developing supratherapeutic levels. For such patients, check serum magnesium level 4 hours after the loading dose and then every 6 hours as needed or if symptoms suggest magnesium toxicity. Patients are monitored hourly for signs and symptoms of magnesium toxicity:
¢ Loss of patellar reflexes at 8 to 10 mEq/L
¢ Respiratory depression or arrest at 12 mEq/L
¢ Mental status changes at 12 mEq/L followed by ECG changes and
arrhythmias
¢ If magnesium toxicity develops, check the patient’s vital signs, stop mag-
nesium and check plasma levels, administer 1-g calcium gluconate IV over
3 minutes, and consider diuretics (eg, furosemide, mannitol).
• Phenytoin (Dilantin) is a secondary agent for eclamptic seizure
• Phenytoin (Dilantin) is a secondary agent for eclamptic seizure prophylaxis. Magnesium was clearly superior in a large randomized clinical trial and is pre- ferred. It may, however, be contraindicated, as in patients with myasthenia gravis.
¢ The loading dose is maternal weight based. For 50 kg, load 1000 mg; for
50 to 70 kg, load 1250 mg; and for 70 kg, load with 1500 mg phenytoin.
¢ Thefirst750mgoftheloadingdoseshouldbegivenat25mg/minandtherest at 12.5 mg/min. If the patient maintains normal cardiac rhythm and has no history of heart disease, ECG monitoring is not necessary at this infusion rate.
¢ Check the serum phenytoin level at 30 to 60 minutes after infusion.
¢ A therapeutic level is 12 μg/mL; recheck level in 12 hours.
¢ If the level is 10 g/mL, reload with 500 mg and check again in 30 to
60 minutes.
¢ If the level is 10 to 12 g/mL, reload with 250 mg and check again in 30 to
60 minutes.
• Antihypertensive therapy is indicated for patients with a systolic blood pressure of
160 mm Hg or greater or diastolic blood pressure of 110 mm Hg or greater. Acute treatment aims to reduce blood pressure in a controlled manner without compro- mising uteroplacental perfusion.
• It is reasonable to reduce the patient’s systolic blood pressure to 140 to
155 mm Hg and the diastolic blood pressure to 90 to 100 mm Hg.
• While administering magnesium, useful antihypertensive agents for acute man-
agement include the following:
¢ Immediate release oral nifedipine: This is particularly useful in patients
without IV access. It has an onset of action of 15 minutes and reaches a peak by 1 hour. Initial dose should be 10 mg orally. Subsequent doses can be given every 20 minutes. Subsequent doses should be 20 mg. A total of three doses every 20 minutes can be attempted to reduce blood pressure. If at any point the patient’s blood pressure is reduced below 160/110 mm Hg, she can be observed. While administering short-acting antihypertensives, the blood pressure should be checked at least every 20 minutes. Once blood pressure is below 160/110 mm Hg, the blood pressure should be checked every 10 minutes for 1 hour, then every 15 minutes for 1 hour, then every 30 minutes for 1 hour, and then every hour for at least the next 4 hours. If three doses of nifedipine do not improve the patient’s blood pressures, you should use one of the two following agents.
¢ Hydralazine hydrochloride: Administered intravenously, it has an onset of action within 10 to 20 minutes. The duration of action is 4 to 6 hours.
¢ Begin with a 5- to 10-mg IV bolus or push over 2 minutes, and recheck
a blood pressure in 20 minutes. If severe blood pressures persist, an ad- ditional 10 mg should be administered. No more than 20 mg should be administered over a 20-minute time period. If the blood pressure remains elevated after two doses, an additional antihypertensive should be used. If the blood pressure is reduced below 160/110 mm Hg, the blood pressure monitoring as described above should be initiated.
¢ Labetalol hydrochloride: Administered intravenously, it has an onset of ac- tion within 5 to 10 minutes and has a duration of 3 to 6 hours. It is contra- indicated in greater than first-degree maternal heart block and should be used cautiously in severe asthmatics.
¢ Begin with a 20-mg IV bolus or push over 2 minutes and then check a repeat blood pressure in 20 minutes. If severe range blood pressures persist, 40 mg intravenously should be administered (over 2 or more minutes) and blood pressures checked in 20 minutes. If severe range blood pressures per- sist, administer 80 mg intravenously. If the blood pressure remains elevated at this time, an additional antihypertensive should be used. If the blood pressure is reduced below 160/110 mm Hg, the blood pressure monitoring as described above should be initiated.
¢ When administering IV labetalol, there should be a maximum dosing of 300 mg/24 hr.
• Fluid management: Patients with preeclampsia are frequently hypovolemic due to third spacing from low serum oncotic pressure and increased capillary permea- bility. These same abnormalities also increase risk for pulmonary edema. Diuretics may be used to treat pulmonary edema but should not be used as the primary antihypertensive in preeclamptic patients.
• Oliguria is defined as urine output of 100 mL in 4 hours. It is treated with 500-mL crystalloid bolus if the lungs are clear. If there is no response, another 500-mL bolus can be administered. If there is no response after 1 L, central hemodynamic monitoring can be considered.
¢ Central venous pressure monitoring does not correlate well with pulmonary capillary wedge pressure. Rarely, a Swan-Ganz catheter may be required to help guide fluid management and prevent flash pulmonary edema. More practically, evaluation with lung exam every 2 hours can help identify onset of pulmonary edema.
• Patients usually begin to effectively diurese about 12 to 24 hours after delivery. In cases of severe renal compromise, it may take 72 hours or more for adequate diuresis to resume.
• Maternal complications of severe preeclampsia require a high index of clinical sus- picion and include renal failure, acute cardiac failure, pulmonary edema, thrombo- cytopenia, disseminated intravascular coagulopathy, and cerebrovascular accidents.
• Perinatal outcome: There is a high perinatal morbidity and mortality in pregnan- cies complicated by severe preeclampsia. Fetal mortality rates range from 5% to more than 70% depending on the gestational age.
HELLP SYNDROME
HELLP syndrome often presents with nonspecific complaints such as malaise, ab- dominal pain, vomiting, shortness of breath, or bleeding.
• The differential diagnosis for HELLP syndrome includes the following:
• Acute fatty liver of pregnancy
• Thromboticthrombocytopenicpurpura
• Hemolyticuremicsyndrome
• Immunethrombocytopenicpurpura
• Systemic lupus erythematosus flare
• Antiphospholipidantibodysyndrome
• Cholecystitis
• Fulminant hepatitis (of any cause)
• Acutepancreatitis
• Disseminatedherpeszoster
• Management is the same as for severe preeclampsia. Transfusion of red cells, plate- lets, or factors may be required immediately prior to delivery depending on severity of anemia and thrombocytopenia. Short-term expectant management in order to allow for administration of betamethasone for fetal lung maturity may be possible in a very select group of patients with HELLP prior to 34 weeks; however, there are no data suggesting improved perinatal outcomes with this approach.
ECLAMPSIA
ECLAMPSIA
Eclampsia should be the presumed diagnosis in obstetric patients with seizures and/or coma without a known history of epilepsy. The incidence of eclampsia is between 1 in 2000 and 1 in 3500 pregnancies in developed countries. Eclampsia occurs in about 1% of patients with preeclampsia. Virtually, all eclampsia is preceded by preeclampsia.
• The pathophysiology of eclamptic seizures is unknown but is related to arte- rial vasospasm and may occur when mean arterial pressure exceeds the capacity of cerebral autoregulation, leading to cerebral edema and increased intracranial pressure.
• Eclampsia can occur antepartum, peripartum, or postpartum and has been reported as late as 3 to 4 weeks postpartum. Patients may have associated hypertension and proteinuria; a small percentage has neither.
Eclampsia
• Management of eclampsia is an obstetric emergency that requires immediate treat- ment, including
• Appropriate management of ABCs (airway, breathing, and circulation) with
measures taken to avoid aspiration
• Seizure control with 6-g MgSO4 IV bolus. If the patient has a seizure during or
after the loading dose, an additional 2-g IV bolus of MgSO4 can be given.
• Treat seizures refractory to MgSO4 with IV phenytoin or a benzodiazepine
(eg, lorazepam).
• Treat status epilepticus with lorazepam 0.1 mg/kg IV at a rate 2 mg/min. Pa-
tients with status epilepticus may require intubation to correct hypoxia and aci-
dosis and to maintain a secure airway.
• Prevent maternal injury with padded bedrails and appropriate positioning.
• Control of severe hypertension (see medications above)
• Delivery is indicated after maternal stabilization.
¢ During acute eclamptic episodes, fetal bradycardia is common. It usually re-
solves in 3 to 5 minutes. Allowing the fetus to recover in utero from the maternal seizure, hypoxia, and hypercarbia before delivery is optimal. How- ever, if fetal bradycardia persists beyond 10 minutes, abruptio placentae should be suspected.
¢ Emergency cesarean delivery should always be anticipated in case of rapid maternal or fetal deterioration.
• Outcomes depend on the severity of disease. Perinatal mortality in the United States ranges from 5.6% to 11.8%, mainly due to extreme prematurity, placental abruption, and IUGR. The maternal mortality rate is from 1.8% in the devel- oped world to 14% in under-resourced countries. Maternal complications include aspiration pneumonitis, hemorrhage, cardiac failure, intracranial hemorrhage, and transient or permanent retinal blindness.
• Long-term neurologic sequelae of eclampsia are rare. Central nervous system im- aging with computed tomography or magnetic resonance imaging should be per- formed if seizures are of late onset (longer than 48 h after delivery) or if neurologic deficits are clinically evident. The signs and symptoms of preeclampsia usually re- solve within 1 to 2 weeks postpartum. Approximately 25% of eclamptic patients develop preeclampsia in subsequent pregnancies, with recurrence of eclampsia up to 2% of cases.
CHRONIC HYPERTENSION
Chronic hypertension is high blood pressure diagnosed before pregnancy or be-
fore 20 weeks’ gestation or first recognized during pregnancy but persisting lon- ger than 12 weeks postpartum. Note: Chronic hypertension is now defined by the American Heart Association (AHA) as blood pressure 130/80 mm Hg; however, in pregnancy, hypertension is still defined by the criteria above.
Chronic hypertension
CHRONIC HYPERTENSION
Chronic hypertension carries increased risk for superimposed preeclampsia, preterm delivery, placental abruption, and IUGR. Chronic hypertension is present in up to 5% of pregnancies. The definition for chronic hypertension was adjusted by the AHA in 2017. This lowered the criteria for chronic hypertension to blood pressure 130 mm Hg systolic or 80 mm Hg diastolic on two separate occasions, greater than 4 hours apart. This will likely result in a greater number of patients being diag- nosed with chronic hypertension. However, the current definition of chronic hyper- tension affecting pregnancy per American College of Obstetricians and Gynecologists is still blood pressure 140 mm Hg systolic or 90 mm Hg diastolic on two separate occasions, occurring prior to 20 weeks’ gestational age or present prior to conception.
